General Surgery (Board Review Series) 1st Edition

5

Wound Healing and Plastic Surgery

Alan Parungao

1. Wound Healing
2. Stages or phases of wound healing (Figure 5-1)
3. Inflammatory phase(substrate, lag, or exudative phase)

• begins immediately after wounding.
• lasts for 4–6 days in uncomplicated postoperative wound closures (primary intentionhealing).

1. Symptoms and signs of inflammationinclude

• redness (rubor).
• heat (calor).
• swelling (tumor).
• pain (dolor).
• loss of function.

1. The two main cells

• involved in the inflammatory response are macrophagesand polymorphonuclear (PMN) leukocytes.

2. Macrophages

• secrete basic fibroblastic growth factor (bFGF), which stimulates fibroblasts and endothelial cells and enhances angiogenesis.

3. PMN leukocytes

• are the predominant cells for the first 48 hours.
• release many of the inflammatory mediators and bactericidal oxygen-derived free radicals.

4. Macrophages and PMN leukocytes removeclots, foreign bodies, and bacteria, which may inhibit wound healing.

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1. Other factors involved in wound healinginclude

Figure 5-1. The course of the different cells appearing in the wound during the healing process. Macrophages and neutrophils are predominant during inflammation, whereas lymphocytes peak somewhat later and fibroblasts are predominant during the proliferative phase. (Adapted with permission from Wittey MB, Barbul A: General Principles of Wound Healing. In The Surgical Clinics of North America, “Wound Healing.” Edited by Barbul A. Philadelphia, WB Saunders, 1997, p 512.)

• growth factors (GF) [e.g., platelet-derived GF (PDGF), epidermal GF (EGF), insulin-like GF (IGF), transforming GF (TGF)].
• interleukin-1.
• tumor necrosis factor.
• prostaglandins.
• collagenase.
• elastase.

1. In healing by secondary intention

• a contaminated wound is left opento prevent wound infection, allowing inflammatory cells to débride the wound.
• the open full-thickness wound is allowed to close by both wound contraction and epithelialization.
• the inflammatory phase continues until the wound surface is closed by epithelium.
• In a variation of this technique, called delayed primary closure, the skin and subcutaneous tissues are left unopposed and closure is performed after 3–4 days.

2. Proliferative phase(collagen or fibroblastic phase)

• begins only when the wound is covered with epithelium (approximately days 4–42).
• is characterized by the production of collagen and glycosaminoglycansfrom fibroblasts.

1. In an incision site, collagenproduction generally begins within 7 days of wounding and continues for approximately 6 weeks (Figure 5-2).

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Figure 5-2. The deposition of wound matrix components over time. Although fibronectin and collagen type III constitute the early matrix, collagen type I accumulates later, corresponding to the increase in wound breaking strength. (Adapted with permission from Wittey MB, Barbul A: General Principles of Wound Healing. In The Surgical Clinics of North America, “Wound Healing.” Edited by Barbul A. Philadelphia, WB Saunders, 1997, p 516.)

1. Hydroxyproline and hydroxylysine are key amino acids in collagen that require specific enzymes for their synthesis.
2. Hydroxylation of these amino acids requires iron, α-ketoglutarate, and ascorbic acid (vitamin C)as cofactors.
3. Removal of terminal amino acids from the α chains produces tropocollagen, which aggregates to form collagen fibrils that cross-link with other fibrils.
4. Postoperative wounds achieve 80%–90% of their final strength within 30 days.
5. Mechanical stresses, such as movement over a joint, affect the quantity, aggregation, and orientation of collagen fibers.
6. Remodeling phase(maturation stage)

• begins at 6 weeks and may last as long as 2 years in adults and even longer in children.
• is characterized by the maturation of collagen by cross-linking and continued turnover.

1. This cross-linkingis primarily responsible for the wound's tensile strength.
2. There is generally little net collagen productionafter day 42.
3. Maturationleads to flattening of scar.
4. Wound contraction
5. Open wounds healby a bimodal process of epithelial migration and contraction of the wound edges.
6. The main cellresponsible for wound contraction is the myofibroblast, which is a specialized fibroblast with contractile properties.
7. Collagen formationis not essential for wound contraction.

