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OPD Surgery Complete PDF
OPD Surgery Complete PDF
Sample
Sample
Axillary vein
4 – 6 lymph nodes medial or
group Upper extremity
posterior to the vein
(Lateral)
External
I 5 – 6 lymph nodes along the
mammary
lower border of the pectoralis Lateral aspect of the
group
minor contiguous with the lateral breast
(Anterior/
thoracic vessels
Pectoral)
5 – 7 lymph nodes along the
Scapular group posterior wall of the axilla, at the Lower posterior neck,
(Posterior/ lateral border of the scapula posterior trunk,
Subcapsular) continguous with subcapsular posterior shoulder
vessels
Axillary vein, external
3 – 4 lymph nodes embedded in mammary and
Central group the axillary fat, immediately scapular lymph
posterior to the pectoralis minor nodes, directly from
II
the breast
Interpectoral 1 – 4 lymph nodes between the
Directly from the
group (Rotter’s pectoralis major and minor
breast
nodes) muscles
6 – 12 lymph nodes posterior and
Subclavicular All other groups of
III superior to the upper border of
group (apical) axillary lymph nodes
the pectoralis minor
6.
enhancement
Magnetic Resonance Imaging
History
and
• Sensitive but not specific for breast evaluation PE:
Patient > 35 y/o Normal
History Localization and Biopsy
• Useful in patients with:
− Mammographically dense breasts and
PE:
− Axillary disease Normal
− Negative mammogram Negative Positive Localization and Biopsy
• Other uses:
− Can detect extent of tumor within breast
− Can detect residual tumor within breast after lumpectomy Negative Positive Benign Malignant
− Can differentiate between tumor and postsurgical scar
Life is what you make it. Vita qua se facies est! 4
BREAST MASSES 2. Mycotic infections
• Work-up depends on age at presentation • Etiology
− Post-menopausal women: most prone to carcinoma (excise) − Blastomyces
− Women younger than 30 years old: most lesions benign (observe) − Sporothrix schenckii
− Pre-menopausal: between 30 years old and menopause: “Gray − Suckling infant inoculates intraoral fungi to nipple-areola
area” (observe/excise) complex
• Approach: • Presentation
− Mammary abscess in close proximity to nipple-areolar
complex
− Seropurulent material expressed
• Management
− Antifungal agents
− Drainage of abscess
− Partial mastectomy
• Candida albicans
− Erythematous, scaly lesions of the inframammary or axillary
folds
− Scrapings: filaments and binding cells
− Management
(1) Remove predisposing factors, e.g. maceration
(2) Topical nystatin
3. Hidradenitis suppurativa
• Nipple-areola complex or axillary chronic inflammatory condition
originating from the accessory areolar glands of Montgomery or
axillary sebaceous glands
• Predisposing factor – chronic acne
• Management
BREAST IMAGING REPORTING AND DATABASE SYSTEM (BI-RADS) − Antibiotic therapy
CATEGORY ASSESSMENT FOLLOW-UP RECOMMENDATIONS − Incision and drainage
Routine annual screening mammography for − Excision
1 Negative
women over 40 years old − Advancement flaps or split-thickness skin grafts
2 Benign
Routine annual screening mammography for 4. Mondor’s disease
women over 40 years old • Thrombosis of the superficial veins of the anterior chest wall and
3 Probably Benign Initial short-term follow up (6 months) examination breast
Suspicious
4 Usually requires biopsy − Frequently involved veins:
abnormality
Highly suggestive of
(1) Lateral thoracic vein
5 Requires biopsy or surgical treatment (2) Thoracoepigastric vein
malignancy
Known Biopsy- Lesions identified on imaging study with biopsy (3) Superficial epigastric vein
6
Proven malignancy proof of malignancy prior to definitive therapy • Acute pain in the lateral aspect of the breast or anterior chest
wall
INFECTIOUS AND INFLAMMATORY DISORDERS • Tender, firm, cord-like structure following the distribution of the
May be intrinsic (breast) or extrinsic (adjacent structures) major superficial veins
1. Cellulitis/Mastitis/Breast abscess • Indications for biopsy:
• Etiology − Uncertain diagnosis
− Staphylococcus aureus: localized, deep − Mass present near tender cord
− Streptococcus: diffuse, superficial • Management
• Presentation − Benign and self-limited (4 – 6 weeks)
− Point tenderness, erythema, hyperthermia − Anti-inflammatory medications
− Occur within first few weeks of breastfeeding − Application of warm compress along vein
− May result to abscess in the ff. areas: − Restriction of motion of ipsilateral extremity and shoulder,
(1) Subcutaneous brassiere support of breast
(2) Subareolar − Excision of involved vein segment: when symptoms persist or
(3) Interlobular/periductal are refractory to therapy
(4) Retromammary
• Pre-op ultrasound: delineate required extent of drainage BENIGN LESIONS OF THE BREAST
• Management: 1. Fibrocystic disease (Chronic Cystic Mastitis)
− Drainage via circumareolar incisions/incisions parallel to • Broad term for various benign breast changes characterized by
Langer’s lines nodularity with or without pain
− Biopsy of abscess cavity wall at the time of I/D: to rule out • Presentation:
underlying breast CA or necrotic tumor − Breast tenderness
− Local wound care − Older women
(1) Application of warm compress − Nevus on breast
(2) Administration of IV antibiotics • Result of prolonged cyclic stimulation of repeated menstrual cycle
(a) Penicillins • NOT premalignant EXCEPT those with atypical hyperplasia
(b) Cephalosporins • Diagnosis:
• Chronic/recurrent abscess − History and PE
− Culture: identify acid-fast bacilli anaerobes, aerobes, fungi, − Mammography
uncommon organisms − Biopsy
• Hospital-acquired puerperal infections • Treatment:
− Milk stasis or non-infectious inflammation − Reassurance and pain management
− Epidemic puerperal mastitis: − Aspiration of cystic lesion
MRSA transmitted via suckling neonate − Proven effective by RCT:
Purulent fluid expressed from nipple (1) Caffeine free diet
− Non-epidemic/sporadic puerperal mastitis: (2) Abstinence from smoking
Interlobular connective tissue involvement (3) Danazol
Nipple fissuring, milk stasis, retrograde bacterial infection 2. Fibroadenomas
− Management: • Predominantly in younger women (15 – 25 years old)
(1) Breast suction pump • 1 – 2 cm diameter, stable but may enlarge
(2) Antibiotic therapy − Disorder: large fibroadenomas (≤ 3 cm)
(3) Surgical therapy − Disease:
• Zuska’s disease (recurrent periductal mastitis) (1) Giant fibroadenomas (> 3 cm)
