Plastic and Reconstructive Surgery Board Review Pearls of Wisdom 3th

25/11/2025 • by Bs CKI Phẫu thuật tạo hình, tái tạo và thẩm mỹ Trương Hoài Anh • cổ
Bìa sách Plastic and Reconstructive Surgery Board Review Pearls of Wisdom Second Edition

Giới thiệu về cuốn sách Pearls of Wisdom Plastic & Reconstructive Surgery Board Review

Cuốn sách Pearls of Wisdom: Plastic & Reconstructive Surgery Board Review, Third Edition được biên soạn nhằm mục đích trở thành một công cụ hỗ trợ học tập đắc lực cho các bác sĩ nội trú, nghiên cứu sinh và các bác sĩ phẫu thuật tạo hình mới vào nghề. Nội dung sách được thiết kế để giúp người đọc chuẩn bị tốt nhất cho các kỳ thi chuyên ngành, bao gồm kỳ thi ABPS (American Board of Plastic Surgery).

Nội dung chính và Tóm tắt

Phiên bản thứ ba này được cấu trúc thành các phần bao gồm 93 chương, đề cập đến các chủ đề thường được kiểm tra nhất trong Phẫu thuật Tạo hình và Tái tạo. Sách sử dụng định dạng câu hỏi và câu trả lời nhanh (rapid-fire), cho phép người đọc lướt qua một lượng lớn thông tin một cách hiệu quả.

Các nội dung chính bao gồm:

  • Phẫu thuật Thẩm mỹ (Aesthetic Surgery): Bao gồm các chương về phẫu thuật vùng quanh mắt, nâng mũi, căng da mặt, và các thủ thuật không xâm lấn như Botox và Filler.
  • Phẫu thuật Ngực (Breast): Giải phẫu, phẫu thuật nâng ngực, thu gọn ngực, và các kỹ thuật tái tạo ngực sau ung thư.
  • Bàn tay và Chi (Hand and Extremities): Giải phẫu bàn tay, điều trị chấn thương gân, thần kinh, gãy xương và các dị tật bẩm sinh.
  • Đầu và Cổ (Head and Neck): Chấn thương hàm mặt, ung thư đầu cổ, và các kỹ thuật tái tạo phức tạp.
  • Nhi khoa (Pediatrics): Các hội chứng sọ mặt, khe hở môi vòm, và các dị tật bẩm sinh khác.
  • Tái tạo (Reconstruction): Nguyên tắc lành thương, ghép da, vạt da, và vi phẫu thuật.

Đánh giá

Đây là một tài liệu tham khảo ngắn gọn, súc tích và hiệu quả cao, tập trung vào các sự kiện và khái niệm “phải biết” (must-know). Cuốn sách không chỉ hữu ích cho việc ôn thi mà còn là một nguồn tra cứu nhanh cho các bác sĩ trong thực hành lâm sàng hàng ngày.

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What is the incidence o pharyngocutaneous stula?
3% to 65% o all laryngectomies.

What are the risk actors or pharyngocutaneous stula ormation?
Several actors have been associated with the development o pharyngocutaneous stula including:
• Hgb < 12.5
• Neck dissection
• Prior radiation and chemoradiation

What is the incidence o salvage laryngectomy?
Salvage laryngectomy is per ormed a ter ailure o radiation to cure and occurs at a requency o 31% to 36% a ter
radiation but is lower at 16% to 28% a ter chemoradiation.

Does prior radiation increase the incidence o pharyngocutaneous stula a ter laryngectomy?
I laryngectomy is per ormed as the initial curative intervention, the rate o stula is 14.3% whereas i it is
per ormed in the setting o salvage laryngectomy then it is nearly double at 27.6%.

What morbidity and mortality is associated with pharyngocutaneous stula?
Pharyngocutaneous stula results in delays in adjuvant treatment, prolonged hospital stays, reoperation, aspiration
pneumonia, and possibly atal carotid blowout.

What are the reconstructive options or reconstruction a ter salvage laryngectomy?
T e most requently used are pedicled pectoralis major, ree jejunal, ree radial orearm, ree anterolateral thigh
(AL ) ap. Choice is in uenced by whether there is suf cient pharyngeal mucosa le t, whether there is a total
laryngopharyngectomy de ect, and whether there is a substantial cutaneous component to reconstruct as well.

What reconstructive option provides better speech outcomes?
Fasciocutaneous reconstruction with an AL has better speech outcomes than enteric ap options with less “wet”
sounding phonations.

What are appropriate anastomotic targets in the irradiation neck?
While easible, anastomoses to the carotid and jugular systems should be avoided as these tend to be encapsulated
in scar and are riable. Better options are those outside the radiated eld and include the transverse cervical,
thoracoacromial, and even the internal mammary arteries.

What is osteoradionecrosis?
It was initially de ned as “an area > 1 cm o exposed bone in a eld o radiation that had ailed to show any
evidence o healing or at least 6 months.” T ere have since been varying de nitions but the consensus is that there
is a history o radiation, there is mucosal breakdown with resultant exposed bone, exposed bone is necrotic, and
most importantly it occurs in the absence o recurrent tumor or metastasis.

How long a ter radiation does it occur?
Most authors agree that it usually will arise 3 to 6 months a ter completion o radiation therapy but can occur up
to 45 years a ter implying a li etime risk. T is is in contrast to normal healing in irradiated mucosa which can take
1 month.

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What is the incidence o osteoradionecrosis?
8.2% o radiated head and neck patients.

What is the pathophysiology o osteoradionecrosis o the mandible?
T e mandible is the most requently a ected and radiation’s e ects damage to its blood supply are thought to be
key. T e primary blood supply, the in erior alveolar artery, undergoes vessel narrowing and obliteration while the
smaller caliber collateral circulation provided by the acial artery via muscular attachments and periosteal vessels
undergoes brosis.

What are the risk actors or osteoradionecrosis?
Risk actors include:
• radiation dose: > 65 Gy in standard ractions con ers at 11- old risk increase
• radiation particle: high rates o severe osteoradionecrosis has been reported with neutron therapy
• tumor characteristics (stage III/IV, recurrences, advanced stage, location): invasion into bone is associated with a
signi cant increase in incidence
• poor hygiene

What are the indications or a tooth’s extraction in the prevention o osteoradionecrosis?
Historically all teeth in the radiation eld were removed. Current indications include:
• grossly carious
• advanced periodontal involvement
• poor prognosis (likelihood o retention < 12 months)
• patient unwilling/unable to maintain oral care

What is the timing o dental extraction in relation to radiation therapy?
Extraction is usually per ormed 2 to 3 weeks prior to the initiation o radiation therapy as tooth socket osteoid
ormation and epithelial repair is usually complete in 3 weeks. Any earlier and the risk o osteoradionecrosis is
actually increased.

What are the indications or surgical debridement?
While 60% o cases resolve with antibiotics, local wound care, and oral hygiene, the indications or surgery
include:
• large intraoral ulcerations
• orocutaneous stula
• pathologic racture
• radiographically evident osteolysis o in erior mandibular border

What is crucial in the surgical treatment o osteoradionecrosis?
All necrotic tissue must be removed (bone and involved so t tissue).
Radiation Craniofacial Grow th Disturbances

What head and neck tumors are treated with radiation?
Sarcoma (rhabdomyosarcoma, Ewing’s sarcoma, neuro brosarcoma), retinoblastoma, leukemia.

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What is the incidence o cranio acial growth disturbance in children receiving radiation or head and neck
tumors?
73% to 100% o survivors.

At what radiation dosages is cranio acial growth altered?
So t-tissue e ects are seen at 4 Gy and bony e ects are seen at 30 Gy.

What is pathophysiology o growth disturbances o the irradiated ace?
T e acial skeleton (viscerocranium) orms rom intramembranous ossi cation and is reliant upon the periosteum
or blood supply. T e periosteal blood ow is diminished rom radiation. In addition, the overlying so t-tissue
envelope becomes contracted and hypovascular.

What reconstructive options are best suited or reconstructing the irradiated pediatric patient’s bony de cits?
Despite being irradiated, orthognathic surgery and corrective osteotomies have been reported as success ul. In
addition, bone gra ting and o course vascularized bone ree aps can be utilized as well. Alloplastic options carry
the risk o in ection/extrusion.

What reconstructive options are best suited or reconstructing the irradiated pediatric patient’s so t tissue de cits?
T e degree o so t-tissue contour loss can be addressed with autogenous at gra ting but larger de cits may require
ree ap reconstruction. T e scapular ree ap is a avored option.
BREAST RECONSTRUCTION AND RADIATION

What are the di erent elds targeted in breast irradiation?
T e chest wall (including the mastectomy scar) and the three nodal basins: axillary, supraclavicular, and internal
mammary artery.

What are the current practice guidelines or irradiating each?
T e American Society o Clinical Oncology (ASCO) Guidelines outline the current evidence-based
recommendations or radiation therapy or each target eld:
• chest wall (single most important target in PMR )
• otal dose: 50 Gy
• Fractions: 1.8 to 2 Gy daily ractions over 5 d/wk
• Boost: 10 to 16 Gy ( ocused dose to mastectomy scar vs. treatment o chest uni ormly)
• Bolus: common (application o material with XR absorption equivalent to skin)
• Axillary nodal radiation
• Full axillary XR should NO be routinely given in patients with complete or level I/II dissections
• Supraclavicular nodal radiation
• Risk o supraclavicular recurrence contingent upon degree o axillary involvement
• > 4 nodes: 45 to 50 Gy in 1.8 to 2 Gy ractions
• 1 to 3 nodes: not recommended
• IMA nodal irradiation
• Insuf cient evidence as data are limited are contradictory; in addition increased risk or cardiac/pulmonary
toxicity
• Most series demonstrate IMA recurrence a rarity even when no XR
• Most XR delivery plans to chest wall may include nodal basin anyway

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What are the controversies in breast radiation treatment indications?
Several studies aim to evaluate broader indications or use o radiation therapy or breast cancer and ocus on
number o nodes with metastases, tumor size alone, and positive margins.

What is the usual timing o radiation delivery a ter mastectomy?
PMR is generally initiated within 4 to 8 weeks a ter mastectomy. I adjuvant chemotherapy is added, a delay o
up to 6 months to initiate PMR does not appear to comprise local-regional control. T e optimal time or PMR
in 2-stage implant-based reconstruction is controversial however.

