Accepted Manuscript

Comprehensive surgical management of CIMDL

Giacomo Colletti, MD Luca Autelitano, MD Matteo Chiapasco, MD Federico Biglioli,MD Federica Giovanditto, MD Marco Mandalà, MD Fabiana Allevi, MD

PII: S0278-2391(14)00326-7

DOI: 10.1016/j.joms.2014.03.013

Reference: YJOMS 56260

To appear in: Journal of Oral and Maxillofacial Surgery

Received Date: 21 January 2014

Revised Date: 8 March 2014

Accepted Date: 10 March 2014

Please cite this article as: Colletti G, Autelitano L, Chiapasco M, Biglioli F, Giovanditto F, Mandalà M,Allevi F, Comprehensive surgical management of CIMDL, Journal of Oral and Maxillofacial Surgery(2014), doi: 10.1016/j.joms.2014.03.013.

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Comprehensive surgical management of CIMDL

Giacomo Colletti MD1, Luca Autelitano MD,1 Matteo Chiapasco MD,2 Federico Biglioli MD,1

Federica Giovanditto MD,1 Marco Mandalà MD,3 Fabiana Allevi MD,1

1 University of Milan, Department of Maxillo facial surgery, San Paolo Hospital, Milan, Italy

2 University of Milan, Department of Oral Surgery, San Paolo Hospital, Milan, Italy

3 University of Verona, Department of Otolaryngology, Verona, Italy

Corresponding Author

Giacomo Colletti

Via di Rudinì 8,

20142 Milan, Italy

Tel.: +39281844593

Fax: +39281844704

Mail: giacomo.colletti@gmail.com

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Abstract

Purpose: This article presents a review of the literature and proposes a protocol for managing

midfacial cocaine-induced acute and chronic injuries.

Methods: We report a series of four patients affected by cocaine-induced midline destructive

lesions (CIMDL). Three of the patients came to our attention after 18 months of drug

withdrawal and underwent surgical treatments to restore nasal and palatal morphology and

function, while the fourth patient was referred due to acute cocaine-induced destructive

lesions and was treated by aggressive debridement. An 18-month drug-free period is planned

before beginning any reconstructive procedures in this latter patient.

Results: Long-term follow-up showed stable results without relapse of palatal fistulas and

good esthetic nasal appearance in all three patients undergoing reconstruction. The fourth

patient did not show any disease progression and will be monitored for drug withdrawal.

Conclusion: Chronic cocaine consumption may cause multiple types of damage to the soft and

hard tissues of the midface. Acute lesions must be addressed with aggressive debridement. As

a result of chronic injury, the palate and the nose are deformed in a very complex way and the

vascularity of remaining local tissues may be compromised or inadequate for flap harvesting.

Palatal and nasal reconstructions are very delicate operations and they should be addressed

separately to maximize the predictability of the result.

Introduction

Cocaine is an alkaloid obtained from Erythroxylum coca plant leaves. The earliest known use

of cocaine was by sub-Andean Indians as a stimulant, while Koller first introduced its use in

medicine as local anesthetic in 1884.1

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More recently, cocaine has been used as a recreational drug because of its stimulating effects,

resulting in socioeconomic and physical damage. Cocaine is most commonly administered

intranasally, and the snorting of this drug has been associated with chronic rhinitis, epistaxis,

nasal septum perforations, lateral nasal wall destruction, and hard palate involvement with

oronasal communication.2,3 Cocaine inhalation damages the mucosal lining of the nose,

resulting in ischemia and necrosis, which lead to exposure and perforation of septal cartilage

and bones. As the disease progresses, the load-bearing structures of the nose can be lost with

consequent nasal collapse and central midface deformation.4 This is caused by a central

midfacial granulomatous destructive process, simulating other aggressive pathologies, such as

systemic lupus erythematosus, Wegener’s granulomatosis, tertiary syphilis, and

lymphoproliferative disorders, and is described in the literature as cocaine-induced midline

destructive lesions (CIMDL).5–7 A diagnosis of CIMLD is confirmed when two of the three

following signs are present: nasal septum perforation, lateral wall nasal destruction, and/or

