Posted in Trauma

Metabolic Response To Trauma

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Posted in Trauma

Midface Fracture Overview

MANAGEMENT OF MIDFACE INJURIES

 

The midface is defined as the area between a superior plane drawn through the zygomatiocofrontal sutures tangential to the base of skull and an inferior plane at the level of the maxillary dental occlusal surfaces.  These  planes do not parallel each other but coverage posterior at a level approximating that of the foramen magnum.  The mid face can therefore be considered a triangular region with its widest dimension facing anteriorly.  This arrangement helps protect vital posterior structures such as the proximal spinal cord as well as cranial nerves and vessels entering and exiting the cranium.

Different functional and anatomic units joined by direct sutural connections form the midface.  it is a composite arrangment with contributions from the orbits.  naso-or-bital-ethmoid (NOE) complex, zygomatic complex, and maxilla.  Consequently, injuries to this region may involve these structures and their soft tissue contents to varying extents.  The comprehensive management of midface injuries therefore involves a mandatory evaluation of these structural neighbors as well as corrective measures that take into account the separate complexes and their respective functions.

Surgical Anatomy

In this section, several issues that relate directly to the pattern and subsequent treatment of midface injuries are discussed.  The bony morphology and important soft tissue structures are also described.

Bony Architecture

Areas of Weakness  As previously stated, the midface is composed of the maxilla, orbits, NOE complex, and paired zygomatic complexes.  Developmental sutures between these structures represent potential areas of weakness and are often the sites of fracture. Common sutural fracture sites are the frontozygomatic suture, zygomaticomaxillary suture, zygomaticosphenoid suture, nasofrontal suture, maxillofrontal suture, nasomaxillary suture, and midpalatal suture.

Fractures are not confined to these junctions but also occur in areas of relative weakness.  B ones are less resistant to external forces when they surround an anatomic space of neurovascular bundle.  Areas weakened in this manner include the mid-maxilla containing the maxillary sinuses bilaterally, the posterior maxilla where the pterygomaxillary junction separates the maxilla from the pterygoid plates, the midfraorbital rims advancement to the infraorbital foramen, the medial orbital walls overlying air cells of ethmodial sinus, and the lateral orbital walls, which are thinned out to accommodate the globe and adnexae medially and the temporalis muscle laterally.

Areas of Strength Fractures also result from the diversion of forces from areas of relative strength of weaker adjacent sites.   Strength is imparted to regions where bone is thickened, contains a higher ratio o cortical to cancellous bone, or surrounds hard tissue structures that help absorb forces without disruption.  An analogy has been drawn to architectural concept of support, and this has led to the characterization of these areas as vertical and horizontal pillars of the face.  The horizontal pillars are composed of the supraorbital rims joined by the nasal process of the frontal bone, the infraorbital rims, and the alveolar process of the maxilla.  Vertical support is derived from the zygomatic butteresses, pyfiform apertures (continuing superiorly as the frontal processes of the maxilla), and pterygomaxillary junctions.  These areas provide structural reinforcement to the midface and help maintain its integrity unless excessive force is applied.

Soft Tissue Attachments

Lining Tissues the Midface skeleton is characterized by the presence of several air-filled cavities.  Where present, soft tissue invests the bones on two sides.  The outer or facial surfaces are covered by a firmly attached periosteal layer.  This primitive structure contains a rich nonaxial network of vascular and neural elements that supplies the underlying bone.  The periosteum is also a repository of undifferentiated mesenchymal cells that, under certain conditions, undergo transformation to osteogenic cells.  The inner surfaces of the midface (i.e., surfaces adjacent to anatomic spaces) and; covered by specialized forms of epithelium that support the particular function of the space.  The maxillary sinus and nasal cavity, for instance, are lined with ciliated epithelium containing secretary cells.  This membrane also contains a rich vascular network, providing the bones of the midface with multiple nutrient sources.  Thickened areas of the midface that do not contain spaces (e.g., the zygomatic buttress) derive an additional endosteal vascular supply from the cancellous marrow.  This combination of periosteal, endosteal, and lining vascularity supports the survival of separate fracture segments even when gross communution is present.

Muscular Attachments Unlike the mandible, the midface is a static structure.  Consequently, muscular forces applied to this region are reduced in magnitude.  Closed reduction techniques or the fixation of fractures with wires and small bone plates are therefore more likely to be successful.  Three muscles of mastication derive  origins from different portion of the midface: the masseter (zygomatic arch) and the medial and lateral pterygoids (pterygoid plates).  Fractures extending into these sites rarely undergo significant displacement.  This reflects the relatively broad area of muscles attachments that tend to splint the fracture interfaces.  other muscles connected to the midface include the various facial mimetic muscles (zygomaticus major and minor, lavatory superioris, levator anguli oris, levator superioris alaeque nasi, and risorius), the extraocular muscles, and the buccinator.  Aside from the extraocular muscles, which provide movement to the globe, and the buccinator, which functions as a diaphragm, the remaining muscles insert into the overlying skin and subcutaneous tissues.  Lack of firm anchorage reduces the ability of mimetic muscles to displace fractured segments.  However, their orientation and tone are responsible for facial form and symmetry, and failure to reestablish their bony attachments may create an alteration of the soft tissue drape.

Lefort classification

Classic descriptions of midface injuries invoke the patterns described by French surgeon Rene LeFort, who observed three levels of fracture determined by the magnitude and direction of an externally applied blunt force.  Fractures occurred along lines of relative weakness and avoided areas of strength, as described previously.  The Lefort I fracture is a horizontal fracture through the maxilla above the level of  the alveolar process.  It extends through the midportion of the pyriform rims and nasomaxillary suture anteriorly and continues posteriorly below the zygomticbuttresses before culminating as a horizontal fracture of the pterygoid plates.  Such fractures permit separate mobility of the maxilla relative to the rest of the midface.  A LeFort 1 fracture is also known as a Guerin fracture.  LeFort II fracturesinvolve seperation of the nasofrontal suture anteriorly.  These continue posteriorly through the thin medial orbital walls and weakened infraorbital floor and rim adjacent to the infraorbital canal and foramen and extend inferiorly through the anterior maxilla aand backward below the zygomatic buttresses and pterygoid plates.  This fracture, also known as a pyramidal fracture, allows the central portion of the midface and maxilla to be mobilized independently from the cranial base, but the lateral orbital walls remain intact.  The leFord III fracture is also known as a craniofacial dysjunction, because the entire midface is separated from the skull base.  This is a result of fractures through the nasofrontal suture, medial orbital walls, orbital floors, lateral orbital walls, zygomaticofrontal sutures, zygomatic arches, maxilla (below the buttresses), and ptergoid plates.

Fracture patterns in the midface are the result of multivariate interactions between the forces applied to the skeletal components and the resistance offered by these structures.  The amount of force obviously affects the type and pattern of fracture.  A less known variable is the angle of impact.  It has been suggested that forces applied obliquely to the horizontal pillars of the midface tend to provide leForT III fracture.

 

Posted in Trauma

Management Of Oral Maxillofacial Surgery Patients With Anaemia

Management Of Oral Maxillofacial Surgery Patients With Anaemia

Anaemia: DEFINITION

As a reduction below normal in the volume of packed red cells as measured by the hematocrit or reduction in the Hb conc of blood.

In physiological terms it is defined as a reduction in the O2 transport capacity of the blood.

SYMPTOMS AND SIGNS

  • Lassitude
  • Fatigue
  • Breathlessness on exertion
  • Palpitations
  • Throbbing in head n ears
  • Dizziness
  • Tinnitus
  • Headache
  • Dimness of vision
  • Insomnia
  • Paresthesia in fingers n toes
  • Angina
  • Pallor of :-
  1. Skin
  2. Mucous membranes
  3. Palms of hand
  4. Conjunctivae
  • Tachycardia
  • Cardiac dilatation
  • Systolic flow murmurs
  • Oedema

IRON DEFICIENCY ANAEMIA

Iron deficiency is the most common cause of anaemia in the world affecting almost 500 million people.

Causes of iron deficiency are :

  • Increased iron utilization
  1.      Adolescent growth spurts
  2.      Postnatal growth spurts
  • Physiologic iron loss
  1.       Menstruation
  2.       Pregnancy
  • Pathologic iron loss
  1.       Genitourinary bleeding
  2.       Gastrointestinal bleeding
  3.       Pulmonary hemosiderosis
  4.       Intravascular hemolysis
  • Decreased iron intake
  1.      Cereal-rich, meat-poor diets
  2.      Pica
  3.      Elderly and indigent
  4.      Food faddists
  5.      Malabsorption

CLINICAL FEATURES

  • Brittle nails
  • Spoon shaped nails (koilonychia)
  • Atrophy of the papillae of the tongue
  • Angular stomatitis
  • Brittle hair
  • Plummer-Vinson syndrome

Diagnostic features

  • Hb level  Variably reduced
  • MCV     Reduced
  • Erythrocyte count Normal or reduced
  • Blood film Hypochromia, Microcytosis, Oval & elliptical cells poikilocytes in more severe cases
  • DLC     Normal
  • Platelet Count    Normal or raised
  • Bone marrow iron stores   Empty
  • Plasma Transferrin     Raised
  • Plasma iron   Reduced
  • Serum ferritin   Reduced

MANAGEMENT OF IRON DEFICIENCY ANAEMIA

Oral iron is all that is required in most cases. Best preparation is ferrous sulphate (200 mg tablet contains 60 mg elemental iron) which is given every 8th hourly.

Absorption is much better if the iron preparations are taken in empty stomach.

If the patient has side effects like nausea, diarrhea or constipation. Taking tablets with food or reducing the dose may reduce the symptoms. Dose is reduced by using preparation with less iron like ferrous gluconate (35mg elemental iron per 300mg tablet)

Parenteral iron therapy is indicated only when :

  •   Oral iron is not tolerated.
  •   Failure to absorb oral iron.
  •   Non-compliance to oral iron.
  •   In presence of severe deficiency with chronic bleeding.

Continue reading “Management Of Oral Maxillofacial Surgery Patients With Anaemia”

Posted in Trauma

Nerve Injuries

 

NERVE INJURIES AND ITS MANAGEMENT

 Introduction

Injuries to the peripheral branches of the fifth (Trigeminal) and the seventh (Facial) cranial nerves are ever-present risks during surgical procedures performed in the oral cavity and associated maxillofacial region. Trauma is also a major cause for these type of nerve injuries. The resulting loss of sensory or motor function in an area of the body that is highly visible  and in which important functions are located can be distressing or even devastating in those patients where spontaneous recovery does not occur.

Contrary to  previous opinion, nerve injuries do not always heal spontaneously. Besides traumatic nerve injuries, there is an increase in iatrogenic causes with wider use of orthognathic and reconstructive surgical procedures. Unlike the other soft tissue injuries and skeletal injuries, the nerve injury is often left  undetected at the initial phase of injury which result in troublesome patient suffering.

Advances in microsurgical technique that has evolved over the past 30 years have made it possible for surgical repair of the injured maxillofacial peripheral nerve in a predictable fashion when done in a timely fashion.

Neuroanatomy

The knowledge of the internal structure of a nerve is essential in understanding the pathophysiological mechanisms of nerve injuries and in evaluating various methods of their surgical repair. There is no anatomic or physiologic distinction between a motor or sensory nerve. Moreover, a sensory nerve is often used as an autogenous nerve graft in the surgical repair of facial nerve.

The anatomic structure of a nerve is similar to the structure of the telephone cable. The axon, which transmits electrical impulse is the functional unit of the nerve. The nerve trunk comprises of four connective tissue sheaths. These are the mesoneurium, epineurium, perineurium and endoneurium. The axons are surrounded by a layer of connective tissue endoneurium.  A number of axons are grouped into fascicles which are in turn surrounded by perineurium. A nerve might contain one or more fascicles. The fascicles are covered by epineurium and mesoneurium.

The mesoneurium is a connective tissue sheath that suspends the nerve tissue within the soft tissue. It contains the segmental blood supply of the nerve and it is continuous with the epineurium.

The epineurium is the loose connective tissue that defines the nerve trunk and protects the nerve against mechanical stress. It is composed of longitudinal oriented collagen bundles which resists both compressive and stretch forces. They occupy 22% – 88% of the cross-sectional diameter of the nerve. Nerves with an abundant cross-sectional area of epineurium are more capable of withstanding compressive forces than tensile forces. The inferior alveolar nerve and lingual nerve have little intra neural epineurium, so these nerves can’t resist prolonged retraction (Compressive force ). Epineurium has epifascicular layer that surrounds the entire trunk and lies superficial to the fascicles, and an interfascicular layer that occupies the area among the fascicles. The vasa nervosum, the longitudinal blood vessels course through the epineurium and give off branches that penetrate the perineurium to connect with the endoneurial capillaries. The epineurial blood vessels are more susceptible to compression than endoneurial vessels. Compression or excessive dissection of the nerve trunk can result in epineural oedema that may lead to epineural fibrosis.  Epineurium also contains the lymphatic vessels which are not found within the fascicles.

The perineurium delineates the fascicles. In a living nerve, perineurium is a white glistening layer devoid of blood vessels.  This is a continuation of the pia-arachnoid mater of the central nervous system. It is composed of two layers: an outer layer of dense connective tissue with collagen arranged perpendicular to the longitudinal axis of the nerve and an inner cellular layer made of a multiple-layered continuous sheets of flat squamous cells ( perineurial epithelium ). The perineurial epithelium form lamellae that vary with the diameter of the fascicle. Larger the fascicle, the greater the number of lamellae. Blood vessels transverse the perineurium to connect the vasa nervosum and endoneurial capillaries. The perineurium has the following functions:

  1. Act as diffusion barrier – prevents certain molecules from penetrating the perineurial and blood-brain barrier, thus it regulates the composition of the endoneurial fluid.
  2. Active transport of certain molecules.
  3. Maintains positive pressure inside the fascicle.
  4. Gives structural support to the enclosed neural tissue.