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Table 5-1. Local and Systemic Factors that May Impair Wound Healing

Local Factors Systemic Factors Infection Malnutrition Ischemia Cancer Cigarette smoking Diabetes mellitus Radiation Uremia Previous trauma Alcoholism Venous insufficiency Chemotherapeutic agents Local toxins (e.g., spider venom) Jaundice Mechanical stress Old age Blood flow Chronic steroid therapy Bacterial contamination

1. Factors impeding wound healing (Table 5-1)
2. Local factors affecting wound closure
3. Hematoma formationprovides a medium for bacterial proliferation and inhibits foreign body removal.
4. Foreign bodies, including sutures, decrease the number of bacteria required to cause a wound infection.
5. Impaired local host defensesalso inhibit healing.
6. Without impaired host defensesor the presence of hematomas or foreign bodies, a wound can withstand a level up to 10⁵ organisms per gram of tissue and still heal successfully.
7. An exception is wounds contaminated with β-hemolytic streptococci, which can cause a wound infection if present in significantly lower numbers.
8. Oxygen deprivation
9. Tissue hypoxiais the most common cause of poor wound healing.
10. Oxygen is important in cell migration and multiplication, and protein and collagen synthesis.
11. The oxygen gradient determines the rate of angiogenesis.
12. Conditions that lower oxygen delivery to tissues include hypotension, hypovolemia, anemia, lung disease, low inspired oxygen concentrations, hypothermia, alkalosis, and edema.
13. Systemic factors affecting wound closure
14. Cytotoxic drugs

• such as 5-fluorouracil, methotrexate, and cyclophosphamide impair wound healing by suppressing collagen synthesis and fibroblast replication.

1. Chronic glucocorticoid therapy
2. Glucocorticoids

• can prevent macrophages from migrating into the wound.

1. The inflammatory responseis decreased.

• There is a delay in angiogenesis, fibroblast proliferation, and synthesis of collagen and proteoglycan.

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2. Supplemental vitamin A

• may counteract the deleterious effects of steroids.
• increases the fibroblast receptor for EGF and increases fibroblast multiplication.
• stabilizes the lysosomal membrane, opposing the effect of glucocorticoids.

1. Diabetes mellitus

• is associated with inhibition of the early inflammatory response and proliferation of fibroblasts and endothelial cells.

1. Hyperglycemiainterferes with the cellular transport of ascorbic acid into fibroblasts and leukocytes and inhibits leukocyte chemotaxis.
2. Other indirect effectsthat may contribute to poor wound healing include dehydration, metabolic acidosis, and inadequate tissue perfusion.
3. Excessive wound healing: hypertrophic scars and keloids (Table 5-2)
4. Squamous cell carcinoma
5. Some wounds may rarely developa focus of squamous cell carcinoma years after the original injury.
6. These lesions characteristically present as a persistent nonhealing ulcerat the site of previous injury, and are frequently referred to as Marjolin ulcers.
7. Appropriate managementof suspicious lesions involves prompt biopsy with subsequent resection of cancerous lesions.
8. Skin Grafts and Tissue Flaps
9. Classification of skin grafts by thickness (Figure 5-3)
10. Split-thickness skin graftsinclude the epidermis and part of the dermis.
11. The dermal skin appendageswithin these grafts (e.g., sweat glands, hair follicles, and sebaceous glands) contribute to epithelialization.
12. Thinner graftsare associated with a higher percentage of graft survival.

• Thicker grafts are associated with less wound contraction.

1. Advantagesinclude

• large supply of donor areas.
• ease of harvesting.
• availability of donor site for reuse in 10–14 days.
• coverage of large surface areas.
• ability to be stored for later use.

1. Disadvantagesinclude

• cosmetic inferiority to full-thickness skin grafts.

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• decreased durability.
• hyperpigmentation.
• increased secondary contracture.

Table 5-2. Characteristics of Hypertrophic Scars and Keloids

Hypertrophic Scars Keloids Causes Increased degree and time of inflammation (e.g., healing by secondary intention), unnecessary tensionthat produces uncontrolled would contraction Pre-disposition to excessive scar formation. Clinical appearance Collagen mass remains within the original bounds of the wound Collagen mass extends beyond the original bounds of the wound, lesion is raised and firm, overlying skin is often darker than normal surrounding skin Common location Anywhere Sternum, mandible, deltoid (rarely occurs distal to wrist or knee) Natural history Usually regresses with time Does not regress Microscopic Histologically similar to keloids; collagen tends to whorl about clusters of macrophages, fibroblasts and vessels; perivascular necrosis Thick, homogenous bands of collagen; paucity of cellular elements; perivascular necrosis; density of fibroblasts and collagen similar to hypertrophic scars Treatment Z-plasty to change direction of scar, direct pressure, intralesional steroids (Surgical treatment is possible because the healing mechanisms are normal.) Intralesional steroids (i.e., triamcinolone every 3–4 weeks) followed by excision, excision followed by radiation therapy (alternative), experimental pharmacologic manipulations [e.g., penicillamine, colchine, vitamin A (as retinoic acid), interferons α and γ]

2. Full-thickness skin graftsare comprised of the epidermis and the full thickness of dermis without subcutaneous fat.
3. The greater the proportion of dermisthe less contraction that occurs during healing.

• This provides better coverage, but is less likely to survive than a split-thickness skin graft because the greater thickness leads to slower revascularization.