When is delayed reconstruction avored over immediate autologous reconstruction?
Delayed autologous reconstruction is traditionally avored to avoid (1) a potential delay in the time to radiation
delivery, (2) potentially compromising the actual delivery o radiation to the chest wall, and (3) the avoidance o
radiation induced morbidity to an otherwise success ul ap reconstruction.

What is a primary result o aps exposed to radiation therapy?
Flap brosis, WHICH might lead to a rmer, less ptotic breast.

Do complication rates and ap compromise as a result o radiation therapy di er signi cantly be ore and
a ter autologous breast reconstruction?
Many studies have tried to address questions related to ap complications ollowing radiation therapy. Large
studies have demonstrated no signi cant di erences in total ap loss, wound healing complications, in ection,
hematoma, seroma, and at necrosis be ore or a ter autologous reconstruction.

What might prevent success ul radiation therapy ollowing breast reconstruction?
T e presence o a reconstructed breast, whether the breast was reconstructed with autologous tissue or an implant,
can compromise the design o the radiation elds to treat the internal mammary lymph node basin.

What is the ideal timing o delayed breast reconstruction ollowing radiation therapy?
Reconstruction needs to be postponed until any possible side e ects o radiation therapy have been diminished.
Pre erably, implant-based reconstruction needs to be avoided. Instead, additional coverage with nonradiated tissue
needs to be provided to cover the implant.

What is the risk o implant-based reconstruction ollowing previous radiation therapy?
Delayed implant-based reconstruction ollowing radiation therapy is associated with increased risk o capsular
contracture and revision surgery. Failure rates between 13.2% and 40% have been described.

What type o immediate reconstruction is recommended in postmastectomy patients who are in need o
additional radiation therapy?
When immediate reconstruction is being per ormed autologous reconstruction is pre erred over implant-based
reconstruction.

Does the implant reconstructed breast a ect oncologic outcomes (i.e., is it oncologically sa e)?
T us ar there has not ound to be a di erence either in recurrence nor survival with patients that underwent
implant-based reconstruction prior to radiation as compared to patients that had radiation completed and then
had reconstruction.

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What is the general rate o complication with implant-based reconstruction with a radiated patient?
T e rate o major complication (that requiring operative intervention) is 21.2% to 45.4% while only 70.1% o
patients retain their original implant.

What is the rate and onset o breast contracture?
While contracture can certainly occur in the absence o radiation, it is a known risk actor. T e 10-year risk o
contracture is 17% to 20% in irradiated patients versus 7% to 8% in patients that did not. Development o
contracture can take 5 to 7 years to occur though most severe contractures tend to appear within the rst
2 years post op.

What is the risk o in ection and what are causative organisms?
T e risk o in ection is 4.88 times greater with radiation and can occur in up to 24% o patients. T e most
commonly cultured organisms are Staphylococcus aureus and Serratia marcescens.

What is the incidence o implant extrusion?
16.5% in patients having received radiation.

What are some o the dif culties encountered when patient has already had their breast irradiated
(i.e., breast conserving therapy [lumpectomy and radiation])?
T ere is an increase in ap necrosis (18%) as compared to nonradiated patients (7%). Previously radiated chest
wall skin provides additional technical dif culty as there can be more pain, less over expansion o the skin
envelope, rib cage contour de ormity. T e resultant breasts tend to be harder, asymmetric, lack projection, and
are in more need o capsulotomies. T e rate o complication and poor aesthetics can be up to 60%.

What surgical strategies are available to mitigate the e ects o radiation upon the implant-reconstructed
breast?
iming reconstruction prior to radiation, capsulotomy, and acellular dermal matrix (ADM) interposition gra t,
and at gra ting.

What can the addition o ADM a ter capsulotomy provide?
T ere is mounting evidence that the addition o acellular dermal matrix (ADM) decreases capsule ormation by
decreasing the amount o contractile myo broblasts, the severity o brosis, and the degree o in ammation.
However, the data at the time being is limited to basic science studies and larger clinical studies have yet to be
published.

What utility can at gra ting provide?
Fat gra ting can certainly address contour de ormities and is relatively sa e. Patients with prior radiation tend to
require more repeat injections. Whether at gra ting can truly alter the capacity o radiated tissue to heal and/
or mitigate capsular contracture is less clear. While an early report demonstrated dramatic healing o radiation-
induced wounds the sample size was small (20 patients). T us ar case reports only suggest at gra ting may
improve contracture.

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de ects: prospective, randomized trial. J Otolaryngol Head Neck Surg. 2010;39:448–453.
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radiotherapy. Int J Radiat Oncol Biol Phys. 2006;66(1):76–82.
Mustoe A, Porras-Reyes BH. Modulation o wound healing response in chronic irradiated tissues. Clin Plast Surg. 1993;20(3):
465–472.
Nahabedian MY, Momen B. T e impact o breast reconstruction on the oncologic ef cacy o radiation therapy: a retrospective analysis.
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O’Donovan DA, Yeun I, Zeman V, Neligan PC, Pan CY, Forrest CR. Radiation-induced cranio acial bone growth inhibition:
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949–956.

231
Jacques A. Machol IV, MD and
John B. Hijjawi, MD, FACS

De ne gynecomastia.
Enlargement o the ductal, stromal, and adipose components o the male breast.

What is pseudogynecomastia?
Enlargement o the adipose tissue o the male breast; o ten seen in obesity.

In what three age distributions does gynecomastia peak?
Neonatal, pubertal, and adult.

What is the incidence o gynecomastia in each age group?
Neonates: 60% to 90%
Pubertal: 66%
Adults: 30% to 65%
Overall incidence is 35%.

What is the Simon classi cation o gynecomastia?
I: Small but visible breast development, no skin redundancy.
IIa: Moderate breast development, no skin redundancy.
IIb: Moderate breast development with skin redundancy.
III: Severe breast development with large skin redundancy.

Name the hallmark location and clinic chest examination ndings o gynecomastia.
Concentric mass directly beneath the nipple. O ten described as a palpable, tender, rm, mobile, disc-like mound.
Gynecomastia
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Name the three histopathologic classi cations.
Florid—increase in vascularity and ductal tissues, early nding < 4 months.
Fibrous— ewer ducts and stromal brosis, typically present a ter 1 year.
Intermediate—Mixture o the two as Florid transitions to Fibrous

What is the normal average areolar diameter in the male nipple areola complex?
25 to 30 mm.

What is the most common male nipple areola complex shape and location?
Oval and 20 cm rom the sternal notch.

What is symptomatic gynecomastia?
Breast pain and tenderness.

What is the incidence and cause o newborn gynecomastia?
60%; transplacental passage o estrogens.

Name the our clinical etiologies o gynecomastia.
Physiologic (neonatal, pubertal, senescent),
Pathologic
Pharmacologic
Familial

What is pathologic gynecomastia?
Gynecomastia secondary to underlying disease, that is,
• adrenal tumors
• hypogonadism (acquired or congenital)
• tumors
• liver disease

How is amilial gynecomastia genetically transmitted?
X-linked recessive.

What are the clinical characteristics o pubertal gynecomastia?
Glandular tissue is greater than 4 cm in diameter, resembling early emale breast development.

What is the pathogenesis o pubertal gynecomastia?
Imbalance o androgen to estrogen ratio, o ten occurring in early puberty.
Commonly seen in midpuberty with anner stage 3 to 4 pubic hair and testicular volumes o 5 to 10 mL
bilaterally.

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233

What are the Tanner stages?
Tanner I
Male: Prepubertal genitalia
Female: Prepubertal genitalia, no glandular breast tissue; areola ollows chest wall
Pubic Hair: Vellus pubic hair, no sexual hair
Tanner II
Male: Genital enlargement and change in skin texture
Female: Breast budding
Pubic Hair: Sparse, long, pigmented downy hair
Tanner III
Male: Growth in penile length and circum erence
Female: Continued breast enlargement, no separation o contour
Pubic Hair: Darker, coarser, curlier
Tanner IV
Male: Penis enlarged in length and circum erence. Enlarged testes
Female: Areolar and papillae elevation and secondary mound ormation
Pubic Hair: Adult in quality but decreased distribution
Tanner V
Male: Adult genitalia
Female: Mature emale breasts
Pubic Hair: Adult in quality, may spread onto medial thighs

What is the typical course o pubertal gynecomastia?
Sel -limited in 75% to 90% o adolescents, regressing over 1 to 3 years.

What is the pathogenesis o senescent gynecomastia?
Primary testicular ailure resulting in hypogonadism, and increased adipose tissue, leading to increased production
o estrogens by aromatase.

Which drugs are strongly associated with gynecomastia?
• Digoxin
• Estrogens
• Ketoconazole
• Cimetidine
• Spironolactone
• Flutamide
• Anabolic steroids
• Marijuana

What is the pathogenesis o drug-induced gynecomastia?
Administration o exogenous estrogens (i.e., prostate cancer hormone therapy, topical estrogen creams)
Reduction o serum testosterone (i.e., ketoconazole, alkylating agents)
Direct gonadal suppression, (i.e., chemotherapy agents)
Blockade o androgen action (i.e., cimetidine, spironolactone, marijuana)

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Elevated levels o which gonadotropins lead to gynecomastia?
Luteinizing hormone (LH) and human chorionic gonadotropin (HCG).

How does primary testicular ailure cause increased estrogen to androgen ratio and gynecomastia?
Reduced androgen production and increased aromatase activity in Leydig cells, resulting in increased estrogen
levels.

By what mechanisms do testicular tumors increase estrogens?
Steroid-producing tumor cells and paraneoplastic production o HCG.

What mechanisms are thought to cause gynecomastia associated with hyperthyroidism?
Increased peripheral conversion o androgens to estrogens and increased sex hormone binding globulins.

What two mechanisms result in gynecomastia in liver tumor patients?
Increased HCG secretion and increased aromatization o circulating adrenal androgens.

What endocrinopathies lead to gynecomastia?
Hypogonadism, hyperthyroidism, and adrenal disorders.

What tumors are associated with pubertal gynecomastia?
Endocrine (pituitary, adrenal, and testicular), liver, and breast.

