Nasal Reconstruction (updated 06/06)

SW1. Review the blood supply to the nose.

SW2. What are the aesthetic subunits of the nose? How does this apply to nasal
reconstruction? Arch Facial Plast Surg Jan-Mar 1999.

AA3. Name some common local flaps used in nasal reconstruction. Be prepared to draw
each.
Dorsal Nasal Flap
The dorsal nasal flap is a modified rotation flap that recruits redundant skin from the glabella. The flap can
be used to repair skin defects of the nasal tip, dorsum, and sidewall. It utilizes the entire dorsal nasal skin
to facilitate repair. Can repair relatively large lower and midnasal defects measuring 2.5 cm or less with
matching adjacent tissue.

Laterally based pivotal flap, pedicle centered in the region of the medial canthus
Pivotal flap: based on branches of the angular artery
Disadvantage: tip elevation/rotation, elevation of ala in lateral nasal defects

Bilobe Flap:
Flap of choice for the lower 3rd of the nose. It is a double transposition flap. The primary
flap is used to repair the nasal defect and the secondary flap repairs the donor site, donor
site of the secondary lobe is closed primarily.
Whenever possible base bilobe flaps laterally. They are ideally suited for defects <1.5cm
located on the central or lateral nasal tip without extension to the ala. The defect should
be at least 0.5 cm above the margin of the nostril. Defects of the upper half of the nose
are not suited for bilobe recon because the flap requires skin from the medial canthus that
is thin and immobile.
Design: a point is marked in the alar groove, this is the pivotal point for the 2 lobes. 2
arcs are drawn from their centers at the marked point. 1st arc passes through the center of
the defect and the other makes a tangent with the most distal border of the defect. The
width of the 1st lobe is equal to the width of the defect. The height of the 2nd lobe is
approximately 1.5-2cm greater than the height of the first lobe. The axis passing through
V-to-Y Island Pedicle Advancement Flap: small defects of the anterior alar groove,
caudal lateral nasal sidewall, lateral nasal tip for defects up to 1.5cm.

Interpolated Melolabial Flap: defects of ala, lateral tip, columella, caudal nasal sidewall.
Blood supply: not based on a specific named vessel but rather on a directionally oriented
subdermal plexus that courses parallel to the melolabial crease and the angular artery
(random pattern). Not a good match for defects of the dorsum and cephalic nasal
sidewall which have less sebaceous glandularity.
Types: pivotal, advancement, hinge
2 stage – flap inset in 3 weeks
Design: may be based either superiorly or inferiorly. The closure line of the donor defect
can be positioned IN or parallel to the melolabial crease.
Advantage: The preservation of the alar facial sulcus
Disadvantage: multi stage procedure
Paramedian Forehead Flap: medium (>2cm) to larger (>3cm) defects
Ideal for reconstructing large or full thickness defects of the caudal 2/3rds of the nose
including nasal tip, ala, columella, dorsum, and nasal sidewall.
Blood Supply: supratrochlear artery
2 stage procedure:
1st Stage: cut a pattern from foil to match the defect, most of the flap should be
dissected in a supraperiosteal subfascial plane. At 2 cm above the supraorbital bony rim
dissection is carried out in a SUB periosteal plane to protect the supratrochlear artery.
2nd Stage: pedicle is divided and flap is debulked and inset
AA4. Can pin cushioning of a local flap be avoided?
Adequately restore adequate lining to full thickness defects. In addition to failures of lining, failure
of adequate reconstruction of cartilaginous support frequently results in unsatisfactory nasal
reconstructions.
Consequently, we advocate the liberal use of cartilage grafts for reconstruction. Cartilage grafts
are often required even if the native cartilage is not ablated at the time of initial Mohs
resection. Certainly, if upper lateral cartilage, lower lateral crural, middle, or medial crural
cartilages are removed with the extirpation, anatomic grafting should be done. It should be noted
that although the anatomic normal alar rim contains no cartilage, an alar rim defect that is
reconstructed without a nonanatomic rim graft has high risk of later deformity.

From Goldman’s Book:

Pin Cushioning aka Trapdoor Phenomenon:
?related to wound contraction of nonsupported tissue.
To lessen the degree of encircling contraction, wide undermining around the flap Is
recommended.
Tacking the flap also helps adhere to more rigid structures (bone, cartilage)
Thin the distal aspect of the flap so that upon inset, the flap appears concave rather than
flush w. the surface.

Commonly occurs with flaps of curvilinear design. Seems to results mainly from scar
contraction occurring on several levels. Persistent lymphedema plays some role.

Thin thin thin

Appropriate size – flap cannot be too big compared to the size of the defect

Square defects have less pin cushioning than round defects

For thick sebaceous skin, recipient bed should be cartilage or bone.