1. These grafts are frequently usedon the

• facebecause they provide a better color match than split-thickness grafts.
• fingerto decrease contracture formation.

1. Advantagesinclude

• cosmetic superiority to split-thickness skin grafts.
• decreased secondary contractures.
• increased durability.

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1. The main disadvantage

• is the limited number of donor sites.

Figure 5-3. A split-thickness skin graft (STSG) includes epidermis and a portion of the dermis. Because dermis is left behind, the donor site heals by epithelialization. A full-thickness skin graft (FTSG) includes the epidermis and all layers of the dermis. Because no dermis is left behind, the donor wound must be closed primarily. (Adapted with permission from Marks MW, Marks C: Grafts and Implants. In Fundamentals of Plastic Surgery, 1st ed. Edited by Marks MW, Marks C. Philadelphia, WB Saunders, 1997, p 67.)

1. Skin graft survival
2. Initially, both types of grafts survive

• via diffusionof nutrients from the recipient bed, a process called plasma imbibition.

2. Three to five days after graft placement

• revascularization occurs by ingrowth of vessels from the recipient site.

3. Common reasons for graft lossinclude

• hematoma or seromaformation under the graft (most common); meshing the skin graft allows for seroma drainage.
• shearing forces between the graft and recipient site (e.g., poor immobilization of an extremity).
• poorly vascularized recipient site (e.g., bone).
• infection.

4. Poorly vascularized bedsthat generally are not good recipient sites for skin grafts include

• bare tendons.
• cortical bonewithout periosteum.
• irradiated wounds.
• infected wounds.

1. Flaps

• consist of tissues transferred from their bed to an adjacent or distal area while retaining a functioning vascular attachmentor pedicle.

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1. Flaps classified by surgical technique
2. In pedicled flaps, the arterial and venous vessels remain in their native bed.
3. In free flaps, the arterial and venous vessels are anastomosed by microvascular techniques to recipient vessels.
4. Skin flaps

• include random pattern, axial pattern, and island flaps.

1. Random pattern flaps lack specific vesselsbut are based on a random blood supply from the intradermal and subdermal plexus, which limits the length of these flaps.
2. Rotation flapsare semicircular flaps of skin and subcutaneous tissue that rotate about a pivot point (Figure 5-4).
3. Transposition flapsare rectangular or square flaps of skin and subcutaneous tissue that transpose around a pivot point into an adjacent wound such as Z-plasty (Figure 5-5).
4. Advancement flaps depend on stretchingof the skin in a straight line to fill a wound or defect.
5. An axial pattern flapis a single-pedicled flap with a defined arteriovenous system running along its long axis.
6. Island flapsare dissected so that the flap is attached only by axial vessels.
7. This improves flap mobility, thus permitting rotation through an arc of 180° or greater.
8. A neurovascular island flap includes a nerve within the pedicle, thereby permitting the skin to retain sensation.

Figure 5-4. A rotation flap. A semicircular flap of skin and subcutaneous tissue is rotated about a pivot point into the defect. (Adapted with permission from Marks MW, Marks C: Grafts and Implants. In Fundamentals of Plastic Surgery, 1st ed. Edited by Marks MW, Marks C. Philadelphia, WB Saunders, 1997, p 84.)

3. Muscle and musculocutaneous flaps

. A muscle may be detached from its origin and insertion sites and transposed on its vascular pedicle to an adjacent area.

• Alternatively, the vascular pedicle may be detached at its origin and reattached by microvascular techniques.

1. Muscle flaps provide

• additional blood supplyto the recipient area.

1. Muscle can obliterate large cavities

• and aid in combating low-grade infections.

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1. The exposed surface of muscleprovides

• an excellent recipient area for split-thickness skin graftif skin is not transposed with the muscle unit.

1. Commonly used muscle flapsinclude

• temporalis or trapezius muscle flaps for head and neck defects.
• pectoralis major, latissimus dorsi, rectus abdominis, or gluteus maximus flaps for defects of the trunk.
• tensor fascia lata, gracilis, rectus femoris, gastrocnemius, or soleus muscle flaps for defects of the lower extremity.

4. Fasciocutaneous flaps

• are well vascularized and easy to manipulate.
• avoid the need for sacrifice of a muscle.

Figure 5-5. A transposition flap. The flap is elevated and transposed into an adjacent defect. The donor defect is either closed primarily or grafted. (Adapted with permission from Marks MW, Marks C: Grafts and Implants. In Fundamentals of Plastic Surgery, 1st ed. Edited by Marks MW, Marks C. Philadelphia, WB Saunders, 1997, p 85.)

III. Hand Surgery

1. Anatomic considerations
2. Compromise of the skin's surface areaor elasticity

• will inhibit range of motionand constrict circulation.

2. Fascia anchors palmar skin to bone

• to make pinch and grip stable.