What chronic diseases are associated with gynecomastia?
• Ulcerative colitis
• Cystic brosis
• HIV
• Liver disease
• Malnutrition
• Renal ailure

What congenital orm o primary gonadal ailure has gynecomastia as a common nding?
Kline elter syndrome (47XXY karyotype).

Which congenital cause o gynecomastia is associated with an increase in breast carcinoma?
Kline elter’s. T ese patients may have up to a 50- old increase risk or breast cancer versus the regular male
population.

What pertinent physical examination ndings should be assessed?
Pubertal development stage, presence o any testicular masses, breast and axilla examination.

I the testicles are asymmetric in a man with gynecomastia, what test should be ordered and why?
Ultrasound to rule out testicular tumor.

CHAPTER 27 Gynecomastia
235

What percentage o testicular tumors present with gynecomastia?
5% to 10%.

What physical examination ndings help to dif erentiate gynecomastia rom breast cancer?
Gynecomastia is characterized by a concentric disc o subareolar tissue.
Breast cancer is usually an ill-de ned subareolar eccentric mass, which is hard, painless, ulcerated, and immobile,
may have nipple retraction, and exhibit discharge.

What should be suspected with an eccentric breast mass?
Malignant mass.

When should radiographic studies be used to evaluate gynecomastia?
o rule out malignancy when an eccentric breast mass is noted.

What radiographic modalities can be used to evaluate gynecomastia?
Ultrasound and mammography.

Describe the mammographic patterns seen with gynecomastia.
Nodular, dendritic/ brous, and di use glandular patterns.

Which laboratory tests should be obtained in pubertal gynecomastia?
No routine tests. est i abnormalities are suspected rom the history and physical examination. Consider
Endocrinology consultation.

What is the most common treatment in pubertal gynecomastia a ter an unremarkable complete work up?
Observation and reassurance as pubertal gynecomastia i o ten sel -limited.

When is surgical intervention considered or pubertal gynecomastia?
A ter a period o observation o at least 12 months, in nonobese males with persistent gynecomastia and no
improvement in breast pain or tenderness. Marked psychosocial distress also an indication.

List other indications or surgical correction o gynecomastia.
Social behaviors negatively a ected by the condition, brotic or symptomatic male breasts, and/or patients at risk
or carcinoma o the breast (Kline elter syndrome).

What patient history in ormation is important in the gynecomastia patient?
Onset, duration, decreased libido, erectile dys unction, in ertility, medication history, nipple discharge, amilial
history, and history o chronic disease.

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Which laboratory tests should be obtained in adult onset gynecomastia?

What is the typical serum prolactin level in patients with gynecomastia?
Normal.

Which conditions cause elevated prolactin levels in association with gynecomastia?
Prolactin-secreting pituitary neoplasms and hypothyroidism.

Name the modalities or treating gynecomastia.
Surgery and pharmacologic.

What medical treatments have shown to be ef ective or gynecomastia?
• Danazol and anastrozole
• amoxi en and raloxi ene
• estosterone

What ef ect does tamoxi en have on gynecomastia?
Reduction in breast pain and a slight decrease in breast size.

What percentage o patients experience reduction in breast size with tamoxi en use?
80% experience reduction, 60% achieve complete regression a ter 3 months. amoxi en may also be used to
prevent gynecomastia secondary to f utamide therapy. Surgery is the mainstay treatment.

How success ul is radiation in reducing gynecomastia?
Incidence o gynecomastia decreased to 28% i radiation was given prophylactically to prevent gynecomastia
secondary to f utamide treatment. Radiation not typically used to treat other orms o gynecomastia.

What surgical options are available to treat gynecomastia?
Liposuction, subcutaneous mastectomy through various approaches, arthroscopic shaving, and combination
therapy.

For which types o gynecomastia might standard liposuction be adequate?
Simon grade 1 or grade 2A. Simon 2b as well, but may require staged skin excision.

How is standard liposuction use ul in gynecomastia?
Reduces bulk o breast ullness when a high percentage o breast tissue is at and aids in contouring.
• Electrolytes
• Liver unction tests
• T yroid unction tests
• Blood urea nitrogen and creatinine
• estosterone and estradiol
• Follicular-stimulating hormone, LH, and HCG

CHAPTER 27 Gynecomastia
237

What technique is most use ul or brous gynecomastia without skin excess?
Ultrasound-assisted liposuction (UAL).

What is the Rohrich classi cation system in terms o work up or UAL?
Grade I: Minimal hypertrophy (< 250 g o breast tissue) without ptosis
Grade II: Moderate hypertrophy (250–500 g o breast tissue) without ptosis
Grade III: Severe hypertrophy (> 500 g o breast tissue) with grade I ptosis
Grade IV: Severe hypertrophy with grade II or III ptosis

Name skin excision techniques.
Circumareolar incision encompassing the superior or in erior hal o the areola. Also, omega, concentric circle, and
in ramammary incisions.

What technique can be used with severe gynecomastia?
Free nipple gra ting with crescent excision.

Where should an incision be placed to maximize the cosmetic outcome o male mastectomy?
Periareolar incision.

Why are incisions in the areola avoided?
Scars in the pigmented areolar skin are white.

What is the concern about incisions into the skin lateral to the areola?
Increased likelihood o hypertrophic scarring.

How deep should the periareolar tissue be incised and undermined to avoid nipple inversion?
A 5- to 10-mm-deep incision with 1 cm o tissue le t beneath the areola prevents an inverted nipple and adherence
to the chest ascia.

Where should drains be placed or best cosmetic result?
T rough the axilla or through a periareolar incision.

List the complications associated with surgical resection.
• Inversion o nipple or areola
• Doughnut/saucer de ormities
• Necrosis o nipple areolar complex
• Contour de ormity
• Un avorable scarring
• Skin redundancy
• Inadequate excision
• Asymmetry
• Hematoma/seroma
• In ection

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Plastic & Reconstructive Surgery Board Review

What is the “doughnut” or “saucer” de ormity?
Over resection beneath nipple areolar complex causing a concave appearance.

How do you avoid the saucer de ormity?
Maintain adequate thickness on the nipple areolar f ap.

How can one treat the saucer de ormity?
Release o the nipple scarring to the pectoralis ascia and interposition o at gra ting.

How can chest concavity be avoided ollowing male mastectomy?
Leave a layer o subcutaneous at over the pectoralis ascia.

What is the most common complication with direct excision?
Hematoma or seroma (immediate), underresection (long term).
REFERENCES
Beer GM, Budi S, Sei ert B, Morgenthaler W, In anger M, Meyer VE. Con guration and localization o the nipple-areola complex in
men. Plast Reconstr Surg. 2001;108(7):1947–1952.
Bostwick J III. Aesthetic problems. In: Plastic and Reconstructive Breast Surgery. 2nd ed. St Louis, MO: Quality Medical Publishing;
2000:584–607.
Braunstein GD. Clinical practice. Gynecomastia. New Eng J Med. 2007;357:1229–1237.
Daniels IR, Layer G . Gynaecomastia. Eur J Surg. 2001;167:885–892.
Hammond DC. Surgical correction o gynecomastia. Plast Reconstr Surg. 2009;124(1Suppl):61e–68e.
Hultborn R, Hanson C, Kop I, Verbiene I, Warnhammar E, Weimack A. Prevalence o Kkline elter’s syndrome in male breast cancer
patients. 1997;17(6D):4293–4297.
Laituri CA, Garey CL, Ostlie DJ, St Peter SD, Gittes GK, Snyder CL. reatment o adolescent gynecomastia. J Pediatr Surg. 2010;45:
650–654.
Lemaine V, Cayci C, Simmons PS, Petty P. Gynecomastia in adolescent males. Semin Plast Surg. 2013;27(1):56–61.
Narula HS, Carlson HE. Gynecomastia. Endo Metab Clin North Am. 2007;36:497–519.
Petty PM, Solomon M, Buchel EW, ran NV. Gynecomastia: evolving paradigm o management and comparison o techniques. Plast
Reconstr Surg. 2010;125(5):1301–1308.
Rohrich RJ, Ha RY, Kenkel J, WP Adams. Classi cation and management o gynecomastia: de ning the role o ultrasound-assisted
liposuction. Plast Reconstr Surg. 2003;111:909–923.
Volpe CM, Ra etto JD, Collure DW, Hoover EL, Doerr RJ. Unilateral male breast masses: cancer risk and their evaluation and
management. Am Surg. 1999;65:250–253.
Wise GJ, Roorda AK, Kalter R. Male breast disease. J Am Coll Surg. 2005;200:255–269.

239
Theodore T. Nyame, MD

Where does the nipple–areolar complex (NAC) get its innervation rom?
Predominately rom the lateral cutaneous branches o the ourth intercostal sensory nerve. T ese bers course
deep within the pectoralis ascia be ore rising to innervate the NAC rom its posterior sur ace in 93% o cadaveric
specimens.

What is the sensory innervation to other areas o the breast?
T e upper pole is innervated by the supraclavicular nerves, which come rom the third and ourth branches o
the cervical plexus. T e medial and lateral breast is innervated by the anterior and lateral cutaneous branches o
intercostals nerves II to VII.

What is the dominant vessel in the arterial supply to the breast?
T e major blood supply comes rom the internal mammary artery (IMA) per orators (estimated 60% total), with
signi cant collaterals rom the lateral thoracic artery, the thoracoacromial trunk, the thoracodorsal artery, as well as
numerous intercostal per orators rom interspaces 3 to 5.

What are some relative preoperative indications that a ree-nipple gra t may be required during reduction
mammoplasty?
• Nipple transpositions > 25 cm
• Smokers
• Patients with diabetes

What determines the cup size o a bra?
Cup size is a common re erence point when patients describe their goals or breast reduction and describes the
relationship o breast girth to chest girth. I breast girth exceeds chest girth by 1 in, the cup size is an A; 2 in is a B;
3 in is a C, 4 in is a D, and 5 in is a DD.
Breast Reduction and
Mastopexy
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What is Regnault’s correlation between chest girth and the amount o glandular resection required to
approximate bra cup size?

What is the management o the dusky postoperative NAC?
1. Release the sutures holding the NAC to make sure there is no tension-related problem.
2. I no brisk change in appearance, the ap should be opened in the operating room to check or pedicle-kinking
or hematoma that could explain the ischemia.
3. Application o nitroglycerin paste to the NAC or a vasodilation e ect should be considered.
4. I these maneuvers are ine ective, a ree-nipple gra t should be per ormed on a deepithelialized bed.
5. T ere are several case reports o salvage o ischemic NACs with hyperbaric oxygen.

