Head and Neck Carotid Sheath

Local condensation of the Prevertebral, Pretracheal

and Investing layers of the deep cervical fascia

• LATERAL – Internal Jugular Vein

• MEDIAL – Common and Internal Carotid artery

• POSTERIOR – Vagus nerve

SUPERFICIAL / SUBCUTANEOUS
• DEEP / FASCIA COLLI
o Investing Layer
o Pretracheal layer
o Prevertebral layer

Platysma - thin broad muscular sheet embedded in

the superficial fascia of the neck Hyoid Bone
- Part of muscles of Facial expression
innervated by the Facial nerve

Sternocleidomastoid
– strong thick muscle crossing the neck

Anterior border covers the carotid arteries, IJV,

deep cervical LN and partly overlaps the thyroid
gland

Posterior border related to the cervical plexus of

nerves, Phrenic nerve and upper part of the
Brachial plexus

ACTION: Rotation of the Head to the opposite side The only bone that does not articulate with another
and flexion of the neck bone

U-shaped consisting of paired LESSER HORNS

Trapezius LATERALLY
– large triangular paired muscle located on the
Paired GREATER HORNS POSTERIORLY
posterior aspect of the neck and thorax
Serves as a moveable base for the tongue
ACTION:
Hyoid – at the level of C 3
Upper – elevates and upwardly rotates the scapula

Middle – adducts the scapula

Lower – depresses and help in rotating the scapula

 Anterior Triangle
• Bounded by:

o Ant border of SCM

o Anterior midline of neck

o Inferior border of the mandible

Triangles of the Neck

BOUNDARIES OF THE NECK:

o Superior – Lower border of mandible

o Inferior – Clavicle

o Anterior – Anterior midline of neck

o Posterior – Trapezius

Submental Triangle
Boundaries

o Apex: symphysis menti

o On each side: Ant. Belly of digastric m. o Ant. Midline of neck

o Base: body of the Hyoid bone o Ant. Border of SCM

o Floor – Mylohyoid Posterior Triangle

Contents: • Bounded by:
o Submental lymph nodes o Post border of SCM
o Submental vessels o Anterior border of Trapezius

o Superior border of clavicle

• Subdivided into:

o Supraclavicular

o Occipital

Digastric/Submandibular Triangle
• Boundaries
o Ant. and Post. Bellies of Digastric m.
o Inferior border of mandible
• Floor – Mylohyoid
Occipital Triangle
• Apex contains portion of occipital bone
• Occipital artery is found in superior part
• Accessory nerve crosses the triangle
• Accessory nerve Lesions
o weakness of the TRAPEZIUS muscle,

Carotid Triangle o difficulty in elevating the scapula / shrugging the

shoulder
• Boundaries
o difficulty in laterally rotating the scapula during
o Superior belly of omohyoid abduction of

o Posterior belly of digastric the arm

o Ant. border of SCM

• Carotid Pulse

o Bifurcation of the Common Carotid artery into the

Internal and External Carotid arteries can easily be
palpated just beneath the

anterior border of SCM at the level of the

SUPERIOR border of the Thyroid cartilage

Muscular Triangle
Supraclavicular Triangle
• Boundaries
• A.K.A. Subclavian Triangle; Omoclavicular
o Superior belly of omohyoid
• Superficial landmark is supraclavicular fossa
• Crossed by external jugular vein and subclavian
artery
• INFERIOR DEEP CERVICAL – lie on the
INTERNAL JUGULAR
VEIN near the Subclavian vein
• EMPTY into the THORACIC DUCT on the LEFT
side and the
RIGHT LYMPHATIC DUCT on the RIGHT side

Level IA – Submental nodes;

• medial to the ant. belly of Digastric, symphysis of
mandible
superiorly and hyoid inferiorly
Level IB – Submandibular nodes;
post. to the ant. belly of Digastric, ant. to post. belly
of Digastric and inferior to the body of mandible
Level IIA – Jugulo-digastric nodes;
• deep to SCM, post. to post. belly of Digastric,
superior to hyoid,
inferior to CN XI
Level IIB – Submuscular;
• superior to CN XI
Level III – Middle Jugular;
• inferior to hyoid, superior to Cricoid, deep to SCM
Level IV – Lower Jugular;
• inferior to Cricoid, superior to clavicle, deep to
SCM
Level VA – lateral to SCM,
• inferior and medial to splenius capitis and
Superficial Cervical Lymph Nodes trapezius, superior
• Lie ABOVE the investing layer of the deep to CN XI
cervical fascia Level VB – lateral to SCM, medial to trapezius,
• Lie along the EXTERNAL JUGULAR VEIN in the inferior to
Posterior Triangle CN XI, superior to clavicle
and along the ANTERIOR JUGULAR VEIN in the Level VI – Ant. Compartment nodes;
Anterior Triangle • inferior to hyoid, superior to suprasternal notch,
• DRAIN into DEEP CERVICAL NODES medial to
o Submental strap muscles
o Submandibular Level VII – Paratracheal nodes;
o Occipital • inferior to suprasternal notch
o Anterior Cervical
o Superficial cervical

Deep Cervical Lymph Nodes

• SUPERIOR DEEP CERVICAL – lie along the
INTERNAL JUGULAR
VEIN in the Carotid Triangle of the neck
 Each lobe is Pear shaped, Apex directed upward –
lamina of thyroid cartilage; Base at the level of the
fourth or fifth tracheal rings

Surrounded by Pretracheal layer of deep fascia

20 gms

PYRAMIDAL LOBE is often present; projects

upward from the isthmus, usually to the LEFT of the
midline

ZONE I – includes the root of the neck and extends Fibrous or Muscular band frequently connects the
from clavicles pyramidal lobe to the hyoid bone – LEVATOR
and manubrium to the level of INFERIOR border of GLANDULAE THYROIDEA
the CRICOID
cartilage
• Structures at risk – cervical pleurae, apices of
lungs, thyroid and
parathyroid glands, trachea, esophagus, common
carotid
arteries, jugular veins and cervical region of the
vertebral
column
ZONE II – extends from the Cricoid cartilage to the
level of ANGLE
of the MANDIBLE
• Structures at risk – superior poles of the Thyroid
gland, Thyroid
and Cricoid cartilages, larynx, laryngopharynx,
carotid arteries,
jugular veins, esophagus and cervical region of the
vertebral
column
ZONE III – ABOVE the level of ANGLE of the
MANDIBLE
• Structures at risk – salivary glands, oral and nasal
cavities,
HEAD AND NECK (PSGS)
oropharynx, nasopharynx
REMEMBER:
• Injuries to Zones I and III obstruct the airway and The regional lymphatic drainage of the neck is
have the divided into seven levels. These levels allow for a
greatest risk for morbidity and mortality standardized format for radiologists, surgeons,
• Injury to Zone II are most common, but morbidity pathologists, and radiation oncologists to
and mortality communicate concerning specific sites within the
are lower because vascular damage may be neck
controlled by direct
pressure and structures involved are easily Level I—the submental and submandibular nodes
visualized and
treated Level Ia—the submental nodes; medial to the
anterior belly of the digastric muscle bilaterally,
symphysis of mandible superiorly, and hyoid
Thyroid Gland inferiorly
Right and Left lobes connected by a narrow
ISTHMUS (second, third and fourth tracheal rings) Level Ib—the submandibular nodes and gland;
posterior to the anterior belly of digastric, anterior to
the posterior belly of digastric, and inferior to the
body of the mandible

Level II—upper jugular chain nodes

Level IIa—jugulodigastric nodes; deep to

sternocleidomastoid (SCM) muscle, anterior to the
posterior border of the muscle, posterior to the
posterior aspect of the posterior belly of digastric,
superior to the level of the hyoid, inferior to spinal
accessory nerve (CN XI)

Level IIb—submuscular recess; superior to spinal

accessory nerve to the level of the skull base

Level III—middle jugular chain nodes; inferior to

the hyoid, superior to the level of the cricoid, deep
to SCM muscle from posterior border of the muscle TNM
to the strap muscles medially
T1 <2 cm
Level IV—lower jugular chain nodes; inferior to the T2 2-4 cm
level of the cricoid, superior to the clavicle, deep to T3 >4 cm
SCM muscle from posterior border of the muscle to
the strap muscles medially T4A- Resectable/ Advanced/ with adjacent
Anatomic Involvement
Level V—posterior triangle nodes
T4B - Unresectable/ Very Advanced
Level Va—lateral to the posterior aspect of the
SCM muscle, inferior and medial to splenius capitis Head: Nasopharynx, Pterygoids, Foramen
and trapezius, superior to the spinal accessory Ovale, Sphenoid
nerve
Neck: Spine ( Cervical Fascia), Carotids
Level Vb—lateral to the posterior aspect of SCM
muscle, medial to trapezius, inferior to the spinal
accessory nerve, superior to the clavicle

Level VI—anterior compartment nodes; inferior to

the hyoid, superior to suprasternal notch, medial to
the lateral extent of the strap muscles bilaterally

Level VII—paratracheal nodes; inferior to the

suprasternal notch in the upper mediastinum

Supraomohyoid Neck Dissection - used with oral

cavity malignancies, removes lymph nodes in levels
I to III

Lateral Neck Dissection - used for laryngeal

malignancies, removes those nodes in levels II
through IV

posterolateral neck dissection - used with thyroid

cancer, removes the lymphatics in levels II to V
1.A neck dissection that preserves lymphatic
compartments normally removed as part of a
classic RND is termed a selective neck dissection
(SND)

Types of SND include the supraomohyoid neck

dissection, the lateral neck dissection, and the
posterolateral neck dissection

2. The classic RND removes levels I to V of the

cervical lymphatics in addition to the SCM, internal
jugular vein, and the spinal accessory nerve (CN
XI). Any modification of the RND that preserves
nonlymphatic structures (i.e., CN XI, SCM muscle,
or internal jugular vein) is defined as a modified
radical neck dissection (MRND).
BREAST BOUNDARIES OF THE BREAST

EMBROLOGY
SUPERIOR 2nd or 3rd Rib
▰ Two ventral bands of thickened ectoderm
(mammary ridges, milk lines) on 5th or 6th
week of fetal development
▰ Paired breasts develop along ridges 6th or 7th Rib (Inframammary
INFERIOR
▰ Base of the forelimb (future axilla) to fold)
hind limb (inguinal area)

MEDIAL Lateral Margin of the Sternum

LATERAL Anterior Axillary Line

Fascia of pectoralis major,

The primary bud, in turn, initiates the development
of 15 to 20 secondary buds. Epithelial cords
develop from the secondary buds and extend into
the surrounding mesenchyme. Major (lactiferous)
ducts develop, which open into a shallow mammary
pit. During infancy, a proliferation of mesenchyme
transforms the mammary pit into a nipple. If there is
failure of a pit to elevate above skin level, an
inverted nipple.
This congenital malformation occurs in 4% of
infants.
At birth, male and female are identical
serratus anterior, and External
POSTERIOR oblique abdominal muscles
and upper extent of rectus
sheath
Retromammary bursa (space): posterior aspect
of the breast between the investing fascia of the
breast and the fascia of the pectoralis major muscle
Boundaries of dissection for MRM:
● Anterior margin of latissimus dorsi muscle
laterally
● Midline of the sternum
● Subclavius muscle superiorly and
● caudal extension of breast, which is 3 to 4
cm inferior to the inframmary fole inferiorly

The breast remains undeveloped in the female until AXILLARY TAIL OF SPENCE
puberty,
- Extends laterally across anterior axillary fold
Responds to ovarian estrogen and progesterone in - Upper outer quadrant contains a greater
puberty volume of tissue than other quadrants
- Lower inner: 5%, right lower: 10 %
Breast compete development at the time of - Upper inner: 15% Upper outer: 45%
pregnancy. - Areolar: 25%

FUNCTIONAL ANATOMY NIPPLE – AREOLA COMPLEX

-Sebaceous glands
The breast is composed of 15 to 20 lobes which are -Sweat glands
each composed of several lobules. Fibrous bands -Montgomery’s tubercles
of connective tissue travel through the breast
(Cooper’s suspensory ligaments), insert
perpendicularly into the dermis, and provide
structural support. Causes the dimpling of the skin
and nipple retraction.
BLOOD SUPPLY ✔ Central group
✔ Subclavicular group (apical)
ARTERIAL SUPPLY VENOUS ✔ Interpectoral group (Rotter’s)
DRAINAGE
The boundaries for lymph drainage of the axilla are
Medial mammary arteries Veins correspond to the not well demarcated, and there is considerable
arise form: arteries variation in the position of the axillary lymph nodes.
The 6 axillary lymph node groups recognized by
- Internal mammary - Internal thoracic surgeons are (1) the axillary vein group (lateral); (2)
artery vein the external mammary group (anterior and
- 2nd to 4th anterior - Posterior pectoral); (3) the scapular group (posterior and
intercostal intercostal veins subscapular); (4) the central group; (5) the
perforators - Tributaries of the subclavicular group (apical); and the interpectoral
axillary vein group (Rotter’s)
Lateral mammary arteries
arise from: Venous drainage is The lymph node groups are assigned levels
toward the axilla
- Lateral branches
of the posterior
intercostal arteries
- Branches from the
axillary artery
(highest thoracic,
lateral thoracic
and pectoral
branches of the
thoracoacromial
artery)

VENOUS DRAINAGE

3 principal groups of veins:

- Perforating branches of the internal thoracic

vein
- Perforating branches of the posterior
intercostal veins
- Tributaries of the axillary vein
- Provides a route for breast cancer
metastases : Vertebrae, skull, pelvic bones,
central venous system
- Batson’s vertebral venous plexus
● Invests the vertebrae and extends
from the base of the skull to the
sacrum
LYMPH DRAINAGE
according to their anatomic relationship to the
pectoralis minor muscle. Lymph nodes located
lateral to or below the lower border of the pectoralis
minor muscle are referred to as level I lymph nodes,
which include the axillary vein, external mammary,
and scapular groups. Lymph nodes located
superficial or deep to the pectoralis minor muscle are
referred to as level II lymph nodes, which include the
central and interpectoral groups. Lymph nodes
located medial to or above the upper border of the
pectoralis minor muscle are referred to as level III
lymph nodes, which consist of the subclavicular
group.