1. In the form of sheathsand pulleys fascia holds tendons in the concave portions of arched joints.
2. Fascial compartmentsprovide an avenue for dissemination of infection.
3. Across the wristthe dense carpal ligament forms a roof over the bony carpal canal (carpal tunnel).

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• All eight finger flexorsas well as the flexor pollicis longus and median nerve pass through this canal.

3. The four joints of each fingerinclude

• distal interphalangeal (DIP).
• proximal interphalangeal (PIP).
• metacarpophalangeal (MCP).
• metacarpocarpal (MCC).

4. Flexor tendons and extensor tendons

• control motor function of the hand.

1. Flexor digitorum superficialis

• inserts on the base of each middlephalanx.

1. Flexor digitorum profundus

• inserts on the base of each distalphalanx.

1. Long extensor tendons

• insert at the base of the middlephalanx.

1. Lateral bands

• originating from the lumbricals and interossei travel on each side of the finger and insert on the distal phalanx to act as MCP flexors and IP extensors.

1. No Man's Land(Figure 5-6)

• is the zone from the middle of the palm to just distal to the PIP joint.
• is where the superficialis and profundus tendons lie ensheathed together.
• is where recovery of function is difficult after injury.

Figure 5-6. Flexor tendon zones of the hand. These zones are defined by their relevance to flexor tendon injuries. Tendon injuries that occur in Zone 2 (No Man's Land) are generally associated with poor recovery of function. (Adapted with permission from Winograd J: Plastic Surgery. In Advanced Surgical Recall, 1st ed. Edited by Blackbourne LH, Fleischer KJ. Baltimore, Williams & Wilkins. 1997, p 1028.)

5. The nerves most important to hand function

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• are the musculocutaneous, radial, ulnar, and median nerves.

1. Together, the musculocutaneous and radial nervecontrol forearm supination.
2. The radialnerve innervates the extensor muscles.
3. The ulnarnerve innervates 15 of the 20 intrinsic muscles.
4. The mediannerve innervates most of the long flexors, the pronators of the forearm, and the thenar muscles.
5. Figure 5-7 demonstrates the sensory distribution of the ulnar, radial, and median nerves.

Figure 5-7. Sensory innervation of the hand. (Adapted with permission from Winograd J: Plastic Surgery. In Advanced Surgical Recall, 1st ed. Edited by Blackbourne LH, Fleischer KJ. Baltimore, Williams & Wilkins. 1997, p 1016.)

1. Hand infections
2. Paronychia

• is an infection at the radial or ulnar side of the nail.

1. Tissue tension that forms about the rigid nail causes exquisite pain.
2. Early treatmentbefore abscess formation involves water-soaked or zinc oxide dressings, elevation, immobilization, and antibiotics.
3. If purulent material forms under the nail, the nail should be removed for adequate drainage.
4. Felon

• is an infection of the volar distal fat pad of the finger.
• The abscess is drained by a longitudinally oriented incisionover the central portion of the fat pad.

3. Tenosynovitis

• is an infection of the synovial tendon sheaths.

1. Kanavel'sfour signs of tenosynovitis include

• flexionof the affected finger.

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• swelling.
• pain with passive extension.
• tendernessover the flexor tendon sheath.

1. Treatmentis by incision, drainage, and irrigation of the tendon sheath.
2. Human bites to the hand

• frequently become infected (see Chapter 4 II C).
• should be treated by aggressive débridement and broad spectrum antibiotics.
• The wound should be left unsutured.

1. Fractures
2. Metacarpal fractures

• are usually transversely oriented and tend to rotate.

1. Rotation of a finger

• causes it to cross over an adjacent finger during flexion.
• interferes with grasping and making a fist.

1. Unstable fractures

• are those that tend to redisplace.
• Treatment involves either percutaneous pinning or open reduction with internal fixation.

1. A boxer's fracture

• is a transverse fracture of the distal fourth or fifth metacarpalwith palmar displacement of the metacarpal head.
• can usually be reduced with traction and application of dorsal pressure on the distal fragment.
• requires percutaneous pinning, if unstable.

2. Proximal and middle phalangeal fractures

• also tend to rotate.
• require percutaneous pinning or fixation.

3. Nondisplaced distal phalangeal fractures

• may be treated by splinting at the DIP joint for 2–3 weeks.

1. Noninfectious inflammatory disorders of the hand
2. Trigger fingeris a stenosing flexor tenosynovitis of the proximal digital pulley.
3. Pain is felt over the DIP joint and the digit may be locked in flexion.
4. The patient may notice a painful “click” as the finger goes into extension.

• This occurs as the bulge in the tendon passes through the tight pulley.

2. de Quervain tenosynovitisinvolves the pulley over the radial styloid.
3. This pulley houses the abductor pollicis longus and extensor pollicis brevis.