hard palate involvement.6 Nasal septum perforation represents the most common

complication in cocaine abuse, affecting 5% of abusers.8 These adverse physical effects were

first described by Owens in 1912.9 Cocaine abuse has become a growing public health

problem, because of the rarity of short-term medical adverse effects and the poor

socioeconomic level of most abusers.1

Several methods have been reported for reconstructing the nose and palate damaged by

repeated cocaine inhalation. This article presents a series of four patients affected by CIMDL

who underwent surgical treatments for acute cocaine-induced granulomatous lesions in one

case and to restore nasal and palate morphology and function in three cases.

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Due to the retrospective nature of this study, an exemption was granted by the internal IRB of

our institution. This study was performed in adherence to the World Medical Association

Declaration of Helsinki.

Patient 1

Patient 1 was a 43-year-old man who was referred to our surgical department because of

severe cocaine-related midfacial destructive lesions. He reported prolonged cocaine abuse

lasting 10 years, but he stopped this habit 2 years before the first visit, which was confirmed

by serial urine analysis.

The patient presented wide midline destructive lesions, characterized by extensive oronasal

communication, with posterior hard palate defect, absence of nasal septum, and collapse of

the nasal pyramid. He complained of rhinolalia and oronasal regurgitation of solids and

liquids (Figs. 1–5).

Preoperative computed tomography (CT) showed complete absence of the nasal septum, the

lateral nasal walls, and the hard palate. The patient underwent two surgical procedures over

the last 2 years. The first surgery was performed for closure of the oronasal communication

using a partially deepithelialized radial fasciocutaneous free flap10 (Fig. 6). During the second

surgery, we performed an open rhinoplasty approach and freed the external soft tissues of the

nose. At the end of this phase, it was decided that the available soft tissues were sufficient and

therefore only reconstruction of the skeletal support of the nose was required. A costal

osteochondral cantilever graft was harvested, placed in the soft tissue pocket, and fixed with a

Kirschner wire (Figs. 7–10).

After 24 months, no relapse of the fistula was detected and the nasal reconstruction was

stable with good esthetic results.

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Patient 2

Patient 2 was a 46-year-old woman who came to our attention because of severe nasal

pyramid collapse following an intense period of cocaine abuse lasting 9 years. She presented a

wide cutaneous fistula of the left nasal ala and marked oronasal communication (Figs. 11–13).

On first examination, she reported that she had stopped abusing cocaine 2 years previously,

which was confirmed by multiple urine analysis. She was unable to breathe through her nose

because of complete collapse of the dorsum-ala complex. As she was unhappy with her

esthetic condition and complained of the passage of liquid and food in the nose, she sought

medical attention and underwent surgery to reconstruct the hard palate and nasal pyramid.

She underwent the first surgery to reconstruct the hard palate with a partially

deepithelialized radial fasciocutaneous free flap10 (Fig. 14). In a second surgery, the borders of

the nasal ala fistula was incised, all of the synechiae of the internal lining were freed, and the

defect was covered with an island melolabial flap. Three months later, we created a pocket

between the newly created internal lining and the external skin with an open rhinoplasty

approach. A costochondral graft was harvested and placed as a cantilever graft to reconstruct

the dorsum and the tip. The graft was secured in place with a Kirschner wire. Fifteen months

after the last surgery, the results were stable: no residual fistula was noted and the esthetic

results of nasal reconstruction had not changed over time (Figs. 15,16).

Patient 3

Patient 3 was a 36-year-old woman who was referred to our surgical department due to wide

oronasal communication and nasal pyramid collapse caused by cocaine abuse. The patient’s

main complaints were the inability to breathe through the nose and the nasal regurgitation of

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solids and liquids. She confirmed a 5-year history of cocaine abuse and complete drug

withdrawal lasting 18 months, which was confirmed by urine analysis. First, she underwent

surgery to reconstruct the hard palate with a radial fasciocutaneous free flap.10 Then, surgery

was performed to reconstruct the nasal pyramid. A first session was needed to reconstruct

the internal lining. This was performed with a grafted forehead pericranial flap, rotated

through a soft tissue tunnel at the level of the glabella. Three months later, with open

rhinoplasty access, a pocket was created in which a costochondral graft was placed and

secured to the nasal bones with a Kirschner wire.