6 axillary lymph node groups include

✔ Axillary vein group (lateral)
✔ External mammary group (anterior
and pectoral)
✔ Scapular group (posterior and
subscapular)
PHYSIOLOGY Lactation: Less common, but a common
presentation to breast specialists
Hormonal stimuli
Intrinsic: Abnormalities of the breast
Estrogen: initiates ductal development
Periductal mastitis
Progesterone: differentiation of epithelium and
lobular development Extrinsic: Infection in an adjacent structure

Prolactin: primary hormonal stimulus for Sebaceous cyst

lactogenesis in late pregnancy and post partum
period BACTERIAL INFECTION

DEVELOPMENT AND FUNCTION ▰ S. aureus and Streptococcus species from

nipple discharge
A dramatic increase in circulating ovarian and ▰ Breast abscess: staphylococcal infection
placental estrogens and progestins is evident during ▻ Point tenderness, erythema,
pregnancy, which initiates striking alterations in the hyperthermia
form and substance of the breast. The breast ▻ Lactation: within first few weeks of
enlarges as the ductal and lobular epithelium breastfeeding
proliferates, the areolar skin darkens, and the
accessory areolar glands (Montgomery’s glands) Typically breast abscesses are seen in
become prominent. In the first and second staphylococcal infections and present with point
trimesters, the minor ducts branch and develop. tenderness, erythema, and hyperthermia.
During the third trimester, fat droplets accumulate in ● Progression may result to abscesses on:
the alveolar epithelium, and colostrum fills the ○ Subcutaneous
alveolar and ductal spaces. In late pregnancy, ○ Subareolar
prolactin stimulates the synthesis of milk fats and ○ Interlobular / periductal
proteins. After delivery of the placenta, circulating ○ Retromammary (unicentric or
progesterone and estrogen levels decrease, multicentric)
permitting full expression of the lactogenic action of Staphylococcal
prolactin. Milk production and release are controlled ○ More localized
by neural reflex arcs that originate in nerve endings ○ Deep
of the nipple-areola complex. Maintenance of Streptococcal
lactation requires regular stimulation of these neural o Diffuse
reflexes, which results in prolactin secretion and milk o Superficial
letdown. Oxytocin release results from the auditory, Management
visual, and olfactory stimuli associated with nursing.
Oxytocin initiates contraction of the myoepithelial ▰ Previous: incision and drainage
cells, which results in compression of alveoli and ▰ Current: antibiotics and repeated aspiration
expulsion of milk into the lactiferous sinuses. After of abscess, ultrasound guided
weaning of the infant, prolactin and oxytocin release ▰ Operative drainage:
decreases. Dormant milk causes increased ▻ Unresolved cases
pressure within the ducts and alveoli, which results ▻ Overlying skin is compromised
in atrophy of the epithelium (Fig. 17-9C). With ▰ Local wound care
menopause, there is a decrease in the secretion of ▰ Warm compress
estrogen and progesterone by the ovaries and ▰ IV antibiotics
involution of the ducts and alveoli of the breast. The ▰ Chronic – culture to identify
surrounding fibrous connective tissue increases in ▰ Acid fast bacilli, anaerobic
density, and breast tissues are replaced by adipose and aerobic bacteria and
tissues. fungi
▰ Biopsy – rule out breast cancer
INFECTIOUS AND INFLAMMATORY DISORDERS

Postpartum: Most common time to occur

 Women with chronic acne are predisposed
Mimics other chronic inflammatory states
Involvement of axillary skin is often multifocal
and contiguous
Treatment
● Antibiotic therapy
● Incision and drainage
● Excision of involved areas
● Advancement flaps or split-thickness
skin grafts
Zuska’s disease

▰ Recurrent periductal mastitis

▰ Recurrent retroareolar infections and
abscesses
▰ Risk factor: smoking
▰ Management: symptomatic
▻ Incision and drainage
▻ Antibiotics
▻ Wide debridement

Mycotic infection
COMMON BENIGN DISORDERS AND
▰ Blastomycosis or sporotrichosis DISEASES
▰ Initiated by inoculation of intraoral fungi from
suckling infant Abberations of Normal Development and
▰ Present as mammary abscess in close Involution (ANDI)
proximity to NAC
▰ Rare Principles:
▰ Treatment:
▰ Antifungal agents for systemic ▻ Normal processes of reproductive
(noncutaneous) infection life and involution
▰ Surgical: drainage of abscess or ▻ Spectrum: normal – disorder –
partial mastectomy for persistent
disease
fungi
▻ Pathogenesis and degree of
abnormality

EARLY REPRODUCTIVE YEARS (15-25)

FIBROADENOMAS

▰ Age 15 to 25 years
▰ 1 to 2 cm in diameter
▰ Stable
▰ Small <1cm
▰ Disorder: <3cm
▰ Disease: Giant >3 cm
▻ Multiple: >5
▰ Fibroadenoma are benign tumors are Atypical proliferative diseases
typically well circumscribed and are
comprised of both stromal and glandular Ductal and lobular hyperplasia may
elements. display features of CIS
Hypertrophy
Women with atypical ductal and lobular
▰ Disorder: Presents as adolescent hyperplasia
hypertrophy
▰ Disease: Gigantomastia - 4-fold increase in breast cancer
▰ Etiology: Unknown risk
Nipple inversion

▰ Disorder of duct development

▰ Prevents normal protrusion of nipple
▰ Disease: Subareolar abscess
▰ Mammary duct fistula
▰ Arise when nipple inversion
predisposes major duct obstruction
▰ Leading to Recurrent subareolar
abscess and mammary duct fistula

LATE REPRODUCTIVE YEARS (25-40)

CYCLICAL MASTALGIA &

NODULARITY

▰ Normal: associated with premenstrual

enlargement of breast
▰ Cyclical pronounced mastalgia and
severe painful nodularity
▰ Disorder: Painful nodularity >1 week
PATHOLOGY OF
INVOLUTION NONPROLIFERATIVE DISORDERS
(35-55)
1. No risk for cancers
▰ When stroma involutes too quickly 2. Proliferative: some of them has no
▻ Alveoli remain or slightly risk: no risk: sclerosing
▻ Form microcysts
▻ Precursor for macrocyst adenosis, and intraductal
▻ Common, papilloma
subclinical, do not
require treatment
 3. Atypical: you have atypia, size, fine, linear,
moderate increase risk, 4 fold branching
increase

-Atypical proliferative lesions have some

features of carcinoma in situ but either
lack a major defining feature of CIS or FIBROADENOMAS Abundant stroma with
histologically normal
have the features in less than fully cellular elements
developed form Hormonal dependence

Non-proliferative disorders of the breast

account for 70% of benign breast ADENOMAS
conditions and carry no increased risk
for the development of breast cancer. ▰ Well-circumscribed
▰ Benign epithelium with sparse stroma –
histologic feature differentiating from
Of paramount importance for optimal fibroadenoma
management of benign breast disorders ▰ Tubular
and diseases is the histologic ▰ Young, nonpregnant
differentiation of benign, atypical and ▰ Lactating
▻ Pregnancy, post-partum
malignant
HAMARTOMAS
MACROCYSTS -Involutional disorder
-High frequency of ▰ Discrete breast tumors
occurrence ▰ 2 to 4 cm, firm, sharply circumscribed
-Multiple
ADENOLIPOMAS
DUCTAL ECTASIA -Dilated subareolar
ducts
-Palpable ▰ Sharply circumscribed nodules of fatty
-Thick nipple discharge tissue
-Primary event 🡪 ▰ Contain normal breast lobules and ducts
stagnation of secretions,
epithelial ulceration, FIBROCYSTIC DISEASE
leakage of duct
secretions 🡪 local ▰ Nonspecific
inflammatory process 🡪 ▰ Diagnostic term to describe symptoms,
periductal fibrosis and rationalize need for biopsy, explain biopsy
nipple retraction results
▰ Spectrum of histopathologic changes that
PERIDUCTAL Weakening of ducts 🡪 are best diagnosed and treated specifically
MASTITIS secondary dilatation

CALCIFICATIONS Calcium deposits PATHOLOGY OF PROLIFERATIVE DISORDERS

Most are benign WITHOUT ATYPIA
Cellular
secretions, debris,
trauma or
inflammation
Cancer
Microcalcifications,
vary in shape and
density, <0.5mm
 SCLEROSIN Childbearing and
G ADENOSIS perimenopausal years
No malignant potential
Proliferative and involutional
Distorted breast lobules,
multiple microcysts, palpable
mass
Benign calcifications
RADIAL Central necrosis, epithelial
SCARS & proliferation, apocrine
COMPLEX metaplasia, papilloma
SCLEROSIN formation
G LESIONS
Radial scars
Up to 1cm diameter
Site of terminal duct branching
Complex sclerosing lesions
Larger lesions
DUCTAL Mild: 3 or 4 cell layers above
HYPERPLAS the basement membrane
IA Moderate: 5 or more layers
above the basement membrane
Florid
Cover 70% of minor duct lumen
>20%: solid or papillary
Increased cancer risk
INTRADUCT Major ducts
AL Premenopausal
PAPILLOMA <0.5cm to 5cm
Nipple discharge: serous or
bloody
Rarely undergo malignant
transformation
No increased risk for breast
cancer development
Malignant transformation
Multiple intraductal papilloma
Less frequently associated with
nipple discharge
PATHOLOGY OF PROLIFERATIVE DISORDERS
WITH ATYPIA
▰ With features of CIS but lack major defining
feature or have less than fully developed
form
▰ Includes:
▻ Atypical ductal hyperplasia
▻ Atypical lobular hyperplasia
ATYPICAL DUCTAL HYPERPLASIA
▰ Similar to DCIS histologically
▰ Monotonous round, cuboidal or polygonal
cells enclosed by basement with rare
mitoses
▰ 2 to 3mm in size (DCIS if >3mm)
▰ Excisional biopsy
▰ Increased risk for breast cancer
development
ATYPICAL LOBULAR HYPERPLASIA
▰ Minimal distention of lobular units
▰ Small monomorphic cells that distend
terminal ductal lobular unit
▰ Acini full and distended
▰ Overall lobular architecture maintained
▰ Classic
▰ Not associated with specific
mammographic or palpable
abnormality
▰ Incidental finding
▰ Increased risk for developing cancer
▰ Pleomorphic
▰ Calcifications or suspicious
mammographic findings
▰ DIAGNOSIS
▰ Immunohistochemical staining
▰ E-cadherin
▻ Lobular (ALH and LCIS)
▻ Lack of E-cadherin
expression
▻ Ductal (ADH and DCIS)
▻ E-cadherin reactivity
RISK FACTORS
HORMONAL
▰ Increased exposure to estrogen= increased
risk for developing breast cancer
▻ Increased number of menstrual
cycles
▻ Older age at first live birth
▻ Obesity
 ▻ Conversion of ▰ Occurrence of 2nd cancer
androstenedione to estrone within the same quadrant
by adipose tissue
▰ Reduced exposure = protective LCIS

NON-HORMONAL ▰ Originates from terminal duct lobular units

▰ Develops only in the female breast
▰ Radiation ▰ Cytoplasmic mucoid globules: distinctive
▻ Radiation therapy features
▻ Somatic mutations (atomic bomb ▰ Presence of neighborhood calcifications
blasts) ▰ Regarded as a marker of increased risk for
▻ Adolescence invasive cancer
▰ Alcohol ▰ LCIS may be observed in breast tissues that
▻ Increased serum estradiol contain microcalcifications, but the
▰ High-fat foods calcifications associated with LCIS
▻ Increased serum estrogen typically occur in adjacent tissues. T
▰ Distention and distortion of terminal duct
BRCA MUTATIONS lobular units by cells
▰ Large
BRCA I BRCA II ▰ Normal nuclear:cystoplastic
ratio
▰ May be observed in breast tissues that
• AD inheritance • AD inheritance contain microcalcifications
• Chr 17q • Chr 13 ▰ Occur in adjacent tissues
• Tumor suppressor • Tumor suppressor
▰ Average age of diagnosis: 45 years
gene gene
• Involved in 45% of • 85% lifetime risk ▰ 15 to 25 years younger than
hereditary breast for Breast CA the age at diagnosis of
CA and 80% of • 6% increased risk invasive breast cancer
hereditary ovarian for Breast CA in
CA men DCIS
• 90% lifetime risk • Associated CA
for Breast CA are well
▰ Also called Intraductal carcinoma: high risk
• Associated CA differentiated and
are poorly express hormone for progression to invasive cancer
differentiated and receptors ▰ Proliferation of epithelium that lines minor
are hormone ducts 🡪 papillary growth within duct lumina
receptor negative ▰ Papillary-cribriform-solid- comedo
• Early onset, ▰ Calcifications occurs in the areas of
bilateral disease, necrosis
CA at other sites ▰ Regarded as a TRUE anatomic precursor of
CARCINOMA IN SITU invasive carcinoma

▰ Cancer cells have not invaded the GROWTH PATTERNS

basement membrane
▰ Broders’ ▰ Papillary
▻ Absence of invasion of cells into Intraluminal projection of cells
surrounding stroma and their ▰ Cribriform
confinement within natural ductal Coalasce and fill the duct lumina
and alveolar boundaries Scatterred, rounded spaces remain between
▻ Multicentricity clumps of atypical cancer cells,
▰ Occurrence of a 2nd breast Hyperchromasia and loss of polarity
cancer outside the breast ▰ Solid growth
quadrant of primary cancer Pleomorphic cancer cells with frequent mitotic
▰ Or at least 4 cm away figures obliterate the lumina and distend the
▻ Multifocality ducts
▰ Comedo
 Cells outstrip their blood supply and become Pathognomonic:
necrotic
Paget cells: Large, pale, vacuolated
cells in rete pegs of epithelium
Must be differentiated from melanoma
Differentiation
S-100 antigen: melanoma
Carcinoembryonic antigen (CEA):
Paget’s disease

INVASIVE DUCTAL CARCINOMA

▰ Most common type (80%)

▰ Axillary LN mets in 60%
▰ Peri/postmenopausal women in their 5th to 6th
decade of life
▰ Solitary, firm mass, poorly defined margins
▰ Central stellate configuration with chalky white or
yellow streaks

MEDULLARY CARCINOMA

▰ 4% of all invasive breast cancers

▰ Frequent phenotype among BRCA1 cancers
▰ Bilateral in 20%
▰ Associated with DCIS in 50%
INVASIVE BREAST CANCER ▰ Soft, hemorrhagic and bulky
▰ Lobular or ductal ▰ Microscopically
▰ Early classifications ▰ Dense lymphoreticular infiltrate of lymphocytes
Lobular – LCIS and plasma cells
Ductal – all other invasive cancers ▰ Large pleomorphic nuclei, poorly differentiated,
▰ 80%: No special type sheet-like growth pattern
▰ Worse than special-type cancers
MUCINOUS CARCINOMA
Foote and Stewart Classification
Paget’s disease of the nipple ▰ 2% of all invasive breast cancers
Invasive ductal carcinoma-80% ▰ Elderly population
Medullary carcinoma- 4% ▰ 66% displays hormone receptors
Mucinous (colloid) carcinoma- 2% ▰ Glistening and gelatinous
Papillary carcinoma – 2% ▰ Microscopic: extracellular pools of mucin
Tubular carcinoma 2%
Invasive lobular carcinoma-10% This cancer is defined by extracellular pools of
Rare cancers mucin, which surround aggregates of low-grade
cancer cells.