Nerve conduction disturbances may result if the perineurium is breached. It also occurs following intrafascicular fibrosis as a sequelae to raise in intrafascicular haemorrhage and oedema.

The endoneurium surrounds the individual nerve fibre and their schwann cells. Endoneurium and perineurium together give elasticity to the nerve. Endoneurium is composed of two layers: an outer layer of collagen fibres and endoneurial fibroblasts and an internal layer of basal lamina and endoneurial capillaries. The capillaries of the endoneurial space are connected to vasa nervosum through the perineurium. The endothelium of the intrafascicular capillaries (endoneurial capillaries) act as a blood nerve barrier, and together with the barrier function of the perineurium they regulate the intrafascicular environment. The endoneurial capillaries are more resistant to compression injury than the epineurial blood vessels. During degeneration the endoneurial space is filled with schwann cells that clean up the myelin and axonal debris. The schwann cells line up to form Büngner bands during the process of regeneration. The endoneurial sheath with prolonged denervation may become collagenized and shrink. Damage to the endoneurium and endoneurial vessels results in solid fibrotic fascicles that prevent regeneration of the axons in spite of intact remnants of fascicular pattern.

The nerve fiber is the functional unit of the peripheral nerve responsible for transmitting stimuli. The nerve fiber is comprised of many different types of axons of diverse diameter, Schwann cells and a myelin sheath in myelinated nerve fibres. The axon is a long projection from the soma ( cell body of neuron ), which can extend for several distance. It is bounded by a semipermeable membrane the axolemma. This is surrounded by basement membrane, which in turn, is encircled by a layer of myelin sheath usually. The myelin sheath is formed by Schwann cells. This is covered by a layer of connective tissue (endoneurium). The axon can be characterised by morphology, conduction velocity and function. The conduction velocity is approximately proportional to the square root of fiber diameter. Based on this Erlanger and Gasser (1937) classified axons into A, B and C. A group is subdivided into alpha (α), beta (β), gamma (γ) and delta (δ).

Classification of axons —  Erlanger & Gasser   1937

A α  Afferents for muscle spindle: the anulospiral end organ and golgi  tendon organs.

A β  Flower spray, touch sensation, pressure & vibratory sensation.

A γ   Motor fibers to muscle spindle

A δ   Large sensory fibres : Temperature and first or fast pain.

B      Autonomic fibres : Sympathetic preganglionic fibers.

C      Unmyelinated fibres Temperature, second or slow pain and sympathetic                                                                                                                                         efferents

 

Lloyd in 1943 classified axons based on the size.

Classification of axons                   Lloyd 1943

Group I           A a                              7 – 16 m m. diameter.                     70 – 120m/sec.

Group II          A b                              6 – 8 m m.                                         30 – 70 m/sec.

Group III         A d                              2.5 – 4 m m.

Group IV        C and B fibres          Smaller diameter, C fibers -1m m.   0.5 – 2 m/sec.

Size of axons in decreasing order

A a      >          A b      >          A g      >          A d      >          B         >          C

A rough estimate on the conduction velocity of the axon can be calculated by multiplying the fiber diameter by 6. Thus a 15m m. nerve fibre conducts impulse at 90 m/s.

The Schwann cells are pluripotential cells that has a variety of functions essential for nerve function. They play an important role in providing essential metabolites to the axon. They ensheath both myelinated or unmyelinated axons. It surrounds several unmyelinated axons to form well-defined units that are inter-spread among myelinated fibers in a fascicle. In myelinated nerve fibers multiple layers of the cell membrane are wrapped around a single axon to form a myelin sheath over a definite segment of axon. The node of Ranvier is 0.3 – 2 m m unmyelinated internode  segment is responsible for saltatory conduction of nerve impulse. The myelin sheath is axon dependant but the schwann cell is not. If the axons degenerates so does the myelin sheath, but the schwann cells survives. All schwann cells are covered with a basement membrane that distinguishes them from fibroblasts, macrophages and mast cells. The axons determine to a large extent the role of schwann cell in myelination process. by a layer of fibroblasts . schwann cells are the most sensitive component to ischemia and irradiation.

The nerve fiber are classified based on the number of fascicles into three fascicular patterns: monofascicular, oligofascicular and polyfascicular.

Monofascicular pattern                  one large fascicle. E.g. Intra-cranial part of facial nerve.

Oligofascicular pattern                   2 – 10 fascicles.

Polyfascicular pattern                     > 10 fascicles. E.g. Inferior alveolar nerve, Lingual nerve.                                                                      ( 18 – 21 fascicles )

The monofascicular pattern is composed of one large fascicle surrounded by concentric layers of perineurium and epifascicular epineurium. The intra cranial course of facial nerve has monofascicular pattern.

The oligofascicular pattern is characterised by two to ten fascicles. All fascicles in oligofascicular pattern are of equal size.

The polyfascicular pattern consists of greater than ten fascicles of different sizes with a prevalence of smaller fascicles. Both inferior alveolar nerve and lingual nerve are polyfascicular, they may contain as many as 18 – 21 fascicles. Polyfascicular nerves are better able to withstand stretch than monofascicular or oligofascicular nerves. The polyfascicular pattern has a large amount of nonfascicular tissue ( epifascicular and interfascicular epineurium ), which increases the malalignment of fascicles during coaptation and epineural fibrosis following injury.

Historical Background of nerve repair .

The first written description of peripheral nervous system is found in the writings of Hippocrates (460 – 370BC) although it is not certain that he differentiated between tendon and nerve.  Galen (130-200AD) has first to study the effects of transection of peripheral nerve.

One of earliest report of nerve repair was by Paget 1847 in which he reported complete recovery of function. Hoffmann and Tinel (1915) reported tingling sensations perceived by patients at increasingly distal point along the trunk of a regenerating nerve.  This sign of nerve regeneration is later known as Tinel’s sign.

Waller and Young 1942 described the characteristic changes seen in the axon distal to the injury. Highly differential function of a single nerve was extensively studied by Erlanger and Gasser (1944), using this they explained compound action potential, nerve fibre conduction and refractory period.  Using these concepts Hodes, Larrabee and German (1948)  developed application of electrophysiology for clinical nerve testing.

The foundation for current science of peripheral nerve surgery was probably laid by Seddon (1948) with innumerable battle casualties. He reported multiple papers on peripheral nerve injuries in all levels. He published nerve grafting techniques (1963), the effect of ischemia on  peripheral nerves (Seddon and Holmes 1945) and measured rate of nerve regeneration after repair (Seddon, Medanour and Smith 1943).  Another British worker Wardhall published large follow up study of peripheral nerve regeneration 1948, where 83%  patients recovered some sensory and motor function after peripheral nerve graft. De Medinaceli 1972 elucidated the role of extracellular calcium in signalling messages to the cell body from the site of injury. Lundborg et al in late 1970s and early 1980s showed that nerve fiber will across a 1-cm space devoid of supporting basal lamina or Schwann cell. He elaborated the presence of neurotrophic factors in nerve regeneration.

It was the incorporation of operating microscope by Millesi and his improved microsuture technique in 1970, that establishes the scientific basis for effective nerve anastomosis and grafting.  Applications of techniques that have been developed largely for injuries to arm, and hand to the maxillofacial region has been reported by Hansamen 1973 and Hansamen and Samii 1974.  Doi and Kuwata (1984) described transfer of microvascularised nerve graft  for reconstruction of large nerve defect.  Extensive studies of neurosensory disturbances following trauma and operative procedures such as tooth extraction, orthognathic surgery and rigid internal fixation of fractures are reported in late 1980 and early 1990.

Peszkowski (1986) studied the neuromas of lingual and inferior alveolar nerves and argued that injury during tooth extraction and 3rd molar surgery is the commonest etiologic factor for these.  Charles C. Alling (1986) studied the sensory disturbances of inferior alveolar and lingual nerves following 3rd molar surgery, About 13% of disorders of lingual nerve persisted for more than one year, where as for inferior alveolar nerve this value is only 3.5%. Nestor D Karas (1990) reported long term study of neurosensory disturbance following various orthognathic surgical procedures.  90% of the sensory deficits where recovered during first post operative year.  Similar study also reported by Schultze – Mosque in 1993, Sorren Hillerup (1994).

Etiology of Peripheral nerve injuries

Peripheral nerve may be injured as a result of

  1. Metabolic or collagen diseases.
  2. Endogenous or exogenous toxins.
  3. Thermal, mechanical or chemical injuries.

Mechanical injuries to peripheral nerves are most common.  Among this lacerating wounds resulting from road traffic accidents, interpersonal violence including stabs, war injuries such as bullet injuries are more common.  Iatrogenic nerve injuries are very common in maxillofacial region. Branches of trigeminal and facial nerve are the nerves commonly injured in maxillofacial region.

Injury to inferior alveolar nerve may result from

  1. Third molar removal.
  2. Mandibular molar endodontics.
  3. Endosteal implant placement.
  4. Orthognathic surgical procedures.
  5. Visor osteotomies.
  6. Mandibular ramus osteotomies.
  7. Mandibular body osteotomies
  8. Sagittal split osteotomy.
  9. Cyst or tumour removal.
  10. Mandibular resection and
  11. Fractures of the mandibular body and angle region.

The lingual nerve may be injured during

  1. Third molar removal
  2. Sialoadenectomy of sublingual and submandibular glands.
  3. Iatrogenic instrumentation of the floor of the mouth.
  4. Sulculoplasties of the lingual vestibule.
  5. Tumour removal.
  6. Mandibular ramus osteotomies.

The infra orbital nerve is infrequently injured but may be involved in

  1. Le Fort I, II and III osteotomies.
  2. Orbital osteotomies.
  3. Caldwell Luc procedures
  4. Fractures of midface and orbit.

Injuries to the other branches of trigeminal nerve are rare. Third molar surgery is commonest cause of lingual and inferior alveolar nerves (Alling CC 1986) out of these lingual nerve injury is more common when lingual split technique is used.  Various orthognathic surgical procedures can cause nerve injury, out of this major role is for sagittal split ramus osteotomy.  The reported incidence of inferior alveolar nerve injury following this is 54-90%. Use of plates and screws for fixation of fractures also lead to injury to inferior alveolar and infra orbital nerves.

The facial nerve might be injured following :

  1. Facial trauma ( lacerations & fractures ).
  2. Orthognathic surgical procedures.
  3. Temporomandibular joint arthrotomy and arthroscopy.
  4. Parotid gland surgery.
  5. Facial aesthetic surgery.

Jones K James (1992) studied the incidence of facial nerve injury in various orthognathic surgical procedures.  He concluded that facial nerve injury in orthognathic surgical procedures are rare.  In a smaller number of cases bilateral intraoral subcondylar osteotomies or sagittal split osteotomies can cause facial nerve injury, mostly by blind and traction injuries by putting retractors posterior to ramus.  Nerve transection is rare. Surgical approach to parotid gland, TMJ and mandible are frequent cause of iatrogenic facial nerve injury. In parotid and TMJ surgeries the main trunk of facial nerve is at risk and the marginal mandibular branch damage is more probable during submandibular incisions. Another cause of facial nerve injury is fractures of mandibular condyle which penetrates the parotid gland.

Classification of Peripheral Nerve Injury

The appropriate and logical management of nerve injuries is based on the accurate description and classification of the injury. A variety of classification have been proposed. To be useful, a classification of peripheral nerve injury should be simple, should correlate the degree of injury with symptomatology and underlying pathology, and should offer prognostic information to determine if and when operative intervention is needed or when spontaneous recovery is probable. There is no entirely a satisfactory classification for nerve injury. Although classifications based on the degree of local nerve injury are of some use, they do not take into account the time between injury and operation nor the sequential changes that might occur in the nerve cell body, motor end plate or target organ.

Seddon 1943 —  Classification of nerve injury

Seddon in 1943 introduced a classification of nerve injuries based on the three fundamental types of nerve fiber injury. It is less complicated and most used today. In this nerve injuries are classified into neurapraxia, axonotmesis and neurotmesis.

Neuropraxia             Local conduction block at the site of injury without Wallerian degeneration

Axonotmesis          Complete interruption of axon and myelin sheath with preservation of connective tissue stroma

Neurotmesis           Complete anatomic severance of the nerve

Neurapraxia is a mild form of nerve injury and denotes a localised conduction block along a nerve.  Axonal continuity is maintained and nerve conduction proximal and distal to the point of injury is preserved.  Recovery is rapid and restoration is normal function occurs with few days or weeks. (Simpson 1970, Spencer 1977, Horn and Crempley 1984, Castaldo 1984).

Axonotmesis is more serious and denotes sufficient damage to disrupt the continuity of axon within the connective tissue of the peripheral nerve.  There will be complete conduction block and distal axon degeneration (Wallerian degeneration).  Prognosis remains good because of continuity of supporting connective tissue, schwann cells and basement membrane.  Spontaneous regeneration with  full functional recovery can be expected.

The most severe injury occurs in neurotmesis, complete anatomic severance of peripheral nerve occurs and no recovery is expected without surgical coaptation of the ends of fibers.  There is distal degeneration as well as some degree of proximal degeneration.

Sunderland  1951 —  Classification of nerve injury

Sunderland 1951, proposed a classification based on five degrees of increasing severity. It is based on the anatomy of the peripheral nerve and on the degree of injury to neural elements and connective tissue structures, the endoneurium, perineurium, and epineurium. Like Seddon’s classification it tries to correlate the degree of damage with clinical symptomatology. Clinically distinction between one grade and other is not possible.

The first degree injury in the Sunderland classification is the same as neurapraxia in the Seddon’s classification. Axonal conduction is temporarily blocked and all tissue components of the nerve trunk are intact. It may be as a result of ischaemia or mechanical demyelination. There are three types of first degree nerve injury based on the proposed mechanism of conduction block.