− Recurrent retroareolar infections and abscesses (2) Multiple fibroadenomas (> 5 lesions/ breast)
Life is what you make it. Vita qua se facies est! 5
• Histologically normal cellular elements, abundant stroma Screening and risk factor management
• Mobile and well circumscribed • Mammography
• Hormonal dependence (estrogen) similar to normal breast − Routine screening for women ≥ 50 years old reduces mortality
− Lactate in pregnancy from breast cancer by 33%
− Involute in postmenopausal period − Controversial for women < 50 years old:
• Diagnosis: ultrasound with core-needle biopsy 1. Breast density is greater, less likely to detect early breast CA
− Features on ultrasound 2. More false-positive test findings, resulting to unnecessary
(1) Oval biopsies
(2) Width larger than AP diameter 3. Younger women less likely to have breast cancer
(3) Gentle lobulations (< 4) • Chemoprevention – selective estrogen receptor modulators, reduce
(4) Well circumscribed margins breast cancer risk by 50%
(5) Homogenous internal echogenicity − Tamoxifen: also reduces incidence of LCIS and DCIS, but with
(6) Thin echogenic capsule adverse effects,
*Vague or thick surrounding echogenicity – malignancy 1. Deep vein thrombosis 1.6x
• Management: 2. Pulmonary emboli 3.0x
− Excision 3. Endometrial cancer 2.5x
− Cryoablation 4. Cataract surgery 2.0x
• Differential diagnoses: − Raloxifene: less adverse effects
− Benign adenoma: sparse stroma • Genetic testing for BRCA mutations, if positive:
(1) Tubular adenoma – young, non-pregnant 1. Prophylactic mastectomy and reconstruction
(2) Lactating adenoma – pregnancy, post-partum 2. Prophylactic oophorectomy and HRT
− Hamartoma: discrete 2 – 4 cm, firm, sharply circumscribed 3. Intensive surveillance for breast and ovarian cancer
− Adenolipoma: sharply circumscribed nodules of fatty tissue 4. Chemoprevntion
with normal lobules and ducts
3. Phylloides Tumor NATURAL HISTORY
• Rapidly growing giant fibroadenomas that are rarely malignant • Untreated patients:
• Rarely metastasizes to axillary lymph nodes − 5 year survival rate: 18%
• Treatment: − 10 year survival rate: 3.6%
− Wide local excision: with normal rim of tissue while small • Most common cause of death – metastatic disease
− Mastectomy: if size is too big • Most common age group affected: 40 – 60 years old
− If with metastasis à Malignant: Axillary dissection • Most common location – upper outer quadrant
4. Intraductal Papilloma − Greatest breast volume
• Unilateral bloody discharge with solitary involvement of duct
• Usually nonpalpable PRIMARY BREAST CANCER
• If mass is present consider malignancy • Presentation
• Treatment: Central duct excision − Breast enlargement or asymmetry
5. Mammary Duct Ectasia − Skin retraction: due to desmoplastic response entrapping and
• Palpable retroareolar mass with nipple discharge or retraction shortening Cooper’s suspensory ligaments in response to cancer
• Common in older women growth and invaions
• Dilatation of subareolar ducts can occur − Peau d’orange (localized edema) with drainage of lymph from
• Treatment: Excision disrupted skin
6. Physiologic Gynecomastia − Ulceration or erythema of the skin of the breast
• Occurs during neonatal, adolescent, senescent periods − Small satellite nodules near primary ulceration
• Causes: − Musculoskeletal discomfort
− Estrogen excess − No breast pain
− Androgen deficiency *Breast pain is associated with benign disease
− Drug-related
− Systemic diseases AXILLARY LYMPH NODE METASTASES
• Most important prognostic correlate of disease-free and overall survival
MANAGEMENT OF CYSTS • Sequential spread from low (level I) to central (level II) to apical (level
• Imaging prior to needle biopsy is preferred, but often the initial test for III) lymph node groups
palpable breast masses is needle biops • Involved LNs are initially ill-defined and soft but become firm or hard
• Two cardinal rules of safe cyst aspiration: and eventually adhere to each other to form a conglomerate mass
1. Mass must disappear completely after aspiration
2. Fluid must not be bloodstained DISTANT METASTASES
• If residual mass exists à ultrasound examination • Most common cause of death in breast cancer patients 10 years after
− Exclude persistent cyst à re-aspirate initial treatment
• If mass is solid à obtain tissue specimen • At the 20th cell doubling or when the primary cancer exceeds 0.5 cm in
• If cystic fluid is bloodstained à 2 mL taken for cytologic exam diameter, the mass acquires its own blood supply (neovascularization);
− Followed by ultrasound thus able to shed cancer cells directly into systemic venous blood:
− Followed by needle biopsy of any solid area on the wall − Axillary and intercostal veins à pulmonary circulation
• Pneumocystography – inject air into cyst then obtain a repeat − Batson’s plexus à vertebral column
mammogram to allow better assessment of cyst cavity for any • Sites of distant metastases:
irregularities − Bone: most common
− Lung
MALIGNANT LESIONS OF THE BREAST − Pleura
Factors for developing Breast Cancer: − Soft tissue
PROTECTIVE FACTORS RISK FACTORS − Liver
Low estrogen states High estrogen states
Late menarche Early menarche THEORIES ON BREAST CANCER SPREAD
Multigravida Nulligravida
1. Halsted Model – breast CA spread follows a course, proven false
Early menopause Late menopause (> 45 y/o)
Early full term pregnancy Older age at 1st live birth (> 35 y/o) 2. Fisher Model – breast CA can spread anywhere because from the
(18 – 25 y/o) Obesity (Peripheral estrogen) beginning it is a systemic disease, currently accepted model
Breast feeding (Prolactin) Hormone replacement therapy
Moderate exercise Oral contraceptives
OTHER RISK FACTORS
Family history of breast CA
Genetic anomalies: BRCA1 (ovarian and breast CA) and 2
(breast CA), Autosomal dominant inheritance
Radiation exposure
Alcohol (estradiol)
High fat diet
*Women who possess no identifiable risk factors account for 85 – 90%
Life is what you make it. Vita qua se facies est! 6
HISTOPATHOLOGY pN0(mol-)
No regional lymph node metastasis histologically, negative molecular
Non-infiltrating (in-situ) Carcinoma findings (reverse transcriptase polymerase chain reaction RT-PCR)
CRITERIA DUCTAL CIS LOBULAR CIS No regional lymph node metastasis histologically, positive molecular
pN0(mol+)
90% are premenopausal findings (RT-PCR)
> 50% are post menopausal pN1mi Micrometastasis (> 0.2 mm, none > 2.0 mm)