Why does a ree-nipple gra t survive when an NAC on a dermal-glandular pedicle will not?
T e metabolic demands o the NAC as a skin gra t are less.

What is the aesthetic appearance o a ree-nipple gra t?
T ere is always some degree o hypopigmentation that may require tattooing, especially in dark-skinned patients.
Excision o the hypopigmented portions is also an option. Following a ree-nipple gra t the nipple lacks projection.

In the rare cases requiring a repeat reduction mammoplasty, what should be done when the previous pedicle
type is unknown?
Strong consideration should be given to a planned ree-nipple gra t. I you do know the previous pedicle design,
the same pedicle should ideally be used to minimize the risk o devascularizing either the NAC or the pedicle itsel .
Studies have shown that repeat reduction can be done sa ely without knowledge o the previous pedicle and
without resorting to a ree-nipple gra t.

Is a deepithelialized dermal pedicle required to maintain NAC viability?
No, although it theoretically provides a greater margin or error. T e NAC can clearly survive on a well-designed
glandular pedicle alone in avorable patients.

What is the advantage o a closed (vs. open) design with a Wise inverted-T pattern-type ap design?
A closed design, one in which the NAC opening is not initially precut in the incision, allows much greater
exibility or placing the nipple at the proper projecting part o the breast as well as allowing adjustments or
symmetry with the contralateral breast.
Chest Circum ference (in)
Am ount to Rem ove for Each
Cup Size Reduction (g)
32–34

100
36–38

200
42–44

300
44–46

400

CHAPTER 28 Breast Reduction and Mastopexy
241

What is the key di erence between the classic Strömbeck and McKissock techniques?
Both are inverted -style designs with bipedicled dermoglandular aps. T ey di er in the pedicle orientation
with the Strömbeck oriented horizontally, while the McKissock “bucket handle” is olded on itsel and oriented
vertically.

What are the odds o f nding an occult breast cancer in a breast reduction specimen?
Retrospectively, this has been estimated between 0.16% and 0.4% in several recent studies.

What is the e ect o reduction mammoplasty on breast cancer risk?
In peri- and postmenopausal women (age 40+ ), there was consistent reduction in relative risk or developing
breast cancer o between 50% and 70%.

What is the reduction in breast cancer risk a ter prophylactic mastectomy?
T e reduction in risk or developing breast cancer is 90% or bilateral prophylactic mastectomy. A unilateral
prophylactic mastectomy a ter developing breast cancer in the contralateral breast approaches a 95% risk
reduction.

Where is the most common place or keloid scarring to occur with breast reductions?
At the medial edge o the transverse incision.

What are the recommendations or mammograms postreduction?
A postreduction mammogram 6 months a ter reduction should be per ormed to establish a new baseline image or
uture comparison.

What is the result o overly long in ramammary old (IMF)-NAC vertical limbs with Wise-pattern in erior
pedicle procedures?
As the length o the vertical limb increases much beyond 5 cm, premature bottoming-out o the tissue has been
requently observed.

Who are the best candidates or good results with suction-assisted lipectomy (SAL) breast reductions?
T e best candidates are breasts with little to no ptosis and a higher- atty composition. Generally, older women
with smaller breasts.

What is the e ect o SAL on breast mammography?
A number o small clinical series have not produced the eared postoperative calci cation that can necessitate
urther workup to rule out malignancy in the short-term ollow-up. However, removal o at alone rom a breast
does increase the density o the breast and so can change the appearance o a mammogram.

What percentage o people may be able to success ully breast- eed a ter reduction mammoplasty?
Up to 68% in some studies. T is is nearly equivalent to the rate o success ul attempts at breast- eeding in women
who have never had breast reduction.

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Plastic & Reconstructive Surgery Board Review

True/False: Patients who have larger breast reductions experience increased relie o symptoms than patient
with smaller reductions.
False: Based on clinical evidence resection weight does not correlate to the degree o symptomatic relie .

True/False: Patients who have larger breast reduction specimens experience increased complications.
rue: Increased resection weights are associated with increased BMI and there ore increased complications.

What is virginal (juvenile) hypertrophy?
T e abrupt development o unilateral or bilateral gigantomastia in adolescent girls presumably secondary
to estrogen hypersensitivity. reatment includes reduction mammoplasty with the addition o tamoxi en
postoperatively to lower the risk o recurrence. Reduction alone has high-recurrence rates.

What are the di erential diagnoses when considering virginal hypertrophy?
• Fibroadenoma
• Cystosarcoma phyllodes
• Breast hamartoma
• Posttraumatic phenomena

What is the role o estrogen in the breast?
Estrogen acilitates ductal growth.

When can you sa ely operate on adolescent patients with virginal breast hypertrophy?
Adolescents with breast enlargement out o proportion to menarche who demonstrate stabilization o breast size
or greater than 1 year may be considered or surgery.

What are the characteristics o the vertical breast reduction technique as described by Dr. Madeline Lejour?
T e Lejour technique includes:
• superior-based NAC pedicle
• a “mosque”-shaped skin excision pattern
• aggressive liposuction sculpturing prior to glandular resection
• liberal lower-pole parenchymal resection
• plication o medial/lateral parenchymal “pillars” to attain projection
• a short vertical limb that does not violate the IMF
An important conceptual change rom previous reduction procedures is the avoidance o relying on the skin
brassiere alone to maintain shape.

How does the Hall–Findlay reduction di er rom the Lejour technique?
T e Hall–Findlay procedure uses a superior-medial pedicle with a liberal lateral-in erior glandular resection.
Liposuction is used or nal contouring and addressing residual axillary ullness rather than early in the procedure
as in the Lejour technique.

CHAPTER 28 Breast Reduction and Mastopexy
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What is the conceptual advantage o many o the medial and superior pedicles to the in erior pedicle?
T e resection o the dependent in erior glandular tissue is maximized, while upper pole ullness is maintained.

What is the upper size limit o reductions that Dr. Lejour believes can be done satis actorily with a VBR
technique?
1,000 g. O note, many surgeons eel aesthetic outcome starts to be compromised at 400 to 500 g with VBR.

What is the immediate postoperative shape characteristic o the VBR?
Frequently, it is described as looking like “an upside-down breast” with exaggerated upper pole ullness, a hollow
in erior pole, downward-projecting nipples, and a bunched vertical limb with a puckered appearance. T is
predictable shape settles out into a pleasing appearance over several months with a low incidence o revisions o
the puckered scar required.

Is the in erior pedicle wise pattern superior to the vertical breast reduction?
T e literature suggests similar relie o symptoms with either technique.

How is breast ptosis graded?
• First degree: nipple position at the IMF
• Second degree: nipple position below the IMF, but above the lowest level o the breast
• T ird degree: nipple position has descended below the lowest level o the breast

What is pseudoptosis?
Where the breast mass descends behind the NAC, but the nipple position remains above the IMF.

What is the most common planning error with breast reduction or mastopexy procedures?
Placing the nipple position too high, resulting in a very di cult to correct de ormity many times.

What are some rough guidelines or deciding nipple position?
A sternal notch-to-nipple distance between 21 and 23 cm and an in erior limb length o 5 to 7 cm are the most
commonly recommended. ransposition o the nipple to the IMF (“Pitanguay’s point”) along the breast meridian
establishes a pleasing grade I ptosis.

When might you commonly have to place a nipple above IMF during a reduction or mastopexy?
When per orming a unilateral symmetry procedure to a contralateral reconstructed breast, which requently have
higher NACs rom the rounded shape and capsular contraction o implant reconstruction.

What are stereotypical changes to the IMF produced by in erior pedicle procedures versus superior or
medial pedicle designed?
T e classic in erior pedicle tends to lower the IMF, while the superior, medial, and superior-medial procedures o
Lejour and Hall–Findlay predictably raise the IMF.

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How do you account or the IMF position when doing a vertical reduction to avoid crossing it with the
vertical limb?
T e lower border o the mosque design will need to terminate several centimeters above the existing IMF.
Recommendations are a 2-cm distance or small reductions and mastopexies, and up to a 6 cm or the larger
reductions (800 g+ ).

Relaxation o what structure allows breast ptosis?
Cooper’s ligaments speci cally, combined with atrophy o the glandular tissue.

What usually determines the need or mastopexy a ter implant explantation?
T e level o ptosis preoperatively, as it usually is not changed signi cantly post removal.

What are some relative contraindications to circumareolar (“doughnut”) mastopexy techniques?
• > 24 cm sternal notch–NAC distance
• Grade 2 or greater ptosis
• Skin laxity
• When breast implants are being signi cantly downsized or removed at the same operation

What are the most common problems with the periareolar mastopexy procedures?
Unpredictable scarring and widening o the NAC over time due to tension. In addition the purse-string e ect has
the e ect o attening the breast and decreasing projection.

How does the Benelli “round block” technique or periareolar mastopexy address problems with the
scarring?
By transmitting the tension away rom the NAC and onto the deeper dermal layer o the surrounding skin with a
permanent circum erential suture that establishes the new areolar width.

What are the two most common techniques or mastopexy in a patient with grade II ptosis?
T e superior pedicle with vertical pattern skin excision and in erior/central pedicle with Wise pattern skin excision
are use ul when moderate ptosis is present.

Where does the arterial blood supply or the superior pedicle come rom?
T e superior pedicle receives its arterial blood supply rom the internal mammary artery at the level o the second
interspace.

Where does the arterial blood supply or the in erior and central pedicle come rom?
T e in erior pedicle and central pedicle receive their blood supply rom intercostal branches o the internal
mammary system rom the ourth interspace.

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How is tuberous breast de ormity classif ed?
ype I: Minor breast constriction with su cient skin envelope, mild ptosis and enlargement o the areola
ype II: Moderate breast constriction with insu cient skin at the lower pole, mild ptosis and moderate herniation
o the areola
ype III: Severe constriction with global skin de ciency, moderate ptosis and severe areola herniation.

What are the principles o addressing the tuberous breast de ormity?
• Augmentation o the hypoplastic breast tissue (may require tissue expansion prior)
• Lowering o the IMF
• Radial scoring o the parenchyma to allow redraping
• Circumareolar reduction o the oversized NAC

What position should the implant be placed or correction o a tuberous breast de ormity?
For tuberous breast correction a subglandular placement allows the prosthesis to shape and expand the constricted
breast tissue.