▰ Cut surface:
▰ Glistening and gelatinous
quality
▰ Variable fibrosis
▰ If abundant, firm consistency
with cancer
▰ >90% display hormone receptors
▰ 33% lymph node metastases
 ▰ 5- and 10-year survival rates are
73% and 59%

PAPPILARY CARCINOMA

▰ 2% of all invasive breast cancers

▰ 7th decade of life
▰ Small, rarely attain a size 3cm
diameter
▰ Low rate of axillary metastasis
▰ Microscopic: Papillae with
fibrovascular stalks
▰ Nonwhite women
▰ Microscopic: Papillae with fibrovascular
stalks and multilayered epithelium
▰ 87% express estrogen receptor
▰ Low frequency of axillary lymph
node metastases
▰ 5- and 10-year survival
▰ Similar to mucinous and
tubular
● 33% reduction in mortality, 30% increase in
TUBULAR CARCINOMA overall survival
● DISADVANTAGE: young women with
▰ 2% of all invasive breast cancers dense breast
▰ Peri/Early menopausal periods ● Microcalcifications are essentially important
▰ Distant metastases are rare sign of cancer in young women in whom it
▰ Micro: Haphazard array of small, may be only mammographic abnormality.
randomly arranged tubular elements
IRADS BIRADS

INVASIVE LOBULAR CARCINOMA

▰ 10% of breast cancers

▰ Multifocal, multicentric, bilateral
▰ Grows insidiously with subtle
mammographic features
▰ Absence of e-cadherin as diagnostic
biomarker
▰ Micro:
▰ Small cells arranged in single
file orientations (Indian file
configuration)
▰ Intracytoplasmic mucin that
may displace the nucleus
(Signet ring cell carcinoma)

DUCTOGRAPHY

▰ Primary indication: nipple discharge,

particularly when the fluid contains blood
▰ Radioopaque contrast media +
mammography
▰ Intraducatal papillomas: seen as small filling
defects
▰ Cancers
▻ Irregular masses
▻ Multiple intraluminal filling defects
ULTRASONNOGRAPHY
▰ 2nd to mammography
▰ Resolve equivocal findings, define cystic
masses, demonstrate echogenic qualities
▰ Used to guide fine-needle aspiration biopsy,
core- needle biopsy, and needle localization
of breast lesions
▰ Cysts: well-circumscribed, smooth margins,
echo free
▰ Benign mass: smooth contours, round or
oval, weak internal echoes, well-defined
anterior and posterior margins
▰ Cancer: irregular walls, smooth margins
with acoustic enhancement
MRI
▰ MRI Screening: recommended in women
with BRCA mutations
▰ Assess response to therapy in the setting of
neoadjuvant systemic treatment
▰ Evaluation of the treated breast for tumor
recurrence
▰ Early age screening with known strong
family history of breast cancer or carry
genetic mutations
▰ Study of contralateral breast
▰ MRI has been advocated by some for
routine in surgical treatment planning based
on the fact that additional disease can be
identified with this advanced imaging
modality and the extent of disease may be
more accurately assessed.
▰ More sensitive than mammography* In
detecting residual disease, occult invasive
breast cancers, multicentric lesions
▰ MRI examination revealing contralateral
breast cancer in a patient diagnosed with
unilateral breast cancer on mammography.
● Image-guided breast biopsy specimens are
frequently required to diagnose nonpalpable
lesions
● The combination of diagnostic
mammography, ultrasound or stereotactic
localization, and fine-needle aspiration
(FNA) biopsy achieves almost 100%
accuracy in the preoperative diagnosis of
breast cancer.
● FNA biopsy permits cytologic evaluation,
core-needle permits the analysis of breast
tissue architecture and allows the
pathologist to determine whether invasive
cancer is present
● Core-needle biopsy is preferred over open
biopsy for nonpalpable breast
● Palpable:
FNA or core biopsy of a palpable breast mass
can usually be performed in an outpatient
setting.
When a breast mass is clinically and
mammographically suspicious, the sensitivity
and specificity of FNA biopsy approaches
100%.
BREAST CANCER STAGING AND
BIOMARKERS
▰ Clinical staging
▰ Pathologic staging
▻ Makes use of TNM status
▰ Parameters:
▻ TNM status
▻ Grade of tumor
▻ Biomarkers (ER PR HER2/neu
status)
● A high Ki-67 level reflects rapidly dividing
tumor cells, althought there is no universal
cut off for measuring Ki- 67 levels.
● According to the ER/PR and HER 2 status
with additional information about Ki-67, 8th
edition identifies four subtypes:
○ Luminal A: HR positive, Her 2
negative, low Ki-67
 ○ Luminal B: HR positive, Her 2
negative, high Ki-67
○ Her 2: Her positive regardless of the
hormone receptor status
○ Basal: both hR and HER negative
○ Luminal A: has best prognosis with
excellent response to endocrine
therapies
○ Luminal B: less responsive to
endocrine therapies and has
WORSE prognosis than luminal A
○ HEr2 type responds to her2
targeting agents and proper
treatment improves prognosis
○ Basal type: triple negative has worst
prognosis
AJCC Anatomic Stage groups
● Both LCIS and DCIS may be difficult to
distinguish from atypical hyperplasia or from
cancers with early invasion
● Bilateral mammography is performed to
determine the extent of the in situ cancer
and to exclude a second cancer.
● Because LCIS is considered a marker for
increased risk rather than an inevitable
precursor of invasive disease, the current
treatment options for LCIS include
observation, chemoprevention, (Tamoxifen)
● and bilateral total mastectomy.
● The goal of treatment is to prevent or detect
at an early stage the invasive cancer that
subsequently develops in 25% to 35% of
these women.
● DCIS and extensive disease
○ >4cm disease or disease
more than 1 quadrant
○ Mastectomy
● Limited disease
○ Lumpectomy and radiation
therapy
EARLY INVASIVE BREAST CANCER
▰ STAGE I, IIa, IIb
▻ Lumpectomy and radiation
▻ Mastectomy with axillary staging and
BCS
▻ Adjuvant chemotherapy
▻ Adjuvant endocrine therapy
▰ NSABP B-06, which is the largest of all the
breast conservation trials, compared total
mastectomy to lumpectomy with or without
radiation therapy in the treatment of women
with stage I and II breast cancer.
▰ After 5- and 8-year follow-up periods, the
disease-free (DFS), distant disease-free,
and overall survival (OS) rates for
lumpectomy with or without radiation
therapy were similar to those observed after
total mastectomy.
▰ However, the incidence of ipsilateral breast
cancer recurrence was higher in the group
not receiving radiation therapy. These
findings supported the use of lumpectomy
and radiation therapy in the treatment of
stage I and II breast cancer and this has
since become the preferred method of
treatment for women with early stage breast
cancer who have unifocal disease and who
are not known BRCA mutation carriers.
▰ Currently, mastectomy with axillary staging
and breast conserving surgery with axillary
staging and radiation therapy are
considered equivalent treatments for
patients with stage I and II breast cancer.
Breast conservation is considered for all
patients because of the important cosmetic
advantages and equivalent survival
outcomes, however, this approach is not
advised in women who are known BRCA
mutation carriers due to the high lifetime risk
for development of additional breast
cancers.
▰ Relative contraindications to breast
conservation therapy include (a) prior
radiation therapy to the breast or chest wall,
(b) persistently positive surgical margins
after reexcision, (c) multicentric disease,
and (d) scleroderma or lupus
erythematosus.
▰ In cases where there is axillary
lymphadenopathy or metastatic disease
noted in a sentinel axillary lymph node 🡪
dissection
▰ Adjuvant chemo
▻ Node-postive cancer, all cancers
greater than 1cm in szie,
▻ Node degative cancer > 0.5cm
▻ Adverse prognostic factors include
blood vessel or lymph vessel
invasion, high nuclear grade, high
histologicgrade, HER-2/neu
overexpression or amplification, and
negative hormone receptor status
▰ Adjuvant endocrine
▻ Tamoxifen or aromatase inhibor
▻ Homronr receptor positve women
grewater than 1 cm
▰ Adjuvant chemotherapy for patients with
early-stage invasive breast cancer is
considered for patients with node-positive
cancers, patients with cancers that are >1
cm, and patients with node-negative
cancers of >0.5 cm when adverse
prognostic features are present. Adverse
prognostic factors include blood vessel or
lymph vessel invasion, high nuclear grade,
high histologicgrade, HER-2/neu
overexpression or amplification, and
negative hormone receptor status.
▰ Adjuvant endocrine therapy is considered
for women with hormone receptor-positive
cancers, and use of an aromatase inhibitor
is recommended if the patient is
postmenopausal.
▰ Trastuzumab is the only HER-2/neu–
targeted agent that is currently approved for
use in the adjuvant setting.
STAGE IIIA, IIIB
▰ Advanced locoregional breast cancer
▰ No clinically detected distant metastases
▰ Surgery with radiation therapy and
chemotherapy
Women with stage IIIA and IIIB breast
cancer have advanced local-regional breast
cancer but have no clinically detected
distant metastases
o provide optimal locoregional disease free
survival and distant disease free survival,
surivaal is integrated with radiona therpy ad
chemotherapy
● Surgical therapy for women with stage III
disease is usually a modified radical
mastectomy, followed by adjuvant radiation
therapy. Chemotherapy is used to maximize
distant disease-free survival, whereas
radiation therapy is used to maximize local-
regional control and disease-free survival. In
selected patients with stage IIIA cancer,
preoperative chemotherapy can reduce the
size of the primary cancer and permit
breast-conserving surgery.
STAGE IV
▰ Not curative, prolong survival and enhance
QOL
▰ Hormone therapy
▰ Systemic chemotherapy
Not directed in curing the disease but
prolonging survival and enhacing quality of
life
Candidates for hormone therapy
Systemic chemotherapy is indicated for
● The 5-year relative survival by race was
reported to be
○ 90.4% for white women
○ and 78.7% for black women
● The 5-year survival rate for
patients with
○ localized disease is 98.6%;
○ for patients with regional
disease is 84.4%;
○ and for patients with distant
metastatic disease is 24.3%
SURGICAL TECHNIQUES
 ● SLN is the first site of drainage from the ◦ Lateral: anterior margin of the
lymphatic vessels of the primary tumor
● Assess the regional lymph- early breast Type of Description
cancers , clinically node negative by Mastectomy
physical examination and imaging studies.
● SLN dissection has also been reported to Simple (or -Most common type of mastectomy to
be accurate for staging of the axilla after total) treat breast cancer
Mastectomy
chemotherapy in women with clinically
node-negative disease at initial -Removal of entire breast, including
presentation the nipple and the areola
● On the day before surgery, or the day of
surgery, the radioactive colloid is injected -Does not remove axillary lymph
either in the breast parenchyma around the nodes or muscle tissue
primary tumor or prior biopsy site, into the Modified -Preserves the PECTORALIS MAJOR
subareolar region, or subdermally in Radical muscle with removal of axillary lymph
proximity to the primary tumor site. Mastectomy nodes
BREAST CONSERVATION -Combines a simple mastectomy+
removal of axillary LN (Axillary LN
❑ Resection of the primary breast cancer dissection)
❑ Segmental mastectomy, lumpectomy,
partial mastectomy, wide local excision -Common subtypes
❑ Currently the standard treatment for women
with stage 0, I, or II invasive breast cancer. 1. Patey: removes the pectoralis
❑ Addition of radiation reduces recurrence by minor to allow complete dissection of
half and improves survival LN (I, II, III)

SURGICAL TECHNIQUES: MRM 2. Madden and Auchincloss-

preserves the pectoralis minor with
▪ Preserves the pectoralis major muscle with dissection of axillary LN levels I and II
removal of level I, II, and III (apical) axillary
lymph nodes. 3. Scanlon- transects the pectoralis
minor m. for complete axillary LN
▪ Preservation of the medial (anterior
dissection (I, II, III) followed by repair
thoracic) pectoral nerve
of the transected m.
▪ Anatomic boundaries
latissimus dorsi muscle
◦ Medial: the midline of the sternum
◦ Superior: the subclavius muscle
◦ Inferior: the caudal extension of the
breast 2 to 3 cm inferior to the
inframammary fold

● Seromas beneath the skin flaps or in the

axilla represent the most frequent
complication of mastectomy and axillary
lymph node dissection
● The use of closed-system suction
drainage reduces the incidence of this
complication.
● Catheters are retained in the wound until
drainage diminishes to <30 mL per day

Type of Description
Mastectomy
 Radical -Removes entire breast,
(Halsted) axillary lymph nodes, and both
Mastectomy pectoral muscles
Skin-sparing -Removes all the breast
mastectomy tissue, the nipple areola
complex (NAC), and the skin
overlying a previous biopsy
site
-Most of the skin over the
breast (other than the nipple)
is left intact
-May not be suitable for large
tumors
Nipple sparing -Combines a skin sparing
mastectomy mastectomy with preservation
of NAC, intraoperative
pathological assessment of
the nipple tissue core, and
immediate reconstruction
-Permits better cosmesis for
patients undergoing total
mastectomy
RARE BREAS CANCER
1. Squamous Cell (epidermoid)
Carcinoma
◦ from metaplasia within the duct
system
◦ devoid of distinctive clinical or
radiographic characteristics.
2. Adenoid cystic Carcinoma
◦ <0.1% of all breast cancers
◦ 1 to 3 cm in diameter at presentation
and are well circumscribe
3. Apocrine Carcinoma
◦ rounded vesicular nuclei and
prominent nucleoli
◦ very low mitotic rate and little
variation in cellular features,
aggressive growth pattern.
4. Sarcomas
◦ large, painless breast mass with
rapid growth
◦ Primary treatment is wide local
excision, which may necessitate
mastectomy
5. Lymphomas
◦ One type occurs in women ≤39
years of age, is frequently bilateral,
and has the histologic features of
Burkitt’s lymphoma
BREAST CANCER DURING PREGNANCY

PATHOPHYSIOLOGY CLINICAL DIAGNOSIS MANAGEMENT

PRESENTATION

• 3% of breast • Pathological • Ultrasound: • Surgery:

cancers lymph node • Mammography
• Average age - 34 involvement with abdominal i. Mastectomy is usually
years old (56-57%) shielding can be the 1st treatment
• Most are invasive • Large tumors performed: ii. Mastectomy, breast-
ductal carcinomas • Lymphovascular • Core-needle conserving surgery, and
• Most are ER- invasion biopsy: axillary surgery can all
negative recommended be performed safely
form of biopsy with no unexpected
complications

• Chemotherapy

i. Avoided during 1st

trimester (risk of
abortion, malformation,
death)

PHYLLOIDES

PATHOPHYSIOLOGY CLINICAL DIAGNOSIS MANAGEMENT

PRESENTATION
• Composed of • Enlarged, tense, • No • Surgery:
epithelial component congested breast pathognomonic
and cellular, spindle with surface mammographic I. Wide local excision
cell stroma forming a ulceration or ultrasound with clear margins
leaf-like structure • Mobile and firm features (1-2cm)
• Classified into in consistency, • Core needle or II. Mastectomy:
benign, borderline, and well- open biopsy recommended for
and malignant delineated from large tumor >10cm,
histotypes the rest of the multiple recurrent
• 15-30% are breast tumors, tumors of
malignant >10cm in a patient
with small breast
III. No need for axillary
dissection

