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 Table of Contents  
Year : 2018  |  Volume : 52  |  Issue : 3  |  Page : 155-166

Hemifacial microsomia

Prof, Department of Oral and Maxillofacial Surgery, Meenakshi Ammal Dental College and Hospital, Chennai, Tamil Nadu, India

Date of Submission11-Nov-2017
Date of Acceptance12-Jun-2018
Date of Web Publication18-Jul-2018

Correspondence Address:
Prof. Anantanarayanan Parameswaran
Af 39, 6th Street, 11th Main Road, Anna Nagar, Chennai - 600 095, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jios.jios_234_17

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Hemifacial microsomia, known also as craniofacial microsomia is a part of the Oculo-auriculo-vertebral spectrum and is generally characterized by a retarded development of the anatomical structures of one side of the head and face. It involves hypoplasia of structures of the first and second branchial arches. This article aims at providing an overview into the current nomenclature, classifications systems, presenting features in patients afflicted with this deformity and guidelines for its successful management. The article focusses on the comprehensive rehabilitation of these unfortunate patients who may present either in their childhood or at a much later stage in life. The highlights of this article include an easy format of presentation with tables, diagrammatic representation and photographs to elicit the various aspects of managing this complex deformity.

Keywords: Hemifacial macrosomia, hemifacial microsomia management, surgery for hemifacial microsomia

How to cite this article:
Parameswaran A, Ramanathan M. Hemifacial microsomia. J Indian Orthod Soc 2018;52:155-66

How to cite this URL:
Parameswaran A, Ramanathan M. Hemifacial microsomia. J Indian Orthod Soc [serial online] 2018 [cited 2019 Feb 19];52:155-66. Available from: http://www.jios.in/text.asp?2018/52/3/155/237102

  Introduction Top

Hemifacial macrosomia (HFM) is a craniofacial disorder which is characterized by hypoplasia of structures of the first and second branchial arches. There is much variation in the nomenclature of this disorder, and the more commonly used alternatives include craniofacial macrosomia (CFM), otomandibular dysostosis, facio-auriculo-vertebral spectrum, and oculo-auriculo-vertebral spectrum. The disorder is classically unilateral in presentation; however, 10%–15% of occurrences have been reported as bilateral. Gorlin and Pindborg were the first to use the term “Hemifacial macrosomia” in the early 1960s. This craniofacial disorder has a wide spectrum of involvement and manifests with varying clinical features [Figure 1] and [Figure 2]. Goldenhar syndrome [Figure 3] is also considered a variant of this disorder in which, apart from the deformities of the head and neck region, the patient also exhibits ocular/epibulbar dermoids and abnormalities of the cervical spine.[1],[2],[3]
Figure 1: Child with right-sided hemifacial macrosomia

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Figure 2: Child with left-sided hemifacial macrosomia and treated bilateral cleft lip

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Figure 3: Adult with Goldenhar syndrome

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  Epidemiology and Etiopathogenesis Top

The incidence of HFM has a wide range between 1 in 3500 and 1 in 26,000 live births, and it is approximately estimated to be 1 in 5000 live births in India which seems close to the global average of 1 in 5600 as reported by Cohen.

The etiology of HFM shows genetic heterogeneity. Familial occurrences have been reported but with a wide range of expression. Poswillo reported that disruption of embryonic arteries in utero and expansion of the resultant hematomas produces abnormalities in the development of the ear and the jaws. The severity of the deformities may be influenced by the size of the hematoma and the amount of tissue damage it produces. A correlation of the various clinical features of the spectrum reveals that this may occur between 30 and 45 days of gestation.

Teratogenic effects of thalidomide, primidone, ethanol, and isotretinoin have also been implicated in the formation of HFM.[1],[3]

  Clinical Features Top

The clinical features of HFM are very diverse and show high degrees of variability, and hence more clinicians are inclined to term it as facio-auriculo-vertebral or oculo-auriculo-vertebral spectrum in the recent years. The features in the head-and-neck region may be segregated into the following subgroups.