Patients Observed only in women
(Same as Invasive Ductal CA) pN1a Metastasis to 1 to 3 axillary lymph nodes
90% are ER (+)
25 – 35% risk for invasive Metastasis in internal mammary nodes with microscopic disease detected
25 – 70% risk for invasive ductal or pN1b
Malignant ductal or lobular CA in 15 by sentinel lymph node dissection, not clnically apparent
lobular CA in 5 years, usually Metastasis in 1 to 3 axillary lymph nodes and in internal mammary lymph
degeneration years, either breast, any
ipsilateral and in same quadrant pN1c nodes with microscopic disease detected by sentinel lymph node
quadrant
Never palpable dissection but not clinically apparent
Characteristics Palpable mass is rare pN2a Metastasis in 4 to 9 axillary lymph nodes (at least 1 tumor deposit > 2.0 mm)
Multicentric, bilateral
Radiographic Metastasis in clinically apparent internal mammary lymph nodes in the
Microcalcifications Usually none pN2b
findings absence of axillary lymph node metastasis
Total mastectomy vs. Conservative Metastasis in ≥ 10 axillary lymph nodes (at least 1 tumor deposit > 2.0 mm),
Management Observation + Tamoxifen pN3a
surgery or in infraclavicular lymph nodes
Infiltrating Malignancies Metastasis n clinically apparent ipsilateral internal mammary lymph nodes
in the presence of 1 or more positive axillary lymph nodes, or in > 3 axillary
1. Paget’s Disease of the Nipples pN3b
lymph nodes with clinically negative microscopic metastasis in internal
• Chronic eczematoid eruption of the nipple mammary lymph nodes
• May progress to ulcerated, weeping lesion pN3c Metastasis in ipsilateral supraclavicular lymph nodes
• Nipple biopsy – pathognomonic: large, pale, M DISTANT METASTASIS
vacuolated cells (Paget cells) in the rete pegs of the epithelium MX Presence of distant metastasis cannot be assessed
• Treatment – lumpectomy, mastectomy, modified radical M0 No distant metastasis
mastectomy M1 Distant metastasis present
2. Infiltrating Ductal Carcinoma with Productive Fibrosis
• Scirrhous or Invasive Ductal CA AJCC STAGE GROUPINGS AND TREATMENT OPTIONS
• Most common form of breast cancer (75 – 80%) STAGE TNM TREATMENT
• Affects 40 – 60 years old age group Lobular Cis – Observation with Tamoxifen, Bilateral
• Presentation mastectomy with reconstruction
0 TisN0M0 Ductal Cis – Total mastectomy (gold standard), Conservative
− Solitary, hard, non-tender, ill-defined mass breast surgery: lumpectomy, quadrantectomy, segmental
− With skin dimpling (due to profound desmoplastic response) mastectomy and irradiation
• Cut surfaces reveals central stellate configuration with chalky I T1N0M0
white or yellow streaks extending to surrounding breast tissues T0N1M0 Breast conservative surgery with separate axillary node
• Variants of Invasive Ductal Carcinoma: IIA T1N1M0 dissection and irradiation
(1) Medullary Carcinoma – large, soft, hemorrhagic, bulky T2N0M0 Modified radical mastectomy (Total mastectomy with axillary
T2N1M0 dissection)
mass associated with favorable prognosis IIB
T3N0M0
(2) Tubular Carcinoma – most differentiated variant, small,
T0N2M0
non-palpable, best prognosis, found on screening T1N2M0 Modified radical mastectomy (MRM)
mammography IIIA
T3N1M0 Induction chemotherapy + MRM + Radiation
(3) Mucinous Carcinoma (Colloid CA) – bulky, mucinous T3N2M0
tumor with glistening, glaring, gelatinous cut surface T4N0M0
Induction chemotherapy
(4) Secretory Carcinoma (Juvenile CA) – most common form IIIB T4N1M0
Good response à MRM + Radiation
T4N2M0
in children and adolescents, often mistaken for Poor response à Radiation + MRM
IIIC AnyTN3M0
firboradenoma
Locally Advanced Breast Cancer and Inflammatory Cancer
3. Papillary Carcinoma – lowest frequency of axillary nodal involvement Palliation
with good survival rate IV AnyTAnyNM1 Radiation and/or palliative hygienic mastectomy and/or
4. Lobular Carcinoma – from terminal ductures of lobules, often bilateral, chemotherapy and/or hormonal therapy and/or biologic
multicentric, multifocal therapy
5. Inflammatory Carcinoma
• Worst prognosis (T4) MANAGEMENT
• Presentation – erythema, Peau d’ orange, skin ridging LOCAL CONTROL
• Subdermal lymphatics and vascular changes permeated with foci 1. Surgery
of highly undifferentiated tumor • Classical Radical Mastectomy (Halsted, Father of Modern Surgery)
− Removes:
TNM STAGING OF BREAST CANCER (1) Whole breast
T TUMOR (2) Overlying skin
TX Primary tumor cannot be assessed (3) Axillary lymph nodes
T0 No evidence of primary tumor (4) Pectoralis major and minor
Carcinoma in situ; Intraductal CA, Lobular CA in situ; Paget’s Disease of the • Modified Radical Mastectomy ( Patsy & Madded)
Tis
Nipple
− Total mastectomy + Axillary lymph node dissection
T1 Tumor ≤ 2.0 cm in greatest dimension
T2 2.0 cm < Tumor < 5.0 cm in greatest dimension
− Most common operation performed for breast cancer in the
T3 Tumor ≥ 5.0 cm in greatest dimension Philippines
T4 Tumor of any size with direct extension to: (1) Chest wall or (2) Skin, • Conservative Breast Surgery (Veronesi & Fischer)
T4a Extension to chest wall − Quadrantectomy/lumpectomy
Edema (including Peau d’ orange) or skin ulceration or satellite skin nodules − Axillary sampling
T4b
confined to the same breast − Radiation of breast (because breast CA is multicentric)
T4c Both of above − Most common procedure done in the USA
T4d Inflammatory carcinoma − Increased recurrent risk compared to MRM
N REGIONAL LYMPH NODES – CLINICAL − Contraindications:
NX Regional lymph nodes cannot be assessed
(1) Tumor > 5 cm
N0 No regional lymph node metastasis
N1 Metastasis to movable ipsilateral axillary lymph node
(2) Poorly defined tumor
Metastasis in ipsilateral axillary lymph node fixed to one another (matted) (3) Large tumor in a small breast
N2a (4) Pregnancy
or to other structures
Metastasis only in clinically apparent ipsilateral internal mammary nodes in (5) Previous irradiation in the same site
N2b
the absence of clinically evident axillary lymph node metastasis (6) Multiple tumors within the breast confirmed to be
N3a Metastasis in ipsilateral intraclavicular lymph nodes malignant
Metastasis in ipsilateral internal mammary lymph nodes and axillary lymph (7) Diffuse microcalcifications on mammography
N3b
nodes
(8) Tumor involves skin or chest wall
N3c Metastasis to ipsilateral supraclavicular lymph nodes
(9) Presence of vascular collagen disorders (e.g.