What options exist or severe tuberous breast de ormities not amenable to single stage correction?
Staged reconstruction with tissue expansion is a use ul option or ype III de ormities with insu cient skin and
sever lower-pole constriction.

When combining breast augmentation and mastopexy procedures, what are some general recommendations
or placing the NAC in relation to the sternal notch?
T e li t achieved rom the augmentation can reduce the distance necessary to elevate the NAC. Some guidelines
espoused or predicting this relationship include:
• 225 cc or less implants = > NAC should be placed at approximately 21 cm
• 250 to 325 cc implant = > NAC placed at 22 cm
• 350 cc and above implants = > NAC placed at 23 cm

When should a staged mastopexy/augmentation procedure be considered?
When more than 3 cm o nipple elevation is required, the predictability o the combined procedure starts to get
more di cult and has been suggested by some to be a guideline or staging the procedures or best results.

What is the unique eature o the Goes mesh mammoplasty technique?
Support o the breast mound with an internal Vicryl-polyester mesh tacked down to pectoralis ascia, which
maintains the shape postoperatively in part due to scarring around the mesh.

What are other techniques used to support the in erior pole a ter mastopexy?
Experience rom using dermal allogra t and xenogra t material rom reconstructive surgery has led to the
incorporation o the in erior “dermal sling” concept. In this technique, the material is sewed to the chest wall
along the in ramammary old to of oad tension on the in erior pole skin.
Gra and Biggs have long written o the technique o passing mammoplasty pedicles through parts o the
pectoralis major muscle (“pectoral loops”) to accomplish similar support o the lower pole.

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REFERENCES
Antony AK, Yegiyants SS, Danielson KK, et al. A matched cohort study o superomedial pedicle vertical scar breast reduction
(100 breasts) and traditional in erior pedicle Wise-pattern reduction (100 breasts): an outcomes study over 3 years. Plast
Reconstr Surg. 2003;132(5):1068–1076.
Benelli L. A new periareolar mammaplasty: the “round block” technique. Aesthetic Plast Surg. 1990;14:93–100.
Courtiss EH, Goldwyn RM. Reduction mammaplasty by the in erior pedicle technique. An alternative to ree nipple and areola gra ting
or severe macromastia or extreme ptosis. Plast Reconstr Surg. 1977;59:500–507.
Hall-Findlay EJ. A simpli ed vertical reduction mammaplasty: shortening the learning curve. Plast Reconstr Surg. 1999;104:748–759.
Hester R Jr, Bostwick J III, Miller L, Cunningham SJ. Breast reduction utilizing the maximally vascularized central breast pedicle.
Plast Reconstr Surg. 1985;76:890–900.
Hidalgo DA. Improving sa ety and aesthetic results in inverted scar breast reduction. Plast Reconstr Surg. 1999;103:874–886.
Lassus C A 30-year experience with vertical mammaplasty. Plast Reconstr Surg. 1996;97:373–380.
Lejour M. Vertical mammaplasty and liposuction o the breast. Plast Reconstr Surg. 1994;94:100–114.
Rohrich RJ, Ha RJ, Kenkel JM, Adams WP Jr. Classi cation and management o gynecomastia: de ning the role o ultrasonic-assisted
liposuction. Plast Reconstr Surg. 2003;111:909–923.

HAND AND EXTREMITIES
Section III

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249
Simon G. Talbot, MD and
Amir H. Taghinia, MD
EMBRYOLOGY
General Organization of the Limb

What tissues comprise the limb bud?
Mesenchyme covered by ectoderm. T e limbs grow by proli eration o mesenchyme.

Which genes regulate patterning in limb development?
Homeobox-containing (HOX) genes.
Timing

When do the limb buds rst appear?
oward the end o the 4th week o development, at which time a group o mesenchymal cells in the lateral
mesoderm are activated. T e buds are visible by day 26 to day 27.

When is the critical period or upper limb development?
wenty- our to 36 days a ter ertilization.

When are nger buds visible?
T e end o week 6.

When does ossi cation occur?
Between weeks 8 and 12, ossi cation o the cartilaginous ramework occurs. Epiphyses gradually ossi y until the
termination o puberty.

What are the last bones to ossi y within their cartilaginous ramework?
T e carpal bones in which ossi cation begins during the rst year o li e.
Hand Anatomy/
Embryology
CHAPTER 29

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Does sensory or motor innervation occur rst?
Sensory axons enter the limb a ter motor axons and use these or guidance.

When is nervous system myelination completed?
Around 2 years o age.
Axes of Development

What is responsible or proximodistal development?
T e apical ectodermal ridge (AER), which expresses endogenous broblast growth actors.

What is responsible or radioulnar development?
T e zone o polarizing activity, ound in the posterior margin o the limb bud, and activated by broblast growth
actors rom the AER that cause Sonic hedgehog (SHH) gene expression.

What is responsible or dorsoventral development?
Expression o wingless-type MM V integration site amily member 7A WN 7 and engrailed-1 (EN1) rom the
dorsal and the ventral epidermis, respectively.
Tissue Differentiation

What process is responsible or syndactyly occurrence?
Apoptosis, likely mediated by bone morphogenic proteins signaling GF-β.

How common is syndactyly and which digits are most commonly a ected?
Occurs in 1 in 2,200 births, most commonly a ecting the webspace between the middle and ring ngers.

Which arteries supply the limb buds?
Dorsal intersegmental arteries arising rom the aorta.
Congenital Deformities

Outline the American Society or Surgery o the Hand classi cation o congenital de ormities o the hand.
T e original classi cation scheme was proposed by Swanson:

i. Failure o ormation
ii. Failure o di erentiation
iii. Duplication
iv. Overgrowth

v. Undergrowth
vi. Constriction band syndromes
vii. Generalized anomalies and syndromes

CHAPTER 29 Hand Anatomy/Embryology
251
HAND ANATOMY
Surface Anatomy

What is the anatomic snu box?
T e area bounded by the tendons o the abductor pollicis longus (APL) and extensor pollicis brevis (EPB)
anteriorly and the tendon o the extendor pollicis longus posteriorly. T e f oor is ormed by the scaphoid and
trapezium, and it is a requent site o tenderness a ter scaphoid racture (see Fig. 29-1).
Figure 29-1 Diagram demonstrating boundaries o the anatomic snu box.
APL
EPB
Radial
artery
Dorsal sensory branch
of radial nerve
ECRL and
ECRB
EPL

Where is the metacarpophalangeal (MCP) joint relative to the MCP palmar exion crease?
Proximal.

What is the “ xed unit” o the hand?
T e distal carpal row and second and third metacarpals.
Soft Tissue
Fingertip

What is a elon?
A subcutaneous abscess o the distal digital pulp. It involves the septal compartments and causes compartment
syndrome o the distal phalangeal pulp. I the pad is not involved, then it is an “apical in ection” instead.

What is the normal value or moving two-point discrimination o the ngertip?
wo to 3 mm, with best discrimination occurring in individuals in their 20s and in ulnar-sided digits. A score o 7
out o 10 correct answers determines the value o two-point discrimination.

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Nail and Nail Bed

What is the perionychium? Paronychium? Hyponychium? Eponychium? Lunula?
T e perionychium includes the nail bed, nail old, eponychium, paronychium, and hyponychium. T e
paronychium is the skin on either side o the nail bed. T e hyponychium is skin distal to the nail bed. T e
eponychium is the skin proximal to the nail that covers the nail old. T e white arc in the proximal nail is the
lunula and is the distal extent o the germinal matrix. Distal to this is the sterile matrix (see Fig. 29-2).
Figure 29-2 Perionychium (E), lunula (F), nail bed (G), germinal matrix (H), sterile matrix (I), nail plate (J), hyponychium (K), and distal
groove (L).
E
F
J
H
I

Which tissues contribute to nail growth?
T e germinal matrix produces approximately 90% o the nail, while the sterile matrix adds a thin layer o cells
underneath the nail to ensure its adherence.

What is a paronychia?
Acute paronychia is in ection o the paronychial tissues.

How long does a nail take to grow?
Approximately, 6 months or the entire nail to regrow.
Muscles

Name the median innervated intrinsic muscles o the hand.
T e intrinsic muscles o the hand are innervated by the ulnar nerve, except the radial two lumbricals, opponens
pollicis, abductor pollicis brevis, and super cial head o the f exor pollicis brevis (mnemonic: Meat-LOAF).

Which muscle is most involved in lateral epicondylitis (“tennis elbow”)?
Extensor carpi radialis brevis (ECRB).

What are the unctions o the palmar and dorsal interossei?
T e interossei originate rom the metacarpal sha ts and orm the lateral bands, aiding in the unction o the
lumbrical muscles. In addition, the Palmar interossei ADduct the ngers and the Dorsal interossei ABduct the
ngers (mnemonic: PAD-DAB).

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What is a lumbrical plus de ormity?
A lumbrical plus de ormity is characterized by paradoxical extension o the proximal interphalangeal (PIP) joint
with attempted digital f exion. T is is due to excessive tension on the lumbrical muscles through the FDP tendon
with f exion causing pull on the lateral bands, o ten the result o FDP retraction a ter a distal amputation.

Name the thenar muscles. What order are they in?
Super cial to deep, they are:
• abductor pollicis brevis
• f exor pollicis brevis
• opponens pollicis
• adductor pollicis

Name the hypothenar muscles.
• Palmaris brevis
• Abductor digiti minimi
• Flexor digiti minimi brevis
• Opponens digiti minimi

Which muscle group in the orearm is most susceptible to compartment syndrome?
T e f exor digitorum pro undus.

Name the muscles o the mobile wad.
Brachioradialis, ECRB, extensor carpi radialis longus (ECRL).

How can you test or extensor pollicis longus (EPL) unction?
Ask the patient to rest their hand palm down on a table and li t the thumb—only the EPL can move li t the
thumb dorsal to the plane o the palm.
Fascia and Ligaments

What are Cleland’s and Grayson’s ligaments?
Cleland’s ligaments connect the digital ascia to the sides o the phalanges and are not involved in Dupuytren
disease. T ey lie dorsal to the neurovascular bundle. Grayson’s ligaments connect the tendon sheath to the digital
ascia and are o ten involved in Dupuytren disease. T ey lie volar to the neurovascular bundle.