• Radiation
therapy:

i. If free margins is
not obtainable
PEDIATRIC SURGERY
GENERAL CONSIDERATIONS
a. Fluid and electrolytes
● Infant’s physiologic day: 8 hours
● Total body water:
○ 12 weeks AOG: 94cc/kg
○ Full term: 80cc/kg
○ 1 yearoflife 60-65cc/kg
● Normal daily maintenance fluid
○ 100mL/kg for the first 10 kg, plus
50 mL/kg for 11 to 20 kg, plus 25
mL/kg for each additional
kilogram of body weight
thereafter
● Sodium requirements - 2 mEq/kg per
day in term infants and up to 5 mEq/kg
per day in critically ill preterm infants as
a consequence of salt wasting.
● Potassium requirements - 1 to 2 mEq/kg
per day.
Acid-base equilibrium
● Metabolic acidosis
○ inadequate tissue perfusion
○ intestinal ischemia from
necrotizing enterocolitis (in the
neonate), midgut volvulus, or
incarcerated hernia.
○ chronic bicarbonate loss from the
gastrointestinal tract or acid
accumulation as in chronic renal
failure
● Respiratory acidosis
○ Hypoventilation
● Respiratory Alkalosis
○ Hyperventilation
● Metabolic Alkalosis
○ Gastric acid losses (pyloric
stenosis), Aggressive diuretic
therapy
Blood volume and blood replacement
● Hemoglobin transfusion trigger: 70g/L
○ Higher threshold for symptomatic
anemia or impaired
cardiorespiratory function
● Transfusion requirements: 10ml/kg
increments
● Consideration for the administration of
10mg/Kg of packed RBC as soon as
possible if the child’s perfusion is
inadequate despite administration of 2-3
boluses of 20ml/kg of isotonic
crystalloid.
Coagulation deficiencies: after extensive
blood transfusion (more than 30ml/Kg)
Plasma: 10-20ml/kg
Platelet: 1 unit/5kg
● Furosemide: 1 mg/kg may help facilitate
excretion of extra fluid load
● Massive transfusion protocol: pediatric
patients who have lost greater than
30mL/Kg, with ongoing bleeding
○ 1:1:1 of RBC’s, plasma and
platelets
Parenteral alimentation
● Prolonged parenteral nutrition is
delivered via a central venous catheter
● Should include copper, zinc and iron
● Major complication: parenteral nutrition-
associated cholestasis which can
progress to liver failure
○ Prevention: concomitant enteral
feedings
cholestasis eventually resolevs in most cases
after parenteral nutrition is discontinued
Venous access
● Should be placed in the least invasive,
least risky, and least painful manner,
and in a location that is most accessible
and allows for use of the catheter
without complications for as long as it is
needed
○ Antecubital fossa, external
jugular vein, facial vein, or
proximal saphenous vein
○ Infants over 3kg and in older
children: subclavian, internal
jugular, or femoral veins are
 accessed using the Seldinger
technique.
Thermoregulation
● Infants and children are thermolabile
● Premature infants: unable to shiver and
lack stores of fat
● In the operating room: keep the infant
warm by the use of heating lamps,
heating blanket, warming of inpired
gases and coverage of extremities and
head with occlusive materials
● Constant monitoring of the temperature
in a lengthy procedure
● Hypothermia: cardiac arhythmias and
coagulopathy
Pain control
● All children including neonates
experience pain
● Pain management options:
○ General anesthesia, IV pain
meds, topical anesthetic
ointment (EMLA cream), regional
anesthesia such as caudal blocks
and epidural or incisional catheter
infusions
Pain control should be collaborative with
anesthesiologists with expertise in pain
management
NECK MASSES
Lymphadenopathy
● Enlarged tender lymph nodes: bacterial
infection (staph or strep)
○ Treatment of the primary cause
(eg. otitis media or pharyngitis)
with antibiotics
○ Fluctuant nodes: incision and
drainage
● Chronic forms of lymphadenitis: atypical
mycobacteria, cat-scratch fever,
infectious mononucleosis are diagnosed
based on serology
● Excisional biopsy: nodes that are firm,
fixed, presence of nodes in the axilla
and groin or history suggestive of
lymphoma
Thyroglossal duct remnants
● Pathology and clinical manifestation
○ Thyroid gland buds off the foregut
diverticulum in the region of the
foramen cecum at 3 weeks of
embryonic life and descends until
it rests in its normal position
○ Residual thyroid tissue during the
descent: midline of the neck as
thyroglossal duct cyst (at or
below the hyoid bone)
○ Most are asymptomatic
○ Rarely: malignant degeneration
● Treatment
○ Abscess: incision and drainage
then antibiotics
○ Sistrunk procedure following
resolution of inflammation: 90%
curative
○ Recurrence:
■ >2 infections prior to
surgery, age under 2
years, and inadequate
initial operation
Branchial cleft anomalies
● Paired branchial clefts and arches
develop early in the fourth gestational
week
● Branchial cleft sinus: drainage of clear
fluid from the anterior border of the
lower third of the SCM
Treatment
● Complete excision of the cyst and sinus
● Abscess: incision and drainage,
antibiotics, excision
Lymphatic Malformation (cystic
hygroma/lymphangioma)
● Sequestration or obstruction of
developing lymph vessels (1 in 12,000
births)
● Most common site: posterior triangle of
the neck, axilla, groin and mediastinum
 ● Most present at the age of 2
Treatment
● Image-guided sclerotherapy
● Cyst excision
● unroofing/partial excision with
preservation of adjacent structures
Torticollis
● Lateral neck mass
● With rotation of the head towards the
opposite side of the mass
● Fibrosis of the sternocleidomastoid
muscle with deposition of collagen and
fibroblasts around the atrophied muscle
cells
Treatment
● Physical therapy: passive stretching
● Rarely, surgical transection
RESPIRATORY SYSTEM
Congenital Diaphragmatic hernia
(Bochdalek)
● Incomplete development of the septum
transversum
● Septum tranversum: precursor of the
diaphragm which normally completed
development posterolaterally
● Allows abdominal viscera to fill the chest
cavity:
○ Abdominal cavity is small and
underdeveloped and remain
scaphois after birth
○ Both lungs are hypoplastic, with
decreased bronchial and
pulmonary artery branching
● Immediate respiratory distress
○ Air-filled bowel compresses the
mediastinum
○ Pulmonary hypertension
develops
○ Affected lung becomes
hypoplastic
● Require ventilation and intensive care
● Mortality rate: 50%
Treatment
● Directed towards managing the
pulmonary hypertension
● Low or “gentle” settings of mechanical
ventilator
● paCO2 range 0f 50-60 mmHg or higher
is acceptable as long as the pH remains
>7.25
ECMO (extracorporeal membrane
oxygenation)
● Maintained until pulmonary hypertension
is resolved and lung function is
improved
● (within 7-10 days)
Criteria for ECMO
● normal cardiac anatomy
● absence of fatal chromosome anomalies
● expectation that the infant would die
without ECMO
Operative repair of the diaphragmatic hernia
may be accomplished either by an abdominal
or transthoracic approach and can be
performed either via open or minimally invasive
techniques.
Then post operatively, All infants are ventilated
to maintain preductal arterial oxygenation of 80
to 100 torr and Very slow weaning from the
ventilator is necessary to avoid recurrent
pulmonary hypertension.
Congenital Lobar Emphysema
● Progressive hyperexpansion of one or
more lobes of the lung
● Hyperexpansion: shifts the mediastinum
to the opposite side and compromises
the other lung.
● Cause: poor bronchial cartilage
development
Diagnosis
● Chest x-ray
 ○ Hyperlucent affected lobe with
adjacent lobar compression and
atelectasis

Treatment

● Resection of the affected lobe (several

months of age) The five major varieties of esophageal atresia
● Prognosis: excellent and tracheoesophageal fistula.

Bronchiectasis The most commonly seen: esophageal atresia

with distal tracheoesophageal fistula which
● Irreversible dilatation of the bronchi and would be the type C, which occurs in
bronchioles approximately 85% of the cases in most series.
The next most frequent is pure esophageal
Diagnosis atresia or type A, occurring in 8% to 10% of
patients, followed by tracheoesophageal fistula
● chest x-ray, chest CT without esophageal atresia or the type E. This
occurs in 8% of cases and is also referred to as
Treatment an H-type fistula. Esophageal atresia with
fistula between both proximal and distal ends of
● Antibiotics the esophagus and trachea or the type D is seen
● Postural drainiage in approximately 2% of cases, and type B,
● Bronchodilator esophageal atresia with tracheoesophageal
● Lobectomy or segmental resection fistula between distal esophagus and trachea, is
● Foreign Bodies seen in approximately 1% of all cases.
● Airway ingestion
● Most common aspirated: peanut Esophageal atresia and tracheoesophageal
● Most common location: right main fistula
stem bronchus
● Chest X-ray: radiopaque foreign body, Clinical presentation:
hyperexpansion of the affected lobe on Esophageal ends either as a blind pouch or
an expiratory film or fluoroscopy. fistula
Excessive drooling
Treatment: Rigid bronchoscopy Choking
Coughing
Epinephrine: minimizes bleeding Abdominal distention
Pulmonary dysfunction
ESOPHAGUS Pneumonitis

Esophageal atresia and tracheoesophageal Diagnosis:

fistula
4 weeks AOG: diverticulum forms off the
anterior aspect of the proximal foregut which
extends caudally creating a separate trachea
and esophagus
Variaties of EA and TEF
Esophageal fistula:
Inability to pass orogastric tube
Contrast study: confirms diagnosis of EA and
occasionally document TEF
Tracheo-esophageal fistula:
Air in the gastrointestinal tract
Plain abdominal radiograph

Associated congenital anomalies:

VACTERRL syndrome
Cardiac defects: 38%
Skeletal defects: 19%
Neurological defects: 15%
Renal defects: 15%
Anorectal defects: 8%
Other abnormalities: 13%
Initial management:
Attention to the respiratory status
Decompression of the upper pouch
Appropriate timing of surgery
Search for other defects
Head elevated at 30 degrees
Sump catheter is placed on the upper pouch
IV antibiotics, warm electrolytes
Definitive management:
Rarely a surgical emergency
Definitive repair: 1 to 2 days after birth
Primary surgical correction:
Primary esophagoesophagostomy
Posterolateral thoracotomy: Retropleural
approach to widespread contamination of the
thorax
Corrosive injury of the esophagus
Most common: toddlers
Strong acids: coagulative necrosis
Strong alkali: liquefactive necrosis
Strictures occur at the anatomic narrowed
areas: cricopharyngeus, midesophagus, and
gastroesophageal junction
Extent of injury
Circumferential injuries with necrosis:
stricture formation
Management
Gastrostomy tube insertion, dilatation after 3-4
weeks
Esophageal replacement: for severe stricture,
failed dilatation
Gastroesophageal reflux
Diagnosis:
Barium swallow: obstruction of the stomach
or duodenum, malrotation
24-hr pH probe: most accurate in determining
the presence of GERD
Esophageal endoscopy with biopsy:
determine presence of esophagitis, presence
of Barett’s esophagus
Treatment:
Conservative: thickening the formula
Medical therapy: gastric acid reduction by H2
blockers/proton pump inhibitors
Surgical management:
Nasojejunal/gastrojejunal tubes:
stomach is bypassed
Fundoplication: definitive treatment
GASTROINTESTONAL TRACT
Hypertrophic pyloric stenosis (HPS)
Clinical presentation:
Non-bilious projectile vomiting
Complete gastric outlet obstruction:
unsuccessful feeds, dehydration
Hypochloremic, hypokalemic metabolic
alkalosis
Diagnosis:
Physical examination: palpation of “olive” like
structure, visible gastric waves
Ultrasound: 95% accuracy
Criteria: Criteria for US diagnosis include a
channel length of over 16 mm and pyloric
thickness over 4 mm
Treatment:
Never a surgical emergency
Fluid resuscitation
Electrolyte and metabolic alkalosis correction
Fredet-Ramstedt pyloromyotomy
Intestinal obstruction in the newborn
Clinical presentation:
Cardinal symptom: Bilious emesis
Proximal intestinal obstruction: bilious emesis
and minimal abdominal distention
Distal abdominal distention: bilious emesis with
abdominal distention
Duodenal obstruction:
Clinical presentation
Bilious vomiting: entry of bile duct is proximal
to the level of obstruction in 85% on infants
Diagnosis:
Abdominal Surgical correction of the small intestinal
radiograph: atresia should be performed relatively urgently,
“double- especially when there is a possibility of
bubble” sign volvulus.
Contrast
upper GI At laparotomy, one of several types of atresia
series will be encountered. In type 1 there is a
Treatment: mucosal atresia with intact muscularis. In type
Orogastric 2, the atretric ends are connected by a fibrous
tube: band. In type 3A, the two ends of the atresia
are separated by a V-shaped defect in the
mesentery. Type 3B is an “apple-peel”
decompression deformity or “Christmas tree” deformity in which
IV fluids: adequate urine output the bowel distal to the atresia receives its blood
Surgery: for suspected malrotation and midgut supply in a retrograde fashion from the ileocolic
volvulus or right colic artery. In type 4 atresia, there are
multiple atresias with a “string of sausage” or
Duodenoduodenostomy: duodenal stenosis “string of beads” appearance.
or atresia, annular pancreas
During surgery, there will be a disparity in
Intestinal atresia lumen size between the proximal distended
Occur anywhere at any point of the intestinal bowel and the small diameter of collapsed
tract bowel distal to the atresia and this has led to a
Clinical presentation: number of innovative techniques of
Bilious vomiting and pregressive abdominal anastomosis. However, under most
distention circumstances, an anastomosis can be
performed using the end-to-back technique.

Malrotation and midgut volvulus

Embryology

6th week AOG: herniation of the midgut into

the umbilical cord

10th to 12th week: midgut returns to the

abdominal cavity. 270 degress
counterclockwise rotation around the SMA

Duodenum: acquires C-loop during rotation

BCL6 mutation: absence of left-sided

expression of its transcript lead to
Diagnosis:
Physical examination malrotation, reversed cardia orientation and
Plain abdominal radiographs defective ocular development
Barium enema: if with diagnostic uncertainty
Treatment: Incomplete rotation: cecum remains in the
epigastrium but the bands fixing
Emergency laparotomy
the duodenum to the retroperitoneum and
Anastomosis: end-to-back technique cecum continue to form
Ladd’s bands: extend from the cecum to the
lateral abdominal wall crossing the duodenum,
creating potential for obstruction.