Widely undermine the recipient bed
Place anchoring/tacking suture
Maximize eversion

Pincushioning was more commonly noted on the nose and upper lip, in defects greater
than or equal to 15 mm, after bilobed or rhombic flap repair, and when dermal sutures
extruded postoperatively. Of the nasal subunits, the nasal ala was more likely to develop
a complication (relative risk [RR] ¼ 1.747, 1.435; ►Table 5), more likely to develop flap
pincushioning (RR ¼ 4.765, 3.504; ►Table 6), and more likely to require intralesional
corticosteroid injection (RR ¼ 2.423, 1.931) than either the entire face or other areas of
the nose, respectively. Larger defects were more likely to develop pincushioning, which
may have been related to the greater need to use transposition flaps in their repair.
Transposition flaps, such as rhombic or bilobed flaps, have long been known to develop
pincushioning more frequently, as seen also in our series; this has been attributed to the
near circumferential nature of the scars around these flaps and the cumulative inward
contractile scar forces at work.5 This finding also correlates with the increased risk of
requiring intralesional corticosteroids after rhombic flaps; the smaller number of
bilobed flaps used may have prevented achievement of statistical significance.
Successes, revisions, and postoperative complications in 446 Mohs defect repairs.
Sclafani AP, Sclafani JA, Sclafani AM.
Facial Plast Surg. 2012 Jun;28(3):358-66. Epub 2012 Jun 21.

CB5. A 70 year-old male is referred by a Moh's surgeon for management of a 1cm full-
thickness defect at the tip of his nose. What are the reconstructive options?
TT6. The Moh's surgeon was so impressed by your results in the previous patient, he
now sends you a patient with a full nasal alar defect… Plast Reconstr Surg
2000;105:1940 and Arch Fac Plast Surg 2001;3:91-99.
TT7. Give us the scoop on the midline forehead flap.
CB8. Describe the methods available for reconstruction of the bony nasal framework.
CB9. Discuss the management of a septal perforation.

AA10. Rhinophyma!
Rosacea is a common condition characterized by symptoms of facial flushing and a
spectrum of clinical signs, including erythema, telangiectasia, coarseness of skin, and an
inflammatory papulopustular eruption resembling acne. When rosacea reaches this
advanced stage, rhinophyma may develop. Rhinophyma is characterized by an enlarged,
bulbous, and red nose resulting from the enlargement of the sebaceous (oil-producing)
glands beneath the surface of the skin on the nose.

Phymatous rosacea is defined as marked skin thickenings and irregular surface

nodularities of the nose, chin, forehead, one or both ears, and/or the eyelids. Four distinct
histologic variants can occur with rhinophyma (associated changes of the nose) that
include glandular, fibrous, fibroangiomatous, and actinic. The mainstays of treatment are
isotretinoin topical application and surgical correction. This varies from other rosacea
subtypes.
Rhinophyma occurs more often in men than women. Treatment options for this advanced
stage of rosacea include medications and surgery.
Rhinophyma is a slowly progressive condition due to hypertrophy of the sebaceous
glands of the tip of the nose often seen in cases of long-standing acne rosacea; it is not a
neoplasm. It presents as a pink, lobulated mass over the nose with superficial vascular
dilation; it mostly affects men past middle age. Patients seek advice because of the
unsightly appearance of the enlargement, or obstruction in breathing and vision.
Treatment consists of paring down the bulk of the tissue with a sharp knife or carbon
dioxide laser and allowing the area to re-epithelialise. Sometimes, the tissue is completely
excised and the raw area skin-grafted.

Epidemiology: United States Accurate incidence data are not available; however,
rosacea is a common skin condition that disproportionately affects persons of fair-
skinned European and Celtic origin.

Treatment:
Cosmetic improvement of rhinophyma may be produced by mechanical dermabrasion,
carbon dioxide laser peel, and surgical shave techniques.
Loop Electrocautery
Surgery to reshape the nose is the best known treatment for rhinophyma. Surgery may be
done with a laser, scalpel, or a rotating brush (dermabrasion). There have been reports of
good results from using certain acne medications.

Pathophysiology
The etiology of rosacea is unknown. However, several factors, such as vasculature,
climatic exposures, dermal matrix degeneration, chemicals and ingested agents,
pilosebaceous unit abnormalities, microbial organisms, ferritin expression, reactive
oxygen species (ROS), increased neoangiogenesis, and dysfunction of antimicrobial
peptides (AMPs), likely play a role in its development.[4] Furthermore, the distinct
subtype of rosacea is likely determined by a patient's unique sensitivity to these triggers.
Vasculature

Increased blood flow to the blood vessels of the face and increased numbers of blood
vessels that are closer to the surface of the face are thought to be responsible for the
redness and flushing associated with rosacea. Furthermore, vasodilatation, the normal
response to hyperthermia, is thought to be more pronounced or exaggerated in those
individuals with rosacea.

Climatic exposures

Some evidence suggests that harsh climatic exposures damage cutaneous blood vessels
and dermal connective tissue. This also includes exposure to solar irradiation, which may
explain why rosacea predominately affects the facial convexities and has a tendency to
flare in the spring. However, other studies suggest the contrary, in that most patients'
symptoms do not worsen in the sunlight and do not flare with an acute exposure to
ultraviolet (UV) light.