pN REGIONAL LYMPH NODES – PATHOLOGIC
Regional lymph nodes cannot be assessed (previously removed, or not
Scleroderma) resulting to poor radiation assimilation
pNX
removed for pathologic study)
pN0(i-) No regional lymph node metastasis histologically, negative IHC results
No regional lymph node metastasis histologically, positive IHC results, no
pN0(i+)
IHC cluster > 0.2 mm
Life is what you make it. Vita qua se facies est! 7
2. Radiation GALLSTONE DISEASE S
• Indications: RECALL: ANATOMY AND PHYSIOLOGY OF THE BILIARY TREE
− Tumor size > 5 cm
− Multiple (≥ 4) involved axillary nodes GALLBLADDER – concentrates and stores hepatic bile, and delivers bile into
− Extracapsular extension of nodal tumor duodenum in response to a meal
− Locally advanced breast cancer a. Right hepatic duct
− Skin involvement b. Left hepatic duct
c. Common hepatic duct
SYSTEMIC CONTROL d. Portal vein
1. Chemotherapy e. Hepatic artery
• Adjuvant chemotherapy – given before initiation of local therapy f. Gastroduodenal artery
• Advantages: g. Left gastric artery
− Reduction of initial tumor burden before surgery h. Common bile duct
− Ability to treat potential systemic disease without delay i. Fundus of the gallbladder
− Ability to assess response of tumor to treatment rendered j. Body of the gallbladder
• Standard treatment – 4 cycles Doxorubicin + 4 cycles Taxane k. Infundibulum
• Response: l. Cystic duct
− Complete response: tumor disappeared m. Cystic artery
− Partial: > 50% tumor burden disappeared n. Superior pancreaticoduodenal
− Non-response: proceed to Cobalt therapy artery
− Progression: worsens after therapy
2. Hormonal therapy
• Ideal when patient is ER (+) and PR (+) • Shape – small avocado fruit hanging from a branch (cystic duct=stem)
− ER (+), PR (+): Diploid, well-differentiated = 80% response • Size – 7 to 10 cm long and 3 to 5 cm wide
− ER (+), PR (-): Aneuploid, not differentiated = 10% response • Peritoneum – visceral peritoneum of the liver attaches its fossa to inferior
− ER (-), PR (+): 45% response surface of the liver
− ER (-), PR (-): Progressive, bad prognosis • Parts
• Anti-estrogen agents: (1) Fundus
(1) Tamoxifen 20 mg daily for 5 years − Inferior blind end normally extending 1 to 2 cm beyond the
− Most common form of hormone therapy liver’s margin (at the inferior border of the liver)
− Blocks ER sites preventing estrogen effects − Mayo-Robson’s point – at the level of the tip of the 9th cc,
− For pre/post menopausal patients with T > 1 cm, (+) intersecting the linea semilunaris, at the transpyloric line of
axillary lymph nodes, ER/PR (+) Addison
− Adverse effects (< 5%) − Contains smooth muscles of the organ
o Endometrial cancer (2) Body (Corpus)
o Thromboembolic events − Average capacity of 30 to 50 ml
(2) Aromatase Inhibitors: Letrozole, Anastrazole, Exemestane − When distended, can distend and contain up to 300 ml
− Blocks conversion of steroids to estrogen − Main storage area and contains most of elastic tissue
− For post menopausal women and estrogen rich tumors − Underneath the liver, directed supero-medially tapering to
− Adverse effects: the porta hepatis
o Bone fractures (3) Neck – funnel shaped, angles down, continues as cystic duct
o Muscle and joint pains (4) Hartmann’s pouch (Infundibulum) – distended neck or upper body,
o Cardiovascular side effects lies in the deepest part of the gallbladder fossa
(3) Others: Diethylstilbestrol, Aminogluthatimide (5) Spiral valve of Heister – spiral mucus folds regulating flow of bile at
3. Biological therapy the neck and cystic duct with great concentration of smooth
• Human Epidermal Growth Factor Receptor 2 (HER2 gene) muscles
− Helps control how cells grow, divide, and repair themselves • Neurovascular supply
− HER2 (+) tumors are aneuploids, grow fast, and are − Cystic artery from the Hepatic artery
aggressive (poor prognosis) but respond well to HER2 *Landmarks: Triangle of Calot
antibody therapy Superior border – Inferior surface of the liver
− Fluorescence in situ hybridization (FISH test): amplified when Right border – Cystic duct
HER2 is positive Medial border – Common Hepatic duct
− Transtuzumab (Herceptin): − Cystic vein which drains to the Portal vein
o Recombinant humanized monoclonal antibody against − Celiac plexus formed by sympathetic and parasympathetic
the extracellular domain of HER2 NEU or ERB-2 vagal fibers
o Reduces risk of recurrence by 50% and death by 33%
• Bevacizumab BILIARY TREE *By order of bile flow:
− Humanized monoclonal antibody against Vascular a. Bile canaliculi
Endothelial Growth Factor Receptor (VEGF) b. Bile ductules
c. Bile ducts
FOLLOW-UP AND PROGNOSIS d. Hepatic ducts
• 80% recurrence within the first 5 years e. Common hepatic duct
• 65 – 85% of recurrences detected by history and PE f. Cystic duct
• Improved survival among patients who later become pregnant g. Common bile duct
• Metastatic disease generally cannot be cured, median survival of 2 Joined by the:
years h. Main pancreatic duct of
Wirsung
REFERENCES: • The Common bile duct and
1. Benign Disorders of the Breast by Fernando L. Lopez, MD, FPCS, FPSGS, Main pancreatic duct
FACS, Professor, Department of Surgery Faculty of Medicine and penetrate the poster-medial
Surgery University of Santo Tomas border of the wall of the 2nd
2. Malignant Disorders of the Breast by Rey B. Malilay, MD, FPCS, FPSGS, part of the duodenum to
FACS, Professor, Department of Surgery Faculty of Medicine and open in the Greater duodenal
Surgery University of Santo Tomas papilla
3. Brunicardi, C.F., et al. (2010). Schwartz’s Principles of Surgery, 19th ed. • Ampulla of Vater or hepato-
McGraw-Hill Companies Inc.: New York. pancreatico ampulla –
4. D’Orsi CJ, Mendelson, EB, Ikeda, DM, et al. (2003). Breast Imaging dilatation at the terminal part
Reporting and Data System. American College of Radiology. of the joined common bile
5. James, W.D., et al. (2006). Andrew’s Diseases of the Skin: Clinical and Main pancreatic duct
Dermatology, 10th ed. Saunders Elsevier Inc.: Canada. o. Sphincter of Oddi – muscle fibers
6. Jarrell, B.E., et al. (2008). National Medical Series for Independent Study: surrounding the Ampulla of
Surgery, 5th ed. Lippincott Williams & Wilkins: Baltimore. Vater
Life is what you make it. Vita qua se facies est! 8
COMMON BILE DUCT • Integral in differential diagnosis of obstructive jaundice
• Length – 6 to 15 cm • Spiral CT scan gives additional information for staging: vascular
• Position involvement
− At the right side of the hepatic artery 5. Percutaneous Transhepatic Cholangiography