The cranial involvement in its true sense is restricted to the hypoplasia of the squamous part of temporal bone. Most individuals affected with HFM do demonstrate hypoplasia of the zygomatic bone which along with the involvement of the maxilla is expressed as orbital dystopia. The deficiency of the zygomatic bone may also lead to alterations in the morphology of the glenoid fossa.


Facial deformities may either be soft tissue or skeletal abnormalities.

The soft tissue deficits can be categorized into four main groups (i) auricular – external ear, (ii) ocular – eye and associated adnexa, (iii) preauricular – cheek and lips, and (iv) temporal. The auricular problems include anotia, microtia, and dysmorphic ears [Figure 4]. The preauricular abnormalities include preauricular skin tags, blind sinus tracts in the cheek [Figure 5], and in many few individuals, macrostomia or lateral facial clefts [Figure 6]. Ocular anomalies range from anophthalmia or microphthalmia to coloboma of the eyelids, absence of the lateral canthi, and epibulbar dermoid cysts which show high rates of presentations. Temporal hollowing due to hypoplastic temporalis may also be evident in the affected.
Figure 4: Adult with right-sided anotia

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Figure 5: Adult with left-sided hemifacial macrosomia demonstrating macrostomia and skin tags

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Figure 6: Child with macrostomia (lateral facial cleft)

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Skeletal abnormalities of the maxillomandibular region are primarily due to deficient development of structures of the first and second branchial arches. These present as unilateral facial deformities with diminished dimensions of facial bones in all three axis – anteroposterior, vertical, and mediolateral producing gross asymmetry of the face and compensatory secondary changes in the contralateral side of the face.

Middle ear and hearing related

Deformities may be present as small sized external auditory canal to totally absent auditory canals. The degree of involvement of the middle ear may be better appreciated with a computed tomography scan, and a thorough audiological evaluation may be necessary to assess the individuals' hearing function.

The full spectrum of possible involvements and associated clinical features has been enumerated in [Table 1].
Table 1: Clinical features of hemifacial microsomia and the spectrum of associated anomalies

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  Head and Neck Top

Maxillary and mandibular asymmetry with hypoplasia on the affected side

  • Microphthalmia
  • Hypoplastic adnexal structures
  • Coloboma
  • Zygomatic hypoplasia
  • External ear abnormalities or atresia
  • Internal ear abnormalities
  • Temporomandibular joint (TMJ) hypoplasia or absence
  • Hypoplastic dentition or oligodontia
  • Parotid hypoplasia or agenesis
  • Plagiocephaly
  • Torticollis.

  Associated Congenital Anomalies Top

  • Cardiac defects (tetralogy of Fallot, ventricular septal defect, aortic coarctation, and patent ductus arteriosus)
  • Lung hypoplasia
  • Renal agenesis, ectopic kidney, multicystic dysplastic kidney, vesicoureteral reflux, or ureteropelvic junction obstruction
  • Vertebral anomalies
  • Mental retardation,  Arnold- Chiari malformation More Details More Details, encephalocele.

  Classification Systems Top

Numerous classifications have tried to group this spectrum to its full extent. They are enumerated below:

  1. SAT classification [Table 2] [4]
  2. OMENS classification [Table 3][5]
  3. Kaban's modification of Pruzansky's classification.[6]
Table 2: SAT classification

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Table 3: OMENS classification

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The SAT and the OMENS classification provide a more comprehensive system of classification which enables us to understand the spectrum better inclusive of the soft extended skeletal deformity, soft tissue defects, and neurological involvement. However, the Kaban-Pruzansky classification has stood the test of time and has been considered as the “Gold Standard” for classifying the deformity of the mandible, masticatory muscles, and associated TMJ and maybe more useful for orthodontics and maxillofacial surgeons who are interested in reestablishing the morphology of the mandible and masticatory apparatus. This classification involves four classes – The Type 1, Type 2A, Type 2B, and the Type 3.