Dermal matrix degeneration

Rosacea involves associated damage to the endothelium and degeneration of the dermal
matrix. However, it is not known whether the initial damage is in the dermal matrix and
this leads to poor tissue support of cutaneous vessels, causing pooling of serum,
inflammatory mediators, and metabolic waste, or whether the initial abnormality exists in
the cutaneous vasculature and this leads to leaky vessels and delayed clearance of serum
proteins, inflammatory mediators, and metabolic waste, thus resulting in matrix
degeneration.

Chemicals and ingested agents

Spicy foods, alcohol, and hot beverages were traditionally thought to trigger flushing in
patients with rosacea. However, most evidence does not support dietary factors playing a
central role in the pathogenesis. Moreover, certain medications, such as amiodarone,
topical steroids, nasal steroids, and high doses of vitamins B-6 and B-12, may cause
flares for patients with rosacea.

Perivascular versus perifollicular inflammation

An inflammatory infiltrate may exist in a perivascular and/or a perifollicular location;

however, evidence is conflicting regarding which location predominates. To answer this
question, more studies need to be designed to categorize subtypes of rosacea because the
answer varies depending on the subclassification.

Microbial organisms

Demodex species (mites that normally inhabit human hair follicles) may play a role in the
pathogenesis of rosacea. Some studies suggest that Demodex prefers the skin regions that
are affected in rosacea, such as the nose and cheeks.[5] Research also supports that an
immune response of helper-inducer T-cell infiltrates occurs, surrounding the Demodex
antigens in patients with rosacea. Yet, conflicting evidence indicates that Demodex does
not induce an inflammatory response in patients with rosacea. Moreover, Demodex is
found in large numbers of healthy individuals without rosacea. More studies need to be
performed to determine whether Demodex truly is pathogenic.

Additionally, inconclusive evidence suggests that Helicobacter pylori is associated with

the etiology of rosacea. However, many of the studies have not controlled for
confounding variables that influence H pylori prevalence, such as sex, age,
socioeconomic status, and medications. Furthermore, these studies were not statistically
powered to account for the ubiquitous nature of H pylori infection.

Ferritin expression

Iron catalyzes the conversion of hydrogen peroxide to free radicals, which leads to tissue
injury by damaging cellular membranes, proteins, and DNA. At the cellular level, iron
that is not metabolized is stored as ferritin. In a 2009 study, skin biopsy specimens from
patients with rosacea were immunohistochemically analyzed, and the number of ferritin-
positive cells was significantly higher in affected individuals compared with control
subjects. Additionally, higher ferritin positivity correlated with more advanced subtypes
of rosacea. Thus, increased release of free iron from proteolysis of ferritin can result in
oxidative damage to the skin, which may contribute to the pathogenesis of rosacea.[6]

Reactive oxygen species

Early in the inflammatory process, reactive oxygen species (ROS) are released by
neutrophils, which are postulated to have a central role in the inflammation associated
with rosacea. Free radicals, such as superoxide anions and hydroxyl radials, in addition to
other reactive molecules, such as molecular oxygen, singlet oxygen, and hydrogen
peroxide, comprise many of the ROS that lead to oxidative tissue damage. Several
mechanisms explain how ROS result in skin inflammation, most notably the deactivation
of natural defenses caused by excessive oxidant stress from ROS; chemical and oxidative
modification of proteins and lipids by ROS; alteration of the lipid balance in rosacea
patients, which, in normal proportions would suppress the creation of ROS; production of
cytokines and other inflammatory mediators by keratinocytes, fibroblasts, and endothelial
cells damaged by ROS; and the generation of ROS by cathelicidins, which are found in
greater amounts in the facial skin of affected individuals.[7]

Neoangiogenesis and vascular endothelial growth factor (VEGF)

overexpression

Studies performed using video capillaroscopy on erythematotelangiectatic rosacea lesions

showed increased neoangiogenesis and blood vessel enlargement. Multiple
immunohistochemistry studies showed increased VEGF expression in vascular
endothelium in lesional versus nonlesional skin of rosacea patients. Cuevas et al[8] used
topical dobesilate, an inhibitor of angiogenic growth factor, for the treatment of
erythematotelagiectatic rosacea and reported an improvement in erythema and
telangiectasia after 2 weeks.[4]

Antimicrobial peptides

AMPs are small molecular weight proteins that are a part of the innate immune response
and have demonstrated broad-spectrum antimicrobial activity against bacteria, viruses,
and fungi. They are rapidly released upon injury and/or infection of the skin, and they
have been implicated in the pathogenesis of many inflammatory skin diseases.
Cathelicidins and β-defensins are 2 well-known types of AMPs, of which the former has
been shown to be expressed in abnormally high levels in patients with rosacea.

Specifically, the LL-37 peptide form of cathelicidin, in addition to proteolytically

processed forms of LL-37, have been found in significantly different amounts in rosacea
patients compared with healthy individuals. LL-37 is expressed by polymorphonuclear
leukocytes and lymphocytes. LL-37 interacts with endothelial cells and stimulates
angiogenesis both in vitro and in vivo. It also modulates the expression of VEGF.[4]
Injection of LL-37 and these novel peptides derived from LL-37 into mice induced
inflammation, erythema, and telangiectasia; therefore, researchers hypothesized that an
excess of cathelicidins coupled with abnormal processing caused disease.[9]