Mesenteric takeoff: confined to the

epigastium.
Results to a narrow pedicle suspending
all the branches of the SMA and entire
midgut.
Volvulus: occur around the mesentery.
Cuts off the blood suply to the midgut

Prognosis: excellent

With early detection and correction

Diagnostic delay: mortality or short gut

syndrome
Presentation and management
Bilious vomiting Meconium ileus
Bloody stools
Eryhtema and edema of the abdominal wall Pathogenesis and clinical presentation

Radiograph: Cystic Fibrosis >abnormal chloride secretion

paucity of gas in the intestines > water-poor meconium
with few
Due to mutations in CFTR gene
scattered air-
fluid levels The diagnosis of
meconium ileus
#early surgical is confirmed by a
intervention is con-trast enema
mandatory that typically
demonstrates a
when volvulus is microcolon as
suspected demonstrated in
the image
Volvulus is reversed

“Turn back the hands of time”

Management
Ladd’s procedure - This operation does not Uncomplicated meconium ileus: non-
correct the malrotation, but it does broaden the operative
narrow mesenteric pedicle to prevent volvulus Dilute water-soluble contrast
from recurring. N-acetyl cysteine
Absorption of fluid from bowel wall into the Inotropes
intestinal lumen: risk for fluid and electrolyte Intubation and mechvent
imbalance TPN
Enema repeated every 12 hrs for several days
Management Intussusception
Complicated meconium ileus: exploratory Leading cause of intestinal obstruction
laparotomy in pediatric patients
Operative irrigation Usually terminal ileum extending distally
Resection and ileostomy with mucus fistula to the ascending, transverse, descending
or rectum
Necrotizing Enterocolitis
Clinical features
Mortality rate: 10-50%
Risk factors:
Prematurity
Inititation of enteral feeding
Bacterial infection
Intestinal ischemia (birth asphyxia, umbilical
artery cannulation, persistence of a patent
ductus arteriosus, cyanotic heart disease,
maternal cocaine abuse)
Pathogenesis: Pathogenesis
Indigenous intestinal microbial flora Hypertrophy of the peyer’s patches in the
Usually occurs 10 days postnatally terminal ileum
(colonization by coliforms) Invagination of terminal ileum into adjacent
Common bacterial isolates:Escherichia coli, distal bowel
Enterobacter, Klebsiella, and occasionally, Occurs in 6-24 months of age: beyond this
coagulase-negative Staphylococcus species age, a pathologic lead point must be
Activation of the TLR4 (toll-like receptor 4) considered
activation by colonizing bacteria leads to NEC
Clinical features Pathologic lead points
Involves single or multiple segments (MC: Polyps
terminal ileum) Malignant tumors (lymphoma)
Gross findings: Enteric duplication cysts
Distention with patchy areas of thinning, Meckel’s diverticulum
pneumatosis, gangrene, or frank perforation.
Microscopic: full thickness necrosis Clinical manifestations
Crampy abdominal pain and intermittent
Clinical manifestation vomiting, normal in between attacks
Bell’s stage I: feeding intolerance (presence of Currant jelly stools
large residual volume from a previous feeding) Without intervention: gangrene and perforation
Bell’s stage II: not immediate life-threatening may ensue
NEC Elongated mass in the right upper quadrant or
Abdominal distention and tenderness, bilious epigastrium. Absence of bowel in the right
nasogastric aspirate, bloody stools lower quadrant (Dance’s sign)
Bell’s stage III: advance form of NEC
Presence of pneumoperitoneum Treatment
Assess for peritonitis
Treatment Resuscitation and IV antibiotics
Feeding discontinued Asses for radiographic vs surgical reduction
NGT
Antibiotics Treatment
Pneumatic reduction/air enema: should ot
exceed >120mmHg
Successful if with free reflux of air into multiple
loops of small bowels and with symptomatic
improvement.
Unsuccessful: may do repeat attempt after a
few hours
Hydrostatic reduction may be useful
Treatment
Pneumatic reduction/air enema:
Overall success rate: 60-90%
Open surgery
Right lower quadrant incision
Reduction: gentle distal pressure
(intussusceptum is milked out of the
Intussuscepiens
Appendectomy
Recurrence: 5-10%
Repeat enema is usually successful
3 or more episodes of intussusception:
pathologic lead point must be considered
After 3rd episode: exploratory laparotomy
Appendicitis
Presentation
Children: atypical presentation
<5 y/o: unable to describe the location and
quality of their pain leading to diagnostic delay
Higher tendency for perforation
Diagnosis
Clinical
Boys: prompt exploration if with localized right
lower quadrant tenderness with associated
fever and leukocytosis
Girls: ovarian or uterine pathology must be
considered
Diagnostic laparoscopy: negative ultrasound
findings
Diagnostic uncertainty: child may be observed,
hydrated, and reassesed
Surgical treatment
IV fluids
IV antibiotics
open/laparoscopic surgery
Surgical treatment of perforated appendix
Surgery through open/laparoscopic approach
Adhesions lysed, abscess cavities are
drained, appendix is removed
<4-5 years old: do not localize or isolate
inflammatory process
Require early surgical intervention
Meckel’s diverticulum
Remnant of a portion of the vitelline duct
Location: 2 feet from the ileocecal valve,
Antimesenteric border
Perforation: impaction of food
Treatment
Narrow base with no mass: wedge resection,
transverse closure of the ileum
Broad base, palbable ectopic tissue, wide
base, inflamed: resection with end-to-end
ileoileostomy
Hirschprung’s disease
Pathogensis:
Absence of ganglion cells in auerbach’s plexus
and hypertrophy of associated nerve trunks
Defect in the migration of neural crest cells
Normally: migration is from cephalad to caudal
(completed at 12 weeks)
Migration of midtransverse colon to anus takes
4 weeks (vulnerable to defects in migration)
Pathogensis:
Mutations in several genes: GDNF, its and removed down to the anus
receptor Ret, or its co-receptor Gfra-1 Ganglionic colon is anastomosed to
>Chemoattractive for neural crest cells the anus via a perineal approach
Clinical presentation C. Soave
1 in 5000 live births Dissection entirely within the rectum
Aganglionic colon: does not permit normal Rectal mucosa is stripped from the
peristalsis muscular sleeve
Children: Functional distal intestinal obstruction Ganglionic colon is brought through
Newborn: abdominal distention, failure to pass the sleeve and anastomosed to the
meconium, bilious emesis anus
Clinical presentation Main complications
Dehydration Enterocolitis
Leukocytosis Constipation
Increase in circulating band forms Anastomotic stricture
Forceful expulsion of feces Recurrent hirschprung’s disease
Treatment: rehydration, systemic antibiotics, Long term results
nasogastric decompression, rectal irrigations Excellent
No response: decompressive stoma Anorectal malformations
Diagnosis: Imperforate anus
Contrast enema: demonstrate location Persistent cloaca
of the transition Occurs approximately in 1 in 5000 live births
zone between males=females
the dilated Pathogenesis:
ganglionic Failure of descent of the rectum through the
colon and the external sphincter complex
distal Rectal pouch ends blindly in the pelvis
constricted Communicates more distally with the
aganglionic genitourinary system or the perineum through a
rectal segment fistula
Diagnosis: Anatomic description:
Rectal biopsy High: above the levator ani muscle complex
(samples of Males: fistula into the membranous
mucosa and fistula
submucosa females : Persistent cloaca
2cm, 2cm and Low: below the levator ani muscle complex
3cm from Males and females: fistula to the
dentate line) perineum
Histopathology: Classification propsed by Pena
Absence of ganglion cells Males:
Increased acetylcholinesterase staining Cutaneous perineal fistula
Presence of hypertrophied bundles Rectourethral bulbar fistula
Treatment: Rectourethral prostatic fistula
Surgical approach (multiple stage procedure) Rectovecsicular fistula
Colostomy Females:
Definitive pull-through Cutaneous perineal fistula
A. Duhamel Vestibula fistula
Dissection confined to the MC: urinary tract defect: 50%
retrorectal space Skeletal defects: sacrum
Ganglionic colon is anstomosed Spinal cord: tethered cord
posteriorly just above the anus Gastrointestinal: esophageal atresia
B. Swenson Cardiac:
Rectum is dissected in the pelvis VACTERLL syndrome
Management: Acholic stools
Diagnosis of the type of defect Progressive failure to thrive
Evaluating the associated anomalies Stigmata of liver failure and portal hypertension
Orogastric tube placement (splenomegaly and esophgeal varices)
Monitor for appearance of meconium (in or Diagnosis
around perineum, urine) Serum bilirubin
Surgical Management: TORCH infection titers and viral hepatitis
Low lesions: perineal operation Ultrasound: choledochal cyst, absence of
High lesions: gallbladder
Colostomy (newborn) Non-dilated intrahepatic bile ducts
Pull through (2 months) Percutaneous liver biopsy
Persistent cloaca: *when these tests point to or cannot exclude
Evaluation of the urinary tract the diagnosis of biliary atresia, surgical
Colostomy exploration is warranted
Determine need for vesicostomy Inspissated bile syndrome
Surgical Management: Persistent obstructive jaundice with normal
Pull through biliary tracts
Posterior sagittal anorectoplasty (PSARP Increased viscosity of bile and obstruction and
procedure) obstruction of the canaliculi
Patient placed in prone Parenteral nutrition
jack-knife position Hemolysis
JAUNDICE Cystic fibrosis
Approach to the jaundiced infant No etiologic factor
Present in the first week of life Treatment
Term: 60% If diagnosis of biliary atresia is confirmed
Preterm: 80% intraoperatively, surgical treatment is
Newborns: high level of circulating undertaken at the same setting
hemoglobin, relative immaturity of the 1st line: hepatoportoenterostomy
conjugating machinery Promote bile flow into the intestine
Transient accumulation of bilirubin in Treatment
tissues Kasai’s procedure
Physiologic jaundice Transection of fibrous tissue in
Evident by the 2nd to 3rd day of life the porta hepatis
Resolves within approximately 5-7 days Construction of intestinal conduit
Pathologic jaundice (roux-en-y of jejunum)
Persist beyond 2 weeks Liver biopsy
Biliary obstruction, increase hemoglobin load, Kasai’s procedure
liver dysfunction <60 days of life: more likely to achieve
Biliary atresia success and long term biliary drainage
Pathogenesis >12 weeks: less favorable
Fibroproliferative obliteration of the biliary tree Still reasonable to proceed with surgery
Progress to hepatic fibrosis, cirrhosis, end- as alternative is certain liver failure
stage liver failure Choledocal cyst
Incidence: 1 in 8,000 to 1 in 18,000 Classification
Pathogenesis Type 1: fusiform (MC)
Proposed theories Type II: isolated diverticulum
Defects on hepatogenesis, prenatal Type III: choledochoceles
vasculogenesis, immune disregulation, Type IVa: multiple intra and
infectious agents, exposure to toxins extrahepatic dilatations
Recent: genetic mutation in the CfC1 gene Type IVb: multiple extrahepatic
Clinical manifestation Dilatations
Jaundice at birth Type V: multiple intrahepatics
(Caroli’s disease) Generally: asymptomatic
Incarceration: abdominal pain, bilious emesis,
tender hard mass protruding from the umbilicus
Mandates immediate exploration and repair of
hernia
Asymptomatic child: surgical correction is
delayed until 5 years
Repair of uncomplicated umbilical hernia
Outpatient procedure
Curved incision into the crease of the umbilicus
Repair of the fascial defect (interrupted sutures
in a transverse plane)
Skin closure
“Common channel” Postoperative recovery: uneventful
Weakening of the bile wall by gradual Recurrence: rare
enzymatic destruction Patent urachus
Leads to dilatation, inflammation, cyst Persistence of the tract between the abdominal
formation wall and urinary bladder
Clinical presentation Presentation:
females>males (4:1) Moisture or urine flow from the umbilicus
Classic symptom traid Recurrent urinary tract infection
Abdominal pain Urachal cyst: inflammatory mass inferior to
Mass umbilicus
Jaundice Treatment: drainage of the infected cyst
Newborns: symptoms similar to biliary atresia, Excision: once inflammation is resolved
with abdominal mass Diagnosis:
Diagnosis Umbilical exploration
Abdominal ultrasound - Cystic structure Treatment:
arising from the biliary tree Excision of the urachal tract
CT scan - Confirmatory Closure of the bladder
ERCP Omphalocele
MRCP Presentation:
Treatment Congenital defect of the abdominal wall:
Surgical excision bowel and viscera are covered by peritoneum
Biliary-enteric reconstruction and amniotic membrane
(roux-en-y limb of jejunum) Incidence: 1 in 5000
Prognosis: excellent Associated syndromes:
Complications: Extrophy of the cloaca (vesicointestinal
Anastomotic stricture, cholangitis, fissure)
intrahepatic stone formation Beckwith-weidmann (macroglosia,
DEFORMITIES OF ABDOMINAL WALL macrosomia, hypoglycemia, visceromegaly,
Failure of development omphalocele)
Cephalic fold: sternal defects Cantrell’s pentalogy (lower thoracic wall
Caudal: extrophy of the bladder malformations, ectopia cordis, epigastric
Lateral folds: omphalocele omphalocele, anterior midline diaphragmatic
“Gastroschisis”: intrauterine rupture of a hernia, cardiac anomalies)
hernia of the umbilical cord Treatment:
Umbilical Hernia Immediate : omphalocele should be covered
Failure of umbilical ring to close No pressure should be placed on the
Central defect in the linea alba omphalocele sac (risk of rupture, interferenc
Hernia <1cm: spontaneous closure by with the abdominal venous return)
4-5 years of life Prophylactic broad-spectrum antibiotics
Treatment: Surgical closure: 1-2 weeks
Immediate : omphalocele should be covered Atresia during closure: reduce bowel at 1st
No pressure should be placed on the operation and return after several weeks to
omphalocele sac (risk of rupture, interferenc correct atresia
with the abdominal venous return) Prune-belly syndrome
Prophylactic broad-spectrum antibiotics Presentation:
Treatment: Extremely lax lower abdominal musculature,
Primary repair dilated urinary tract and bilateral undescended
Resection of the omphalocele membrane and testis
closure Pathophysiology: mesodermal arrest
of the fascia Significantly higher incidence in males
Giant omphalocele Comorbidities:
Cannot be closed primarily (inadequate Pulmonary hypoplasia
intraperitoneal Skeletal abnormalities
domain Treatment:
Treatment: Abdominal reconstruction: 6-12 months of age
Primary repair Testis: invariably intraabdominal
Resection of the omphalocele membrane and Bilateral orchidopexy
closure Inguinal hernia
of the fascia Embryology
Giant omphalocele Failure of the closure of the processus
Cannot be closed primarily (inadequate vaginalis: normally closes a few months prior
intraperitoneal to birth (high incidence in premature infants)
domain Treatment
Gastroschisis Incarcerated hernia: reduced with light
Presentation: sedation
Defect in the anterior abdominal wall Gentle application of pressure on the
No overlying ac sac
Size of the defect is usually <4cm Admitted for observation
Located at the junction of the umbilicus and Herniorrhaphy: after 24 hours
normal skin Irreducible/strangulated: emergency surgery
Almost always to the right of the umbilicus Laparotomy and bowel resection
Gastroschisis
Presentation: TRAUMA IN CHILDREN
Associated anomalies: 10% intestinal atresia
Treatment: Injury: leading cause of death > 1yr old
Require urgent surgical treatment
Vigorous fluid resuscitation: 160-190 cc/kg/day Trauma: accounts for more than half of all
Gastroschisis: pediatric deaths
Treatment:
Intestines returned to abdominal cavity and Mechanism of injury:
primary repair is performed
Increased abdominal pressure: may lead to Blunt: most common
compression of the inferior vena cava,
respiratory distress, abdominal compartement Penetrating: gun violence, fall, penetration by
syndrome glass
Measure bladder or airway pressure
during reduction 14-18y/o: contact sports, gun violence, motor
Plastic spring-loaded Silo : for thickened and vehicular accidents
edematous intestines that cannot be reduced
Daily reduction as the edema of the bowels Infants and toddlers: fall
Decrease
Similar with adults Rapid deceleration