What are natatory ligaments?
T is is another name or the super cial transverse metacarpal ligaments and these help to create the webspaces.
T ese coalesce distally with the spiral bands and may be involved in Dupuytren’s disease.

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What are the boundaries and contents o the carpal tunnel?
1. Roo : transverse carpal ligament
2. Floor: carpal bones
3. Radial border: scaphoid and trapezium
4. Ulnar border: pisi orm and hamate
5. Contents: the median nerve and nine tendons (f exor digitorum super cialis [FDS], f exor digitorum
pro undus [FDP], and f exor pollicis longus [FPL])

What are the boundaries and contents o Guyon’s canal?
1. Roo : volar carpal ligament and pisohamate ligament
2. Floor: transverse carpal ligament
3. Ulnar wall: pisi orm
4. Contents: ulnar nerve and artery

What is the oblique retinacular ligament?
A ligament running between the f exor tendon sheath at the proximal phalanx and the terminal extensor tendon,
linking f exion and extension between the interphalangeal joints.

What is the transverse retinacular ligament?
T ey are ligaments that span the edge o the f exor tendon sheath to the conjoined lateral bands, preventing dorsal
shi t o the lateral bands, and thus preventing a swan neck de ormity.

What are the pulleys? What do they do? How many pulleys are there? Which pulleys are the most important?
T ickened areas o the synovial sheath. T ey prevent bowstringing o the f exor tendons. T ere are ve annular
and our cruciate pulleys in each o the ngers and two annular and one oblique pulley in the thumb. A2, A4, and
the oblique pulleys are essential to prevent bowstringing (see Fig. 29-3).
Figure 29-3
A5
C3 A4
C2
A3
C1
A2
A1

What is a boutonniere de ormity?
PIP hyperf exion with distal interphalangeal (DIP) hyperextension, which may be caused by extensor mechanism
injury, synovitis, or iatrogenic causes.

What is a swan neck de ormity?
PIP joint hyperextension with DIP joint f exion, which may be due to multiple potential causes including FDS
loss, synovitis, mallet de ormity, or iatrogenic causes.

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Bursae and Spaces

Name the seven potential spaces and two bursae in the hand.
1. T enar space
2. Midpalmar space
3. Hypothenar space
4. Interdigital webspace
5. Dorsal subcutaneous space
6. Dorsal sub-aponeurotic space
7. Parona’s space
In addition to the above, the radial and ulnar bursae.

What is a collar button abscess?
A webspace abscess in which in ection tracks both volarly and dorsally. T ese in ections usually start on the volar
sur ace but dense attachments o the palmar ascia to the skin limit the volar extension causing it to track dorsally
orming an hourglass shape.

What is a horseshoe abscess and why does it occur?
T is is an abscess ormed by communication or rupture between the ulnar and the radial bursae o the hand
through Parona’s space (region between FPL, FDP, and pronator quadratus).

What is the ultimate result o an untreated compartment syndrome?
Decreased capillary per usion pressure leads to tissue necrosis and ultimately may result in a Volkmann’s
contracture.

What are Kanavel’s signs?
T ese are used to diagnose in ectious tenosynovitis:
1. Pain and tenderness along the course o the tendon
2. Flexed resting posture
3. Uni orm and symmetric swelling
4. Pain on passive extension
Bones and Joints
Joints

What is the pathophysiology o a Boutonnière de ormity?
A Boutonnière de ormity occurs with injury to the central slip o the extensor tendon with associated or secondary
attenuation o the triangular ligament. T e lateral bands migrate volarly and f ex the PIP joint.

What type o joints are ound in the thumb?
T e thumb MCP is a hinge joint. T e thumb carpometacarpal (CMC) is a saddle joint (allowing f exion,
extension, abduction, adduction, and circumduction).

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What is the sa e position or splinting the hand and why?
T e intrinsic plus or sa e position: the MCP joints are f exed to 60 to 70 degrees, the interphalangeal joints are ully
extended, the wrist is at 10 degrees less than maximal extension, and the thumb is abducted. Owing to the nature
o the cam o the joint, the collateral ligaments o the MCP joints are maximally stretched when the joint is ully
f exed and o the interphalangeal joints are maximally stretched when the joint is ully extended (see Fig. 29-4).
Figure 29-4 Note that in extension, the metacarpophalangeal collateral ligaments are loose and at risk or shortening.
Extension

Flexion

Which is the most mobile CMC joint?
T e rst CMC joint.

Where are the epiphyses in the bones o the hand?
Proximally on all phalanges and the thumb metacarpal, and distally on the other metacarpals.

What extensor compartments is Lister’s tubercle between?
T e second and third extensor compartments.

What structure in the nger prevents a hook nail de ormity?
T e distal tu t which supports the sterile matrix.

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Fractures

What is a Seymour racture?
A juxtaepiphyseal racture o the terminal phalanx o the nger—analogous to a mallet injury in an adult. T e
terminal tendon is attached to the proximal epiphyseal ragment, and the pro undus tendon, attached to the distal
ragment, causes it to f ex. T e distal segment gets displaced (herniates) above the eponychial old. T e old then
prevents reduction o the racture. Usually needs operative repair.

What is a jersey nger racture?
raumatic avulsion o the f exor digitorum pro undus tendon.

What is an extra octave racture?
A Salter–Harris 2 racture o the proximal phalanx o the small nger with ulnar angulation o the small nger.

What is a boxer’s racture?
Metacarpal neck ractures o the ulnar digits.

Name the types o mallet injuries.
ype I: closed with tendon rupture
ype II: laceration
ype III: abrasion with tissue loss
ype IV: with racture

What is a Stener lesion?
T is occurs in ulnar collateral ligament injury in the thumb when the adductor aponeurosis interposes between
the distally avulsed ligament and its insertion into the base o the proximal phalanx.

What is the most common physeal racture in the hand?
Salter-Harris type II. It most commonly a ects the proximal phalanges. ypically, some degree o angulation is
tolerated in the plane o motion, but little to no angulation is tolerated in the plane 90 degrees to the plane o
motion. Fractures near the growth plate have signi cant remodeling potential in younger patients.

T e articular anatomy o which carpal bone allows it to be used or reconstruction o the PIP joints o the
ngers?
T e hamate. Originally described by Hastings in 1999, the hemi-hamate arthroplasty procedure has become the
choice reconstruction or unstable, late-presenting racture/dislocations o the PIP joint.

What are the most common carpal bone ractures in order o requency?
Carpal bone ractures in order o highest to lowest requency are: scaphoid, triquetral, trapezium, lunate, and
hamate. riquetral ractures typically appear as small dorsal avulsion ractures on lateral view o plain lms.
Physical examination shows tenderness on the dorsal/ulnar wrist. Cast immobilization or a ew weeks is the
treatment o choice, and recovery is usually 100%.

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Flexor System

What are the origins and insertions o the lumbrical muscles? What is their unction?
Originate rom the f exor digitorum pro undus tendons and insert into the radial aspect o the extensor
mechanism distal to the MCP joint. T ey help f ex the MCP joint and extend the interphalangeal joint.

What prevents pro undus tendons rom retracting ully when cut?
T ey may be tethered by the lumbricals, vinculae, and adjacent tendons (with which they share a muscle belly).

How are the exor tendons arranged in the carpal tunnel?
T e FDP tendons lie on the f oor side by side. T e FDS tendons to the ring and middle ngers are super cial to
the index and small ngers. FPL lies radially.

How o ten is the palmaris longus tendon absent?
Between 7% and 20% o people do not have a palmaris longus.

What is Camper’s chiasm?
T is is where the FDS slips bi urcate (to allow passage o the FDP tendon). T e slips then rejoin on the volar
sur ace o the middle phalanx. Proximal to this location, the pro undus tendon is deep to the super cialis tendon.

How is the FDP to the index nger unique?
It has an independent muscle belly.

How do exor tendons receive nutrition?
T ey receive nutrition through the parietal paratenon, bony insertions, muscle bellies, and the longitudinal
vincular system on the dorsal aspect o the tendon—including the vinculum brevis super cialis, vinculum brevis
pro undus, vinculum longum super cialis, and vinculum longum pro undus (see Fig. 29-5).
Figure 29-5
Long vinculae
Short vinculae

CHAPTER 29 Hand Anatomy/Embryology
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What are the exor tendon zones (see Fig. 29-6)?
Zone 1: distal to FDS insertion
Zone 2: rom the A1 pulley to FDS insertion
Zone 3: rom the distal edge o the carpal ligament to the proximal edge o the A1 pulley
Zone 4: the carpal tunnel
Zone 5: proximal to the carpal tunnel
Extensor System

Name the insertions o the extrinsic extensors.
T e base o the proximal, middle, and distal phalanges.
Figure 29-6
I Distal to FDS insertion
II From A1 to FDS insertion
III From carpal tunnel
to A1 pulley
IV Carpal tunnel
V Proximal to carpal tunnel

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Name the extensor tendon zones (see Fig. 29-7).
Figure 29-7
T I
T II
T III
T IV
T VI
IX
VIII
VII
VI
V
IV
III
II
I
Zone I: DIP joint
Zone II: middle phalanx
Zone III: PIP joint (MCP joint in thumb)
Zone IV: proximal phalanx (metacarpal in thumb)
Zone V: MCP joint (carpometacarpal join in thumb)
Zone VI: metacarpal
Zone VII: dorsal retinaculum/carpal bones
Zone VIII: distal orearm
Zone IX: mid and proximal orearm

CHAPTER 29 Hand Anatomy/Embryology
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How many dorsal extensor compartments are there at the wrist? What are their contents?
T ere are six, whose contents are as ollows (see Fig. 29-8):
Figure 29-8 APL, abductor pollicis longus; EPB, extensor pollicis brevis; ECRL, extensor carpi radialis longus; ECRB, extensor carpi radialis
brevis; EPL, extensor pollicis longus; EDC, extensor digitorum communis; EIP, extensor indicis proprius; EDM, extensor digiti minimi;
ECU, extensor carpi ulnaris.
III EPL
II ECRL and ECRB
I APL and EPB
IV EDC and EIP
V EDQ
VI ECU
1. APL, EPB
2. ECRL, ECRB
3. EPL
4. EDC, EIP
5. EDM
6. ECU

Which digits have their own unique extensor tendons? Where are these located?
T e index and small ngers each have proprius tendons (EIP and EDM) that typically lie both ulnar and volar to
their EDC tendons. T e EIP tendon typically has a more distal muscle belly than its EDC counterpart.