First degree, type I injury results from nerve trunk manipulation, mild traction or mild compression such as that might occur during sagittal split ramus osteotomy, inferior alveolar nerve repositioning, or lingual nerve manipulation during sialadenectomy of the sublingual or submandibular gland. The mechanism of conduction block is presumed to be anoxia from the interruption of the segmental or epineural blood vessels, but there is no axonal degeneration or demyelination. Normal function returns within several hours ( 24 hrs.) following the restoration of circulation.

First degree, type II injury results from moderate manipulation, traction or compression of a nerve. This conduction block is as a result of intrafascicular oedema following injury to endoneurial vessels. Normal function returns within 1 –2 days following the resolution of intrafascicular oedema, which generally occurs within 1 week after nerve injury.

 

1st degree       Corresponds to Seddon’s neurapraxia

Type I               Conduction block due to anoxia from interruption of the segmental or epineural blood vessels, but there is no axonal degeneration or demyelination. Resulting from nerve trunk manipulation, mild traction or mild compression. Recovery is rapid following restoration of sensation.

Type II              Conduction block due to intrafascicular oedema following rupture of endoneurial capillaries as a result of trauma of sufficient magnitude. Recovery of senses within 1 – 2 days following resolution in the intrafascicular oedema.

Type III             Segmental demyelination or mechanical disruption of the myelin sheaths following severe manipulation, traction or compression. Recovery takes 1 – 2 months

2nd degree    Axon and myelin are interrupted, but the endoneural sheath and other supporting connective tissue stroma including epineurium and perineurium are preserved. Wallerian degeneration distal to the lesion and complete loss of motor, sensory and autonomic innervation.

3rd degree      Disruption of  axon, myelin sheath; damage to internal structures of the fascicles with loss of endoneural integrity. Epineurium and perineurium are preserved

4th degree      Interruption of all neural and supporting connective tissue stroma, except for epineurium. The fascicular pattern is lost, and the nerve may appear as a thin strand of connective or as a neuroma in continuity.

5th degree       Loss of continuity of nerve trunk with complete loss of motor, sensory and autonomic function. Pathologic overgrowth of regenerating axons might result in neuroma formation.

6th degree      Mixed combinations of previous five levels of injury. (Added lately by MacKinnon & Dellon 1988.)

First degree, type III injury is as a result of segmental demyelination or mechanical disruption of the myelin as a result of severe manipulation, traction or compression. Sensory and functional recovery is complete within 1 – 2 months after nerve injury.

Electrophysiologically, the conduction block in first degree injury is confined to the injured area, distal conduction is normal. Microreconstructive surgery is not indicated unless there is a foreign body irritant.

The second and third degree injury overlap with Seddon’s axonotmesis. In second degree injury the afferent and efferent axons are damaged along with myelin sheath and they undergo degeneration and regeneration. The remaining component of the nerve trunk (epineurium, perineurium & endoneurium) remain intact. Axonal interruption results in wallerian degeneration distal to the lesion and complete loss of motor , sensory and autonomic innervation. The signs and symptoms are generalised paresthesia with localised anaesthesia.  Surgical intervention is not usually required unless there is a foreign body irritant. Recovery usually takes months or years.

The third degree injury is characterised by damage to the intrafascicular components, the axon and the endoneurium. There is wallerian degeneration distal to the lesion. There is usually intrafascicular fibrosis blocking the path of the regenerating axons. Clinically, there is complete loss of motor function, sensory and autonomic function distal to the lesion with electrophysiologic evidence of denervation. Recovery is poor, usually delayed and incomplete depending on the severity of intrafascicular. The incidence of neuroma –in-continuity is low as the perineurium  and epineurium are intact with this degree of injury.

The fourth and fifth degree injury corresponds to Seddon’s neurotemesis. The fourth degree injury involves interruptions of all neural and supporting connective tissue except for the epineurium. The fascicular pattern is lost , and the nerve may appear as a thinned strand of connective tissue or as a neuroma-in-continuity. Regenerating axons enter grossly disrupted intrafascicular planes with few, if any, fibers reaching the distal trunk. There is complete motor loss, sensory and autonomic loss. Surgical repair is mandatory and often requires nerve grafts.

The fifth degree injury consists of complete loss of continuity of the nerve trunk involved with complete motor, sensory and autonomic dysfunction distal to the injury. Pathologically, outgrowth of regenerating axons in the proximal stump results in neuroma formation. A few axons reach the distal stump, but this is usually not associated with any functional recovery. Intraosseous fifth degree injury may show spontaneous recovery of some degree of sensibility if the canal is intact. Soft tissue fifth degree injury have poor prognosis for recovery and hey require surgical adaptation and coaptation. There is usually some residual disability even after surgical correction.

The sixth degree injury was added by MacKinnon and Dellon (1988 ) to describe a mixed combination of five degrees of injury, within the same nerve trunk.

Intra-operative grading of peripheral nerve lesions – Gentili 1985

Gentili et al 1985, graded intraoperative findings of nerve injuries into three groups based on the fascicular pattern and the time interval between the injury and surgical intervention.

  • Divided peripheral nerve
  1. Injury to examination interval < 3 weeks
  2. Injury to examination interval > 3 weeks

2             Lesion in continuity

  1. Injury to examination interval < 3 months
  2. Injury to examination interval > 3 months

3             Mixed 1 and 2

Group I lesion includes lesion associated with gross anatomic disruption of the nerve. Group 2 include lesions in continuity. Group 3 includes mixed type of lesions.

Symptomatic classification

Patients with sensory disturbances following nerve injury present with subjective complaints of numbness. This can be broadly classified into anaesthesia, paresthesia, and dyesthesia

Anaesthesia.            Complete loss any stimulus detection and perception including mechanoreceptors and nociceptor stimuli.

Paresthesia. Alteration in sensibility with abnormal or normal stimulus detection and perception which may be perceived as unpleasant but not painful.

Dyesthesia.  Alteration in sensibility with abnormal stimulus detection and perception which may be perceived as unpleasant and  painful.                                                                               Types  : Allodynia, Hyperpathia.

Anatomic classification

Nerve injuries can be classified anatomically as intraosseous or soft tissue injury. The management of and prognosis of the injured nerves contained within osseous canal is different from that for the injured nerve lying in soft tissue.

Intraosseous nerve injury

Soft tissue nerve injury

Osseous canals provide protection from mechanical trauma unless the integrity of the canal is breached. Conversely, the closed space of the osseous canal predisposes the enclosed nerve trunk to compartment syndrome, which starts as a cascade of events following acute phase of trauma. Compression causing increased vascular permeability, resulting in oedema and increased endoneurial pressure, producing ischaemia and nerve function dysfunction. The chronic effects of compression also results in nerve dysfunction due fibroblast invasion producing scarring and fiber deformation  – degeneration. Generally no surgical intervention is required for mechanical injuries if the canal remains intact and the nerve is not compressed by foreign body or there is no oedema within the canal. The prognosis for nerve function recovery without any surgical intervention is good. Foreign bodies such as implants, tooth fragments, bone fragments should be removed early to alleviate the compression and prevent the unfavourable cascade resulting from compression.

Nerves located within soft tissue are not afforded the protection from mechanical trauma. Lacerations and trasections of the nerves located in soft tissue are more likely to form neuromas and are less likely to undergo spontaneous regeneration because of the formation of scar tissue between the injured ends.

Features / Effects of Peripheral nerve injury

Following peripheral nerve injury the motor function, sensory and autonomic function of the nerve is disrupted resulting in their dysfunction.

Motor Functions

When a peripheral nerve is severed at a given level all motor functions of nerve distal to injury is lost.   All muscles supplied by that nerve becomes paralysed and atonic.  Significant electromyographic changes are not apparent for 8-14 days.  Spontaneous fibrillation on needle insertion is evident 2-4 weeks, this coincide with onset of atrophic changes within muscle fibers. Atrophy of muscle fibers progress rapidly to 50-70% in following 2 months.  Then continues at slower rate.  Striations and motor and plate configuration will retain for more than 12, months, by that time empty endoneurial tube will shrink to 1/3rd of its original size.  Complete disruption of muscle fibers may not occur till 3 years.

In cases of facial nerve injuries total paralysis of facial muscles is not often evident.  There are reports of many cases in which despite deep lacerations of parotid gland and definite damage to facial nerve branches no traumatic paresis was not seen or any immediate facial paralysis were recorded.  The reason for such an observation include nerve’s  Strong resistance to mechanical damage, due to its considerable longitudinal elasticity and Existences of anastomosis between facial nerve  branches from opposite side.  When the total severance of  main trunk occurs, complete paralysis of affected side will result.

Sensory function

Sensory loss usually follow a definite anatomic pattern, although the factor of over lap from adjacent nerves may cause confusion.  After severance of a peripheral sensory nerve only a small area of complete sensory loss is found.   This area is supplied exclusively by this nerve and is called autonomous zone or isolated zone for that nerve.  A some what larger area of tactile or thermal anaesthesia is readily delineated and correspond more closely to gross anatomic distribution of nerve.  This  larger areas is known as intermediate zone.

The autonomous zone becomes smaller within first few days or weeks after injury  long before regeneration is possible.  Livingston believed this is caused by in growth of adjacent nerves, to autonomous area.  This phenomenon gives a false impression of nerve regeneration.

The sensory modalities are affected in the order of decreasing frequency as follows.  Proprioception, touch, temperature, and pain.   Sympathetic fibers are most resistant to lower degrees of nerve injuries.

Autonomic function

Interruption of peripheral nerve is followed by loss of sweating and of pilomotor response and by vasomotor paralysis in the autonomous zone.  The area of Unhydrosis  usually corresponds to but may be slightly larger than the sensory defect.  Vasodilation occurs in higher degree injuries and the area affected at first warmer and pinker than the adjacent area.   After 2-3 weeks the affected area becomes colder and skin may become pale, cyanotic and mottled.  This changes may extend even beyond the maximal zone of injured nerve.

The motor sensory and autonomic deficit make the affected region liable to injury.  In order to protect the tissue from damage and to reduce atrophic changes various therapeutic measures are suggested.  These include massage, oedema control, skin care, splinting, and regular physiotherapy with muscle stimulation and biofeed back. (Chin and Ishi 1986).

Wound Healing in Peripheral nerves -Regeneration and Degeneration

When a nerve is injured there are responses that occur distal to the injury, at the site of injury, proximal to the injury and within the central nervous system.

Neuron :

The neuron undergoes hypertrophic changes beginning on the third or fourth day following injury to the axon and peaks between the tenth and twelfth day. Neuronal RNA content increases, and synthesis of glycoprotiens increase.  This preparatory period last for 24 hours. The neuron enters anabolic proteosynthetic phase with an increase in RNA content, this is maintained as long as the nerve is in active regeneration. The hypertrophic changes are more pronounced in more proximal location of the nerve injury. Nerve repair should ideally be done 14 –21 days after injury to take into account the cells metabolic response.

Proximal nerve trunk.

One hour after injury there is marked swelling on the proximal segment as far as 1 cm. The cross sectional area of the nerve increases to three times normal size and this swelling persists for 1 week or more. On the 2nd or 4th day there is clear demarcation of the proximal nerve stump. Proximal to nerve  injury the axon undergo limited degeneration up to the last preserved internode.   By seventh day there is vigorous sprouting of axons from the proximal stump. Regeneration is by sprouting of newly formed neurofibrills out of the proximal axon.  This sprout is known as growth cone Ramon and Cajol (1928). Tennyson (1970) studied this growth cone, electron microscopically and demonstrated multiple cytoplasmic process called filopodia that protrude and retract in an ameboid manner which direct the growth of cone.  Letourneau (1981) explained that a large number of filopodia extend from the surface of growth cone and sensed by this they will attach to the Schwann cell membrane and will pull the growth cone forwards.   The direction of filopodia is controlled by some neutrotrophic factors. ( Laminin and type 4 collagen – secreted by Schwann cells).Each axon may have as many as 50 collateral sprouts. Axon buds begin advancing across the point of injury 14 to 21 days after injury. They cross the point of injury by 28th day and by 42nd day a considerable amount of axons occupy distal segment. The delay in crossing the site is greater for more proximal injuries and in blast injuries because of the local inflammatory response. When one sprout establishes contact with target organs (Muscle spindle, sensory organs etc.)  the axon gets matured while others disintegrate.  Some sprout may be branch or grow back on themselves in an  arbitrary manner.  The  manner of  myelination of new growing sprout is determined by the original proximal axon and not by the end organ.

The direction and shape of growth cone are influenced by  mechanical  factors along its path.  Impermeable scar causes a change in direction of growth of advancing axon or cause it to branch (Büngner  1984) .  In  ideal situations the growth cone will enter the  distal stump where longitudinally arranged Schawnn cell will direct it to end organ.

Site of injury:

Within hours of injury there is proliferation of macrophages, perineural fibroblasts, schwann cells and epineural fibroblasts. There is cellular proliferation in the proximal and distal stumps . Schwann cell is most active by 7th day. Schwann cells are responsible of debridement by phagocytic function. Schwann cell response is dependant on the amount of injury. Tubules ( Bands of Büngner ) composed of schwann cells and surrounded by collagen guide the axons towards the distal nerve trunk. The mesenchymal and neuroectodermal scar remains after the debridement by Schwann cells. This tissue is not longitudinally arranged and the axonal regeneration may be twisted and resulting in a neuroma.