Type 1

In this classification, the mandible joint morphology is normal and masticatory muscle has adequate bulk and function. The mandible is slightly hypoplastic with retrusion and may exhibit a mild asymmetry with deviation of the chin to the affected side [Figure 7].
Figure 7: CT scan of patient with left-sided Type 1 Kaban-Pruzansky deformity

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Type 2A

In this type, the joint is slightly involved with a change in its position. The whole joint is shifted anteriorly and medially than its counterpart, though the morphology of the condyle and glenoid fossa is retained. The joint is functional with moderate hypoplasia of the associated musculature. The mandible shows moderate hypoplasia, the chin is deviated to the affected side, and the patient demonstrates occlusal canting or open bites.

Type 2B

There is moderate-to-severe involvement of the joint here. The condyle is grossly hypoplastic and so is the glenoid fossa. The joint shows rotation of the condyle and near normal function. There is evidence of involvement of other facial bones. The muscle of mastication is deficient to a clinically evident level. The patient demonstrates severe occlusal canting with or without an open bite [Figure 8].
Figure 8: CT scan of patient with right-sided Type 2B Kaban-Pruzansky deformity

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Type 3

Here, the patient shows gross facial asymmetry with severely hypoplastic muscle of mastication which may at times be absent. The patient shows severe deformity of the skull and orbitozygomatic complex also. They may often present with orbital dystopia. The mandible is severely affected with a “floating mandible” appearance where the condyle and the ramus are absent [Figure 9]. These children may show severe degrees of mandibular retrusion and many often present with a compromised airway.
Figure 9: CT scan of patient with right-sided Type 3 Kaban-Pruzansky deformity

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Sat classification

The skeletal, auricle, and soft tissue (SAT) classification system of hemifacial microsomia

Skeletal categories

S1 = Small mandible with normal shape

S2 = Condyle, ramus, and sigmoid notch identifiable but grossly distorted; mandible strikingly different in size and shape from normal

S3 = Mandible severely malformed, ranging from poorly identifiable ramal components to complete agenesis of ramus

S4 = An S3 mandible plus orbital involvement with gross posterior recession of lateral and inferior orbital rims

S5 = The S4 defects plus orbital dystopia and frequently hypoplasia and asymmetrical neurocranium with a flat temporal fossa.

Auricle categories

A0 = Normal

A1 = Small, malformed auricle retaining characteristic features

A3 = Rudimentary auricle with hook at cranial and corresponding to the helix

A3 = Malformed lobule with rest of pinna absent.

Soft tissue categories

T1 = Minimal contour defect with no cranial nerve involvement

T2 = Moderate defect.

  Omens Classification Top

  1. Orbit

  2. 0 = Normal

    1 = Small size

    2 = Poor position

    3 = Both small size and poor position.

  3. Mandible

    • Type I
    • Type IIA
    • Type IIB
    • Type III.

  4. Ear

    • Type I = Small ear but most of the normal structure
    • Type II = Severely affected external anatomy with rudimentary auricle present
    • Type III = External ear is only a small rudiment with no pinna
    • Type IV = Anotia.

  5. Nerve (cranial nerve VII)

  6. 0 = Normal

    1 = Upper branches impaired

    2 = Lower branches impaired

    3 = Upper and lower branches impaired.

  7. Soft tissue

  8. 0 = Normal

    1 = Mild hypoplasia

    2 = Moderate hypoplasia

    3 = Severe hypoplasia.

  Principles of Management of Craniofacial/hemifacial Microsomia Top

The principles involved in the management of CFM are described below with more focus on the mandible and TMJ and involved masticatory musculature. For ease of understanding, the management of the patient may be age related as not only the presenting complaints and features may vary but also so would the method or technique of management [Figure 10].
Figure 10: Diagrammatic representation of interventions necessary at different ages

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  Interventions in Neonates and Infants Top

The severity of the deformities may produce morphological as well as functional compromise of the child's airway. The presence of a compromised airway may alter the child's ability to swallow or ingest food. Hence, the primary focus of management in a neonate or an infant is in the stabilization of the airway and assisted feeding.[3],[7]


A grossly compromised airway may necessitate neonatal distraction (early distraction osteogenesis) or in rare instances a tracheostomy to maintain the patency of the child's airway and facilitate the child to thrive.[8]


Most children presenting with airway compromises may require assisted feeding which may vary from postural changes during feeding to the use of nasogastric tubes for a few weeks to a couple of months. The use of a feeding gastrostomy also may be an option that is used in instances.