What is a juncturae tendinae?
Connections between the common extensor tendons that prevent independent nger extension.

What is the primary MCP joint extensor?
T e extrinsic system, while the intrinsic system is its primary f exor.

What is the Elson test?
T e Elson test assesses the integrity o the central slip. T e PIP joint is passively maximally f exed (usually over
the edge o a table) and held there by the examiner, while the patient attempts active extension. I the central slip
is intact, the DIP joint remains ‘f oppy’ without any extension tone. However, in a central slip injury attempted
extension by the patient allows extension o the DIP joint by the lateral bands.
Vascular

Name the vascular arches in the hand.
1. Super cial palmar arch (anastomosis between the ulnar artery and the super cial branch o the radial artery).
2. Deep palmar arch (extension o the radial artery a ter giving o the princeps pollicis artery).
3. Dorsal carpal arch (anastomosis o the radial and ulnar dorsal carpal branches).

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Where do digital arteries originate?
Common digital arteries originate rom the super cial palmar arch.

How can radioulnar anastomosis be tested?
An Allen’s test is used—the ulnar and radial arteries are occluded by the examiner, blood is removed rom the hand
by making a st, and each artery is released in turn to test patency.

Why may an upper arm tourniquet not suf ciently prevent bleeding in the hand?
Blood may be shunted via nutrient vessels present in the humerus. A tourniquet should be placed as high as
possible to avoid this.

What is the dominant vascular supply to the hand?
Most commonly the ulnar artery—66% ulnar artery, 30% radial artery, and 4% persistent median artery.

Which are the dominant proper digital arteries or each digit?
1. T umb and index: ulnar digital artery
2. Middle and ring: codominance
3. Small nger: radial digital artery

What is Buerger disease?
Buerger disease, or thromboangiitis obliterans, is an inf ammatory vasculitis ound in smokers resulting in severe
ischemia and ulceration o the digits. Angiography typically demonstrates “corkscrew” appearances o the arteries
with multiple occlusions and stenosis.

Name the draining lymphatic beds o the arm.
Axillary, supraclavicular, and in raclavicular.

Between which musculotendinous structures is the radial artery located at the wrist and distal orearm?
Between the brachioradialis and the f exor carpi radialis.

Between which musculotendinous structures is the posterior interosseous artery located in the orearm?
Between extensor carpi ulnaris and extensor digiti minimi.

What is hypothenar hammer syndrome?
Hypothenar hammer syndrome is a trauma-induced thrombosis o the ulnar artery, typically the results o chronic
vibrational or blunt trauma.
Nerves

Where does the motor branch o the median nerve arise within the carpal tunnel?
Around hal are extraligamentous, approximately 30% subligamentous, and approximately 20% transligamentous.

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Where is the palmar branch o the median nerve ound?
T is sensory nerve arises approximately 6 cm proximal to the transverse carpal ligament between FCR and
palmaris longus and running distally along on radial aspect o the carpal tunnel. Overly radial placement o a
carpal tunnel release incision may cause injury to this nerve.

Which nerve is most at risk o injury in a de Quervain release?
T e super cial branch o the radial nerve.

What does the anterior interosseous nerve supply? What does the posterior interosseous nerve supply?
T e anterior is a branch o the median nerve supplies FPL, FDP to index/long ngers, and pronator quadratus. T e
posterior is a branch o the radial nerve and supplies ECRB, EDC, EDM, ECU, supinator, APL, EPL, EPB, and EIP.

Which nerve supplies the exors o the hand and wrist?
T e median nerve supplies all f exors except the f exor carpi ulnaris and f exor digitorum pro undus to the ring and
small ngers (which are supplied by the ulnar nerve).

Describe the path o the median nerve in the orearm.
As it traverses the orearm, the median nerve passes in between the deep and super cial heads o the pronator teres
muscle. A ter emerging rom the pronator teres, it passes deep to the brous arch created by the two heads o the
FDS origin. It then travels between the FDS and f exor digitorum pro undus until more distally where it emerges
super cial in between the FDS and the f exor pollicis longus muscles.

Describe the path o the radial nerve in the orearm.
T e radial nerve can be ound between the brachialis and brachioradialis muscles in the anterior elbow. Beyond
the elbow, it splits into the super cial radial nerve (sensory) and the posterior interosseous nerve (motor). T e
super cial branch passes into the orearm deep to the brachioradialis, but about 8 cm rom the radial styloid, it
emerges between the brachioradialis and the ECRL. T e PIN, pierces the supinator and then, as it extends more
distally, it courses between the EDC and ECRB muscles where it is usually seen in the T ompson approach to the
proximal radius.

Are digital nerves dorsal or volar to digital arteries?
Volar.

Which nerve trans er is most appropriate in an isolated high-ulnar nerve injury?
Anterior interosseous nerve trans er to the motor branch o the ulnar nerve in the mid to distal orearm.

List the Sunderland classi cation o nerve injuries.
Grade I is a neurapraxia (the axon is preserved with altered conduction).
Grade II is an axonotmesis (the axonal integrity is disrupted).
Grade III is neurotmesis (disruption o supporting structures) with preservation o the perineurium.
Grade IV is neurotmesis with preservation o the epineurium.
Grade V is complete transaction o the nerve trunk.
Grade VI (MacKinnon modi cation) is a mixed injury.

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Plastic & Reconstructive Surgery Board Review
Anastomoses

What is a Riche–Cannieu anastomosis?
A communication between the deep branch o the ulnar nerve and the recurrent motor branch o the median
nerve in the palm.

What is a Martin–Gruber anastomosis?
A communication o motor bers rom the median to ulnar nerve in the orearm.
Compression Syndromes

Name the possible sites o ulnar nerve compression in ulnar nerve entrapment.
T ese include the ollowing:
1. intermuscular septum (arcade o Struthers, medial septum, medial head o triceps)
2. medial epicondyle
3. epicondylar groove
4. cubital tunnel (between the heads o the f exor carpi ulnaris)
5. f exor–pronator aponeurosis
6. Guyon’s canal

Name the possible sites o median nerve compression in pronator syndrome.
T ese include the ollowing:
1. bicipital aponeurosis
2. ligament o Struthers
3. between the heads o pronator teres

What is the di erence between de Quervain and intersection syndromes?
De Quervain syndrome is a stenosing tenosynovitis o the rst extensor compartment with pain elt at the wrist,
whereas intersection syndrome is caused by the tendons o the rst extensor compartment crossing over those o
the second compartment and pain is elt proximal to the wrist joint.
REFERENCES
E-hand. T e Electronic extbook of Hand Surgery. Accessed March 22, 2010.
Green DP, Hitchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. 5th ed. London, UK: Churchill Livingstone; 2005.
Greer SE, Benhaim P, Lorenz HP, Chang J, Hedrick MH, eds. Handbook of Plastic Surgery. New York, NY: Marcel Decker; 2004.
Laub DR Jr. Congenital Hand Deformities. Accessed March 22, 2010.
Lin SJ, Hijjawi JB. Plastic and Reconstructive Surgery Board Review. New York, NY: McGraw-Hill; 2006.
Moore KL, Dalley AF. Clinically Oriented Anatomy. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999.
Moore KL, Persaud VN. T e Developing Human—Clinically Oriented Embryology. 7th ed. Philadelphia, PA: Saunders; 2002.
Sinnatamby CS. Last’s Anatomy: Regional and Applied. 10th ed. London, UK: Churchill Livingstone; 1999.
Weinzweig J. Hand and Wrist Surgery Secrets. Philadelphia, PA: Hanley & Bel us; 1999.
Wheeless CR. Wheeless’ extbook of Orthopaedics. Accessed April 11, 2010.

265
Michel Saint-Cyr, MD, FRCS(C) and
Hanif Ukani, MD, FRCSC
BASIC NERVE CELL PHYSIOLOGY

What is the resting potential value o a nerve cell membrane?
All cells have a resting potential: an electrical charge across the plasma membrane with the interior o the cell
negative with respect to the exterior. T e size o the resting potential can vary, but in excitable cells it is about
–70 millivolts (mV).

What determines the resting potential o a nerve cell?
T e resting potential arises rom two activities:
1. T e sodium/potassium A Pase, which moves three sodium ions outside the cell or every two potassium ions
inside the cell and produces a net loss o positive charges and results in a negative intracellular charge.
2. Facilitated di usion o potassium outside the cell.

Describe the ionic relations in the cell or sodium, potassium, chloride, and calcium ions.
1. T e sodium/potassium A Pase produces:
a. A concentration o Na+ outside the cell that is some 10 times greater than that inside the cell.
b. A concentration o K+ inside the cell some 20 times greater than that outside the cell
2. T e concentrations o chloride ions (Cl–) and calcium ions (Ca2+) are maintained at greater levels outside the
cell.

Describe the depolarization o a nerve cell membrane.
Be ore an action potential can be ormed, the nerve cell membrane is depolarized by either a mechanical stimulus
(sound, stretch, etc.) or a neurotransmitter (e.g., acetylcholine). T is allows the acilitated di usion o sodium into
the cell, which reduces the resting potential at that area on the cell and creates an excitatory postsynaptic potential
or EPSP.
Anesthesia
CHAPTER 30

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Plastic & Reconstructive Surgery Board Review

Describe the ormation o an action potential.
I the initial depolarization stimulus reaches a threshold voltage o −50 mV, then an action potential will be
generated rom that area o the cell membrane. T is opens hundreds o voltage-gated sodium channels and creates
a massive in ux o sodium. T e sudden complete depolarization o the membrane opens up more o the voltage-
gated sodium channels in adjacent portions o the membrane. In this way, a wave o depolarization sweeps along
the cell. T is is the action potential, or nerve impulse.

Why is the action potential an all-or-nothing event?
I the critical threshold o a −50 mV membrane depolarization is reached, then an action potential will be
produced, i not, then no action potential will result. Strong stimuli produce no stronger action potentials than
weak ones.

How is membrane repolarization reestablished?
1. Di usion o potassium ions out o the cell.
2. Closure o sodium channels.