− In front of the portal vein • Able to assess intrahepatic bile ducts
• Location – within the hepato-duodenal ligament • Little role in uncomplicated gallstone disease
• Parts: • Useful in patients with bile duct strictures and tumors
(1) Supraduodenal • A small needle is passed under fluoroscopic guidance into the bile
(2) Retroduodenal duct à Guidewire is passed à Catheter is passed over the wire à
(3) Infraduodenal Cholangiogram and therapeutic interventions (e.g. Biliary drain
(4) Intrapancreatic insertion, Stent placement)
− At the head of the pancreas
− Surrounded by Sphincter choledochus of Boyden –
constricting muscle fibers
− Joins the Main pancreatic duct of Wirsung
MANAGEMENT
Cholecystectomy
ACUTE CHRONIC
CHOLELITHIASIS
CHOLECYSTITIS CHOLECYSTITIS
Cholecystectomy Routine procedure NOT Definitive Laparoscopic –
recommended Advised within 72 procedure of
May be considered in hours of admission choice
select patients: high risk, Laparoscopic –
areas with high procedure of
incidence of choice
gallbladder cancer,
porcelain gallbladder In surgically unfit:
(risk of malignancy) Antibiotics +
Laparoscopic 6
weeks to 2 months
later
Or Percutaneous
Cholecystostomy
Open Cholecystectomy
1. Right subcostal incision
2. GB moved off liver, usually starting at the top
3. Cystic duct and artery ligated and divided during the course of the
operation
• Begins at the Deep inguinal ring and continues for about 4 cm, ending
at the Superficial inguinal ring
1. Deep (internal) inguinal ring
− Beginning of the inguinal canal
− Beginning of the tubular evagination of the Transversalis
fascia that forms one of the coverings of the spermatic cord
in men (Internal Spermatic Fascia) or round ligament of the
uterus in women HESSELBACH’S TRIANGLE (Rectus abdominis, Inguinal ligament, Inferior epigastric artery)
− Location:
o Midway between ASIS and pubic symphysis CLASSIFICATION SYSTEMS OF HERNIAS – for standardization in comparing
o Just above inguinal ligament outcomes of various hernias (little clinical significance)
o Immediately lateral to the Inferior Epigastric Vessels 1. Gilbert’s classification system– intraop assessment of location and size
2. Superficial (external) inguinal ring Type 1 Small internal ring, indirect
− End of the inguinal canal
Type 2 Medium (moderately dilated internal ring), indirect
− Beginning of the tubular evagination of the Transversalis
Type 3 Large (internal ring > 2 fingerbreadths), indirect
fascia that forms one of the coverings of the spermatic cord
Type 4 Complete disruption of entire inguinal floor, direct
(External Spermatic Fascia)
− Located superior to the pubic tubercle Type 5 With small (< 1 fingerbreadth) diverticular opening, direct
− Triangle-shaped opening in aponeurosis of External oblique Type 6 Combined direct and indirect (Pantaloon)
o Base – pubic crest Type 7 Femoral
o Sides of triangle – medial crus and lateral crus attached 2. Nyhus classification system – location, size of defect + integrity of
to pubic symphysis and pubic tubercle respectively inguinal ring and floor
o Apex – points superolaterally; intercrural fibers hold the Indirect, internal abdominal ring normal,
Type I
two crura together to prevent further widening of ring typical in infants, children, small adults
Indirect, internal ring enlarged w/o impingement on inguinal floor
Type II
Does not extend to scrotum
Type IIIA Direct, size not taken into account
Indirect, large enough to encroach upon posterior inguinal wall
Type IIIB
Usually includes indirect sliding or scrotal hernias, Pantaloon
Type IIIC Femoral hernia
Type IV Recurrent hernia
3. Schumpelick classification system – adds orifice sizing
Type I < 1.5 cm L – Lateral indirect site
Type II 1.5 – 3.0 cm M – Medial direct site
Type III > 3 cm F – Femoral
• Anterior wall
− Formed along its entire length by aponeurosis of External oblique
ETIOLOGY
− Reinforced laterally by medial fibers of Internal oblique which
• Congenital defects
originate from lateral 2/3 of inguinal ligament
• Loss of tissue strength and elasticity due to aging or repetitive stress
o Adds additional covering over Deep inguinal ring: potential
• Trauma (especially operative trauma)
point of weakness
• Increased intra-abdominal pressure due to:
o Contributes Cremasteric fascia containing Creamsteric
− Heavy lifting
muscle to coverings of structures traversing inguinal canal
− Coughing, asthma, COPD
• Posterior wall
− Bladder outlet obstruction (e.g. BPH)
− Formed along its entire length by Transversalis fascia
− Prior pregnancy
− Reinforced along medial 1/3 by the Cojoint tendon (Inguinal falx)
− Ascites and abdominal distention, obesity
− Reinforces Superficial inguinal ring
• Roof (Superior wall)
DESCRIPTIVE TERMINOLOGY
− Formed by arching fibers of Transversus abdominis and Internal
• Reducible – contents can be pushed back into abdomen
oblique passing from lateral points of origin from inguinal ligament
• Incarcerated – cannot be pushed back
to common medial attachment as Cojoint tendon
• Obstructing – contains loops of bowel that is kinked and obstructs GIT
• Floor (Inferior wall)
• Strangulated – contents are ischemic and will necrosedue to
− Formed by medial ½ of Inguinal ligament
compromise of blood supply
− Rolled-under, free margin of lowest part of aponeurosis of external
• Sliding – wall of sac is partly formed by retroperitoneal structure such as
oblique forms gutter on which contents of inguinal canal are
colon or bladder instead of peritoneum
positioned, reinforced by lacunar ligament
• Richter’s hernia – only one side of bowel is trapped in the hernia (usually
antimesenteric side) rather than entire loop, at risk for perforation
Life is what you make it. Vita qua se facies est! 12
INGUINAL HERNIAS PHYSICAL EXAMINATION
• 75 – 85% of hernias occur in the groin (inguinal) area • Always perform same examination on the other side to:
− 8 – 10%: Incisional hernias − Compare affected area vs. contralateral normal area
− 3 – 8%: Umbilical hernias − Investigate whether there is bilateral involvement
• Protrusion or passage of a peritoneal sac with or without abdominal • Examine patient in standing position with groin
contents through a weakened part of the abdominal wall in the groin area fully exposed
• Peritoneal sac enters the inguinal canal either: − Increases intra-abdominal pressure so that
hernia can be more easily elicited
INDIRECT INGUINAL HERNIA DIRECT INGUINAL HERNIA • Inspection:
Enters through posterior wall of − Is the abnormal bulge along the groin? Or
Enters through deep inguinal ring within the scrotum?
inguinal canal
− Is the bulge not obvious?