1st priority: airway Spleen

Blunt trauma
Child has larger head and shorter neck, Grading of splenic injuries
smaller anterior larynx, floppy epiglottis, short Management is governed by the
trache, large tongue injury grade
Current treatment: non-operative
ET size: (age + 16)/4 approach in most cases
Extended period of bed rest
Breathing

Relief of gastric distention: compromises Extremely restricted activity: 2 weeks

respiration longer than the grade of injury

NGT: placed early during the resuscitation Eg: grade 4 injury: 6 weeks of
restricted activity
Initial management
Exploration: ongoing fluid
Volume depletion requirement/when blood transfusion is
required
20ml/kg: saline or lactated ringer’s
Splenectomy: prophylactic antibiotics and
No response to 3 boluses: blood should be immunization
transfused: 10ml/kg
Liver
Common sites of beeding: chest, abdomen,
pelvis, extremity fractures, large scalp wounds Blunt trauma

Evaluation of injury Non-operative mangement is usually

Abdominal CT scan (IV and oral contrast): successful

ALL cases with significant abdominal
tenderness anda MOI that could cause intra- Associated injuries: more significant
abdominal injury
predictors of outcome
FAST/focused abdominal exam: not widely
accepted in the management of pediatric blunt Criteria for surgery: hemodynamic
abdominal trauma:
instability
Non-operative treatment for most soli-
organ injuries Pediatric GCS

Liver and spleen: most commonly injured Modified from the original
after direct abdominal trauma
glasgow coma scale
Duodenal injuries: blunt trauma
Main difference: Verbal response
Small intestinal injurie: jejunum (ligament of
treitz) Interpretation
>13: mild TBI

9-12: moderate TBI

<8: severe TBI

 PLASTIC SURGERY – BURN
“A burn is defined as damage to the skin and
underlying tissues caused by heat, chemicals,
or electricity. “ - ABA
Initial evaluation of the burned patient should
follow the same initial priorities of all trauma
patients and involves four crucial Assessments
namely..
- With direct thermal injury to the upper airway
or smoke inhalation, rapid and severe airway
edema is potentially lethal. Anticipating the
need for intubation and establishing an early
airway are critical
AIRWAY MANAGEMENT
Signs of Impending Respiratory Compromise:
Adult
• Subjective complaint of Dyspnea
• Hoarseness of Voice
• Wheezing
• Stridor
• Perioral Burns and Singed nasal hairs
Pedia
• Hoarseness of Voice
• Increased work of breathing
• Tachypnea
• Use of accessory muscles or sternal
retractions
“ Burned patients are trauma patients and
evaluated with a primary survey in
accordance with Advanced Trauma Life
Support guidelines”
The Primary survey consists of the following:
1. Airway maintenance with cervical spine
protection : ASSSESSED BY USING
CHIN LIFT OR JAW THRUST
MANEUVER; OR OROPHARYNGEAL
AIRWAY PLACEMENT IF PT IS
UNCONCIOUS
2. Breathing and ventilation : ASSESSED
BY CHEST AUSCULTATION BY
VERIFYING EQUAL BREATH
SOUNDS, RATE AND DEPTH OF
BREATHING AND PRESENCE OF
CIRCUMFERENTIAL FULL-
THICKNESS BURNS ON THE TRUNK
AND NECK
3. Circulation and Cardiac Status with
hemorrhage control : ASSESSED BY
CHECKING BP, PR, AND SKIN COLOR
Associated trauma may also cause internal
bleeding, resulting in tachycardia and
hypotension. Maintain a high index of suspicion
if the injury mechanism suggests possible non-
burn trauma (i.e. fall as a result of the burn
event and motor vehicle crash).
Disability, Neurological Deficit and Gross
Deformity assessment : ASSESSED USING
GCS SCORING
Exposure and Environmental Control:
ASSESSED BY Completely undressing the
patient, Examining for associated injuries and
maintaining a warm Environment.
ESTIMATION OF BURN
The “rule of nines” is a crude but quick and
effective method of estimating burn size .
*It is important to note Superficial or first-
degree burns should not be included when
calculating burn size, and thorough cleaning of
soot and debris is mandatory to avoid confusing
soiled skin with burns.
Just a recap, In adults, the anterior and posterior
trunk each account for 18%, each lower
extremity is 18%, each upper extremity is 9%,
and the head is 9%. In children under 3 years
old, the head accounts for a larger relative
surface area and should be taken into account
when estimating burn size. The head and neck
represent 18% TBSA, twice that of an adult.
Each lower extremity represents 14% TBSA in
the infant.
For scattered, smaller or odd-shaped burns,
the “rule of the palm” where the palmar surface
of the PATIENTS hand, including the digits, is
1% TBSA is useful.
For a more precise and accurate way of
calculating the burned TBSA. We use the LUND
AND BROWDER CHART. The Lund and
Browder chart gives a more accurate
accounting of the true burn size in children and
adults, and it is the one being used in Burn
Centers. It is used by Estimating the % TBSA
burn by the sum of the individual areas
Thermal burns have 3 subtypes: flame, contact
and scald. Flame burns are the most common
cause for hospital admission of burns, and
have the highest mortality. This is primarily
related to their association with structural fires
and the accompanying inhalation injury and/or
CO poisoning.
Electrical burns make up 3% of U.S. hospital
admissions but have special concerns,
including cardiac arrhythmia and
compartment syndrome with concurrent
rhabdomyolysis. A baseline ECG is
recommended in all patients with an electrical
injury, and a normal ECG in a low-voltage
injury (<1000 V) may preclude hospital
admission. Because compartment syndrome
and rhabdomyolysis are common in high-
voltage electrical injuries, vigilance must be
maintained for neurologic or vascular
compromise, and fasciotomies should be
performed even in cases of moderate clinical
suspicion. DC causes a single strong muscle
contraction, often throwing its victim away from
the energy source, while AC causes cont.
muscle contraction, causing the patient to
unable to let go of the source.

*NOTES: Long-term neurologic symptoms

and cataract development are common with
high-voltage electrical injuries, thus neurologic
and ophthalmologic consultation should be
obtained to define baseline patient function.

Chemical burns also comprise 3% of admitted

burn patients and result in potentially severe
burns. Typically, acid chemical burns result in
coagulation necrosis and alkali chemical burns
cause liquefactive necrosis (with an exception
of hydrofluoric acid, which also causes
liquefactive necrosis).

DEPTH INVOLVED SYMPTOMS/REM

STRUCTUR ARKS
E

1. Epidermis - painful but do

Superficia not blister
l (first- - not included on
degree) fluid requirement
computation
2. Partial- Superficial - extremely
thickness Dermis painful are
(second- Deep weeping
degree) Dermis and with
a. Sup blisters
erfi - Blanching Jackson described three zones of tissue injury
cial when following burn injury. The zone of coagulation
b. De pressed is the most severely burned portion and is
ep - Can result typically in the center of the wound. As the
to name implies, the affected tissue is coagulated
contractur
and sometimes frankly necrotic, much like a
es
full thickness burn, and will need excision and
Full- Up to -leathery, grafting. Peripheral to that is a zone of stasis,
thickness Subcutaneo painless, and with variable degrees of vasoconstriction and
(third- us Fat nonblanching resultant ischemia, much like a second degree
degree) burn. Appropriate resuscitation and wound care
may prevent conversion to a deeper wound,
but infection or suboptimal perfusion may result
Fourth- Up to
degree underlying in an increase in burn depth. This is clinically
Soft tissues relevant because many superficial partial-
thickness burns will heal with nonoperative
management, and the majority of deep partial-
thickness burns benefit from excision and skin
grafting. The outermost area of a burn is called
the zone of hyperemia, which will heal with
minimal or no scarring and is
most like a superficial partial thickness burn or
first-degree burn.
FLUID RESUSCITATION
The most common cause of mortality in the 1st
48 hours following a burn injury is inadequate
fluid resuscitation. Patients with moderate and
major burns will require fluid rescucitation via
intravenous route, while patients with minor
burns are encouraged to increase oral intake.
Fluid rescucitation should be started as early
as possible in the ER and even before other
diagnostic exams.
The management of injury encompasses
several dimensions which can be roughly
divided into two phases: Initial/Resuscitative
period (first 48 hours) and the Definitive
management period (after 48 hours).
In electrical injuries, the %BSA involved does
not correspond to the extent of injuries of the
underlying soft tissues. There may be areas of
soft tissue sustaining injuries secondary to the
passage of electrical current but with normal
looking skin over it.
8. Weigh patient and record. This step is very
important. In cases where it is impossible to
weigh the patient weight can be estimated
using the formula:
For children: Wt (kg)=[2x(age in years)] + 5
For adults: Wt 9kg)=0.9x [(ht in cms)-100]
In the presence of increased capillary
permeability, colloid content of resuscitation
fluid exerts little influence on intravascular
retention during the initial hours
postburn→consequently crystalloid fluids are
given.
If urine output and pigment clearing do not
respond to fluid resuscitation, 12.5g of
cosmetic diuretic mannitol may be added to
each liter of resuscitation fluid. Since hama
tigments are more soluble in alkaline medium,
NaHCo3 can be added to IVF to maintain a
slightly alkaline urine.
NOTE: In electrical injuries, fluid volume for
resuscitation should be adjusted to maintain a
urine output of 75-100 ml/hr and mannitol 12.5-
25g may be infused to promote dieresis.
1. Get a complete history regarding the
circumstances surrounding the burn. A
burn injury sustained in an enclosed
space raises the possibility of an
inhalation injury.
Parkland Formula (3-4 ml/kg/%TBSA/24 hours)
st st nd
- 1 half is given during the 1 8 hours after burn and 2
half given over the subsequent 16 hours
Modified Brooke Formula (2 ml/kg/%TBSA/24 hours)
“Consequently, crystalloid fluid is the
cornerstone of resuscitation for burn patients.
Lactated Ringer’s (LR) is the fluid of choice for
burn resuscitation because it is widely available
and approximates intravascular solute content”.
-ABA
Common Parameters for Titration for Burn
Resuscitation:
• Blood Pressure
• Urine Output
Adults: 0.5 ml/kg/hour (or 30-50 ml/hour)
Young Children (weighing ≤ 30kg): 1
ml/kg/hour
Pediatric (Weighing > 30 kg,up to age 17): 0.5
ml/kg/hour
Adult patients with high voltage electrical
injuries with evidence of myoglobinuria: 75 –
100 ml/hour until urine clears.
• Critically Ill patients: MAP of 60mmHg
Medicatio Advantage Disadvantages thickness
n s burns

A. Silver Wide range Used as Useful in

Sulfadiazin of prophylaxis rather Meshed
e antimicrobia than treatment of skin grafts
l activity existing infection

Inexpensive Causes E. Silver Can be Limits serial

, easily Neutropenia Impregnate used for wound
applied and d Dressing donor examinations
with Causes Allergic (Aquacel sites, skin
soothing Reaction to Sulfa Ag) grafts, and
qualities component partial
thickness
Not burns
Destroys Skin
absorbed grafts
systemically Can be
used to
Delays healing in
avoid daily
partial thickness
dressing
wounds
change
B. Effective Painful if applied
F. MEBO Promotes Expensive
Mafenide even if with to partial
(Moist cell
Acetate Eschar thickness wounds
Exposed regeneratio
Burn n and
Used as Can cause Ointment wound
prevention Metabolic healing
and Acidosis
treatment
Less
for ongoing
dressing
infection
changes
(every 3-4
Can be days)
used for
fresh skin
grafts General wound care recommendations:
C. Silver Has broad Can cause
Superficial Partial thickness burns
Nitrate spectrum hyponatremia and
antimicrobia rarely
l activity methemoglobinem SPT’s and donor sites of split thickness skin
ia grafts can benefits from closed/occluded
Inexpensive dressings for long period (about a week)
Causes
Black/Dark stains • Humid, heat preserving modern
dressings are preferred (e.g.
D. Useful for Can cause
Foam, hydrocolloid, hydrofiber)
Bacitracin, smaller nephrotoxicity
Neomycin, burns or • Moist dressing/conventional for
polymyxin nearly Cannot be used in
low-resource settings (e.g. Silver
healed burns large burns sulfadiazine wet-to-dry dressing)
and
Superficial If infection is being entertained (eg. Delayed
Partial presentation, use of inappropriate burn first aid
such as wounds covered with sand, dirt or
toothpaste:
Dressing should be done more often
(every 2-3 days) to allow inspection and
cleansing with proper antimicrobacterial
solutions
Closed/Occluded dressings is the rule for
DPT’s and full thickness burns
DPT/FT’s avascular nature predisposes
these burns to bacterial colonization and
subsequent infection
Eschar remains soft allowing tangential
excision
Protect the eschar from infection
Prolongs contact of antimicrobial agent with the
eschar
Prevents desiccation, fluid and heat loss
Consensus: use of antimicrobials dressing
(Silver, Povidone) favored over antibiotics
creams
• Less bacterial resistance
Once eschar has separated, these wounds can
be dressed/prepared as raw area wounds with
closed dressing
Early Excision
This is done within the 1st 7 days post-burn,
while the burn wound is not yet colonized by
microorganism; thus reducing chances of
infection and promoting good graft take
Preparation for OR- Prerequisites
1. Stable vital signs
2. Not in septic shock
3. Afebrile
4. Blood type and crossmatch for OR use.
Estimated amount to replace losses during
tangential excision at 200-400 ml/% BSA
excised
5. Albumin us normal (38-51g/L)
6. No medical contraindications for surgery
Conduct for OR
1. Make sure that the OR table is covered by
sterile linen before the patient is transferred
onto the table
2. Keep the OR warm
3. Prep the patient using betadine soap and
betadine paint for the donor sit, betadine soap
for the wound
4. Prep the donor site
5. Drape the donor site separate from the burn
wound
Tangential excision
• Most common Technique
• Sequential debridement of burn tissue
until a layer of viable vascularized tissue
is encounter
Fascial excision
 • Enbloc removal of skin and
subcutaneous tissue up to the investing
fascia using electrocautery
• Ideal for large, deep and life threatening
burn wound

SKIN GRAFT HEALING

Plasma imbibition: 24 to 48 hours – consist of

simple diffusion of nutrients from recipient bed
to skin graft

Inosculation: Day 3-5 Capillary buds from the

recipient bed line up with graft vessels to form
open channels and establish blood flow FULL THICKNESS SKIN GRAFT

Revascularization: Day 4 to day 7: Newly • Contains entire epidermis and dermis

formed vascular connection differentiate into
afferent and efferent vessels
Care of the skin graft
1. First graft opening could be as early as the
3rd post-op day or as late as 5th post-op day.
Open early if the skin graft is suspected to be
infected as when it has a foul-smelling odor
• Better cosmetic results, reduced
scarring, less contraction
• Eyelid burns, finger, face/hands
• Donor site close primarily
• Back of ear, clavicle, inguinal,
lower abdomen