Thirteen months after the second procedure, the palatal and nasal results are stable and the

patient no longer shows oronasal regurgitation.

Patient 4

Patient 4 was a 39-year-old woman who was referred to our institution because of CIMDL

after 10 years of cocaine abuse. The patient had not ceased drug consumption at the time of

referral. Acute lesions on the nasal septum, columella, nostrils, premaxilla, and palate were

clearly evident. These areas were characterized by the presence of granulation tissue and pus.

Bone, cartilage, and soft tissues of the nasal septum and lateral nasal wall were missing, and a

wide palatal fistula was present (Figs. 17,18).

These chronic inflammatory lesions endured for months despite conservative treatment with

antibiotics and gentle debridement. Then it was decided to perform aggressive debridement

and all of the areas involved by the process were surgically removed under general

anesthesia. No signs of new acute lesions were found several months after the operation (Figs.

19,20). The patient has since reported complete drug withdrawal. Urine analysis is performed

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every 2 months to confirm withdrawal, and an 18-month drug-free period is planned before

commencement of any reconstructive procedures.10

Discussion

Midfacial osteocartilaginous lesions as a result of cocaine abuse were first reported in 1988.11

Cocaine abuse is becoming increasingly common in Western countries, and cocaine use is

being seen among younger and younger people.10 Snorted cocaine induces intense

vasoconstriction, which in turn leads to severe ischemic necrosis of the affected tissues

associated with osteomyelitis and chondritis, with eventual destruction of the sinonasal and

midfacial bones and soft tissues.2 Necrosis of nasal tissues is caused by the added effects of

cocaine and topical decongestant; the caustic effects of adulterants such as talc, amphetamine,

and lidocaine; and the anesthetic effects of the drug resulting in trauma and thermal injuries,

favoring local infections. The midfacial complications of cocaine abuse are well documented.

Approximately 5% of cocaine abusers show nasal septal perforation, which is the most

frequent local complication of intranasal cocaine use.1 All of the surrounding structures, i.e.,

the lateral nasal wall and hard and soft palate, then show progressive damage, until reaching a

condition described as CIMDL.

Nasal septal perforation is usually well tolerated by these patients, while they are usually

troubled by external nasal collapse and by the oronasal fistulas that cause rhinolalia and

passage of liquids and food into the nose.

In 2005, Goodger et al. suggested that women may be more susceptible to wide palatal

necrosis and connective tissue disorders than men.2 In addition to cocaine abuse, multiple

other conditions can induce midfacial destructive lesions, including tertiary syphilis, tumors,

traumas, chronic infections (actinomycosis and tuberculosis), Wegener’s granulomatosis,

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systemic lupus erythematosus, and midline granulomas, often caused by angiocentric T-cell

lymphoma.1,2 In patients who do not admit to cocaine abuse, the differential diagnosis

between Wegener’s granulomatosis and cocaine-induced midfacial osteocartilaginous lesions

may be difficult because both diseases are c-ANCA-positive and show vascular lesions. The

absence of renal and pulmonary involvement does not exclude limited Wegener’s

granulomatosis; therefore, histopathology represents the gold standard for obtaining a

reliable diagnosis. Nonspecific histopathological changes are more frequent in cocaine-

induced lesions than in Wegener’s disease; fibrinoid necrosis, leukocytoclastic vasculitis,

perivenulitis, and microabscesses in the vascular wall are usually present in both pathologies;

and extravascular changes such as stromal granulomas with giant cells, microabscesses, and

deeply localized necrosis are pathognomonic features of Wegener’s granulomatosis that are

not present in CIMDL.12–14

Drug abusers are difficult patients as they are prone to lie regarding their condition and often

show poor compliance. However, there is little information in the literature regarding the

general treatment of these patients.