• Palpation:
− Place index finger into the scrotum, aimed toward external
inguinal ring to palpate inguinal canal
− Ask patient to cough or bear down to protrude hernia contents
(Valsalva’s maneuver)
• Inguinal occlusion test
− Place finger over the internal inguinal ring, ask patient to cough
− Controlled cough impulse felt on tip of finger = Indirect
− Uncontrolled Cough impulse felt on dorsum of finger = Direct
• Femoral hernia – palpable below inguinal ligament
More common in men – possibly because men have larger inguinal canal MANAGEMENT
Bimodal – peaks before 1 year of age and after 40 years of age
90% of inguinal hernia repairs are performed in men
Most common type of inguinal hernia Most common type of inguinal hernia
in women
Pathology – congenital*: partially/ Pathology – acquired: secondary to
completely patent processus either raised intra-abdominal
vaginalis pressure, damage to nerves of
anterior abdominal wall, weakening
of walls of inguinal canal
Sac passes lateral to inferior Sac passes medial to the inferior
epigastric vessels epigastric vessels (usually through
weakened posterior wall of inguinal
canal), in Hesselbach’s triangle
Extent of excursion down canal Does not traverse entire length of
depends on amount of processus inguinal canal but may exit through
vaginalis that remains patent (may superficial inguinal ring Diagnosis
pass through spermatic cord, • For clinically ambiguous cases such as:
scrotum) − Obese patients
*During the third trimester, the testes descend from the intra-abdominal space into the − Hernias not elicited on PE
scrotum accompanied by the processus vaginalis (finger-like projection of peritoneum). − Recurrent inguinal hernias
At the 36th – 40th weeks AOG the processus vaginalis closes and eliminates the peritoneal • Laparoscopic confirmation – gold standard
opening at the internal inguinal ring. Failure of the peritoneum to close results in patent
• Ultrasound
processus vaginalis (PPV) common in preterm babies. But PPV usually closes within the first
few months of life. − Least invasive
− Positive intra-abdominal pressure is used to elicit herniation of
FEMORAL HERNIA abdominal contents
• Pass through femoral canal into the medial aspect of the anterior thigh − (+) Movement of contents used to diagnose hernia
• Femoral canal − Lack of movement may be false negative
− At the medial edge of the femoral sheath which contains the − Normal movement of spermatic cord and posterior abdominal
femoral artery, femoral vein, lymphatics wall against the anterior may be false positive
− The neck is narrow thus prone to trapping bowel within the sac, • MRI
hence irreducible and susceptible to strangulation − Most sensitive
• Usually acquired − Delineate groin anatomy, demonstrate presence of groin hernia,
• More common in women because of wider pelvises rule out differentials that may affect management plans
Life is what you make it. Vita qua se facies est! 14
THYROID DISORDERS S THYROID GLAND
Recall: Thyroid Anatomy and Physiology • Normally brown, firm, weighs 20 g, located posterior to strap muscles
• Blood supply:
TRIANGLES OF THE NECK − Superior thyroid artery (from External Carotid Arteries)
The trapezius and sternocleidomastoid muscles divide the neck into the − Inferior thyroid artery (from Thyrocervical Trunk): crosses the
anterior and posterior triangles on each side. Recurrent Laryngeal Nerve
− Thyroidea ima (from the Aorta or Innominate artery)
Borders: • Innervation:
ANTERIOR TRIANGLE POSTERIOR TRIANGLE − Recurrent laryngeal nerve (from the Vagus nerve)
Median vertical line of neck Middle 1/3 of clavicle o Innervates intrinsic muscles of larynx except Cricothyroid
Inferior margin of the mandible Anterior margin of trapezius o Injury results to:
Anterior margin of Posterior margin of − Unilateral: adducted = weak voice, abducted = hoarse
sternocleidomastoid sternocleidomastoid voice and ineffective cough
− Bilateral: airway obstruction (Stridor)
− Superior laryngeal nerve (from the Vagus nerve)
o Innervates Cricothyroid muscle
o Injury results to inability to tense ipsilateral vocal cord =
difficulty hitting high notes, projecting the voice, voice
fatigue
• Lymphatic drainage
IODIDE
à Na/I Symporter in Thyroid
gland basement
membrane
à Pendrin in Thyroid gland
apical surface
à Thyroglobulin
à Thyroid Peroxidase:
Organification – Iodide +
Tyrosyl residues
à Thyroid Peroxidase:
Coupling
à T3, T4
à Exocytosis, Proteolysis
à Release
à Peripheral metabolism
POSTERIOR TRIANGLE
The inferior belly of the Omohyoid further divides the posterior triangle of the
neck into: superiorly, Occipital triangle, and inferiorly, Sublavian triangle
OCCIPITAL SUBCLAVIAN
Contents CN XI Subclavian artery, vein
Cervical sympathetic ganglia Thyrocervical trunk
Splenius capitis Costocervical trunk
Levator scapula Apex of the lung
Scalenus posterior, medius, anterior Brachial plexus
Low •
•
Primary hypothyroidism
Subclinical hypothyroidism
TSH > 4 μ IU/mL 0.4 > TSH < 4 μ IU/mL TSH < 0.4 μ IU/mL Normal • Early phase of treatment of primary hypothyroidism with
HIGH
levothyroxine
• TSH-producing adenoma causing thyrotoxicosis
PROBABLE EUTHYROID Free T4 levels High
• Generalized resistance to thyroid hormone (genetic) – rare
HYPOTHYROIDISM
4. Thyrotropin Releasing Hormone – evaluates pituitary TSH secretion
• Procedure:
FT4 normal 0.4 > TSH < 4 μ IU/mL FT4 elevated
− Administer 500 µg TRH
− Monitor TSH levels after 30 and 60 minutes
Free T3 levels 0.4 > TSH < 4 μ IU/mL HYPERTHYROID − Normal result: increase at least 6 µU/ml from baseline
5. Thyroid antibodies
• Do not evaluate thyroid function
• Elevation indicates an underlying disorder
FT3 normal 0.4 > TSH < 4 μ IU/mL FT3 elevated − Most common: Autoimmune thyroiditis
− 80% Hashimoto’s Thyroiditis
− Also seen in:
SUBCLINICAL HYPERTHYROID
HYPERTHYROID
(1) Grave’s disease
0.4 > TSH < 4 μ IU/mL (2) Multinodular goiter