Distal nerve trunk :

The distal nerve trunk undergoes wallerian degeneration in preparation for the arrival of sprouting axons. A reactive schwannoma may form from the proliferating supportive elements and block the neurotization. Wallerian degeneration is initiated because all distal neural elements die. By 7th post injury day most of the distal neural elements break down. Majority of the cellular debris are phagocytosed by 21st day by the Schwann cells. Within 42nd day debridement is complete and part of the fascicular anatomy persist. The endoneurial tube either shrinks or collapse and some are obliterated as a result of active cellular proliferation and abundant collagen deposition. The diameter of the endoneurial tubes shrink by 50% at 3 months postinjury and may be only 10% to 25% of their original diameter by 12 months. The entire distal nerve shrinks ( distal atrophy) and in time the shrinkage becomes irreversible. Collagen accumulated during the repair process does not diminish when reinnervation occurs, unlike the collagen of cutaneous skin. The metabolic activity of the schwann cells in the distal stump increases with the arrival of sprouting axons. New myelin is deposited around the sprouting axon which is never as good as the original one. The size of the axon is diminished with shorter nodes of Ranvier resulting in slower conduction of impulse.

Rate of regeneration of axons

Axonal regeneration occurs in following stages.

  1. Initial delay : the time required for axons to sprout and advance as far as the lesion site. It is usually 2-3 weeks.
  2. Site delay : the time required for axons to cross the lesion site or anastomosis. This is for 1- 2
  3. Outgrowth period : the time during which axons transverse the distal nerve stump by following the basement membranes of the schwann cells that had supported the original nerve fibers. This is inversely proportional to length of the distal stump.
  4. Terminal delay : the period that begins with axonal reconnection at an appropriate end organ, includes the recovery of fiber diameter and the reversal of end-organ atrophy, and ends with recovery of function.

The rate of growth of axon depend on a number of factors.  Average growth rate through a scar  tissue is  0.25mm/day).  After entering the endoneurial tube the rate of growth  varies from 1.0 – 8.5 mm/day.  The rate of nerve regeneration is inversely proportional to the distance from the cell body (Tinnel 1971).  Clinically the advancement of growth cone can be detected  by Tinel’s signs in which taping on growth cone or proximal stump will elicit paresthesia or muscle twitching.  Sunderland 1968 reported regeneration rates of nerve at various regions which are sustained a second degree crush injury.  This is 8mm or more/day in upper arm, 6mm in proximal forearm, 1-2mm in wrist, 1-1.5mm in hand.  Ferxis 1988 reported that the rate of nerve regeneration through non vascularised nerve graft is 3-4mm/day.

Neuropathic events following nerve injury.

There are four basic types of neuropathy ( pathological changes ) seen after a nerve injury. Collateral macrosprouting, peripheral neuroma, cervical sympathetic pathosis and central pathosis. These are clinically manifested as anaesthesia dolorosa, causalgia or sympathetically maintained pain, allodynia and hyperpathia. The incidence of chronic pain following peripheral nerve injury range from 2.5 to 60 %.

Collateral Macrosprouting :

Collateral macrosprouting from the injured or from the adjacent uninjured nerves will produce a dyesthetic pattern due to neuroma like collaterals invading the injured zone. This is traumatic collateral macrosprouting. If inferior alveolar nerve is injured, adjacent nerves such as the cervical cutaneous branches, the mylohyoid nerve, long buccal nerve or the contralateral mental nerve might send branches into the uninjured zone. This can be verified by blockage of the inferior alveolar nerve which will not eliminate pain. The possible collateral branches to be blocked for pain relief. Microreconstructive surgery is not effective unless the collateral branches are addressed.

Neuromas :

Neuromas are characterised by disorganised microsprouting and formation of disorganised mass of collagen and randomly oriented small neural fascicles. Many factors may detract the growth cone from establishing continuity to end organ.  This may be scar tissue or foreign bodies between the proximal and distal axon  terminals.  In such situations the growth cone may continue the proliferate at the site of injury in an aimless manner and a tumour of small nerve fiber or a neuroma forms.  The growth of  neuroma depends on local factors such as nerve growth factor, a substance secreted by fibroblasts (McCarthy 1990), local infection, foreign body, or repeated irritation from pressure or friction. (Herudon 1982) These factors will tend to increase the size of neuroma.

Neuroma

Peripheral neuromas can be classified into : amputation or stump neuroma, central or neuroma in continuity and eccentric neuromas.

The amputation or stump neuroma is a knobby, disorganised mass of axons and collagen associated with the proximal nerve stump and completely separated from the distal nerve stump. This type of neuroma is the result of Sunderland’s fifth degree injury.

The central or neuroma in continuity is a fusiform expansion or fibrotic narrowing of the nerve with variable degrees of fascicular disruption and disorganisation. There is no breach in epineurium. This type of neuroma is as a result of Sunderland’s fourth degree or fifth degree injury in which the continuity between the proximal and the distal stump has been re-established.

There are two types of eccentric neuroma: lateral exophytic and stellate neuroma. The lateral exophytic neuroma is an outgrowth of axons and collagen forming a terminal knob like bulb in an otherwise intact nerve. Here only a few superficial fascicles are disrupted owing to an incomplete transection of the nerve or from a poor coaptation of the distal and proximal nerve stumps. There is recognisable breach of epineurium at the site of lateral exophytic neuroma. The Stellate neuroma has two or more branches ending in the adjacent soft tissue or mucosa. In contrast to lateral exophytic neuroma, the epineurium is intact and the branches end in soft tissue. These type of neuroma is seen with inferior alveolar nerve in the third molar region where the branches are seen penetrating the cortical plates to end in the adjacent soft tissue. If stellate neuroma is symptomatic it is necessary to ligate theses branches.

The  fibers of neuroma rarely matures and get myelinated.  They will be having a low threshold for stimulation, and will result in intermittent pain and bizarre paresthesia.  This phenomenon is explained as artificial synapses by Wall 1974 in an attempt to explain the trigeminal neuralgia.  It is estimated that as few as 7% (Wilson 1981) or as many as 30% of neuromas are  painful. Handrous 1982.  Mactren and Peckock 1972 stated that there is no relation between size and configuration of neuroma and the presence of symptoms.  Wilson 1981 explained that painful neuromas are tend to be large and soft where as asymptomatic neuromas are likely to have a firm fibrous outer capsule and are smaller in size. John M Greg 1990 studied the neuromas histologically and found that painful neuromas are framed of mechanosensitive  A δ fibers. M J Peszkowski (1990)  studied the intraosseous oral traumatic neuromas.  Tooth extraction  was frequent cause of developing neuroma.

Fibrosis

There are various degree of reactive fibrosis that occur following trauma to a nerve. These have been classified by Millesi et al into type A, B, C, N and S. Type A fibrosis involves epifascicular epineurium and is associated with good prognosis for recovery. Type B fibrosis involves intrafascicular epineurium. The prognosis is guarded and depends on the original damage. Internal neurolysis is indicated for type A and B fibrosis. Type C fibrosis extends into endoneurium and has poor prognosis. Type C requires excision of the fibrosed segment and neurorrhaphy or nerve graft reconstruction. Type N is associated with Sunderland’s fourth degree injury in which epineurium is intact and it is infiltrated by neuroma. Type S is associated with fourth degree injury and the intervening tissue is only by a scar. It requires scar excision and neurorrhaphy or graft reconstruction.

 

Classification of nerve injuries by location of fibrosis         Millesi et al  1989.

Designation

Location

Prognosis

A

Epifascicular  epineurium

Good prognosis

B

Interfascicular epineurium

Depends on original damage

C

Endoneurium

Poor.

N

In a Sunderland class IV injury, the epineural connective tissue that maintains continuity can be  infiltrated by neuroma

Poor

S

Continuity in class IV injury maintained only by scar tissue.

Poor

Grade A, B & C are used in combination  with Sunderland’s classification : I A & I B; II A & II B and III A, III B & III C.

Grade C fibrosis occurs only with class III injury.

Cervical Autonomic pathosis :

This involves collateral macrosprouting from the cervical sympathetic branches into the injured nerve. This results in signs and symptoms of Causalgia or Sympathetically maintained pain. It is diagnosed by blockage of the sympathetic ganglion.

Causalgia or sympathetically maintained pain has clinical feature of burning pain, allodynia and hyperpathia following nerve injury. The onset might be immediate or delayed. It is characterised by spontaneous pain described as constant, burning and exacerbated by light touch, stress, temperature change or movement of the involved part. Associated symptoms include atrophy of skin appendages, secondary atrophic changes in bones, joint and muscles.

A wide variety of theories have been propounded for explaining the mechanism of Causalgia. The theory proposed by Roberts 1986 explains the mechanism of SMP. This is due to chain of events which render the sympathetic efferents capable of driving the neurons that are part of the central afferent nociceptive pathway. Activity of the A δ and C nociceptive stimulus to the trigeminal nucleus and dorsal horn stimulates wide dynamic range ( WDR ) neurons. WDR neurons receive both nociceptive and mechanoreceptor inputs. The sensitised WDR neurons are activated by A fibers to cause a painful sensation. The diagnosis of Causalgia or sympathetically maintained pain is by sympathetic blockade ( stellate ganglion blockade in case of face ). This condition is minimally improved by microneurosurgical technique. This condition is best treated by sympathectomy.

Central Pathosis :

Following peripheral nerve injury there are central anatomical degenerative changes that may result in central hyperactivity. Inputs reach the injured receptive sites in the brain stem from the adjacent uninjured neurons. Depending on the age of the patient, location of the lesion and metabolic status of the injured nerve certain ganglion cells will die. Degenerative changes are also seen in the brain stem as granular degeneration and cell loss. These changes can result in deafferentation and central pain.

Post traumatic neuralgias

During regeneration of a sensory nerve, gradual return of sensory function is experienced that is functional and tolerable in quantity.  But in some patients these become pathologic and intolerable and are referred to as post traumatic neuralgias.  Abnormalities in nerve regeneration is the explained mechanism of this neuralgia.  The predominant among these are anaesthesia dolorosa, neuralgiform pain and causalgia.

Anaesthesia dolorosa occurs in 3-15% of cases.  It is a constant, boring, penetrating or grinding type of pain, experienced in the centre of autonomous zone of injured nerve.  Patient experience this sensation in tissue which is other wise unresponsive to any other sensory stimulation.  The neural mechanism for this is explained to be situated in Central nervous system.  Therefore local surgical management is of little use in controlling this.

Triggered neuralgiform pain may be experienced within first week following injury and continue for few weeks.  The pain is like classic trigeminal neuralgia, fine tactile or mild heat stimulation evoke brief hyperanaesthesia, and sharp tingling or stabbing pain, it is explained as a result of nerve inflammation, caused by foreign bodies, mobile fragments etc. It can also be caused by painful neuromas surgical exploration of the injury site is indicated in this case to get rid of foreign bodies, bony spicules, or for treatment of neuroma.

Diagnostic evaluation of nerve injury

The purpose of diagnostic evaluation is to:

  1. Document whether or not a sensory disturbance exists.
  2. Quantitate the sensory disturbance, monitor the progress of recovery.
  3. Determine whether or not microreconstructive surgery may be needed and
  4. To monitor the progress of sensory recovery following microreconstructive surgery.

This includes a properly taken thorough history, clinical evaluation and some diagnostic testing as nerve blocks and electrophysiological testing of nerve and muscles. The basic clinical examination involves testing for motor function, sensory function and autonomic function.

The motor function is evaluated by testing the motor power of the associated muscle.

The neurosensory testing involves: static light touch, brush directional discrimination, two-point discrimination, pin pressure nociceptive discrimination and thermal discrimination. The area of sensory disturbance is mapped first by brushing from the unaffected area to affected area. Then  the above test are performed both on the unaffected side and the area mapped with sensory disturbance. Static light touch is tested with Weinstein-Semmes filaments or with Von Frey hairs. This assess the integrity of the Merkel Cell and Ruffini endings innervated by A β fibers. Brush directional discrimination tests the proprioception and it tests the integrity of A α and A β fibers. Two point discrimination is a test of tactilegnosis and it assess the quantity and density of functional sensory receptors and afferent fibers. If sharp points are used then A δ and C fibers are evaluated, if blunt points are used then A α fibers are assessed. Pin pressure nociceptive assess the free nerve endings and the small A δ and C fibers. Thermal discrimination is a useful adjunctive test of sensation. Warmth sensation is attributed to A δ fibers and cold sensation is attributed to C fibers.

Diagnostic nerve blocks are important part of the diagnostic evaluation when pain is the symptom. Post traumatic pain may be due to nerve compression, neuroma, anaesthesia dolorosa, causalgia, sympathetic nervous system irritation, central pain etc. the purpose of diagnostic nerve block is to aid in determining the mechanism of pain, identifying the pain pathway, and to help to determine the prognosis for decreasing or eliminating the pain.

Electrophysiological testing of the peripheral nerve injury is an indispensable addition to clinical evaluation of peripheral nerve injury. It provides new and corroborative information about the nature of an injury and can aid in predicting outcome and timing of recovery during the follow up of an acute injury. The studies mainly involve electromyographic( EMG ) and electroneurographic studies. EMG studies are done to evaluate the motor function. Electroneurographic studies ( Trigeminal Sensory Evoked Response testing) are of limited use in maxillofacial region due to minimal amplitude of the response than the brain electrical activity.

Algorithm for managing nerve injuries.

The essential feature of the algorithm for management of nerve injury is serial diagnostic evaluations and to classify the injury as observed or unobserved. Treatment of the observed injury may be initiated immediately, whereas the unobserved may need to be monitored for a period of time before definite treatment is initiated. The timing of nerve repair may be classified as primary, delayed primary and secondary. Primary nerve repairs are completed within hours of injury, delayed primary repairs 14 to 21 days after injury and secondary repairs are done 3 weeks after injury.

An observed nerve injury is any injury or wound that provides direct access to and visualisation of the nerve without extensive surgical dissection. The transected observed nerve is repaired primarily while observed compression or stretch injury is managed by decompression and alleviation of stretch to prevent ischaemia. The unobserved nerve injury requires long follow up because the exact anatomical nature of the injury usually is not known. Microreconstructive surgery for unobserved nerve injury are indicated for painful conditions, prevention of avoidable posttraumatic sensory disturbances and anaesthesia. Microreconstructive surgery are contraindicated in anaesthesia dolorosa, sympathetically maintained pain, deafferentation, atypical facial pain and most instances paresthesia.