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1. A characteristic finding includes local tenderness and pain with active or passive stretching of these tendons (Finklestein's test).
2. Carpal tunnel syndromeis caused by compression of the median nerve as it passes under the volar carpal ligament.
3. Patients experience sleep disturbanceby the aching and numbness over the distribution of the nerve (most often the long and ring fingers).
4. Severe constriction causes paralysisof the abductor pollicis brevis.

• This can manifest itself as atrophy of the thenar eminence.

4. Ulnar nerve compressionmay occur in three places:

• Behind the medial epicondyle (cubital tunnel).
• Between the heads of the flexor carpi ulnaris.
• Guyon's canalfrom the pisiform bone to the hook of the hamate (this canal contains both the ulnar artery and nerve).

5. Dupuytren contractureis a fibrous contraction of the palmar fascia of unknown etiology.

. Risk factors include Celtic origin, epilepsy, diabetes, alcoholism, and a family history of the disease.

1. On physical examination, patients may have nodules or cordlike bandsin their palms that restrict their ability to completely extend the fingers.
2. Treatmentis by partial fasciectomy, although recurrence is common.
3. Tumors of the hand (Table 5-3)

Table 5-3. Tumors of the Hand

Tumor Pathology Clinical Presentation Treatment Ganglion* Protrusion of synovium filled with synovial fluid Most commonly found on the wrist (radiodorsal or radiovolar) Asymptomatic: none Symptomatic: excision Inclusion cyst Subcutaneous mass containing a nidus of epithelial cells Associated with penetrating trauma Excision Xanthoma (giant cell tumor) Yellow, nodule-like tumor containing connective tissue histiocytes May be cystic, solid, or multilocular; often hard and painless Excision Enchondroma Lobules of hyaline cartilage with areas of calcification Frequently presents as a pathologic fracture Curette and bone grafting Glomus Comprised of blood vessels and unmyelinated nerves Found in pad of finger and under nail, associated with cold sensitivity Excision *Ganglion tumors are the most common tumor of the hand.

1. A ganglion

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• is a protrusion of synovium filled with synovial fluid.
• typically appears insidiously, although sudden forceful bending of a joint may be associated with an acute presentation.
• is most commonly located on the radiodorsal or radiovolar area of the wrist.

1. A mucous cystis a DIP ganglion that may deform the nail.
2. Asymptomatic ganglia generally do not require treatment, while symptomatic cysts require surgical excision.
3. An inclusion cyst

• forms when viable epidermal cellsare found deep in the dermis, in subcutaneous fat, or in bone (frequently induced by traumatic injury).

1. With growth of these cells, keratinized cells accumulate into a ball or cyst.
2. These lesions can be removed surgically.
3. Xanthoma (i.e., giant cell tumor)

• is an insidiously growing, benign, often multinodular tumor that arises from the fibrous flexor sheath, ligaments, or fascia.
• is usually hard and painless.

4. Enchondromas

• are benign tumors that constitute 90% of bone tumors of the hand.
• The classic finding is calcific stipplingof the lytic bone defect, which is commonly seen in the proximal phalanges and distal metacarpals.

5. Glomus tumors

• are comprised of blood vessels and unmyelinated nerves of a heat-regulating arteriovenous shunt.

1. Although most patients will have no symptoms, lesions under the fingernail may be associated with severe pain.
2. Treatment is by total excision.
3. Compartment syndromes of the upper extremity
4. This syndrome developswhen a compartment of tissue (e.g., muscle) bounded by noncompliant structures (e.g., fascia, bone) develops a significant increase in pressure.

• The most common causeof compartment syndrome is trauma.

1. Increased pressure leads to inhibition of venous outflowwith a subsequent decrease in arterial inflow, resulting in tissue ischemia.
2. Compartment pressures greater than 30–40 mm Hgsignificantly inhibit muscle perfusion.
3. Volkmann ischemiais irreversible muscle necrosis that may occur within 2 hours of onset of injury.
4. Nerve compression results in paresthesia and hypoesthesia.
5. Flow through major vessels is generally maintained, thus distal pulses may remain palpable, even after irreversible muscle necrosis.

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2. The most common siteof compartment syndrome in the upper extremity is in the anterior forearm compartment.

. Signs and symptoms occur in the following order

• painout of proportion to the injury.
• weaknessof the compartment muscles.
• increased tensenessof the compartment.
• hypoesthesiaof nerves passing through the compartment.

1. Compartment syndrome may present

• as flexion of the digits with resistance to passive extension.

1. The diagnosis

• is clinical, based on a high index of suspicion from the history of a predisposing trauma or medical condition and progressive signs of muscle and nerve ischemia.
• can be confirmedby compartment pressure measurements that are above 30 mm Hg.

3. Prompt surgical decompression by adequate fasciotomyis the only treatment for the early stage of compartment syndromes.