(3) Some thyroid neoplasms
MALIGNANT BENIGN
• Almost all malignant nodules are • Halo used to be believed to represent
hypoechoic but majority of benign benign nodules but sometimes found
nodules are also hypoechoic in malignancy
• Microcalcifications may represent • Sharp borders represent non-invasion
Psammoma bodies but calcifications but majority of malignant nodules also
can be a consequence of bleeding have sharp borders
HYPERTHYROIDISM
Etiology
Increased hormone synthesis Release of preformed hormone
(Increased RAIU) (Decreased RAIU)
1. Grave’s disease (Diffuse Toxic Goiter) 1. Thyroiditis (early stage)
2. Toxic multinodular goiter 2. Thyrotoxicosis
3. Plummer’s disease (Toxic Adenoma)
4. Drug induced – amiodarone
1. Radionuclide imaging
5. Jod-Basedow Syndrome – iodine
• Measures thyroid uptake 6. Thyroid carcinoma
INCREASED UPTAKE DECREASED UPTAKE 7. Struma ovarii
Conditions with increased new thyroid Painless (De Quervain’s) Thyroiditis 8. Hydatidiform mole
hormone production, where iodine is needed Subacute Thyroiditis 9. TSH secreting pituitary adenoma
more to manufacture new hormones: Jod-Basedown Syndrome (Iodine-
Grave’s disease induced Hyperthyroidism)
Toxic nodular goiter Exogenous intake of thyroid hormone
Differential Diagnoses
Ectopic thyroid Based on Type of Goiter
Falsely decreased uptake: TYPE OF GOITER DIAGNOSIS
Iodine deficiency – a lot of room for Exogenous thyroid hormone Normal thyroid gland Graves’ disease, Painless thyroiditis, Factitious hyperthyroidism
radioactive iodine Anti-thyroid drugs Diffuse, non-tender Graves’ disease, Painless thyroiditis
Iodinated contrasts Single thyroid nodule Thyroid adenoma (Plummer’s)
• Agents: Multiple thyroid nodules Toxic multinodular goiter
(1) Iodine 123 Tender painful goiter Subacute thyroiditis (De Quervain’s)
• Preferred agent for imaging studies – taken up by
thyroid gland but non-destructive Based on Laboratories and Ancillaries
• Low dose and shorter half life (12 – 14 hours)
(2) Iodine 131
• High dose and longer half life (8 – 10 days)
• For patients with differentiated thyroid carcinoma with
metastatic disease
• Destroys thyroid follicles
(3) Technetium Tc 99m pertechnetate
• Taken up by mitochondria
• Trapped but not organified
• Shorter half life, less radiation exposure
• For nodal metastases
• Contraindications: Pregnancy, breastfeeding
2. Thyroid Scan
• Usually done with thyroid uptake using the same radioisotope
• Pictures are taken by a gamma camera
• Reported as films, pictures, or computer printouts
• Imaging for:
(1) Determining size and shape of gland
(2) Distribution of functionality – shows us exactly where in the
thyroid gland are the isotopes most intensely taken up
• Cold nodule: traps less radioactivity, higher risk for
malignancy
• Hot nodule: traps more radioactivity = more active
3. Ultrasound
• Advantages:
− Noninvasive and portable tool
− No radiation exposure
1. Graves disease (Diffuse Toxic Goiter)
Life is what you make it. Vita qua se facies est! 17
• Autoimmune disease triggered by either of the following: Advantages Disadvantages
− Post-partum states 1. Rapid, complete, permanent 1. Preoperative preparation
− Iodine intake control of toxicity 2. Morbidity:
2. Removal of mass a. Recurrent and/or Superior
− Infections
3. Treatment of choice for huge goiters Laryngeal nerve injury
− Genetic factors: HLA B8, DR3, HLA DQA10501, CTLA1 b. Hypothyroidism
• Stimulate thyrocytes to grow and produce hormones c. Hypoparathyroidism
• Epidemiology: d. Hematoma, seroma
− Most common cause of hyperthyroidism in North America e. Anesthetic and medical
− Common in females 40 – 60 years old complications
f. Thyroid storm
• Triad:
(1) Diffusely enlarged thyroid gland with increase in
vascularity 2. Toxic Multinodular Goiter
(2) Hyperthyroidism • Common in older patients with history of non-toxic multinodular
(3) Exophthalmos goiter wherein enough nodules become autonomous to cause
hyperthyroidism
• Other clinical manifestations:
− Increased adrenergic stimulation • May be precipitated by:
− Opthalmopathy − Iodide containing drugs (e.g. contrast medium)
− GI symptoms − Amiodarone
− Cardiovascular complications: tachycardia, atrial fibrillation, • Clinical manifestations similar to Grave’s disease but without
congestive heart failure extrathyroidal signs and symptoms
− Thyroid acropachy: subperiosteal bone formation and • Diagnosis:
swelling of metacarpals − Suppressed TSH
− Onycholysis: separation of fingernails from beds − Elevated FT4 and FT3
− Pretibial myxedema − Elevated RAIU
− Females: amenorrhea, decreased fertility, miscarriage • Treatment:
− Children: rapid growth, early bone maturation − Surgical resection: Subtotal thyroidectomy using Hartley-
− Young males: gynecomastia Dunhill Procedure
(1) Total lobectomy on one side
• Diagnosis:
− Suppressed TSH (2) Subtotal thyroidectomy on the other side
− Elevated FT4 and FT3 3. Plummer’s disease (Toxic adenoma)
− Elevated RAIU • Single hyperfunctioning nodule
− Solitary nodule usually 3 cm or larger
− Presence of thyroid receptor antibodies
(1) Thyroid stimulating immunoglobulins • More common in younger patients
(2) Thyroid stimulating antibodies • Linked with gene mutations of TSH-R or gsp
• Medical treatment: • Rarely malignant
• Diagnosis:
− Anti-thyroid drugs
o Inhibit organification and coupling of iodotyrosines − Elevated RAIU (“Hot” nodule)
o Euthyroid state achieved in 4 to 6 weeks • Treatment:
(1) Propylthiouracil – decreases peripheral conversion of T4 − Surgery: lobectomy and isthmusectomy
4. Thyroid storm
to T3, preferred in pregnant or breast feeding women
(less transfer via placenta) • Seen in unprepared patients
(2) Methimazole – longer half life, can be dosed once daily, • Sign and symptoms of thyrotoxicosis are magnified
associated with congenital aplasia • Management:
(3) Carbimazole − Prevention: induce euthyroid state