NERVE REPAIR (NEURORRHAPHY)

Jabaley 1984 described the ideal nerve repair.  This would be with alignment of fascicles that would be perfect at axonal level, without use of sutures.  The stumps should be bonded with a non-inflammatory tissue glue. Epineurium soft tissue should not  be interposed between the stump ends and perfect coaptation would preclude tension free, the nerve will heal in a viable vascular bed without foreign body reaction.  Although this ideal situation is not possible, this principle should remain the goal to strive for.

There are few micro surgical procedures which are generally used for the treatment of maxillofacial nerve injuries.  These are nerve anastomosis (Neurorrhaphy) nerve grafting, nerve decompression and neurotization.

Indication for Surgical Correction

(Philip E Write 1992)

In the presence of traumatic peripheral nerve deficit exploration of nerve is indicated.

(1)        When a sharp injury has obviously divided a nerve.  In such case exploration
can be for diagnostic or therapeutic purpose.  Neurorrhaphy may done at the
time of exploration or later.

(2)       In abraded, avulsed or blasted wounds exploration is done to identify the
condition of nerve and the ends are marked with sutures for later repair.

(3)       When a nerve deficit follows a blunt or closed trauma no clinical evidence of
regeneration has occurred after an appropriate time.

(4)       When a nerve deficit follows a penetrating wound such as low velocity gunshot,
the part is observed for evidence of regeneration for an appropriate time.  Then
if evidence of regeneration is absent, exploration is indicated.

Factors influencing  regeneration after neurorrhaphy:

The following factors seem to influence nerves regeneration:

  1. Age:- Better axonal regeneration and functional recovery is seem in younger                                 individuals (Onne 1972)   Black and Lasek  (1974)   showed that the rate
    of regeneration declines with increasing age.
  2. Timing:- Nerve injury can be primary or secondary.  The  Primary repair is that
    which is done up 48 hours after injury.  Early secondary repair are
    those accomplished within first 3-6 weeks following injury and  late
    secondary repair are those performed after 3 month (McCarthy 1990).

There is no absolute rules with regard  to the timing of nerve repair, and it  should be decided after considering the nature of injury, condition of patient and status of  associated injuries.  It is generally accepted that clean transected injuries are repaired primary.  In cases of severe injuries secondary repair is recommended because viable and non  viable nerve tissues can be better  designated (Buske 1972) Experimental finding showed better results with primary reconstruction Branch 1972, Peakock 1984).

Advantages of Primary repair are: It allows

– Early  correction of  sensory and motor defect.

– Better functional nerve regeneration (Peacock 1984)

– Fascicles can be identified by electrical stimulation (up to 4 days).

-Less time  consuming.

– Degeneration of distal  stump is less.

– Chance of secondary deformity resulting from long term  denervation is less.

Daker 1972 recommended a short delay for nerve repair is consideration of metabolic  response of cell body to injury cell showed peak metabolic regeneration activity after 2 weeks.

Horn and Crumely 1984 advocated a  longer delay because

  1. The state of nerve can be better defined in relation to surrounding tissue.
  2. Intraneural scarring is more apparent in proximal and distal stumps, and this
    facilitate more accurate debridment.
  3. The epineurium is thicker at this time yielding a more  accurate repair.
  4. (4) The surgery can be planned to proceed in an unhurried elective manner.
  5. Proper facilities can be made available,

Young in (1944)  described few disadvantages of delaying the repair.

  1. The longer the delay the greater is the distal endoneurial Shrinkage (due to collagen deposit an the schwamn cell sheath) which prevents successful re-entry.
  2. Prolonged delay may arrest maturation of regenerating axon and the nerves never attain the pre-injury
  3. Longer period of denervation causes atrophy of and organ. In such cases renervation is difficult.  McQuarrie (1986) recommended a  definitive delay in bullet injuries, because the bullet is unlikely to have transected the nerve.  The injury  sustained will be at all the degree.  The delay will help to  resolve Ist and 2nd degree injuries. The injured and functional fascicles can be identified and the  treatment can be  better planned.  According to him for low velocity bullets 8-10 weeks delay is probably sufficient and for high velocity bullets 12-16 weeks delay is required.

Time factors   should be taken seriously.  As the time passes the degenerative changes  are proceeding. Considering all options, early repair should be performed if damage to neural elements can be identified, contamination and  associated trauma are minimal and a  well trained surgical team is available (McCarthy 1990).

  1. Gap between the Nerve Ends:-

Nerves, as in the case of  vessels will retract or severe.  If the cut is sharp the cut ends will retract slightly.  In high velocity, injuries excessive loss of nerve tissue create larger gaps.  Millesi (1981) recommended that if the gap is less than 2.5cm direct end to end coaptation can be done.  Larger gaps required grafting.

  1. The level of Injury :-

The more proximal the injury the more incomplete is the overall return of function especially in more distal structures.  This is because

(a)       Proximal injuries require a greater percentage of total cell mass.

(b)       Regenerating axon has to pass a longer distance to reach the end organ.

(c)       The fascicular topography of nerve is more complicated proximally.

  1. Type of Nerve:

Repair of a pure sensory or pure motor nerve achieve a higher percentage of functional recovery than a mixed nerve.

  1. Cause of nerve injury and associated injuries:

The less a nerve is traumatised the greater is likelihood of functional recovery.  In simple clean lacerations the extend of tissue damage and necrosis is less.  In such cases faster regeneration and better functional recovery is expected.  In high velocity injuries and avulsion injuries, greater amount of nerve tissue is lost and nerve injury will be mixed In such cases regeneration potential is less.  In severe injuries necrosis of  surrounding tissue occurs.  The level of contamination and subsequent ischemia may lead to infection and scar formation in such  cases regeneration will be incomplete.

The other factors influencing are presence of neurotrophic substances in tissue bed and finally the precision of repair which is related to experience and technique of surgeon.

End to End Anastamosis:

This the simplest and most commoly performed nerve repair.  This is indicated for  simple transections without considerable loss of nerve tissue so that the transected ends can be brought together without tension.  For achieving this after planned and adequate exposure of the area the nerve is freed proximally and distally and the ends are brought together and sutured.  Suturing can be done over perineurium or epineurium depending on requirement.

At the onset of nerve exploration, wide exposure of proximal and distal stump is essential.  Dissection should begin at non injured region, tissue are retracted away from nerve.  It is done by putting a longitudinal incision on the normal appearing nerve.  Using a microscisors the epineurium is dissected off towards the lesion.

It is usually white in colour, composed of several layers of lose connective tissue and contain longitudinally oriented blood vessels.  Uninjured fascicles should be identified and preserved.  Before the nerve is raised from the bed marking suture are put on the perineurium at 12 and 6 ‘O clock position to avoid rotational defect.

Epineural Repair:

Epineural repair is the conventional method of surgical coaptation of peripheral nerve.  Its advantage is short execution time, simplicity and need for minimal magnification.  The intraneural contents are not disturbed and there is not intra neural suture foreign body.  This technique is applicable to primary and secondary repair and is easily to perform.

After adequate exposure of proximal and distal stumps  the intraneural and perineural scar tissue should be removed from the injured site and a fresh face of cut end should be  obtained to maintain a uniform fascicle length.  This will help correct approximation.  Excessive neural tissue should not be removed of because this will lead to tension at the nerve is approximated.  To achieve this nerve is held with a nerve holding forceps and cut (Neurotomy) is done  with a micro blade.  Use of scissors will produce more crush injury (Mayer 1980) sectioning starts at the centre of injury end proceed proximally and distally 1mm intervals until the fascicular structure is identified an d relatively free of scar.

Up on transecting a nerve or fascicle, axoplasm will sweep out and collect at the end.  Excessive axoplasmic outflow will interfere with accurate coaptation.  Therefore as a rule, the nerve section should not be done until the last possible moment when the surgeon is prepared to perform suturing.  Bleeding should be controlled with bipolar microcoagulator and damp sponge pressure.

After the nerve ends are make lying without tension opposite each other the magnification is increased to 16x and 10-0 nylon sutures are carefully placed in epineurium.  Before placement of first suture fascicular bundles are matched by noting   features such as  position of longitudinal vessels.  First  suture tie is trimmed long and can be used for retracting.  The second suture is placed 180 o from the first and then at 90o to right and left depending on size of nerve.  The number  of sutures should be kept minimum.  Buckling of nerve ends caused by in appropriately large  suture  ties should be avoided since this leads to wasteful  regeneration and neuroma formation.

If the gap is so large that first 10-0  suture does not hold the nerves together, then a 8-0  suture can be used and it can be replaced at the end of the procedure.  If the nerve gap is more than  2.5cm after mobilisation  nerve grafting  is indicated (Williams 1975).

Cause of failures of  epineural repair are lack of  accurate coaptation of   corresponding fascicles, gapping, over riding, buckling of fascicles.

Perineural (Fascicular) Repair:

This implies the surgical manipulation of corresponding fascicles in the  proximal and distal  stumps to achieve optimum alignment.   Identification of corresponding  fascicle can be  done by intra-operative electro-diagnosis or histochemical identification and this is easy at distal  portions of a nerve owing to  fascicular homogeneity.

For perineural repair, after  exposing the injured nerve, the epineurium is stripped away to expose the underlying fascicles.  Fascicular groups are carefully isolated making sure to observe and maintain the integrity of perineurium which is normally glistening white and devoid of blood vessels.  Intact fascicles if any should not be disturbed.  After careful matching the sutures are placed under high magnification.  Suture is placed to inner epineurium which is adherent  to perineurium.  Care is taken to avoid placing sutures within  endoneurium and to avoid a rotational deformity.  Usually only two sutures are required to complete each coaptation.  Any number of fascicles can be coapted in this manner, but each carries the potential of further intraneural foreign suture materials and subsequent fibrosis.

Millesi (1975) described various “Septa” which separate various fascicular groups.  These Septa can be sutured and thus groups of fascicles can be coapted instead of individual fascicles.  This help to reduce amount of suture foreign body within nerve.  The most frequent indication of epineural repair is reconstruction of partially severed nerves.

The Disadvantages are

–           Intra neural fibrosis by increased dissection and foreign materials.

–           The Technique is tedious and time consuming (Urbanic 1984 and Orgel 1987).

Partial Neurorrhaphy:

When a nerve is partially severed and if some fascicles are intact partial neurorrhaphy is indicated.  For this after adequate exposure of nerve longitudinal incision is made along epineurium for several centimetres.  Then the intact fascicles are dissected out for equal distance on both sides.  Then the ends of severed fascicles are brought together and sutured.  Epineural sutures are adequate.  If not possible perineural sutures are put in each fascicles.  The intact fascicles are then put as a loop.  Cinching of this should be avoided by adequate relief of epineurium. Care should be taken to preserve the integrity of intact fascicles.

Effect of Tension:-   Tension at the site of nerve coaptation invites connective tissue proliferation and subsequent scar formation.  As scar tissue matures it has a tendency to constrict, there by compressing any regenerating axon (Daniel and Terziz 1977).

Millesi (1975) studied the effects of tension on 252 nerve repair in 146 animals and observed that connective tissue proliferation and length of resulting scar between  the two ends of the coapted nerve were directly related to the amount of tension.  The major source of connective tissue out growth was epineurium and the proliferation of the scar begins at the suture line and displaced the suture inwards.  In such cases the cross sectional area for nerve regeneration is decreased.

On the basis of these findings, placement of a nerve graft is believed to be indicated for any nerve defect exceeding 2 to 2.5cm (Moniem 1952) amd Milles 1987)

Nerve Grafting:-

Nerve grafting is indicated in cases of neurotmesis where

  • Reanastomosis can not be done without tension
  • Neurotemesis and  axonotemesis injuries that have resulted in pain and  poor return of sensitivity
  • There is evidence of symptomatic neuroma.

Usually the donor nerves are taken from .

–           Sural nerve, the branch of peroneal nerve.

–           The  medical antebrachial cutaneous nerve.

–           Lateral antibrachial cutaneous nerve

–           Lateral and posterior nerve of thigh

–           Great auricular nerve.

Hiroyasher Noma (1986)  recommended that the great auricular nerve is ideal donor nerve for reconstruction of lingual and inferior alveolar nerve because  It is superficial, having equal diameter, sensory defect is less when compared to sural nerve where the lateral part of sole  loses sensation.

Suzanne E MacKinnon (1994) in a histologic comparison study of fascicular pattern  of sural nerve and medial antebrachial cutaneous nerve conclude that MACN is more suitable for grafting the defects of inferior alveolar and lingual nerves than sural nerve.

Before measuring the length of nerve defect it should be ensured that all the injured non viable nerve tissue is removed.  Adequate length of distal and proximal stumps are freed and the scar tissue is resected away.

Grafts are cut slightly longer than the defect with the surrounding tissues completely extended.  A clean vertical sectioning of nerve is then made proximal and distal to injured area.  Epinurectomy is not indicated because being tension free the proliferation of scar tissue will not occur before revascularisation of graft.  Now the graft is interposed and epineural suturing is done with 10,0 nylon.  Since there is no tension, graft will adhere to nerve tissue by fibrin clot so one or two sutures are adequate.  Suture is carefully placed in inner epineural and outer perineural layer of fascicles and the epineurium graft.  The polarity of the graft is not important.

The nerve graft are revascularised by direct in growth  of vessels instead of the growth from transected ends.  Therefore graft diameter is most important in survival.  Thicker nerves show central necrosis before revascularisation (Smith 1986).  The nerves graft should lie in a well vascularised viable bed devoid of infection, haematoma or foreign bodies.