Management of associated orofacial clefting

The incidence of orofacial clefting occurring with HFM is approximately 10% with the most common forms of clefting apart from labial clefts being macrostomia or Tessier 7 facial cleft. The management of children with associated orofacial clefting is no different from the general principles for management. The cleft is corrected as early as 3–6 months and then the standard protocol is followed.[3],[9]

Soft-tissue deformities

Soft tissue and skin deformities such as preauricular tags and blind sinuses may be managed at the earliest during the correction of the orofacial clefting [Figure 11].
Figure 11: Surgical correction of lateral facial cleft

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  Interventions in a Child Top

The basic goals for management in a child may be enumerated as follows:[3],[10]

Ear reconstruction

Reconstruction of the external ear may be contemplated as early as 7 years [Figure 12] and [Figure 13].
Figure 12: Surgical correction of anotia

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Figure 13: Steps in ear reconstruction with autogenous chondral cartilage

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Cranio-orbital region

Reconstruction of the cranio-orbital region may be accomplished between 7 and 9 years by which time the calvarial growth is almost complete. The use of a split calvarial graft may be the ideal solution for the management of the asymmetry of the cranio-orbital region.

Maxillomandibular correction

Variations in the management of the maxillomandibular complex ranges from early intervention and reconstruction of the mandible to a policy of wait and watch with only dental and orthodontic interventions performed to reduce the impact of the deformity on the dental occlusion and masticatory function. The author personally prefers to wait for the cessation of growth for any definitive interventions for reconstruction of the maxillomandibular complex and the TMJ.[11],[12]

Role of orthodontics/functional appliance therapy

Growth modification with the use of functional appliances does have a role in the management of HFM and is directed toward the less severe forms where the ramus-condyle unit (RCU) shows reasonable integrity for the functional forces to translate into skeletal growth. Literature also shows that the significant point of difference of HFM may lie in the fact that there is associated deficit of the soft tissue also in varying proportions which may influence the final outcomes of functional therapy in a major way. The role of functional appliances in the management of HFM is focused to address the following goals:

  1. To facilitate eruption of the dentition in an optimal fashion
  2. To prevent compensatory mechanisms of the dentoalveolar process from worsening the deformity and increasing the functional deficit
  3. To passively guide the growth of the RCU.

The focus of functional therapy is aimed at repositioning the affected mandibular condyle to a much more inferior and anterior position to enable the condylar process and the mandible to grow and compensate for the intrinsic skeletal deficit.[13],[14],[15]

  Adolescents and Adults Top

Management during the adolescent phase and adults includes definitive reconstruction for skeletal and residual soft-tissue deficits. The management of permanent neurological deficits is also managed at this level [Figure 14].
Figure 14: Diagrammatic representation of skeletal corrections required for hemifacial macrosomia

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  Principles of Management of the Temporomandibular Joint Top

Type 1 and 2A

There is no indication for the reconstruction of the TMJ in Type 1 and 2A deformities. The glenoid and condylar components of the joint are reasonably intact with normal morphology and minimal hypoplasia. The joint exhibits normal movement characteristics, and the patient is able to demonstrate adequate mouth opening and masticatory function.

Type 2B

Type 2B patients exhibit altered functioning of the joint due to gross hypoplasia of both the condylar and the glenoid elements of the joint. This greatly retards the translatory movement of the joint while still facilitating rotation. The authors' personal choice for Type 2A where augmentation of the RCU is needed is the use of distraction osteogenesis for developing the mandibular corpus and corrects the deficiency along with reshaping the glenoid component and condylar process. However, this is contemplated only as the patient nears skeletal maturation. The use of maxillomandibular osteotomies to correct the dentofacial deformity is also performed either concomitantly or in a staged manner as described in the following section. Other options for reconstruction of the RCU which is reported with reasonable levels of success are costochondral grafting.[16]

Type 3

Patients with Type 3 deformities require total reconstruction of the TMJ including reshaping or reconstruction of the glenoid-zygomatic complex region as well as the RCU for optimal functioning. The growing adolescent in final stages of growth may be a candidate for glenoid reshaping and costochondral graft reconstruction of the RCU, while an adult is subjected to alloplastic total joint reconstruction solutions with concomitant orthognathic surgical procedures.