− Beta-blockers: Propanolol (1) Lugol’s solution
o Symptomatic relief of hypermetabolic state (2) Sodium ipodate – decreases iodide uptake and thyroid
o Can also decrease peripheral conversion of T4 to T3 hormone secretion
− Anti-thyroid drugs: PTU can block formation of new thyroid
Advantages Disadvantages hormone and conversion of T4 to T3
1. No morbidity related to surgery 1. High relapse rate − Beta-blockers: reduce symptoms and peripheral conversion
2. Treatment of choice for small goiters 2. Side effects especially in prolonged − Steroids: prevent adrenal exhaustion and block hepatic
and pregnant patients uses: rashes, fever, neuritis, thyroid hormone conversion
agranulocytosis
3. Crosses placenta HYPOTHYROIDISM
4. Hypothyroidism
5. Patient compliance
Etiology
Primary Secondary Tertiary
(Increased TSH) (Decreased TSH)
• Radioactive Iodine Therapy 1. Hashimoto’s thyroiditis 1. Pituitary tumor 1. Hypothalamic
− Emits low dose radiation to destroy thyroid follicles 2. RAI for Grave’s disease 2. Pituitary resection or insufficiency
− Standard dose: 10 mC = 8,500 cGY 3. Post-thyroidectomy ablation 2. Resistance to
4. Excessive iodine thyroid hormone
Advantages Disadvantages 5. Subacute thyroiditis
1. No morbidity related to surgery 1. Cure rate is dose dependent 6. Antithyroid drugs
2. Ease of treatment 2. Hypothyroidism 7. Lithium
3. Highly effective in diffuse goiter 3. Aggravate exophthalmos
4. Treatment of choice for failed 4. Thyrotoxicosis/thyroid storm Differential Diagnosis
surgical management 5. Crosses placenta
6. Infertility in females
7. Increase cancer risk in children
8. Not effective in nodular goiter
• Surgical treatment
− Preoperative preparation: render patient euthyroid
(1) Lugol’s solution
(2) Saturated potassium iodide
− Indications: Total thyroidectomy or Near total thyroidectomy
(1) Coexistent carcinoma
(2) Severe opthalmopathy
(3) Life threatening reactions to medication
(4) Refusal to undergo RAI therapy
− Indication: Subtotal thyroidectomy – all other situations
CLINICAL
DISEASE ETIOLOGY DIAGNOSIS MANAGEMENT
MANIFESTATIONS
Nodular Non-toxic Goiter TSH stimulation secondary to Pressure sensation in neck Patchy RAIU Subtotal thyroidectomy +
inadequate TH synthesis Catarrh Usually euthyroid with Lifelong T4 replacement
Familial (enzyme, iodine Compression symptoms normal TSH, low-normal FT4
metabolism defect), endemic (+) Pemberton’s Sign FNAB if with dominant
(iodine), or sporadic nodule or enlarging nodule
CT scan
Graves Disease Autoimmune: Thyroid-stimulating Diffusely enlarged thyroid â TSH Propylthiouracil,
(Diffuse Toxic Goiter) immunoglobulins and/or Exophthalmos á FT4 and FT3 Methimazole, Carbimazole
antibodies bind to the Myxedema á RAIU Propanolol
Thyrotropin receptor to stimulate (+) Thyroid receptor Radioactive iodine therapy
thyrocytes to grow and produce antibodies Total, near total, or subtotal
hormones thyroidectomy
Toxic Multinodular Goiter Multiple autonomous nodules Multiple palpable â TSH Subtotal thyroidectomy
May be precipitated by: Iodide, nodules á FT4 and FT3 (Hartley-Dunhill procedure)
Amiodarone Purely thyroid signs and á RAIU
symptoms
Plummer’s Disease Gene mutations of TSH receptor Single nodule usually 3 á RAIU Radioactive iodine therapy
(Toxic Adenoma) or GSP cm or larger
Hashimoto’s Thyroiditis Genetic predisposition Diffuse, symmetrically Initially hyper then T4 suppression
(Chronic Lymphocytic Transformation of thyroid to enlarged neck subsequently eu or Surgery
Thyroiditis) lymphoid tissue (+) Pain, tenderness hypothyroid Thyroid hormone
á TSH replacement
(+) Thyroid antibodies
Acute Suppurative Thyroiditis Infection caused by Preceded by URTI or OM Leukocytosis Parenteral antibiotics
hematogenous or lymphatic or Severe neck pain FNAB with Gram’s stain, Drainage of abscess
direct spread, trauma, or radiating to jaws or ear culture, cytology Complete resection of
immunosuppression Fever, chills CT-scan Pyriform sinus fistula if present
Common: Streptococcus, Odynophagia Barium swallow
anaerobes Dysphonia
De Quervain’s Viral or post-viral inflammatory Preceded by URTI Initially hyper then eu then
Granulomatous Thyroiditis response Neck pain radiating to hypo then resolution to Symptomatic treatment
(Painful Subacute Thyroiditis) Genetic predisposition: HLA B35 the jaws or ear euthyroidism Aspirins or NSAIDs
Enlarged, tender, firm â TSH Steroids for severe pain
thyroid á T4 and T3 Short term TH replacement
ESR > 100 Thyroidectomy: if prolonged
â RAIU and unresponsive
Painless Subacute Thyroiditis Autoimmune Normal sized or minimally â TSH Beta-blockers
Sporadic or post-partum enlarged, slightly firm, á T4 and T3 TH replacement
non-tender thyroid gland Normal ESR Thyroidectomy, RAI ablation
â RAIU if recurrent and disabling
Riedel’s Thyroiditis (Invasive Autoimmune Painless, hard, anterior Open thyroid biopsy Surgery
Fibrous Thyroiditis) Thyroid parenchyma replaced neck mass TH replacement +
by fibrous tissue invading Hard, woody thyroid Corticosteroids
adjacent tissue gland with fixation to
surrounding structures
Compression symptoms
REFERENCES:
1. Role of Surgery in Benign and Malignant Thyroid Diseases by Dr. E.H.
Nucum, Department of Surgery Faculty of Medicine and Surgery
University of Santo Tomas
2. The Thyroid Gland by Dr. S. Kho, Department of Internal Medicine
Section of Endocrinology Faculty of Medicine and Surgery University of
Santo Tomas
3. Brunicardi, C.F., et al. (2010). Schwartz’s Principles of Surgery, 19th ed.
McGraw-Hill Companies Inc.: New York.
4. Foster, C., Mistry, N.F., et al. (2010). The Washington Manual of Medical
Therapeutics, 33rd ed. Lippincott Williams & Wilkins: Philadelphia.
5. Longo, D.L., Fauci, A.C., Kasper, D.L, et al. (2013). Harrison’s Principles of
Internal Medicine, 18th edition. McGraw-Hill Companies Inc.: New York.
6. Gray’s Anatomy for Students by Richard L. Drake, Wayne Vogl, and
Adam W.M. Mitchell