Several aspects must be taken into consideration in the management of CIMDL. The first is the

management of acute lesions. As seen in patient 4, these are essentially caused by areas of

nonviable tissue that form crypts where many toxic substances can accumulate if the patient

continues using the drug. The complex of necrotic tissue and harmful substances causes a

mixed acute and chronic inflammatory reaction. Medications such as antibiotics and “light”

debridement will not help in such cases, and meticulous and thorough curettage is needed to

eliminate all of the foci. This surgical step is essential for the tissue to heal, but complete and

definitive withdrawal of the drug is required to avoid relapse.

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The second aspect to consider in the management of CIMDL is reconstruction. Soft and hard

tissues of the nose, maxilla, and the soft and hard palate of cocaine abusers are frequently

destroyed. These anatomical structures are completely lost or left with a complex three-

dimensional deformity in cocaine users. Moreover, the vascularity of the affected areas is

frequently unreliable and therefore local flaps are prone to failure. An integrated

reconstructive protocol will rely on many delicate surgical procedures, which could easily fail

if the patient resumes drug abuse. To ascertain patient motivation to undergo this complex

course of treatment, an 18-month period of drug withdrawal, confirmed by serial urine

analysis, is considered mandatory.15

Comprehensive reconstructive management of CIMDL must address the palatal fistula and the

nasal deformity. In the past, severe hard palate defects were rehabilitated using prosthetic

obturators, with moderate results in term of speech and swallowing. Several disadvantages of

such devices have recently been described, including the lack of stability and retention in

edentulous patients and sensory impairment that leads to problems with mastication,

deglutition, and speech.16

Many surgical techniques have been proposed for reconstruction of nasal and palatal tissues.

However, both local and regional tissue transfer have limitations in cocaine users: oronasal

communication often presents as a wide fistula that cannot be treated with local tissues

(palatal or lingual flap), because of the large size of the fistula and the unreliable results in

terms of flap survival in infected and poorly vascularized donor and recipient beds.

Furthermore, local tissues are often quantitatively unavailable as local flap donors because of

their involvement in drug-induced necrosis.

However, there have been some reports of the successful treatment of small CIMDL palatal

fistulas with palatal or tongue flaps.1,17 The use of temporalis muscle flaps was proposed, but

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cocaine abusers usually present with median palatal defects, which are difficult to reach with

a temporalis muscle flap that requires a very large fenestration through the maxilla.16,18 Even

more complex procedures, such as Le Fort I osteotomy and buccal fat pad flaps, have

occasionally been tried. The validity of such procedures, however, remains to be determined

as only single case reports have been described.19 In 2003, Marshall and colleagues first

described the use of the forearm fasciocutaneous free flap to reconstruct cocaine-related

oronasal fistulas.20 The forearm free flap is a thin versatile flap with a long vascular pedicle

that allows it to reach the cervical region to make use of facial vessels for vascular

anastomosis. Should the facial vessel be inadequate, the length of the pedicle allows switching

to more distant vessels, such as the internal jugular vein and the carotid artery. In patients 1

and 2 in the present study, the facial artery was anastomosed with the radial artery of the flap,

while the facial vein was too small so we used the internal jugular vein to facilitate safe

venous drainage. In patient 3, facial vessels were adequate for microvascular anastomoses.

The use of free flaps in reconstructing CIMDL is particularly suitable because they allow

repair of the defect with abundant reliable well-vascularized soft tissue without tension; in

addition, they yield reliable long-term results. In experienced hands, with a double team

approach, a forearm free flap is not more invasive and does not require more operative time

than harvesting and rotating a temporalis muscle flap.