  Management of the Maxillomandibular Complex Top

Orthodontics for definitive skeletal surgery

Orthodontics for definitive surgical correction of the maxilla and mandible are similar to the conventional presurgical orthodontic protocols and sequenced in the following manner

  1. Arch alignments
  2. Dental decrowding
  3. Occlusal leveling
  4. Arch widening where necessary
  5. Planning for cross bite and open bite corrections
  6. Achieving optimal postsurgical dental intercuspation.

Type 1

The minimal asymmetry and deformity associated with a Type 1 HFM may be amenable to corrections with an isolated chin procedure alone in most cases. Very few of the patients in this group may require any further orthognathic surgical correction [Figure 15].
Figure 15: Diagrammatic representation of surgical management of Type 1 Kaban-Pruzansky (a) deformity with isolated genioplasty for asymmetry correction (b)

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Type 2A

Patients with Type 2A deformities require planned orthodontic interventions to facilitate definitive orthognathic correction of the maxillomandibular complex.[17] This includes bimaxillary surgery to achieve the following goals [Figure 16] and [Figure 17].
Figure 16: Diagrammatic representation of surgical management of Type 2 Kaban-Pruzansky deformity (a). Derotation of the maxilla-mandibular complex by orthognathic surgery (b and c). Midline skeletal correction with a centering genioplsty (d)

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Figure 17: Adult with right Type 2A skeletal deformity corrected by orthognathic surgery

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Maxilla and midface

  1. Leveling of the occlusal canting
  2. Widening of maxilla to facilitate corrections of cross-bites
  3. Derotation of the maxilla to achieve midline corrections
  4. Augmentation of the zygomatic complex where necessary
  5. Asymmetry correction.


  1. The mandible is subjected to either a bilateral sagittal split osteotomy procedure to correct the canting of the occlusal plane and derotation of the displaced dental midline
  2. An inverted “L” osteotomy or a subsigmoid osteotomy may be performed in indicated patients to achieve elongation of the RCU
  3. Correction of skeletal asymmetry.

Simultaneous maxillomandibular distraction described by Monasterio and Molina paved way for an alternate method for achieving maxillary and mandibular corrections with minimal disturbance of the dental cant and occlusion.

Type 2B and 3

As explained earlier, the Type 2B and 3 patients require reconstruction of the TMJ as the primary goal which may be performed either as a Stage 1 correction with maxillomandibular correction as Stage 2 or a concomitant maxillomandibular correction and joint reconstruction. The principles of management of the maxilla, mandible, and the dentition are similar to the protocol followed for Type 2 deformities [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24].
Figure 18: Adult with right-sided Type 2B skeletal deformity corrected by bidirectional distraction osteogenesis

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Figure 19: Radiographs demonstrating mandibular bidirectional distraction for the same patient

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Figure 20: Skeletal correction of patient with Goldenhar syndrome using bimaxillary osteotomies (frontal pictures)

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Figure 21: Profile pictures of the same patient

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Figure 22: Soft tissue correction of patient with Type 2B deformity using dermis – fat grafting technique

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Figure 23: Skeletal correction of patient with Type 3 deformity by single stage alloplastic joint reconstruction and concomitant orthognathic surgery

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Figure 24: Postsurgical radiographs of the same patient demonstrating right sided alloplastic joint reconstruction

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  Controversies in Surgical Management of Hfm Top

Growth considerations and role of early mandibular reconstruction in HFM

Opinions regarding growth in HFM and the indication for early or first-stage reconstruction of the RCU during early childhood, especially in the Type 2B and 3 classes, has mixed reports of success.[3],[11],[12],[18],[19],[20]

When looking at the growth patterns in HFM, most available research shows that the asymmetry in HFM is not a progressive disorder and maintains the same proportional deficiency throughout the growth phase of the child. The child starts with a shorter mandible on one side as compared to the normal and this in untreated children stay the same way, and on cessation of growth, the proportions remain the same showing no progressive deficiency associated with the disorder.