2. Remove the bulky dressing slowly. Take

care not to disturb the skin graft. Use copious
amount of sterile water. Skin graft take is
indicated by pinkish-color of graft and
adherence to graft bed. Gently wash the area
wit betadine soap and rinse with water. Dress
the graft with bulky wet dressing,
MESHED GRAFT
3. Staples can be removed at he 1st dressing
change • Ideal for large burn with limited donor
site
4. Skin grafts can be dressed every day if not • Allows expansion for wider coverage
infected. If with good take, the skin graft can be • Allows seroma/hematoma to drain
left open on the 7th post-op day. Small areas of • Poor cosmetic result (Net Appearance)
graft loss (about thumb size) could be cleansed • Not to be applied to the face, neck and
by mercurochrome hand

SPLIT THICKNESS SKIN GRAFT

• Contains epidermis and various layer of

dermis
• Contract significantly
• Donor site heals by reepithelialization
(may be reharvested)
• Thighs, abdomen, scalp, back
SHEET GRAFTS
• Better cosmetic and functional outcome
• Best for face/neck, hands
• WOF: Seroma/Hematoma formation
• Except dorsum of hand and forearm
MEEK MICROGRAFTS
• Similar to meshed in advantages and
disadvantages
• Autografts cut into small squares and
applied on the pleated gauze
• Technique to expand available skin 4x,
6x to 9x, minimizing donor site
XENOGRAFT/BIOBRANE
BIOBRANE CHECK
CADAVERIC ALLOGRAFTS
DERMAL MATRICES
• Culture studies done -> growth reported
and graded for quality
• Grade A,B,C depending on the
site for infection
• Key indications:
• Applied to debrided acute burns
areas where there are insufficient
autografts
• Applied on top on meshed
autografts to decreased amount
of graft loss
• Undergoes graft take as per autograft,
before being rejected and sloughed off
around 2-3 weeks after
• Short life: 7 days but can be preserved
for about 12 months
SANDWICH TECHNIQUE
• Widely meshed autograft is covered with
meshed cadaveric allograft to prevent
graft loss
• Allograft sloughed-off in 2-3 weeks
revealing vascularized autografts
• Temporary wound coverage (not a true
skin substitute)
• Partial thickness burn -> allows faster
healing and less pain
• Excised burn -> temporary coverage
prior to skin grafting
• Allows fibrin to permeate the mesh and
ingrowth of host fibroblasts
• Checked for adherence after 3-4 days
• Once adherent, patient can take a
shower
• WOF: infection underneath the biobrane
• Dermal scaffold for cell and tissue
regeneration allowing vascular ingrowth
• Composition:
• Collagen
• Chondroitin-6-sulfate
• +/- synthetic cover (Silicone)
• Originally developed for burn
reconstruction
• Applications for exposed:
• Bone without intact periosteum
• Tendon without paratendon
• Cartilage without perichondrium
• Advantages:
• Better skin quality
 • Greater thickness and elasticity
(vs STSG alone)
• Can cover a larger area
• Can temporize wounds until
STSG donor site becomes
available
• Needs METICULOUS wound
care (Higher rate of local infection
-> loss/no revascularization
• Expensive/ not accessible

THE RECONSTRUCTIVE LADDER

PRINCIPLES OF FLAP SURGERY

1. REPLACE LIKE WITH LIKE

2. THINK OF RECONSTRUCTION IN
TERMS OF UNIT

3. ALWAYS HAVE A PATTERN AND A

BACK UP PLAN

4. NEVER FORGET THE DONOR AREA

MALIGNANT SKIN LESIONS
1. BASAL CELL CARCINOMA
· Most common type of skin cancer; less
aggressive
· Arises from basal cell layer of epidermis
· Very slow growing with rare systemic
metastasis; often neglected for years
· Good prognosis
· Subtypes:
o Nodular: most common (70%); appears as
waxy and pearly with rolled edges surrounding
an ulcer
o Superficial spreading: red, scaling lesions;
commonly found in the trunk
o Micronodular
o Infiltrative
o Pigmented: tan to black in color (sometimes
mistaken as melanoma)
o Morpheaform: flat, plaque-like, aggressive,
requires prompt early excision
Treatment:
o Curettage
o Electrodessication – Disadvantage: you may
not have
whole specimen because you will destroy it
Laser vaporization
o Surgical excision (most ideal): provides
complete tumor
removal as well as preservation of the tissue
for lab
evaluation (compared to the first 3, which
destroy the
lesion)
o For large and aggressive lesions
(morpheaform and infiltrative): needs 0.5-1 cm
margin
o In areas of aesthetic value, such as the head
and face (cheek, nose or lip) which are often
the sites of CA (increased sun exposure):
Mohs surgery [1]
§ Involves serial excision in small increments
with immediate microscopic analysis
§ Distinct advantage: ALL specimen margins
are evaluated (vs. traditional histologic
evaluation which selects portions only)
§ Major benefit: ability to remove a tumor
with minimal sacrifice of uninvolved tissue
§ Disadvantage: long procedure and may
require multiple attempts
§ Recurrence and metastasis comparable to
wide local excision
o Excision with flap (for aesthetic purposes):
bigger but
heals more nicely
2. SQUAMOUS CELL CARCINOMA
Arises from epidermal keratinocytes
Less common but more devastating d/t
increased invasiveness and can metastasize
“Bowen’s disease” – in situ SCC
“Erythroplasia of Queyrat” – in situ SCC in the
penis
Tumor thickness & size correlates with
malignant behavior
o > 4 mm thickness: increased recurrence
o > 10 mm diameter: increased metastasis
· Location:
o Less UV and radiation exposure – less
aggressive
o Marjolin’s ulcer (areas of SCC from chronic
burn scars),
chronic osteomyelitis, previous injury – very
aggressive and metastasize early
Treatment:
o Surgical excision (preferred) – at least with 1
cm (or 10 mm) margin and histologic
confirmation of tumor-free borders are
mandatory
o Mohs’ surgery for areas of aesthetic value
o Regional LN dissection for palpable LNs only
(at least N1)
o Prophylactic LN dissection
§ Doing a dissection wherein the lymph nodes
are not yet clinically enlarged or palpable.
§ Evaluate if metastatic then evaluate lymph
node of most probable area of metastasis.
Remove the lymph node.
§ Example of most probable area of
metastasis: arm/chest – axilla; lower
extremities – inguinal; head & neck – neck
dissection
§ Only for lesions arising from chronic wounds
because they are more aggressive
o Metastasis is a poor prognostic sign: 13% 10-
year survival
3. MELANOMA
The age-adjusted incidence of invasive
melanoma in the Us increased from approx. 4-
18 per 100,000 among white males between Prognostic indicators
1973 and 1998. o Histologic type
Pathogenesis complex and remains poorly o Depth of invasion*
understood o Lesions at extremities have 82% 10-year
Risks: transformed melanocytes, dysplastic survival rate than those in
nevi with focus of atypical melanocytes the head, neck, or trunk (68%) because the
(increase in number: increase in the relative head and neck are
risk), strong genetic component lymphatic rich
90% occur in the skin, although the eye and o Ulceration* = due to increased angiogenesis;
anus are notable sites worse prognosis (78%
4% are discovered as metastasis without any to 50% in stage 1 lesion)
identifiable primary site o Females have better prognosis
5-10% are non-pigmented o 2 most important prognostic factors for
Tumor growth occurs radially in the epidermal melanoma
plane
Metastasis doesn’t occur until melanocytes
form dermal nests

Types of melanoma
By decreasing frequency:
o Superficial spreading
§ Up to 70% of melanomas
§ Occurs anywhere in the skin except the
hands and feet
§ Typically flat and measures 1 to 2 cm in
diameter at diagnosis
§ A characteristic prolonged radial growth
phase is seen before vertical extension
occurs
o Nodular
§ 15-30% of melanomas
§ Lack radial growth, thus all are in vertical
growth phase at diagnosis
§ Darker coloration and often raised
§ Prognosis for patients similar to that with a
superficial spreading type of the same depth
o Lentigo Maligna
§ 4-15% of melanomas
§ Most frequent in the neck, face, and hands of
the elderly
§ Tend to be larger but with the best prognosis
since invasive growth occurs late
o Acral Lentiginous
§ 2-8% of melanomas in white populations but
29-72% of all melanomas in dark-skinned
people
§ Mostly on the palms, soles, and subungual
regions
§ Lesions appear as blue-black discolorations
of the posterior nail fold

SOFT TISSUE SARCOMA
· Arises predominantly from embryonic
mesoderm or ectoderm
· Rare tumor that accounts for less than 1% of
cancers in adults and 7% of cancers in children
· Approximately 2/3 arise in the extremities and
the rest in the retroperitoneum, trunk,
abdomen, and head & neck · 5-year survival is
50-60%
· Patients usually die of lung metastasis (rarely
due to growth in size of tumor)
DIAGNOSTICS
Clinical presentation: asymptomatic mass;
detected earlier if superficial in location
Symptoms are elicited when surrounding
structures are compressed
Differential diagnosis: benign lesions
(lipoma, leiomyomas, neuromas)
Radiologic imaging is the mainstay
modality for diagnosis
o Defines local extent, stages, assists in
biopsy procedures and aids in diagnosis
o Ultrasound – often as adjunct to MRI
o CT – preferred for retroperitoneal
sarcomas
o MRI – delineates muscle groups and
distinguishes bone, vascular structures
and tumor especially in extremities
Biopsy Techniques
o Fine Needle Aspiration Biopsy (FNAB) –
guided by ultrasound or CT scan; least
invasive; rule out or confirm the presence of
metastasis and local recurrence; can’t
differentiate the type
o Core needle Biopsy – more recommended;
tells you the type and histologic grade
o Sectional Biopsy – for superficial lesions
§ Punch biopsy
§ Excision biopsy - whole lesion is examined
§ Incision biopsy - only a part of the lesion is
examined
§ Shave biopsy – not recommended
PATHOLOGIC CLASSIFICATION
· Limited metastatic potential
o Desmoid
o Well-differentiated liposarcoma
o Dermatofibrosarcoma protuberans
o Hemangiopericytoma
· Intermediate metastatic spread
o Myxoid liposarcoma
o Extraskeletal chondrosarcoma

· Highly aggressive
o Angiosarcoma
o Clear cell sarcoma
o Pleomorphic and dedifferentiated
liposarcoma
o Leiomyosarcoma
o Rhabdosarcoma
o Synovial sarcoma

Histologic grade
o Most important prognostic factor for
sarcomas o Stage 1: low grade – simple wide excision
o 3-grade system only (minimum of 2 cm margin if possible)
§ G1 – low
§ G2/3 – high o Stage 2: <5cm, high grade – consider
o Features: cellularity, differentiation, adding radiation to surgical resection
pleomorphism, necrosis, and number of
mitoses o Stage 3: >5cm, high grade, nodal –
o Predict development of metastasis and surgical resection + radiation, consider
overall survival chemotherapy
o Metastasis: 5-10% for low grade and 50-60%
for high grade o Stage 4: distant metastasis – consider
neoadjuvant chemotherapy (able to see
Tumor size response of tumor). If good response, consider
o Deep (retroperitoneal, mediastinal, visceral) resection.
o Superficial (fascia)
Surgery
Metastasis o Small (<5cm) primary tumors with no
o Lung – primary evidence of distant metastatic disease
o Also bone, brain, and liver o Extent and type determined by:
Size, grade, and depth § Location, size, and depth
Older age and gender § Contiguous structures
Positive microscopic margin § Need for reconstruction
Early recurrence after resection o Margin involvement affect local recurrence
Expression of markers but not survival
o Ki-67 – poor outcome o Functional compromise determined for
amputation versus wide excision
Soft tissue tumors that are enlarging and >3 o 1X2 cm ideal but sometimes limited by
cm should be evaluated surrounding structures and functionality
o Radiologic imaging (CT or ultrasonography) o Radical lymphadenectomy in isolated
o Tissue diagnosis (core needle biopsy) regional lymph node metastasis
Once a sarcoma diagnosis is established
o Obtain imaging (MRI for extremity lesion; CT · Amputation
for other anatomic locations) o Limb sparing versus amputation
o Evaluate for metastatic disease with chest o 5% of cases
CT for intermediate/high grade tumors (T2 o Addition of radiation increases limb salvage
tumors) rates
If:
§ LIMB SALVAGE – muscle group excision is
done, then radiation to preserve the function of
the limb
o Includes bone, soft tissue
Adjuvant therapy
o Radiation
§ Local control rates of 80-90%
§ Not given to small tumors (T1)
§ Generally given postoperatively
o Systemic THERAPY
§ Metastasis and death remains a problem for
high risk tumors
§ CHEMOTHERAPY – generally poor
response; only doxorubicin, dacarbizine and
ifosfamide