Cocaine abuse causes severe and extremely complex changes in nasal morphology. The entire

process is initiated by necrosis of the nasal mucosa of the septum. When the cartilage is

exposed, it rapidly becomes necrotic, giving rise to septal perforation. The loss of septal

support causes collapse of the dorsum with a typical resulting saddle nose. The same process

afflicts the entire mucosa, and the areas where this mucosa is thinner are more rapidly

compromised. Immediately after the septum, the area that is injured next corresponds to the

internal valve and to the caudal limit of the nasal bones. These areas with time become

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retracted as a consequence of the loss of internal lining, resulting in cephalic migration of the

tip with columellar exposure. In contrast, the area of the ala cartilage is covered by skin and

thus becomes affected only at the very end of the process. Moreover, the deformity is often

asymmetrical as cocaine abusers usually use their dominant hand to introduce the drug and

thus the detrimental effect accumulates more on that side. As a result, there is a worse

contracture of the nose corresponding to the patient’s dominant side and the entire nose

becomes deviated to that side. Often, there is some columellar retraction that pulls the tip

dorsally.21 Reconstructive rhinoplasty of CIMDL must take all of these aspects of the disease

into account.

The first to consider is the internal lining. Although various procedures have been proposed,

no surgical technique is yet available to reconstruct a sufficiently thin soft tissue envelope for

a new nasal septum. The role of microvascular reconstruction of the nasal septum, which ends

with a bulky mass inside the nasal cavity, is questionable and until new techniques are

discovered such procedures are better avoided.22

However, there have been reports of successful reconstruction of the internal lining using free

flaps.23–26 This is required only where there is an almost complete absence of the internal

lining and it is therefore seldom indicated in CIMDL nasal reconstruction.

On the other hand, despite a single report of excellent results obtained with local flaps from

the remaining internal lining,22 other authors have relied on locoregional flaps, typically an

island melolabial flap, to rebuild the lost mucosa.4 While local flaps have the undoubted

advantage of being very thin and thus do not affect respiration, their vasculature can be

unreliable and therefore the results may not be maintained over the long term. Conversely,

melolabial flaps are bulky and may require additional thinning, but they have superior

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vasculature. In our institute, we have used for the second option for internal lining

reconstruction with rotation of an island melolabial flap.

The other aspect of nasal reconstruction for CIMDL is the skeletal framework. The aim is to

rebuild support for the dorsum, the tip, and the ala, and various different approaches have

been reported. Some authors have used composite free flaps containing skin and cartilage,27

while others have transferred prefabricated composite skin-cartilage flaps.23 Again,

considering the general poor color and texture match of distant flaps, these are a second

choice and should be used only if local tissues are truly unavailable.

The best option for reconstruction of CIMDL nasal defects is an open rhinoplasty approach

where the inner lining is carefully preserved. Any breach must be repaired immediately with

watertight sutures.22 When the entire inner lining has been separated then the outer soft

tissues must be widely freed. The tip must be moved anteriorly and downward, and the

surgeon checks the amount of movement obtained while exerting gentle traction on these

outer soft tissues. If there is any tension, then more soft tissue mobility must be obtained by

undermining in the frontoglabellar region and within the cheeks. When a sufficient degree of

freedom has been obtained in the soft tissues, structural skeletal grafting is required. The rib

is acknowledged as the best donor site for major nasal reconstruction,4,22 but some other

grafts are seldom used, such as calvarial bone.28 The technique of skeletal reconstruction with

costochondral grafts in CIMDL is equivalent to the same procedure used in other

circumstances, such as in posttraumatic defects or even in syphilis or leprosy.4 The quality of

local nasal soft tissues, even if injured by many years of chronic drug abuse, is not an issue

and we have not observed any exposure or infection of the grafts, consistent with other

reports in the literature.4,22

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Chronic cocaine abuse may cause a wide range of damage to the soft and hard tissues of the

midface. The aim of acute management is aggressive removal of infected crypts where

injurious substances and bacteria can accumulate. Reconstruction of the affected structures

can be initiated when an 18-month period of drug withdrawal can be confirmed. The palate

and nose are damaged in a very complex way, and the vascularity of remaining local tissues

can be compromised or inadequate to allow for flap harvesting. Palatal and nasal

reconstructions are very delicate, and they should be addressed separately to maximize the

predictability of the result.