Longitudinal studies from New York and Seoul provide evidence for early osteodistraction. The Koreans [17] report that the skeletal stability is poor, and the results are not good as the child grows while the results from New York reveal that early correction may show stable results in mild-to-moderate skeletal deformities (Type 1 and Type 2A).[22] The role of mandibular distraction as a tool may, however, be more relevant in the more severe deformities. The reports from Harvard provide a new perspective and suggest that early intervention may reduce the quantum of correction after growth maturation and make definitive final correction more easy to achieve.

The authors' personal stand on early intervention is guarded and is necessitated only by the presence of a compromised airway. In all other children, a standard protocol of orthodontics with functional appliances is maintained to minimize the dental compensations till skeletal maturity is achieved. Definitive surgical management is then contemplated.

Long-term results

Long-term evaluation of surgical correction depends on two main factors:

  1. The time of intervention
  2. The severity of the skeletal deformity.[7],[18],[19],[20]

Time of intervention

Results are much more stable when the definitive surgical correction is planned toward the final stages of skeletal maturation or growth cessation. Numerous reports of early interventions have also been published with mixed results as discussed earlier.

Severity of skeletal deformity

The more severe deformities demonstrate less stable and favorable results when attempted early. However, literature supporting early intervention to minimize the deficiency and facilitate easier final correction is also available.

The authors personally feel that soft tissue corrections including repair of orofacial clefts, skin tags, and blind sinuses may be managed early with supportive orthodontics and definitive surgical correction is reserved only after skeletal maturation [Figure 25], [Figure 26] and [Table 4]. The only indications in our hand for early skeletal correction maybe (1) compromise of airway necessitating immediate intervention irrespective of age and (2) severe psychological conditions affecting the child in school age.
Figure 25: Long-term results of patient treated with mandibular distraction in childhood. (a) 6 year old with right-sided hemifacial macrosomia. (b) Mandibular distraction for elongation of body and ramus. (c) Demonstration of asymmetry correction 1 year post surgery. (d) Demonstration of re-appearance of asymmetry in the 3rd year after surgery. (e) Persistent asymmetry at the completion of skeletal maturation. Planned for correction by orthognathic surgery. (f) Post orthognathic correction of the Patient, one year following surgery at 19 years of age.

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Figure 26: Flowchart for management of hemifacial macrosomia

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Table 4: Authors personal protocol for management of hemifacial microsomia

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  Authors' Personal Protocol Top

  • Neonate intervention for airway compromise and feeding disturbances
  • 3–6 months Correction of orofacial clefting, removal of skin tags, and blind sinuses
  • 9–18 months Cleft palate correction
  • 6–24 months Cranial vault correction
  • 7–9 years Zygomatico-orbital correction
  • 7 years Ear reconstruction
  • 9 years onward Orthodontics
  • 13–16 years Maxillomandibular correction with TMJ reconstruction in Type 2B/3 (Females)
  • 17–19 years (Males).