PROGNOSIS AND OUTCOME

· Early recognition and treatment of recurrent
disease can prolong survival
· Metastasectomy is an option for single lesion
· History, PE, CT/MRI
o Every 3-6 months for 2-3 years
· Recurrence common for abdominal soft tissue
sarcoma
· Metastasis may occur within 2-3 years of
initial diagnosis
COLON, RECTUM, ANUS
EMBRYOLOGY AND ANATOMY - 4th week of
gestation: beginning of the development of the
embryonic gastrointestinal tract
● Primitive gut is derived from the endoderm
○ Three segments: foregut, midgut, hindgut
○ Midgut and hindgut: contribute to the colon,
rectum, and anus
● Midgut
○ Develops into the small intestine, ascending
colon, and proximal transverse colon
○ Blood supply: superior mesenteric artery
○ 6th week of gestation: herniates out of the
abdominal cavity → 270º counterclockwise
around SMA → returns inside abdominal cavity
during 10th week
• Hindgut
○ Distal transverse colon, descending colon,
rectum and proximal anus
○ Blood supply: inferior mesenteric artery
○ 6th week of gestation: cloaca divided by the
urorectal septum into the urogenital sinus and
rectum
Ectoderm: where the distal anal canal is derived
from
○ Blood supply: internal pudendal artery
○ Dentate line: divides the endodermal hindgut
from the ectodermal distal anal Canal
ANATOMY OF THE COLON
Large intestine: divided anatomically and
functionally into the colon, rectum, and anal
canal
○ From ileocecal valve to the anus
● Four distinct layers: mucosa, submucosa,
muscularis propria (ICOL), serosa
● Colon: Outer longitudinal muscle separated
into 3 teniae coli
○ Converge proximally at appendix,
distally at rectum
● Distal rectum: inner smooth muscle layer
coalesces to form the internal anal sphincter
● Covered by serosa: intraperitoneal colon,
proximal ⅓ of rectum
● No serosa: mid and lower rectum
Arterial Supply
● Superior mesenteric artery branches
○ Ileocolic artery: terminal ileum and
proximal ascending colon
■ Absent in up to 20% of people
○ Right colic artery: ascending colon
○ Middle colic artery: transverse colon
● Inferior mesenteric artery branches
○ Left colic artery: descending colon
○ Sigmoidal branches: sigmoid colon
○ Superior rectal artery: proximal Rectum
Anastomoses:
● Marginal artery of Drummond:
anastomoses between the terminal branches of
the SMA and IMA
● Arc of Riolan: anastomosis between the
middle colic artery of the SMA and ascending
branch of the left colic artery of the IMA Venous
Drainage
● Veins of the colon parallel their
corresponding arteries and bear the same
terminology except for the inferior mesenteric
vein (IMV) ● IMV: ascends into the
retroperitoneal plane over the psoas muscle and
continues posterior to the pancreas to join the
splenic vein
○ Often mobilized independently
and ligated during a colectomy
Lymphatic Drainage
● Follow the regional arteries
● Epicolic nodes: on the bowel wall
● Paracolic nodes: adjacent to the anastomosing
arteries
● Intermediate nodes: around the SMA and IMA
● Main nodes: at the origin of the SMA and IMA
Nerve Supply
● Sympathetic nerve supply (inhibitory): from T6-
T12 and L1-L3
● Parasympathetic nerve supply (stimulatory):
from vagus and the nervi erigentes (S2-S4)
ANATOMY OF THE RECTUM AND ANUS
Anorectal Landmarks
● Rectum: approximately 12-15 cm in length
○ Valves of Houston: 3 distinct
submucosal folds that extend into the rectal
lumen
○ Presacral fascia: separates the rectum
from the presacral venous plexus and pelvic
nerves
○ Rectosacral fascia (Waldeyer’s
fascia): extends anteriorly and caudally and
attaches to the fascia propria at the anorectal
junction at S4
○ Denonvilliers’ fascia: anteriorly
separates the rectum from the prostate and
seminal vesicles in men; from the vagina in
women
○ Lateral ligament: support the lower
rectum
Anorectal Landmarks
● Anatomic anal canal: extends from the dentate
or pectinate line to the anal verge
● Dentate or pectinate line: marks the transition
point between columnar rectal mucosa and
squamous anoderm
● Anal transition zone: includes mucosa
proximal to the dentate line that shares histologic
characteristics of columnar, cuboidal, and
squamous epithelium
● Columns of Morgagni: longitudinal mucosal
folds that surround the dentate line, into which
the anal crypts empty
● Surgical anal canal: begins at anorectal
junction and terminates at the anal verge;
generally longer in men
Landmarks
● Internal anal sphincter: comprised by
thickened inner smooth muscle in the distal
rectum
○ Surrounded by the subcutaneous,
superficial and deep external sphincter
● Deep external anal sphincter: extension
of the puborectalis muscle
● Levator ani muscle: puborectalis,
iliococcygeus, and pubococcygeus muscle
Supply and Venous Drainage
Superior rectal artery: terminal branch of the
IMA Middle rectal artery: from internal iliac
artery Inferior rectal artery: from the internal
pudendal artery, which arises from the internal
iliac artery
Superior rectal vein: drains to inferior
mesenteric vein, then portal vein
Middle rectal vein: drains to internal iliac vein
Inferior rectal vein: drains to internal pudendal,
then to internal iliac vein
Lymphatic Drainage and Nerve Supply
Upper and middle rectum: pararectal nodes,
then to inferior mesenteric nodes
Lower rectum: pararectal nodes then to inferior
mesenteric and internal iliac nodes
Anal canal above dentate line: inferior
mesenteric and internal iliac nodes
Below dentate line: primarily into the medial
group of superficial inguinal nodes
Pelvic plexus
● Sympathetic Nerve Supply (L1-L3): distributed
as preaortic and hypogastric plexus, joins the
nervi erigentes to become the pelvic plexus
● Parasympathetic (S2-S4): known as the nervi
erigentes; joins the hypogastric plexus to become
pelvic plexus
IAS: sympathetic (L5) and parasympathetic (S2-
S4) EAS and puborectalis ms: inferior rectal
branch (S2-S3) of internal pudendal nerve and by
the perineal branch (S4)
PHYSIOLOGY
Motility
○ Intermittent contractions of either low or high
amplitude
○ Low-amplitude, short-duration contractions
occur in bursts and appear to move the colonic
contents both antegrade and retrograde
○ These bursts delay colonic transit and thus
increase the time available for absorption of water
and exchange of electrolytes
○ High-amplitude, prolonged duration,
propagated contractions (HAPCs): occur in a
more coordinated fashion and create “mass
movements”
■ 4-10 times per day, mostly after meals
and awakening
Defecation
○ Complex, coordinated mechanism
○ Colonic mass movement, increased intra-
abdominal and rectal pressure, and relaxation of
the pelvic floor
○ Rectal distention → reflex relaxation of the IAS
(rectoanal inhibitory reflex) → contents make
contact with the anal canal → sensory epithelium
distinguishes solid stool from liquid stool and gas
○ No defecation → rectum relaxes and the urge to
defecate passes (accommodation response)
○ Defecation → increasing intra-abdominal
pressure via Valsalva maneuver with rectal
contraction, relaxation of the puborectalis muscle
and opening of anal canal
● Continence
○ Requires adequate rectal wall compliance to
accommodate fecal bolus, appropriate
neurogenic control of the pelvic floor and
sphincter mechanism, and functional internal and
external sphincter muscles
○ At rest: puborectalis muscle creates a “sling”
around the distal rectum, forming a relatively
acute angle that distributes intra-abdominal forces
onto the pelvic floor
○ With defecation: the angle straightens, allowing
downward force to be applied along the axis of the
rectum and anal canal
○ IAS and EAS: tonically active at rest
■ Innervated by branches of the pudendal
nerve ○ Internal sphincter: responsible for most of
the resting, involuntary sphincter tone (resting
pressure)
○ External sphincter: responsible for most
of the voluntary sphincter tone (squeeze
pressure)
○ Hemorrhoidal cushions (mechanically
block the anal canal) and a formed stool
contribute to maintaining continence
○ Poor rectal compliance, injury to the
internal and/or external sphincter or puborectalis
or neuropathy → impaired continence
LOWER GI BLEEDING
● Most common sources: esophageal, gastric or
duodenal
○ Nasogastric aspiration should always be
performed
○ Return of bile suggests that source of
bleeding is distal to the ligament of Treitz
○ Blood or nonbile secretions or symptoms
suggestive of upper intestinal source:
esophagogastroduodenoscopy should be
performed ● Anoscopy and/or limited
proctoscopy: hemorrhoidal bleeding
● Technetium-99-tagged red blood cell
scan: extremely sensitive but location is imprecise
○ If positive, angiography can then
be both diagnostic and potentially
therapeutic
● Rapid bowel preparation can be
performed to allow colonoscopy in
hemodynamically stable patients
○ Cautery or epinephrine into
bleeding site may be used to control hemorrhage
● SPECT/CT: if other modalities have not
localized source of bleeding
Colectomy may be required if bleeding persists
despite interventions
○ Segmental resection preferred if source
can be localized
○ “Blind” subtotal colectomy may be
required in a hemodynamically unstable patient of
unknown source of colonic hemorrhage
● Intraoperative colonoscopy and/or enteroscopy
● Occult blood loss from GI tract may manifest as
IDA or be detected with FOBT or FIT
○ (+) occult blood should always prompt a
colonoscopy
○ Unexplained IDA: indication for
colonoscopy
● Hematochezia: hemorrhoids or fissure
○ Sharp, knife-like pain with bright red
rectal bleeding with bowel movements: fissure
○ Painless, bright red rectal bleeding with
bowel movements: friable internal hemorrhoid
RESECTIONS
Curative resection of a colorectal cancer
● Proximal mesenteric vessel ligation and radical
mesenteric clearance of the lymphatic drainage
basin of the tumor site
Extent of resection for cancers of the colon
A: Cecal cancer
B: Hepatic flexure cancer
C: Transverse colon cancer
D: Splenic flexure cancer
E: Descending Colon cancer
F: Sigmoid Colon cancer

Resection of a benign process

● does not require wide mesenteric
clearance
Emergency Resection may be required because
of
● Obstruction
● Perforation
● Hemorrhage
Attempt should be made to resect the involved
segment along with its lymphovascular supply
Right colon or proximal transverse colon
● Right or Extended Right Colectomy
● Primary ileocolonic anastomosis can usually
be performed safely as long as the remaining
bowel appears healthy and the patient is stable
Left-sided tumors
● Traditional Approach
○ Resection of the involved bowel and
end colostomy, with or without a mucus fistula
● Primary anastomosis without a bowel
preparation or with an on-table lavage with or
without a diverting ileostomy, may be equally
safe in this setting If the proximal colon appears
unhealthy
● Due to
○ Vascular compromise
○ Serosal tears
○ Perforation
● Subtotal colectomy can be performed with a
small bowel to rectosigmoid anastomosis
Total Proctocolectomy
● Entire colon, rectum and anus is
removed ● Ileum is brought to the skin as
a Brooke ileostomy Restorative
Proctocolectomy (Ileal Pouch-Anal
Anastomosis)
● Entire colon and rectum are resected
● Anal sphincter muscles and a variable
portion of the distal anal canal are
preserved ● Bowel continuity is restored
by anastomosis of an ileal reservoir to the
anal canal
Restorative Proctocolectomy (Ileal Pouch-Anal
Anastomosis)
● Entire colon and rectum are resected
● Anal sphincter muscles and a variable
portion of the distal anal canal are preserved
● Bowel continuity is restored by
anastomosis of an ileal reservoir to the anal
canal
Annual surveillance of the anastomosis and/or
anal
transition zone
● digital rectal exam and anoscopy or
proctoscopy
Proctocolectomy
Neorectum
● Made by anastomosis of the terminal ileum
aligned in a “J,” “S,” or “W” configuration
● J-pouch
○ Simplest to construct
○ Most used configuration
Total proctocolectomy w/ ileal pouch–anal
reconstruction using minimally invasive surgical
techniques
Proximal ileostomy performed to divert succus
from the newly created pouch in an attempt to
minimize the consequences of leak and sepsis
Ileostomy is then closed 6 to 12 weeks later after
a contrast study confirms the integrity of the
pouch
Anterior Resection Resection of the rectum
from an abdominal approach to the pelvis with
no need for a perineal, sacral, or other incision
High anterior resection
● Resection of distal sigmoid colon &
upper rectum
● Appropriate operation for benign
lesions and disease at the rectosigmoid junction
(e.g. diverticulitis) Low Anterior Resection
● Used to remove lesions in the upper
and mid rectum Extended Low Anterior
Resection
● Necessary to remove lesions located in
distal rectum, but several centimeters above the
sphincter
 ○ Low in the rectum
Hartmann’s Procedure ○ In an irradiated field
● Colon or rectal resection without an ○ Immunocompromised or
anastomosis malnourished patient
● A colostomy or ileostomy is created ○ Emergency operations
and the distal colon or rectum is left as a blind ● Loop ileostomy is often constructed
pouch Permanent Ileostomy
● Term is typically used when the left or ● Sometimes required after total
sigmoid colon is resected and the closed off proctocolectomy or in patients with
rectum is left in the pelvis obstruction
● End ileostomy is the preferred
Mucus fistula configuration
● If the distal colon is long enough to 1. Stoma necrosis
reach the abdominal wall 2. Stoma retraction
● Can be created by opening the 3. Dehydration with fluid and
defunctioned bowel and suturing the open electrolyte abnormalities
lumen to the skin 4. Skin irritation
5. Obstruction
Abdominoperineal Resection 6. Parastomal hernia
● removal of the entire rectum, anal 7. Prolapse
canal, and anus with construction of a Colostomy
permanent colostomy from the descending or ● Most colostomies are created as end
sigmoid colon Extralevator abdominoperineal colostomies rather than loop colostomies
resection (ELAPE) ● Most colostomies are created on the
● resection of the levator muscles near left side of the colon
their bony attachments, in order to avoid ● Abdominal wall defect is created and
opening the space between the tumor and the the end of the colon mobilized through it
levator ani ● Protruding stoma is considerably
● useful for low, locally advanced rectal easier to pouch
cancers The distal bowel may be:
● Brought through the abdominal wall as
Anastomoses Configurations: Mucus fistula
● End-to-end ● Left intra-abdominally as a Hartmann’s
● End-to-side pouch
● Side-to-end
● Side-to-side Complications of Colostomy
1. Colostomy necrosis
Submucosal layer of the intestine provides the 2. Retraction
strength of the bowel wall and must be 3. Obstruction
incorporated in the anastomosis to assure 4. Parastomal hernia
healing 5. Prolapse
6. Dehydration
Accurate approximation of two well- 7. Skin irritation
vascularized, healthy limbs of bowel without
tension in a normotensive, well nourished Ulcerative Colitis
patient almost always results in a good outcome Mucosal process - colonic mucosa and
submucosa are infiltrated with inflammatory
Ileostomy cells
Temporary Ileostomy ● atrophic
Complications of Ileostomy ● crypt abscesses
● Used to “protect” an anastomosis that Mucosa is frequently friable and may possess
is at risk for leakage multiple inflammatory pseudopolyps
In longstanding ulcerative colitis
● Colon may be foreshortened
● Mucosa replaced by scar
In quiescent ulcerative colitis
● Colonic mucosa may appear normal
Ulcerative colitis may affect
● Rectum (proctitis) – May produce
tenesmus
● Rectum and sigmoid colon
(proctosigmoiditis)
● Rectum and left colon (left-sided colitis)
● Rectum and entire colon (pancolitis)
A key feature of ulcerative colitis is the
continuous involvement of the rectum and colon
Ulcerative colitis may involve the terminal ileum
● May demonstrate inflammatory
changes (“backwash ileitis”)
Fulminant colitis or toxic megacolon
● Severe abdominal pain and fever,
Physical findings are nonspecific
● minimal abdominal tenderness
● distention
● frank peritonitis
Diagnosis through colonoscopy and mucosal
biopsy
Crohn’s Disease
Transmural inflammatory process
● Can affect any part of the
gastrointestinal tract from mouth to anus
Characteristic pathologic findings
● Mucosal ulcerations
● Inflammatory cell infiltrate
● Noncaseating granulomas
● Chronic inflammation may ultimately
result in fibrosis, strictures, and fistulas
● Characterized by deep serpiginous
ulcers and a “cobblestone” appearance
● Skip lesions or rectal sparing suggest a
diagnosis
● Presence of symptomatic diverticula
● Diverticulitis vs Diverticulosis
● Majority: False Diverticula - mucosa and
muscularis mucosa have herniated through the
colonic wall
● Diverticular bleeding - massive but usually
self-limiting
● True Diverticula: involves all layers
● Most common site of diverticulosis: sigmoid
colon
○ Due to lack of dietary fibers
○ Due to loss of tensile strength and
decreased in elasticity of the bowel as we age
DIVERTICULITIS
Occur in 10 to 25% of people with
diverticulosis
● Perforation → Peridiverticular and
pericolic infections → contamination,
inflammation and infection
● S&S: left-sided abdominal pain, with or
without fever and leukocytosis; mass
● Diagnostics: ○ Plain Radiograph - free
intra-abdominal air ○ CT scan - pericolic
inflammation, phlegmon or abscess
● Contraindications: Barium enema;
endoscopy

Perianal Crohn’s disease - pain, swelling, and

drainage from fistulas or abscesses

Serologic markers to differentiate ulcerative

colitis from Crohn’s disease
● anti-Saccharomyces cerevisiae antibody
(ASCA) ● Perinuclear anticytoplasmic antibody
(pANCA)

DIVERTICULAR DISEASE