Vasscularised nerves Grafts:

When  the extensive nerve grafting is necessary or when the tissue bed is poorly vascularised microvascularised nerve grafting is indicated.  This will assure immediate blood supply to graft so that fibrosis secondary to ischaemia is avoided and this will assure more rapid axonal regeneration (Terziz 1987).  Experimental evidence suggests that regeneration  proceeds in a faster rate in revascularised nerve grafts.  Terziz 1988 shown that Tinel’s sign progresses in such grafts in a rate of 7-12mm per day compared to 3-4mm in conventional grafts.  Fuminori (1992) showed faster return of nerve function is revascularised grafts.

Suitable nerves that may be used for vascularised nerve grafts, are the superficial radial, the Ulnar, sural, anterior tibial superficial peroneal and saphenous (Terzies 1987).  These nerves have got predominant  vessels supplying the  perineurium which  can be used for anastomosis.  In this after the coaptation of nerve the nutrient vessel is microanastomosed with  adjacent vessels.

Nerve Decompression (Neurolysis)

This is the procedure of releasing of  nerve from surrounding scar tissue, foreign,  bodies, bones or tooth fragments by micro dissection,  so that pressure over the nerve is  released and regeneration is facilitated. This can be internal neurolysis and external neurolysis.  In external neurolysis the perineurium is  carefully dissected out of scar tissue a  bony fragment which is compressing the nerves. This is indicated where there is a  commutation of bone across a neurovascular bundle as seen in zygomatic maxillary body fractures across inferior alveolar nerve or during complicated lover 3rd  molar surgery.

Even though the nerve may be visualised with naked eye external neurolysis should be done using  surgical microscope  with 4x or 8x  magnification in order to avoid tearing of epineurium.  Attempt should be made to preserve the extrinsic arterioles that are found within the epineurium and nerve is carefully inspected for interruptions, lateral neuroma or neuroma in continuity. If there is a sign of intraneural injury internal neurolysis or nerve grafting may be required.

Internal  Neurolysis: of  previously  injured nerves is indicated when there is incomplete return of normal sensory function with hyperesthesia or triggered pain.  In internal decompression an  external  release is first made to visualise the nerve and a small amount of  saliva or local  anaesthetic solution is injected  beneath epineurium with a 30 Gauge needle.  Then using micro scissors epineurium is  longitudinally opened to expose the  fascicles.  Then under 16x magnification the  adhesion between the fascicles are  carefully released and continuity of each fascicle is re-established.  The epineurium is closed with 10-12-0 nylon.

Neurolysis procedure is having  complication that it produce some amount of intra neural injury and subsequent scarring.  Therefore it should be restricted to the cases where  scaring due to injury is  more than that expected from surgery.

Non Suture nerve repair:-    Technique for the sutureless repair of nerve with and without grafting have recently shown promise for maxillofacial surgery.   Mtrays 1982 described use of fibrin clot anastomosis for repair of  trigeminal and facial nerve  injuries.  In the non suture technique the injured nerve ends are isolated from the surrounding  scar and they are kept in close proximity using tubes known as nerve conduits, Various materials are described as nerve  conduits.These are

– Psuedosynovial tube  – (Lundborg 1980)

– Autogenous Vein – (Chiu DT 1980)

– Permanent nerve guide (Machinon 1986)

– Bio observable nerve guide ( Seckel 1984)

– Silicon tube ( Vron 1986)

– Autogenous muscle ( Glosby 1986)

– Bioresobable polyglycolic acid ( William A- Crawly 1992)

Neurotization

It is a technique by which the proximal portion of one nerve is anastamosed to the distal end of another nerve. This is indicated in cases where proximal segments are not accessible for microreconstruction. The greater auricular nerve, mental nerve and infra orbital nerve have been used for neurotization of inferior alveolar nerve and lingual nerve. The hypoglossal nerve and contralateral facial nerve along with nerve grafts have been used for facial nerve reconstruction.

Post Operative Care

In order to maximise the functional recovery the area of nerve repair should be  protected for 7-10 days post operatively.  Care is taken in wound closure and even gentle washing of skin over the repair is avoided.  Skin sutures are removed at two weeks.  After this physiotherapy is started and muscle stimulation is carried out.  The patient should be seen for evaluation  at one, 3, 6 and 12 month postoperatively.  The assessment of regeneration is done by noting advancing Tinel’s sign and by electromyographic and electroneurographic studies.

Several methods are used to evaluate motor function return following peripheral nerve injury.  They involve assessment of muscle strength against gravity, against gravity and graded resistance.  British medical research council (BMRC) established the following system for assessing the return  of motor function.

M0      – No Contraction

M1       – Return of perceptible construction in the proximal muscles.

M2      – Return of perceptible contraction in proximal and distal muscles.

M3      – Important muscles are sufficiently power full to act against resistence.

M4      – Return of function as in M3 synergetic and independent movements possible.

M5      – Complete Recovery.

The sensory return is assessed by the following:

Moving Touch, Constant touch, vibratory stimulation, pin prick and two point discrimination.  Pin prick sensation is returned first, followed by low vibratory, moving touch, constant touch, then  high frequency vibration.  Small diameter fibers show faster degeneration.   The BMRC established the following six level grading scale for sensory return.

S0       – Absence of sensibility in autonomous area.

S1        – Recovery of deep cutaneous pain sensibility within autonomous area.

S2       – Return of some degree of superficial cutaneous pain and tactile sensibility
within autonomous area.

S3       – Return of superficial cutaneous and tactile sensibility through out the
autonomous area and disappearance any pevious over response.

S3+     – Return of sensibility as on S3 and there is some recovery of two point
discrimination.

S4       – Complete recovery.

Sensory Reeducation and physiotherapy

Sensory reeducation and physiotherapy are extremely helpful in improving the quality of life after nerve repair. The aim of sensory reeducation is to stimulate the peripheral receptors of touch, pain and temperature which sends impulses to the brain to improve the perception of these sensations.


CONCLUSION

Understanding the clinical manifestations of peripheral and autonomic nerve injury requires a thorough knowledge of the peripheral nervous system and the musculoskeletal system. The clinical evaluation of the peripheral and autonomic nervous system injury should be carefully documented because such documentation along with electrophysiological parameters forms a baseline upon which further decision about operative and non-operative management strategies can be based.

Injuries of nerves in the maxillofacial region is of major concern when considering  the functional deficit as a result of the injury. Introduction of complicated osteotomies to correct dentofacial deformities and ever increasing complex facial trauma have resulted in an increase in  incidence of nerve injuries over the past few years. The results of repair of traumatically damaged nerves have improved considerably with the introduction of newer micro surgical technique, diagnostic modalities such as somotosensory evoked potential (SEP), intra operative Histochemical fascicle  identification etc. Patients require constant evaluation, follow up, sensory reeducation and physiotherapy for an effective outcome following a nerve injury.

Severe to moderate nerve injury can be an injury for life, so it would be ideal to give a realistic assurance to the patient.


REFERENCES

  1. P P Robinson, A R Loescher & K G Smith. A prospective, quantitative study on the clinical outcome of the lingual nerve repair. Br J Oral Maxillofac Surg.2000. 255 – 263.
  2. John P. LaBanc. Reconstructive microneurosurgery of the Trigeminal nerve. Principles of Oral & Maxillofacial surgery. Steven M Roser, Larry J Peterson, Robert D Marciani & A Thomas Indresano. Vol II. Lippincott – Raven publishers. 1997. 1041 –1088.
  3. Roger A Meyer. Evaluation and management of Neurological complications. Complications in Oral & Maxillofacial surgery. Leonard B Kaban, Antohony Pogrel & David H Perrott. 1997. W B Saunders Company. 69 – 88.
  4. Robert M Worth. Anatomy and Physiology of Peripheral nerves. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3099 – 3104.
  5. F Gentili, Alan R Hudson & R Midha. Peripheral Nerve Injuries : Types, Causes & Grading. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3105 – 3114.
  6. Thomas B Pathophysiology of Peripheral nerve trauma. Section on NERVE INJURIES. Neurosurgery. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3115 – 3119.
  7. David G Kline, Earl R Hackett & Austin J Summer. Management of the Neuroma in continuity. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3169 – 3177.
  8. John E McGillicuddy. Techniques of Nerve Repair. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3179 – 3191.
  9. Roger D Madison & Simon J Archibald. Potential value of synthetic tubes for nerve repair. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3193 – 3197.
  10. Irvine G McQuairre. Clinical signs of peripheral Nerve Regeneration. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3199 – 3203.
  11. Suzie C Tindall. Painful Neuromas. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3205 – 3207.
  12. Joseph H Arguelles & Kim J Burchiel. Causalgia and Reflex Sympathetic Dystrophy. Section on NERVE INJURIES. Robert H Wilkin & Setti S Rengachary. 2nd edition. Vol III. McGraw-Hill. 1996. 3209 –3215.
  13. Sujit S. Prabu, John S, Myseror, William C. Broaddur. Clinical Manifestation of peripheral and autonomic nervous system injury. The Practice of Neurosurgery. Vol III. George T Tindall, Paul R Cooper & David L Barrow. 1996 : 2821 – 2829.
  14. Susan E Mackinnon. Techniques of nerve repair. The Practice of Neurosurgery. Vol III. George T Tindall, Paul R Cooper & David L Barrow. 1996 : 2879 – 2908.
  15. Allan H Friedmann. The Practice of Neurosurgery. Vol III. George T Tindall, Paul R Cooper & David L Barrow. 1996 : 2909 – 2921.
  16. James R. Hupp. Facial neuropathy. Contemporary Oral & Maxillofacial surgery. Larry J Peterson, Edward Ellis, James R Hupp & Myron R Tucker. 2nd 1993. Mosby. 697 – 712.
  17. William M Swartz & Joseph C Banis. Facial Paralysis. Head and Neck Microsurgery. Williams & Wilkins. 250 – 265.
  18. Hano Millesi. Basic principles of nerve grafting. Textbook of Plastic, Maxillofacial and Reconstructive Surgery. Gregory S Georgiade, Nicholas G Georgiade, Ronald Riefkohl and William J Barwick. Vol I. 2nd 1992. Williams & Wilkins. 83 – 92.
  19. Nancy Van Laeken & Ralph T Manktelow. Facial paralysis : Principles of treatment. Textbook of Plastic, Maxillofacial and Reconstructive Surgery. Gregory S Georgiade, Nicholas G Georgiade, Ronald Riefkohl and William J Barwick. Vol I. 2nd 1992. Williams & Wilkins. 581 –596.
  • Keith E Brandt & Susan E Mackinnon. Microsurgical repair of peripheral nerves and nerve grafts. Grabb and Smith’s PLASTIC SURGERY. Sherrell J Aston, Robert W Beasley & Charles H M Thorne. 4th 1991. Lippincott-Raven publishers. 79 – 90.
  1. Daniel C Baker. Reconstruction of the paralyzed face. Grabb and Smith’s PLASTIC SURGERY. Sherrell J Aston, Robert W Beasley & Charles H M Thorne. 4th 1991. Lippincott-Raven publishers. 545 – 557.
  2. A Lee Dellon. Wound healing in nerve. Wound healing. Stephen H Miller. Clinics in Plastic surgery. 17 :3 : july 1990 : 545 –570.
  3. John P LaBanc. Scheme for trigeminal nerve injury management. Controversies in Oral & Maxillofacial surgery. Philip Worthington and John R Evans. W B Saunders Company. 1994 : 275 – 287.
  • John Paul LaBAnc. Maxillofacial nerve injuries: Evaluation, classification and management. Oral and Maxillofacial trauma. 2nd edition. Raymond J Fonseca, Robert V Walker, Norman J Betts and H Dexter Barber. Vol II. W B Saunders Company. 913 – 924.
  1. Stephen E Feinberg, Barry Steinberg and Joseph J Helman. Healing of traumatic injuries. Oral and Maxillofacial trauma. 2nd edition. Raymond J Fonseca, Robert V Walker, Norman J Betts and H Dexter Barber. Vol I. W B Saunders Company. 13 – 60.
  2. K. Terzies, Kevin L.Smith Repair and Grafting of peripheral nerves in McCarthy’s PLASTIC SURGERY Volume I 1990.
  3. Philip E Wright and Mark T Job. Peripheral nerve injuries in V Campbell’s Operative Orthopedics Vol. 4 Mosby 1992.

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Posted in Aesthetic Surgery, Oncosurgery, Trauma

Skin Grafts

 Introduction

Skin is the primary protective barrier of the body against external mechanical, chemical or biological threats. Raw areas created on the skin surface by a variety of causes exposes the body to the harmful effects of these threats. Thus it is important to make good any loss of skin or mucosal surface lost by burns, surgical procedures or other injuries.

In managing the defects both of skin and mucous membrane which follow excision of lesions, closure by direct suturing is used when the defect is small enough and is otherwise suitable. Likewise, small defects produced by burns or ulcerations are allowed to epithelise primarily. When the defect is too large, the potential methods of reconstruction are the use of a free skin graft, a local or distant skin flap, a composite flap or a free flap.

Skin grafting is the method commonly used to close superficial defects of skin and mucous membrane. Its main advantages are the technical ease of the procedure and the minimal donor site morbidity. During its transfer from donor to recipient site, a free skin graft is completely, even if only temporarily, detached from the body. While being so detached, such a graft remains viable for a limited period whose precise limit depends on the ambient temperature at which the graft is maintained. In order to survive permanently, it has to become re-attached, and obtain a fresh blood supply from its new habitat. The processes that result in its re-attachment and revascularisation are collectively referred to as ‘take’.


Anatomy of the human skin

The skin is a two-layered organ which forms the protective covering of the body. The outer layer is the epidermis, an avascular cellular structure, and the deeper layer is the dermis, which is essentially a meshwork of collagen and elastic fibres. The two are separated by a lamina, the basement membrane. Downward prolongations of the epithelium penetrate the dermis in the form of eccrine sweat glands and pilosebaceous units like apocrine glands. These specialised structures are collectively called the adnexa. The dermis is also penetrated from below by a network of blood vessels, lymphatics and nerves.