. The important features of the incision used are adequate exposure, maintenance of skin coverage of the median nerve at the wrist, and avoidance of longitudinal cuts across the wrist and elbow skin creases.

1. Judicious débridement of necrotic muscle should be performed.

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Review Test

Directions: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case.

1. Which of the following characteristics of keloids most appropriately differentiates a keloid from a hypertrophic scar?

(A) Decreased fibroblast density

(B) Increased fibroblast density

(C) Increased collagen density

(D) Increased perivascular sclerosis

(E) Growth beyond the incision site

1–E. Unlike hypertrophic scars, keloids typically overgrow the boundaries of the initial incision site. This differentiation is generally made by clinical examination. Light microscopy alone cannot be used to make this differentiation because there are no differences in the architecture or quantity of collagen or the number of fibroblasts. Perivascular sclerosis also occurs in both disorders. Although the specific biochemical cause of abnormal scar production has not been identified, increased collagen production and decreased collagen lysis have been demonstrated.

2. Which of the following is a mechanism of keloid formation?

(A) Altered ratio of collagen production and collagenase activity

(B) Excessive fibroblast proliferation

(C) Excessive collagenase synthesis

(D) Excessive collagen cross-linking

(E) Prolonged acute inflammation

2–A. Studies of the origin of keloids and hypertrophic scars suggest that both excessive collagen production and decreased collagenase activity may be responsible for abnormal collagen formation. Excessive cross-linking and prolonged inflammation are not thought to be primary mechanisms. Although collagen production is increased in hypertrophic scars and keloids, it does not result from an excessive number of fibroblasts in the wound or from specific abnormal types of fibroblasts.

3. A 16-year-old girl sustains a needle prick to the left index finger over the distal palmar surface. Initially, she notices little discomfort. However, 3 days after the injury she develops intense pain in the distal phalanx that wakes her up at night. Regarding this situation, which of the following is the most appropriate statement?

(A) She has an acute paronychial infection

(B) Drainage is accomplished via an incision over the most tender region

(C) Incision through the volar surface of the finger often results in a tender scar

(D) Cultures of the finger will most likely produce a gram-negative rod

(E) Late sequelae of this type of infection seldom involve the bone

3–B. This patient has a felon, not a paronychial infection. Untreated, the infection may progress to involve the distal phalanx. The most likely organisms are gram-positive cocci. The scar on the volar surface may be tender initially, but no more so than a scar elsewhere on the hand. Incision and drainage is indicated in this situation, with the incision placed directly over the point of maximal tenderness.

4. A 62-year-old woman has had a clicking sensation of her thumb for 4 months. On examination, she has tenderness and a palpable nodule at the level of the proximal interphalangeal joint. The thumb exhibits full active and passive range of motion, but active extension results in a clicking noise. Which of the following is the most appropriate initial step in the management of this patient?

(A) Physical therapy

(B) Splinting of the thumb

(C) Oral administration of an anti-inflammatory agent

(D) Injection of a corticosteroid into the flexor tendon sheath

(E) Surgical release of the A1 annular pulley

4–D. This patient has stenosing flexor tenosynovitis of the thumb (trigger thumb). When she flexes or extends her thumb, triggering occurs. Primary, or idiopathic, trigger finger is common, and middle-aged women are most frequently affected. Secondary causes include gout, rheumatoid arthritis, diabetes mellitus, and other diseases that cause connective tissue changes. The most appropriate initial treatment is to inject corticosteroid into the flexor tendon sheath. Splinting and corticosteroid injection are equally effective in treating trigger finger, but corticosteroid injection has been shown to be more successful when the thumb is affected. Surgical release of the A1 annular pulley is indicated when corticosteroid injection fails or if the digit is locked. Physical therapy has no effect on the nodule causing the triggering. Anti-inflammatory agents are not likely to be successful as the sole treatment of this disease.

Questions 5–6

A 16-year-old boy presents to the office immediately after a cut injury to the palm of his right hand. The cut was caused by a clean razor blade. Physical examination reveals a 2-cm laceration at the base of the long finger. The patient is able to flex the metacarpophalangeal (MCP) joint but he cannot flex either interphalangeal joint in that finger.

5. Which of the following is the most likely diagnosis?

(A) Lacerated flexor digitorum profundus tendon

(B) Lacerated flexor digitorum superficialis tendon

(C) Combined laceration of the superficialis and profundus tendon

(D) Laceration of the intrinsic muscle to the long finger

(E) Transection of the radial nerve

5–C. Flexion of the metacarpophalangeal (MCP) joint is accomplished via intrinsic muscles of the hand. This may be preserved even when the extrinsic flexion mechanism is disrupted. The goal of flexor tendon repair is to restore interphalangeal joint flexion. The flexor digitorum superficialis inserts on the base of each middle phalanx and causes proximal interphalangeal (PIP) flexion. The flexor digitorum profundus inserts on the base of each distal phalanx and is responsible for distal interphalangeal (DIP) flexion. Laceration of the intrinsic muscle to the long finger would not explain the patient's inability to flex the PIP and DIP joints. The radial nerve is responsible for the extensors, not flexors, of the hand.