What is the re ractory period?
A second stimulus applied to a neuron less than 0.001 second a ter the f rst will not trigger another impulse.
T e membrane is depolarized, and the neuron is in its re ractory period. Not until the −70 mV polarity is
reestablished will the neuron be ready to f re again.

How long does the re ractory period last?
Varies in some human neurons the re ractory period lasts only 0.001 to 0.002 seconds. T is means that the
neuron can transmit 500 to 1,000 impulses per second.

What is the node o Ranvier?
Myelinated neurons are encased in a atty sheath called the myelin sheath, which is the expanded plasma
membrane o an accessory cell called the Schwann cell. Where the sheath o one Schwann cell meets the next, the
axon is unprotected. T is area is called the node o Ranvier.

Why is conduction in myelinated neurons aster than in unmyelinated ones?
Voltage-gated sodium channels o myelinated neurons are conf ned to the nodes o Ranvier. T e in ow o sodium
ions at one node creates just enough depolarization to reach the threshold o the next. In this way, the action
potential jumps rom one node to the next. T is results in much aster propagation o the nerve impulse than is
possible in unmyelinated neurons.
ACTION OF LOCAL ANESTHETICS

What is a conduction block?
It is the reversible interruption o conduction within a neural structure by a local anesthetic.

CHAPTER 30 Anesthesia
267

When does conduction block occur?
It occurs when local anesthetic molecules occupy enough sodium channels within an axon to interrupt its activity.

How does conduction block by a local anesthetic occur?
Local anesthetics act by binding to open-gated sodium channels causing them to remain inactive, thus preventing
subsequent depolarization.

Why do local anesthetics have a higher potency or nerves with a higher requency o stimulation?
Nerves that have a higher requency o stimulation have more activated open sodium channels that are more
susceptible to the action o local anesthetics.

Why are myelinated nerves easier to block than unmyelinated ones?
In myelinated nerves, only the nodes o Ranvier need to be exposed to local anesthetic or conduction block to
occur. In unmyelinated f bers, the ull length and circum erence o the nerve must be exposed to local anesthetic.

During local anesthesia, what is the sequence o blockade and which nerve bers are a ected?
1. Vasodilation (nerve type B, preganglionic autonomic, sympathetic, light myelin)
2. Loss o pain and temperature sensation (nerve types A-δ and C, moderate and no myelin, respectively)
3. Loss o pressure sensation (nerve type A-β, heavy myelin)
4. Loss o motor unction (nerve type A-α, heavy myelin)

What three structures make up the anesthetic molecule?
1. Aromatic ring (hydrophobic)
2. ertiary amine (hydrophilic)
3. Intermediate chain (contains either an amide or ester bond)

Local anesthetics are classi ed into which two groups?
1. Amino esters
2. Amino amides

What is the pH o local anesthetic solutions?
Local anesthetics are weak base with a pKa ranging rom 7.7 to 9.1. Commercially prepared solutions are prepared
as hydrochloride salts o the cation with a pH o 5.0 to 6.0 without epinephrine and a pH o 2.0 to 3.0 with
epinephrine. T is is why they burn so much.

How can pain rom local anesthetic blocks be minimized?
T e pain associated with use o local anesthetics can be decreased by adding sodium bicarbonate to the anesthetic.
Alkalinization o the local anesthetic solution allows the anesthetic to enter the nerve more quickly thereby
increasing the rapidity o onset and e ectiveness. Normal dose or sodium bicarbonate is 1 mEq/10 mL lidocaine
and 0.1 mEq/20 mL bupivacaine. It can decrease the pain o local anesthetic injection by adding 1-mL sodium
bicarbonate or every 9-mL local anesthetic.

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Plastic & Reconstructive Surgery Board Review

T e pharmacological activity o local anesthetics is determined by which three physiochemical properties?
1. Lipid solubility
2. Protein binding
3. pKa

How does lipid solubility a ect the action o local anesthetics?
Increased lipid solubility o a local anesthetic will increase its potency because nerve cell membranes are highly
hydrophobic. Increased nerve block will occur because o acilitated entry across the nerve cell membrane.

How does protein binding a ect the action o local anesthetics?
Local anesthetics with a higher-protein binding will have greater contact with the nerve membrane and thus a
longer duration o action.

How does the pKa a ect the action o local anesthetics?
T e pKa o a local anesthetic determines the speed o onset o the nerve conduction block. Fi ty percent o the
anesthetic will exist in its basic and cationic orm at a given pKa. T e nonionized basic orm has the highest lipid
solubility and hence highest speed o onset. Because local anesthetics are prepared as hydrochloride salts with a
pH o 5.0 to 6.0, some delay in onset will occur because o physiological bu ering which is required to establish a
signif cant base orm concentration.

In what two ways can the onset o local anesthetics be accelerated?
1. Preparation o the local anesthetic solution as a hydrocarbonate salt instead o a hydrochloride salt.
2. Addition o sodium bicarbonate to the local anesthetic prior to injection.

List our ester local anesthetics.
1. Procaine
2. etracaine
3. Benzocaine
4. Cocaine

List three amide local anesthetics.
1. Lidocaine
2. Bupivacaine
3. Prilocaine
Note that these all have an “i” be ore the “-aine.”

How are esters metabolized?
Esters are rapidly hydrolyzed by plasma pseudocholinesterase that creates a short plasma hal -li e. Products o
metabolism include para-aminobenzoic acid (PABA), which can be associated with hypersensitivity reactions in
certain patients.

CHAPTER 30 Anesthesia
269

How are amides metabolized?
Liver cells metabolize amides intracellularly. Because o this longer process, an accumulation o repeated doses
can cause systemic toxicity. Patients with poor liver unction and congestive heart ailure will have a signif cantly
prolonged amide hal -li e. Normal hal -li e is 2 to 3 hours and unlike esters, true allergies are rare.
TOXICITY OF LOCAL ANESTHETICS

What types o toxicities are related to local anesthetics?
1. Direct tissue toxicity (bu ers, preservatives, potential or intraneural injection)
2. Systemic toxicity (CNS, cardiac, methemoglobinemia)

What actors determine the toxicity o a local anesthetic?
1. Potency or lipid solubility (increased CNS toxicity)
2. otal dose delivered
3. Rate o plasma uptake
4. Protein binding
5. Site o injection (highly vascularized tissues increase the rate o uptake)

How does the addition o epinephrine reduce a local anesthetic’s toxicity?
Produces vasoconstriction which:
1. Decreases vascular uptake
2. Lowers peak plasma levels
3. Slows time course to peak level (reduced CNS toxicity)

What toxic e ects are associated with the addition o epinephrine?
1. Hypertension
2. achycardia
3. Cardiac arrhythmia
4. Myocardial ischemia

Name three actors that decrease seizure threshold and increase the risk o CNS toxicity.
1. Hypercarbia
2. Hypoxia
3. Acidosis

Name two agents that can be used to treat seizures ollowing CNS toxicity.
1. Benzodiazepine (increases seizure threshold and can prevent seizure activity)
2. Sodium thiopental

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Plastic & Reconstructive Surgery Board Review

Describe the evolution o local anesthesia-induced CNS toxicity.
1. CNS excitation (occurs f rst):
a. Dizziness
b. Light-headedness
c. innitus
d. Circumoral numbness
e. Metallic taste in the mouth
. Loss o consciousness
g. Muscular twitching
h. Convulsions
2. CNS depression (occurs later):
a. Respiratory depression
b. Cardiorespiratory arrest

What are the e ects o local anesthetic toxicity on the cardiovascular system?
1. Increased sodium channel blockade within the cardiac conduction system causes:
a. Decreased Purkinje f ber f ring and prolonged conduction time
b. Long PR interval
c. Widened QRS complex
d. Sinus bradycardia and asystole
e. Direct myocardial depressant
. Ventricular arrhythmia (increased reentrant pathway activity)

What measures can be used to prevent or minimize systemic reactions to local anesthetics?
1. Avoid intravascular injections ( requent aspirations while injecting).
2. Always use smallest possible dose and concentration.
3. Add epinephrine (avoid in digits and in patients with ischemic heart disease).
4. Premedication with benzodiazepine (elevates convulsive threshold).
5. Use a small test dose.

What measures can be used to treat toxic systemic reactions to local anesthetics?
1. Always ollow principles o ACLS.
2. Convulsions:
a. Hyperventilation with O2 to reduce PaCO2
b. Diazepam, Midazolam, Pentothal 50 to 100 mg IV

What is the estimated adult toxic dose o lidocaine without epinephrine?
Maximal dose/kg: 5 mg/kg
Maximal single dose: 300 mg

CHAPTER 30 Anesthesia
271

What is the estimated adult toxic dose o lidocaine with epinephrine?
Maximal dose/kg: 7 mg/kg
Maximal single dose: 500 mg

What is the maximum total dose o epinephrine in a healthy adult?
0.25 mg.

How is a concentration o 1:200,000 o epinephrine prepared?
Add 0.05 mg (or 0.05 mL o 1:1,000 concentration) o epinephrine to each 10 mL o local anesthetic solution
used (maximum o 50 mL o local anesthesia).

What is the onset and duration o 1% lidocaine with and without epinephrine?

Describe the various indications and concentrations or lidocaine.
1. Local inf ltration: 0.5% to 1% (45–60 minutes)
2. Intravenous regional anesthesia (IVRA): 0.5% 40 mL total or upper extremity (45–60 minutes)
3. Peripheral nerve block: 1% to 2% (1–3 hours)
4. Motor nerve block: 2% (60–80 minutes)
Lidocaine 1% (m in) Lidocaine 1% w ith Epinephrine (m in)
Onset: 5–10

Onset: 3–5
Duration: 45–60

Duration: 60–120
Agent

Concentration (%) Duration (m in)
2-Chloroprocaine

2–3

30–75
Lidocaine

1–2

45–120
Mepivacaine

1–2

120–300
Bupivacaine

0.25–0.5

300–720
Etidocaine

0.5–0.75

300–720

What common local anesthetics are used or peripheral nerve blocks?

What causes methemoglobinemia?
T e oxidation o hemoglobin rom its erric to errous orm by prilocaine and benzocaine. Visible cyanosis can
occur when concentrations exceed 4 g/dL and tissue hypoxia and cyanosis can be treated with methylene blue.

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