The epidermis

The epidermis has two main elements – the epithelial cells and the pigment system

The epithelial cells

The epithelial cells take the form of stratified squamous epithelium in which the cells, as they mature, move from the deepest layer, the basal layer, towards the surface. In the process of this, the cells become keratinised and flattened until at the surface, they finally desquamate. The thickness of the epidermis varies greatly in different body area, the thickest in the pressure zones and the thinnest in the eyelids.

The differences in the histologic appearance of different layers of the epidermis is caused by the progressive keratinisation of the cells. The structure of the cells alter as they move towards the surface, the nuclei being lost as the cells become part of the keratin layer. This regular orderly progression to maturation which takes place in normal skin from the basal layer of cuboidal shaped cells abutting on the dermis, to the final keratin layer of flattened cells on the surface, is called ‘orthokeratinisation’. The units of the cell line maturing in this way are termed ‘epidermal keratinocytes’, regardless of its stage in the maturation process.

The pigment system

The cells responsible for the production of pigment in the epidermis are the ‘melanocytes’. They are derived from the neural crest ectoderm, from where they migrate early in the foetal life to the epidermis. In the epidermis, they lie among the cells of the basal layer and the cells of the hair bulbs.

The melanocytes are triangular in section with numerous dentritic processes which run between the cells of the basal and supra-basal layers. The pigment which they produce (melanin) is synthesised as granules (melanosomes) in their cytoplasm. According to Wolff (1973), the granules move outwards along the dentritic processes from where they are transferred by phagocytosis into the adjacent keratinocytes. In these cells, the granules cluster together as a pigmented cap over the nucleus. An ‘epidermal melanin unit’ is formed by the melanocyte and the adjoining specific number (between 20 and 36) of keratinocytes subserved for it.

The melanin cuts down the transmission of ultraviolet light through the epidermis, thus reducing its damaging effect. Coloured skin has the same ratio of melanocytes to basal cells as white skin. Its darker colour is due to a greater amount of pigment concentrated in the keratinocytes.

The dermis

The structural basis of the dermis is provided by the interweaving network of collagen and elastic fibres. Its upper surface is irregular, with upward projections called dermal papillae which fit into corresponding irregularities made by rete ridge pattern on the deep surface of the epidermis.

The superficial layer, the papillary dermis has a fine, loose structure and contains fine collagen, elastic and reticular fibres which run vertical to the surface, supporting the capillary loops, lymphatics and terminal nerve fibres. The deeper layer is called reticular dermis in which the collagen network is coarser in structure and runs parallel to the surface of the skin. Its deep surface has a pattern of indentations into which the fat of the superficial fascia extends to surround the secretory coils of the sweat glands.

The basement membrane

This term refers to the lamina between the epidermis and dermis, though it is doubtful if it acts strictly as a membrane. It is not of much significance in skin grafting, as even the thinnest of split-skin grafts contain at least some amount of dermis.

The adnexa

This is the collective term applied to the specialised epithelial prolongations which pass from the epidermis deep into the dermis. They include the pilosebaceous units and the sweat gland apparatus.

The epithelial cells of the adnexal structures constitute a biological cell line distinct from the cells of the epidermis, called adnexal keratinocytes. The distinction is more by means of biological behaviour than histological. One example is their different reaction to solar radiation. Compared with epidermal keratinocytes, the adnexal keratinocytes are relatively resistant to the effects of such radiation. Notwithstanding the differences, there exists a congruence in the basic potential of these cells. Given an adequate stimulus like the loss of surface epithelium from burning or the cutting of a split-skin graft, the adnexal cells are capable of ‘dedifferentiating’ and reverting to their ‘original’ function, of becoming epidermal keratinocytes to resurface on the skin.

The pilosebaceous unit

The pilosebaceous unit is a complex structure incorporating the hair follicle and sebaceous gland. The hair follicle extends into the dermis to varying depths, even reaching the subcutis in the scalp, beard area, upper lip and eyebrows. Towards its deepest part, it expands to form the hair bulb. The hair is formed in the hair bulb, and grows upward through the epidermis to the surface. The hair is surrounded along its length by a multi-layered  sheath of follicular adnexal keratinocytes.

The sebaceous gland buds off from the side of the hair follicle. This has a lobulated structure and opens via a duct into the upper part of the follicle. The sebaceous glands are particularly numerous in the nasal skin and the naso-labial fold, and their prominence and activity in different sites vary greatly in different individuals. In the oral mucosa, they open directly into the mucosal surface. Similar direct openings of the glands into the surface is also seen in the tarsal plates of upper and lower eyelids.

The sweat gland apparatus

The eccrine glands are widely distributed over the entire skin, excluding some particular sites like the red margin of the lips. Structurally, each of these consists of a simple tube which passes downward from the skin surface deep into the dermis and ends in a coil. In some of the glands, the coil reaches a sufficient depth to lie in one of the projections of fat which extends up from the superficial fascia. More than half of the coiled element is secretory; the remainder forms part of the duct element. From the secretory portion, the duct initially continues as part of the coil, but later emerges from it to pursue a gently undulating course up through dermis until it reaches the epidermis. It spirals through the epidermis to reach the surface.

Indications for skin grafting

The common indications for skin grafting include

Large raw surfaces on skin /mucous membrane after excision of benign or malignant lesions.

  1. Gross loss of skin caused by burns and crush injuries.
  2. Non-malignant ulcers or granulating areas (e. g. diabetic ulcers and pressure sores), which have failed to epithelise after routine conservative treatment
  3. Raw skin /mucous membrane surfaces left at the flap donor site, not amenable to direct suturing.
  4. Raw mucous membrane surfaces produced by pre-prosthetic surgical procedures like vestibuloplasty.
  5. Raw bony surfaces produced by maxillectomy, eyeball exenteration, and excision of palatal lesions.
  6. Interpositional material in the treatment of temporomandibular joint ankylosis.

Types of skin grafts

The free skin grafts consist of the entire thickness of the epidermis and a variable amount of dermis. They are designated according to their dermal component as

  1. Full-thickness skin grafts, consisting of epidermis and the entire thickness of the dermis, and
  2. Split-skin grafts, containing epidermis and a variable proportion of the dermis. According to the relative thickness of dermis included, the split-skin grafts are further subdivided into thin, intermediate and thick grafts.

These various categories of grafts are not completely distinct from each other. They merely represent convenient reference points on a continuous scale of decreasing thickness from the full-thickness skin graft to the graft containing little more than epidermis. The real difference in practice is between the full-thickness skin graft and the split-skin graft.

The full-thickness skin graft, once cut, leaves behind no epidermal elements in the donor area from where resurfacing can take place; the split-skin graft leaves adnexal remnants, pilosebaceous follicles and/or sweat gland apparatus as foci from which the donor site can resurface. As a result, the donor site of the split skin graft heals spontaneously, and requires no care other than that usually accorded to any raw surface; the donor site of a full-thickness skin graft has to be closed by direct suture or, if it is too large for this, covered with a split-skin graft. This limits the size of the full-thickness skin graft which can usually be cut in practice. Extensive defects are split-skin grafted; the full-thickness skin graft is restricted to small defects.

The full-thickness skin graft takes less readily than the split skin-graft, and before it can be used, conditions have to be optimal. The full-thickness skin graft remains virtually at its original size; the split-skin graft tends to contract subsequently of circumstances permit, e.g. across a flexure. Within broad limits, the thinner the graft, the more it contracts secondarily. The stability of the graft depends on dermis, and the thicker graft stands late trauma better than the thin graft.

History of skin grafts in oral cavity

Moscovitz in 1916 treated sulcal scarring by the use of skin grafts placed over a mould which was inserted through a submental approach. 10 days later, an intra-oral incision opened the graft pocket into the mouth. Weiser (1918) and Pickerill (1919) used the intra-oral route for placing skin grafts. Gillies and Waldon (1920) and Kilner and Jackson (1921) sued he same technique for correction of post-traumatic scarring and pre-prosthetic problems. Pichler (1931) used grafts in maxillectomy operations to prevent cavity shrinkage and promote early healing.

Schuchardt (1952) suggested suturing the mucosal edge to periosteum and grafting only the periosteal surface to overcome the problems created by the soft tissue-based graft. Obwegesser (1964) and Rehrmann and Pelser (1965) combined a buccal vestibuloplasty using a skin graft with the surgical lowering of the whole floor of the mouth. Hopkins et al (1974, 1980) described the use of a mucosal transposition flap from the lower lip with a skin graft on the donor site and resection of the mylohyoid ridges.

Donor sites

The thickness, appearance, texture and vascularity of skin vary greatly in different parts of the body, and have a strong influence in the selection of donor site appropriate to a particular surgical situation.

Full-thickness grafts

The full thickness skin graft may be harvested from a wide selection of donor sites, the main criteria for selection being colour matching, vascularity and the available area of the donor skin.

Post-auricular skin

The posterior surface of the ear extending on to the adjoining post-auricular hairless mastoid skin makes the best donor skin when the face is being grafted. It gives a most excellent skin colour and texture match, and when replacing eyelid skin, is virtually undetectable. The vascularity both of the graft and the usual sites to which it is usually applied make it the easiest of full-thickness skin grafts to get to take. It is the smallness of area of skin available which limits the size of the defect which can be used to cover. The donor site is closed by direct suture.

Upper eyelid skin

In the adult, skin is nearly always available on the upper eyelid, and this can be useful particularly when the defect is of another eyelid. The match of colour and texture is outstandingly good. The area available is obviously limited, though the redundancy of the upper eyelid skin usually present in the older age-group, the group in which such grafts are more often needed, allows more skin to be harvested than one might expect.

Supraclavicular skin

The skin of the lower posterior triangle of the neck gives a reasonable colour and texture match used on the face although it is distinctly inferior to post-auricular skin. The larger area of skin is available but unless the neck defect is grafted with a split-skin graft, the increase is not sufficient to make it obviously useful. Grafting the neck creates a cosmetic defect of its own and this is likely to be particularly undesirable in the female where the donor area is often exposed. These adverse factors restrict its usefulness considerably and it is not often used.

Flexural skin

The antecubital fossa and the groin are both described as possible donor sites. The dermis is thinner than average, and the skin is mobile on the deeper tissues, but only a limited width is available unless a graft is used to cover the donor site. On the face, the cosmetic result is comparable to that of the supraclavicular skin.

In the antecubital fossa, even if the donor site defect can be closed directly, the resulting scar is very obvious, and if the closure is under much tension, hypertrophy of the scar is a hazard. Its use as a donor site is, therefore, not recommended now. The groin area is useful if a long narrow graft is needed, closure in such circumstances being relatively simple. Its main use is in hand surgery, particularly in managing flexion contractures.

Thigh and abdominal skin

The texture and colour match of thigh and abdominal skin grafted to the face is usually poor. The skin either stays extremely pale or becomes hyperpigmented relative to the rest of the face. An added deficiency is a loss of constantly varying fine play of normal facial expression, the grafted area taking on a rather mask-like appearance, due possibly to its thicker dermis.

Both these sites provide a source of skin for the palm of the hand. The thickness of the dermis in both sites, where there is no ageing skin atrophy, provides a good pad to take the necessary pressure when used on the sole of the foot. If a graft of any size is used, the donor site in its turn must be grafted and even when the donor site can be directly sutured, the scar usually stretches badly.

Split skin grafts

This graft has a much wider usage than the full thickness graft, and within limits, the surgeon is able to control its thickness and make use of that variable in its characteristics and clinical behaviour. The donor site is chosen in any particular instance by taking into account such factors as the amount of skin required, whether a good colour and texture match is possible, local convenience (as in grafting from forearm to hand with need for only one dressing), the necessity of having no hair on the graft, the cutting instrument available, the desirability of avoiding the leg in the aged or out-patient.

The sites usually used as donor sites are:

  1. the thigh,
  2. the upper arm,
  3. the flexor aspect of forearm and
  4. virtually the whole of the reasonably plane surface of the torso.

When these sites are not available or when all possible sites are needed, skin can be taken from:

  1. the other aspects of forearm and
  2. the lower leg.

Harvesting of graft

The full-thickness skin graft is cut with a scalpel while the split-skin graft, of whatever thickness, is usually cut with a special instrument.

Local anaesthesia for graft cutting

Local anaesthesia can be used for harvesting skin grafts by injection of the local anaesthetic agent or by the topical application of the local anaesthetic into the skin area being harvested.

The topical anaesthetic agent commonly used is a mixture of lignocaine and prilocaine. Both agents are very slowly absorbed into the superficial layers of the skin, with negligible absorption into the blood stream, and this allows larger areas to be anaesthetised, though the anaesthesia may not extent to the deeper part of dermis. The area of anaesthesia required is marked out on the skin, and is covered liberally with the anaesthetic cream. As a rule, at least half an hour should be allowed for sufficient absorption to permit the cutting of the graft. Although pallor of the skin area is often seen, it is not a reliable indicator either of the presence of anaesthesia or its surface extent. The patient has to be tested for both.

When the anaesthetic agent is being injected, the addition of hyaluronidase to the solution makes it possible to cut a reasonable size of graft readily. The exact amount of hyaluronidase which has to be used is not critical; 1500 IU added to 100 ml of anaesthetic solution works satisfactorily. The mixture diffuses rapidly and leaves a uniformly flat skin surface. The diffuse increase in tissue turgor also increase the dermal thickness and makes the area slightly more rigid, which is helpful while harvesting thin grafts.