6. Which of the following is the most appropriate treatment plan for this patient?

(A) Immediate tendon repair

(B) Regional anesthesia, extension of the skin wound, and exploration to confirm the diagnosis

(C) Careful cleansing of the wound, placement of the appropriate dressing, and hand immobilization before definitive primary surgical repair

(D) Cleansing of the wound, primary skin closure, hand immobilization, and delayed repair using tendon graft

(E) Observation only

6–C. The goal of flexor tendon repair is to restore interphalangeal joint flexion. Proper wound cleansing, dressing, immobilization, and prophylactic antibiotics allow delay of primary repair if a hand surgeon is not immediately available. With this cut, primary repair of the tendon is the most appropriate operative technique without the need for tendon grafts. Delayed repair (2–6 days after injury) is indicated when the degree of wound contamination is uncertain or if the initial treatment has been delayed beyond several hours. Grossly contaminated wounds, those with significant tendon disruption, or wounds with significant associated injuries to the soft tissue, bone, nerve, or blood vessels are treated by secondary repair in 3–6 weeks, after the wound has healed and edema and callus formation subside.

Questions 7–9

A 45-year-old man suffers a 45% total body surface area (TBSA, partial and full-thickness) burn to the neck, face, trunk, and lower extremities sustained in an industrial explosion. Other injuries include a severe LeFort II maxillary fracture, a pulmonary contusion with rib fractures, and a crush injury to the right arm and hand. The patient is unresponsive with labored respirations and his current blood pressure is 70/40 mm Hg.

7. Which of the following should be the primary concern in the emergency room?

(A) The facial fractures

(B) The 45% TBSA burns

(C) Endotracheal intubation

(D) The crush injury to the right upper extremity

(E) Splinting of the chest for the rib fractures

7–C. Trauma evaluations are generally approached in the same systematic manner to avoid missing life-threatening injuries. The ABCs (airway, breathing, circulation) of trauma is a useful mnemonic for the sequential approach to potential life-threatening injuries during a trauma evaluation. While the crush injury and burns may be quite disfiguring and obvious, in patients with respiratory distress initial attention should be directed toward providing an adequate airway, typically via endotracheal intubation. Facial fractures can also be dealt with once the life-threatening injuries are controlled.

8. The patient is appropriately resuscitated and further work-up reveals no additional thoracic or intra-abdominal injuries. Thirty-six hours after the injury, his blood pressure is 130/85 mm Hg and urine output is maintained at 30 mL/hour. The patient is also awake and alert. Physical examination of his right arm reveals it to be tense and painful. Pulses in the extremity are noted by Doppler examination. Which of the following is the most appropriate next step in the management of this patient?

(A) High-dose corticosteroids

(B) Arm evaluation, analgesics, and close observation

(C) Fasciotomies

(D) Compressive dressings

(E) Burn excision and grafting

8–C. The patient is developing a compartment syndrome secondary to his crush injuries. Immediate treatment includes fasciotomies to prevent irreversible muscle necrosis and nerve damage. There is no role for corticosteroids in the treatment of his compartment syndrome. Arm elevation may be a temporizing measure before fasciotomy but is not adequate for definitive treatment. Compressive dressings may mask his findings and irreversible necrosis can ensue. Pulses may be present even during the late stages of compartment syndrome. Although burn excision and grafting are important, initial attention to release of compartment pressure with fasciotomy is essential.

9. Three days after the initial injury, the patient's wounds are débrided in the operating room. Coverage of the burns to his thorax, abdomen, and lower extremities is best accomplished via which of the following?

(A) Local (random pattern) skin flaps

(B) Free flaps using microvascular transfer

(C) Full-thickness skin grafts

(D) Split-thickness skin grafts

(E) Myocutaneous flaps

9–D. This patient has a large amount of surface area that requires coverage. This is best accomplished using meshed split-thickness skin grafts, which are harvested at a thickness of 12–15 one-thousandths of an inch. Skin and myocutaneous flaps will not adequately cover his wounds, and the donor site morbidity precludes their use. Similarly, full-thickness skin grafts require the donor sites to be covered with skin grafts and this too limits their use. In this patient, split-thickness skin grafts will accomplish the coverage needed while minimizing donor site morbidity.