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References

1 – Marì A, Arranz C, Gimeno X, Lluch J, Pericot J, Escuder O, Monner A, Piulachs P: Nasal

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Br Dent J 198(6): 333-4, 2005

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fistula with forearm radial free flap. J Craniofac Surg 24(5): 1734-8, 2013

11 – Becker GD, Hill S: Midline granuloma due to illicit cocaine use. Arch Otolaryngol Head

Neck Surg 114: 90-1, 1988

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12 – Trimarchi M, Mortini P: Cocaine-induced midline destructive lesion and Wegener

granulomatosis. Neurosurgery 70(5): E1339, 2012

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radiographic, histopathologic and serologic features and their differentiation from Wegener

granulomatosis. Medicine (Baltimore) 80(6): 391-404, 2001

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in cocaine abuser. Ear Nose Throat J 75: 623-27, 1996

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17 – Posnick JC, Getz SB: Surgical closure of end-stage palatal fistulas using anteriorly-based

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18 – Cordeiro P, Wolfe SA: The temporalis muscle flap revisited on its centennial: advantages,

newer uses and disadvantages. Plast Reconstr Surg 98: 980-87, 1996

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osteotomy and the use of bilateral Bichat bulla adipose flap: an effective new technique for

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20 – Marshall DM, Amjad I, Wolfe A: Use of the radial forearm flap for deep, central, midfacial

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21 – Silvestre FJ, Perez-Herbera A, Puente-Sandoval A, Bagan JV: Hard palate perforation in

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Legends

Figure 1: Preoperative picture showing a typically foreshortened nose with right deviation:

the patient is right-handed; the tip is underprojected and deepened nasolabial sulci are

evident. Frontal view.

Figure 2: Preoperative three-quarter view of the same patient showing collapse of the nasal

pyramid caused by CIMDL.

Figure 3: Preoperative lateral view of the same patient: the tip is cranially and dorsally

retracted as a result of the collapsed nasal pyramid.

Figure 4: Preoperative worm’s eye view showing an asymmetric nasal deformity

characterized by tip deviation and collapse of the dorsum.

Figure 5: Preoperative picture showing extensive oronasal communication.

Figure 6: Postoperative result: closure of the oronasal communication was obtained with a

partially deepithelialized fasciocutaneous radial free flap.

Figure 7: Frontal view showing the postoperative result obtained with an open rhinoplasty

approach, a costal osteochondral cantilever graft fixed with a Kirschner wire.

Figure 8: A three-quarter view showing the postoperative result of the same patient:

eumorphic nasal pyramid and nasolabial sulci were obtained.

Figure 9: Lateral view of the same patient where a normally projected tip and a 105° naso-

labial angle are detected.

Figure 10: Postoperative worm’s eye view showing a good symmetry of the tip and nasal alae.

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Figure 11: Preoperative picture showing a patient with a severe nasal pyramid collapse

following intense cocaine abuse lasting 9 years (lateral view).

Figure 12: Preoperative picture showing a patient with a severe nasal pyramid collapse

following intense cocaine abuse lasting 9 years (three-quarter view).

Figure 13: Preoperative picture showing a wide oronasal communication.

Figure 14: Postoperative picture showing the closure of the oronasal communication obtained

by a partially deepithelialized radial fasciocutaneous free flap.

Figure 15: Postoperative picture showing the result obtained after two-step surgery: first, we

freed all of the retractions of the inner lining and reconstructed the resulting defect with an

island melolabial flap; second, a costochondral cantilever graft was placed to reconstruct the

dorsum and the tip (lateral view).

Figure 16: Postoperative three-quarter view of the same patient. A dorsum with good tip

projection and nasolabial angle was obtained.

Figure 17: Frontal view of the fourth patient, affected by acute lesions on the nasal septum,

columella, nostrils, and premaxilla. These areas were characterized by the presence of

granulation tissue and pus. Bone, cartilage, and soft tissue of the nasal septum and lateral

nasal wall were already missing.

Figure 18: Intraoral picture of the fourth patient affected by a wide palatal fistula.

Figure 19: Frontal view of the fourth patient after aggressive debridement: under general

anesthesia all of the areas involved by the process were surgically cleared.

Figure 20: Intraoral picture after aggressive debridement: the resulting severe collapse of the

lower two-thirds of the nose is evident.

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ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT

MANUSCRIP

T

ACCEPTED

ACCEPTED MANUSCRIPT