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Costello B, Ruiz R, Caccamese JF. Oculoauriculo-vertebral spectrum: Staged reconstruction. Fonseca - Oral and Maxillofacial Surgery, 3rd ed., Elsevier, St. Louis, Missouri; 2018.  Back to cited text no. 1
Gorlin RJ, Jue KL, Jacobsen U, Goldschmidt E. Oculoauriculovertebral dysplasia. J Pediatr 1963;63:991-9.  Back to cited text no. 2
Posnick JC. Hemifacial macrosomia: Evaluation and treatment. Principles and practice of Orthognathic Surgery. Elsevier, St. Louis, Missouri; 2014.  Back to cited text no. 3
David DJ, Mahatumarat C, Cooter RD. Hemifacial microsomia: A multisystem classification. Plast Reconstr Surg 1987;80:525-35.  Back to cited text no. 4
Vento AR, LaBrie RA, Mulliken JB. The O.M.E.N.S. classification of hemifacial microsomia. Cleft Palate Craniofac J 1991;28:68-76; discussion 77.  Back to cited text no. 5
Kaban LB, Mulliken JB, Murray JE. Three-dimensional approach to analysis and treatment of hemifacial microso- mia. Cleft Palate J 1981;18:90-99.  Back to cited text no. 6
Nagy K, Kuijpers-Jagtman AM, Mommaerts MY. No evidence for long-term effectiveness of early osteodistraction in hemifacial microsomia. Plast Reconstr Surg 2009;124:2061-71.  Back to cited text no. 7
Tahiri Y, Viezel-Mathieu A, Aldekhayel S, Lee J, Gilardino M. The effectiveness of mandibular distraction in improving airway obstruction in the pediatric population. Plast Reconstr Surg 2014;133:352e-9e.  Back to cited text no. 8
Fan WS, Mulliken JB, Padwa BL. An association between hemifacial microsomia and facial clefting. J Oral Maxillofac Surg 2005;63:330-4.  Back to cited text no. 9
Munro I. Hemifacial micorosmia: The skeletal correction. Operative techniques in Plastic and Reconstructive Surgery 1994;1:77-92.  Back to cited text no. 10
Kaban LB, Moses MH, Mulliken JB. Correction of hemifacial microsomia in thegrowing child: A follow-up study. Cleft Palate J 1986;23(Suppl 1):50.  Back to cited text no. 11
Kaban LB, Padwa BL, Mulliken JB. Surgical correction of mandibular hypoplasia in hemifacial microsomia: The case for treatment in early childhood. J Oral Maxillofac Surg 1998;56:628-38.  Back to cited text no. 12
Ohtani J, Hoffman WY, Vargervik K, Oberoi S. Team management and treatment outcomes for patients with hemifacial microsomia. Am J Orthod Dentofacial Orthop 2012;141(4 Suppl):S74-81.  Back to cited text no. 13
Silvestri A, Natali G, Iannetti G. Functional therapy in hemifacial microsomia: Therapeutic protocol for growing children. J Oral Maxillofac Surg 1996;54:271-8; discussion 278-80.  Back to cited text no. 14
Zanardi G, Parente EV, Esteves LS, Louro RS, Capelli J Jr. Orthodontic and surgical treatment of a patient with hemifacial microsomia. Am J Orthod Dentofacial Orthop 2012;141(4 Suppl):S130-9.  Back to cited text no. 15
Tahiri Y, Chang CS, Tuin J, Paliga JT, Lowe KM, Taylor JA, et al. Costochondral grafting in craniofacial microsomia. Plast Reconstr Surg 2015;135:530-41.  Back to cited text no. 16
Ortiz Monasterio F, Molina F, Andrade L, Rodriguez C, Sainz Arregui J. Simultaneous mandibular and maxillary distraction in hemifacial microsomia in adults: Avoiding occlusal disasters. Plast Reconstr Surg 1997;100:852-6.  Back to cited text no. 17
Murray JE, Kaban LB, Mulliken JB. Analysis and treatment of hemifacial microsomia. J Craniofac Surg 1985;33:377.  Back to cited text no. 18
Murra JE, Mulliken JB, Kaban IB. Twenty-year experience in maxillofacial surgery: An evaluation of early surgery on growth function and body image. Ann Surg 1979;190:320.  Back to cited text no. 19
Ongkosuwito EM, van Vooren J, van Neck JW, Wattel E, Wolvius EB, van Adrichem LN, et al. Changes of mandibular ramal height, during growth in unilateral hemifacial microsomia patients and unaffected controls. J Craniomaxillofac Surg 2013;41:92-7.  Back to cited text no. 20
Suh J, Choi TH, Baek SH, Kim JC, Kim S. Mandibular distraction in unilateral craniofacial microsomia: Longitudinal results until the completion of growth. Plast Reconstr Surg 2013;132:1244-52.  Back to cited text no. 21
Weichman KE, Jacobs J, Patel P, Szpalski C, Shetye P, Grayson B, et al. Early distraction for mild to moderate unilateral craniofacial microsomia: Long-term follow-up, outcomes, and recommendations. Plast Reconstr Surg 2017;139:941e-53e.  Back to cited text no. 22


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 16]

  [Table 1], [Table 2], [Table 3], [Table 4]


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