10. Which of the following statements is correct regarding wound healing and persistent local tissue hypoxia?

(A) Fibroblasts are stimulated by low oxygen tension

(B) High lactate levels inhibit macrophage production of angiogenesis factor

(C) Low oxygen tension is the most common cause of poor wound healing

(D) Collagen synthesis is stimulated by hypoxia

(E) Wound healing is not affected by alterations in tissue oxygen tension

10–C. Oxygen deficiency of the tissues is the most common cause of poor wound healing. Proper tissue oxygenation requires sufficient inspired PO₂, transfer of oxygen to hemoglobin, ample hemoglobin for transport, and adequate vascularity of the tissues. Most healing problems associated with diabetes mellitus, irradiation, small vessel atherosclerosis, and chronic infection are a result of a faulty oxygen delivery system. Transiently low wound tissue oxygen levels stimulates cell migration, growth factor release, and collagenase production. Similarly, high lactate levels stimulate the macrophage to produce angiogenesis factors. Fibroblasts are oxygen sensitive and are inhibited by low tissue oxygen tension. Collagen synthesis is also inhibited by low tissue oxygen.

11. During the first 4 days after an injury, which of the following cells are most critical to wound healing?

(A) Fibroblast

(B) Lymphocyte

(C) Myofibroblast

(D) Platelet

(E) Macrophage

11–E. Macrophages play a critical role in the inflammatory phase of wound healing and in the modulation of collagen production. These cells affect wound healing through multiple secretory factors and receptors. Studies of the role of macrophages have shown a marked inhibition in the process of wound débridement and collagen production with administration of antimacrophage serum early in wound healing. Although lymphocytes also modulate wound healing by secreting interleukin-2, transforming growth factor-β, and other lymphokines, these substances do not appear until inflammation has resolved, approximately 3 days after injury.

12. A 45-year-old, obese man develops a wound infection on postoperative day 10. The patient undergoes wound débridement, followed by dressing changes to the open wound and systemic antibiotics. Allowing this wound to heal by wound contraction and epithelialization (i.e., secondary intention) means that the wound will spend a prolonged period of time in which of the following phases?

(A) Inflammatory

(B) Proliferative

(C) Fibroblastic

(D) Remodeling

(E) Maturation

12–A. In healing by secondary intention, the inflammatory phase continues until the wound surface is closed by epithelium. In this case, coverage with epithelium may not be complete for several weeks to months, depending on the size of the defect. When a wound is closed primarily, the inflammatory phase usually lasts from 4–6 days. The rest of the phases listed should proceed normally once the wound has closed by contraction and epithelialization.

13. Which of the following is the most appropriate option for closing a large wound once the wound appears “clean”?

(A) Split-thickness skin graft

(B) Full-thickness skin graft

(C) Local skin flap

(D) Myocutaneous flap

(E) Cadaveric skin grafting

13–D. The choice for coverage depends on the wound's size and depth. Because bone will probably be débrided before definitive closure, the resulting defect will have a significant amount of dead space. A myocutaneous flap provides excellent coverage and obliterates the dead space. In addition, the added vascularity of the transposed muscle will aid in fighting infection by allowing the egress of inflammatory cells. Skin grafts and a local skin flap will not provide the bulk needed to close the dead space. Cadaveric skin grafts serve as a temporary biologic dressing before definitive closure; they are not appropriate for long-term use.

Directions: Each of the numbered items or incomplete statements in this section is negatively phrased, as indicated by a capitalized word such as NOT, LEAST, or EXCEPT. Select the ONE lettered answer or completion that is BEST in each case.

14. A 65-year-old man with a past medical history of chronic obstructive pulmonary disease (COPD), diabetes mellitus, and peripheral vascular disease undergoes an uncomplicated three-vessel coronary artery bypass grafting (CABG) using both internal mammary arteries. His sternal wound is closed primarily using sternal wires and buried subcuticular sutures using absorbable, synthetic suture. Eight days postoperatively, the patient develops a fever, and on examination there is crepitance in the sternal wound. Factors predisposing the patient to a sternal wound infection include all of the following EXCEPT

(A) Male gender

(B) COPD

(C) Diabetes mellitus

(D) Peripheral vascular disease

(E) Use of both internal mammary arteries versus using only one

14–A. Tissue hypoxia is the most common cause of poor wound healing. Conditions that lower oxygen delivery to tissues include lung disease, cigarette smoking, hypovolemia, anemia, hypotension, and low concentrations of inspired oxygen. Peripheral vascular disease is associated with tissue hypoxia and poor wound healing. Diabetes mellitus has multiple effects on different aspects of wound healing and predisposes this patient to wound infection. For example, diabetes is associated with an inhibition of the early inflammatory response and proliferation of fibroblasts and endothelial cells. The use of bilateral internal mammary arteries for revascularization procedures (e.g., CABG) has recently been demonstrated as being associated with an increased risk of postoperative sternal wound infection, verus using only a single internal mammary artery while maintaining adequate perfusion of the area by the remaining mammary artery. While old age may lead to impaired wound healing, being male does not.