Full-thickness graft

As the full-thickness graft is to be accurately fitted into the defect, a pattern of the defect to be grafted is made to ensure that the graft is at normal skin tension at its new site. Aluminium foil and polythene sheet are the materials most often used for making patterns. The pattern may be made before or after excision. If the defect is irregular, matching points may be tattooed with methylene blue on the defect, and on the graft before it is cut.

While cutting the full-thickness graft with scalpel, it should be carefully cleared of fat on its deeper surface. Time and care should be spent in the cutting of the graft so that no fat is left on its deep surface. This procedure requires both skill and care. Alternatively, the graft may be cut without special regard to the inclusion of fat, the fat being subsequently removed with scissors. This removal of the subcutaneous fat is not considered necessary in case the donor site is upper eyelid or post-auricular region.

The graft is easier to cut if the area is ballooned with fluid, usually I:200,000 noradrenalin. Using the pattern already made, the outline is marked on the skin with methylene blue, and then it is incised and undercut. It often helps to pull the skin of the graft taut over the knife with hooks so that the cutting is done blindly, largely by touch. Alternatively, the graft can be held turned back so that cutting is done under vision. This latter method is less precise and usually results in more fat being left on the graft.

Split skin grafts

Unlike full-thickness grafts, the cutting of split-skin grafts require specialised instruments. The instruments most commonly used are:

  1. The Humby knife and
  2. The power-driven dermatome.

The Humby knife

The instrument originally used to cut split-skin grafts was the Blair knife, which has a blade approximately 25 cm long. The difficulty to cut grafts of uniform thickness with this instrument prompted Humby to add a roller mechanism to it. Modified versions of the Humby knife, of which the Watson modification is the most popular, have since been produced. A scaled-down version called the Silver knife, which uses a razor blade to provide the cutting edge, is useful when only a small graft is required. The Humby knife can be used only on convex surfaces, but despite this disadvantage, its convenience makes it the most frequently used instrument for routine graft cutting.

The donor site most often used is the thigh. While positioning the patient, the leg is placed with the appropriate group of muscles relaxed so that by pressing the muscle group either medially or laterally, the maximum of plane surface is presented to the knife. The same principle may be applied to any donor site.

Graft thickness is controlled by adjusting the distance between the roller and the blade. Despite the presence of a gauge on the instrument, most surgeons assess the thickness by holding the knife up to the light to see the clearance between the blade and the roller. Clearance of a little less than 0.5 mm gives a graft of average thickness. This initial assessment is adjusted as necessary by watching both the graft as it is cut, and the bed from which it is being cut.

Ideally, the blade when cutting moves to and fro smoothly over the skin surface which does not move at all with the knife. Drag, resulting from friction between the blade and the skin, causes the skin to move with the blade, making the graft harvesting more difficult. It cannot be completely eliminated, but lubrication with liquid paraffin of the skin surface and the surface of the blade next to the skin reduces it considerably.

The direction and orientation of the cut depends on the convenience of the surgeon. A little in front of the knife and moving smoothly a fixed distance from it, a wooden board is held pressed down on the skin. This serves the dual purpose of steadying the skin and flattening it as the blade reaches it. The edge of this board is also lubricated with liquid paraffin so that the forward movement of the knife is in unison with the movement of the board.

Assessment of graft thickness

Although a setting of the roller is suggested, the surgeon must be prepared to modify it accordingly. The first few millimetres of the graft cut provides an initial indication of the thickness and the setting can be adjusted accordingly.

The translucency  of the graft is the main index of its thickness. A very thin graft is so translucent that the grey of the blade shows through. Opacity of the graft increases with increasing thickness until the full-thickness graft has the colour and appearance of cadaveric skin. A split-skin graft of intermediate thickness is of moderate translucency. The pattern of bleeding of the donor site gives a further indication of the graft thickness. The thin graft produces a high density of tiny bleeding points; the thicker graft gives a lower density of larger bleeding points.

The thickness of the skin from the point of view of clinical atrophy and graft cutting, and the presence of remnants of the adnexa from which the sites can heal, vary in different parts of the limb. In general, the skin of the lateral aspect is thicker than the medial, and distal is thicker than proximal. In the thigh when atrophy is clinically obvious, the lateral aspect should be chosen if at all possible.

The power-driven dermatome

The power-driven dermatome is a complex and fragile instrument. It consists of a rapidly oscillating cutting blade which is driven electrically or by compressed air. With the skin held steady, and lubricated with liquid paraffin, the instrument is able to move forward smoothly.

The main advantage of the power-driven dermatome is the ability to cut a graft of controlled width and accurately controllable thickness from almost any part of the trunk or limbs. It is also capable of cutting thin grafts much more consistently when compared to other instruments. The straight margin, and the uniform thickness of the graft which it cuts, means that one need not leave any quantity of skin between adjoining donor sites in the knowledge that the whole area will heal uniformly and quickly. This facility makes it practically possible to cut successive crops of skin from the same donor site, which is a valuable property when the skin is at a premium such as in extensive burns.

Storage of skin

By storage at a low temperature, skin cut in excess of current requirements can be preserved for later use as needed. The increase in the use of ‘delayed exposed grafting’ has greatly increased the need for storage. Within the temperature range 0 –37˚ C, the survival time of a stored graft is a function of its temperature; the lower the temperature, the longer the survival time.

The graft is wrapped in gauze moistened with saline and placed in a sterile, sealed container. Unless specially long survival (e.g. up to 21 days) is needed, the storage temperature is not of paramount importance, but it is generally considered that 4˚ C gives the best results.

Preparation of recipient site

Free skin grafts are applied either to raw surfaces surgically created, or at least surgically clean, or to granulating wounds. The practise of grafting and site preparation varies with the two types of surfaces.

The surgically clean surfaces

A completely dry field is essential before the graft is applied, since graft failure is most often due to the presence of haematoma. To achieve this, several measures are used. Time is the single most important factor in this regard. The steps of the operation should be planned to give the area to be grafted the longest possible time for the normal haemostatic mechanism to become effective. While waiting for bleeding to cease, the area should be left covered with gauze soaked in saline.

Only the actual bleeding point should be picked up by the mosquito forceps so that necrosis caused by the short fine catgut is minimal. Bipolar coagulation is a useful alternative. Once the defect is created, the continuous use of suction would keep the bleeding active. Even when a specific clot is to be sucked off, the suction nozzle should not actually touch the tissue.

After the graft is sutured in place, unless the graft bed is dry, it is a good practise to flush out under the graft with saline using a 20 ml syringe with blunt cannula, before the tie-over bolus is applied.

Granulating areas

Healthy granulations are flat, red and vascular, do not bleed unduly readily, are free from a covering surface film, and shows evidence of good marginal healing. Left ungrafted, granulations generally become more fibrous (less vascular) or oedematous. Infection tends to add to the difficulties of grafting.

Systemic antibiotics to which the colonising organisms are sensitive, are ineffective in eliminating them from a granulating surface. An antiseptic (such as chlorhexidene) applied locally is likely to be more effective. The presence of slough created a suitable environment  for continuing infection. Surgical excision is a rapid and highly effective method of eliminating it. In the process, excision of fascia is preferable to excision of fat. The Humby knife with the roller widely open may be used to excise both slough and heavily infected granulations.

Granulations, once clean and free of slough, should be grafted without delay. If this is not possible, the area should be kept adequately covered with a large and thick dressing. Crepe bandages may be used to exert pressure over the area. It is noticed that hydrocortisone ointment sometimes improves unhealthy granulations.

Application of the graft

The full-thickness skin graft, cut to its prescribed pattern, fits the defect accurately and is sutured edge to edge along its margin. Sufficient sutures are inserted to give as accurate edge apposition as possible, care being taken to avoid inversion of the edges. Sufficient sutures are left long to provide a snug tie-over, and the remainder are cut short. The spilt-skin graft is cut large enough to cover the defect with an overlap, and the sutures used to hold it in its overlapped position are left long to provide for the tie-over.

The application of a skin graft depend on whether the graft is being applied on the skin surface or inside the mouth and/or sino-nasal cavity, but in any site, two distinct techniques are available. In the first, pressure is applied to the graft; in the second, the graft is left exposed without pressure being applied to the graft.

The skin surface

Pressure methods

Pressure methods are preferable when the graft is small in area and are invariable when it is full-thickness in type. They are advisable even if the graft is split-skin when the defect is in an area which is inherently mobile (around eyelids and mouth), where the defect is markedly irregular in contour (the pinna), and when the defect is markedly concave (orbital cavity following exenteration). When grafting is carried out primarily (immediately following the creation of the defect) pressure methods are normally used since the pressure, apart from keeping the graft immobile, helps to achieve hemostasis.

The pressure is exerted on the graft surface by a bolus applied directly over the graft and further pressure may be added by the use of additional dressings and crepe bandage and/or Elastoplast. The pressure is not a necessary factor in the take of the graft, and is only a means of providing immobility of the graft and holding it in contact with the bed.

Various bolus materials are used – flavine wool (cotton wool prepared with flavine emulsion), cotton wool moistened with saline or liquid paraffin, cotton waste, and polyurethane foams are some examples. The bolus should be bulky and extent to the margins of the graft, the long tie-over sutures being then tied tightly over the bolus, anchoring the bolus and graft in a single mass. A layer of Sofra-tulle®  laid over the graft before the bolus is applied, might help to ease the first post-operative dressing.

In certain situations, the defect may have to be kept stretched while a split-skin graft is taking. This is to allow  as much skin as possible to be introduced into the defect to mitigate the effect of any subsequent graft contracture. The usual bolus materials are not rigid enough to keep the defect stretched and a bolus of dental impression compound may be used instead. Since it softens in hot water bath and hardens to rigidity on cooling, an accurate impression of the stretched defect may be made from it. The material with the graft draped over its surface is then inserted into the defect. The  sutures are placed in and along the margins of the defect and tied across the bolus drawing the defect over it and stretching it so that as much skin as possible is inserted. This technique has its main application in the reconstruction of upper eyelid defects.

The outer pressure dressing consists of the usual gauze, cotton wool and crepe bandage or Elastoplast. The bulk of dressing may be enough for immobilisation, but plaster of Paris should always be used if necessary to reinforce the dressings.

Exposed grafting

The exposed grafting was initially developed as a solution to the ineffectiveness of bolus grafting in areas which cannot be immobilised. In this technique, the graft is laid on the defect, without dressing of any kind, merely protected from being rubbed off, and allowed to attach by fibrin adhesion alone. While applying the graft, any air trapped under it should be pressed out and the skin allowed to overlap the defect margins. Fibrin adhesion occurs quickly and it helps the graft to tolerate minor movements without interfering with the process of graft uptake.

If exposed grafting is used primarily, control of all bleeding points is essential since pressure is not available to help hemostasis. Since this is practically difficult, a technique called ‘delayed exposed grafting’ is used, where the application of the graft is postponed until natural hemostasis has taken place, the skin being stored at a lower temperature in the interval. The waiting period (usually 2-5 days) is used to free the wound of all the residual blood clot, and the graft can be applied as soon as the surface has been cleared of clot. Late exposed grafting, allowing the wound to granulate, is another option, but it has little application in head and neck regions.

In using delayed exposed grafting, the most important factor to be taken care is that the surface of the defect should not be allowed to dry out. This is particularly important when the forehead and the scalp are the sites concerned.  For this reason, an occlusive dressing should be applied to the defect as soon as it is created.

Exposed grafting demands a degree of co-operation from the patient, and it has to be used with discretion in children. In the head and neck region, however, no elaborate instructions are usually needed; an explanation to the patient of the need for care is often sufficient.

Mesh grafting

The procedure of meshing the grafts considerably help to expand the area which an individual graft is able to cover. The graft, cut in the usual way is passed through an instrument from which it emerges shredded into a regular network of skin. An alternative is to manually create regular slits on the graft using a scalpel. Traction applied to the four corners of the graft expands the mesh, giving a considerable increase in area. Apart from the factor that it provides for a large surface area, meshed grafts also show a higher ease of graft uptake. The main disadvantage is the unpredictable cosmetic outcome, making it unpopular in cosmetically important sites. The chief indication of mesh grafting is to expand the extent of the area the graft is being used to cover.

Oro-nasal cavity

Pressure methods

In the mouth, the nasal cavity or the sinuses, pressure methods either involve the use of a bolus tie-over dressing or, when the bed has a firm bony base, the use of a dental appliance to exert pressure on the graft.

Bolus grafting

This method uses a tie-over bolus in the manner primarily designed for grafting on the skin surface. Unfortunately, with most materials, the bolus rapidly becomes soaked with saliva, food debris, bacteria etc. with resulting offensive smell. Polyurethane foam is considered to be the most suitable bolus material to be used in the mouth. After suturing the graft with sufficient overlap and leaving the sutures long, the surgeon himself compresses the bolus between his fingertips and holds it against the defect, while the assistant completes the tie-over sutures around the bolus. After the compressing finger is removed, the bolus expands to exert its pressure on the graft.

The overlap of the graft may become a difficult slough which may separate spontaneously, but more often it is trimmed off when the bolus is removed 7 days after its insertion. By the time, the part of the graft which is taken, is fixed to the bed. Any area of failure is left to heal spontaneously.

Bolus grafting is most suitable when used in obviously concave areas where mobility is minimal or where the graft bed can provide some stability, as in buccal mucosa or floor of the mouth. It is advisable to insert as much skin as the defect can accommodate to avoid subsequent tenting, and to compensate for graft contraction.

Dental appliance method

This method is used where treatment of the tumour involves resected part of hard palate and upper alveolus. The technique may be discussed under two headings – edentulous and dentulous patients.

In the edentulous patient, an acrylic dental plate is prepared pre-operatively. If the patient already has a denture which fits well, it can be used as well. This provides the basis of the splint which ultimately presses the graft against the bed. The plate fits the area untouched by resection, but a fresh mould of the post-resection defect is required. Dental impression compound and gutta-percha are the available moulding materials for this purpose. Multiple holes are bored in the part of the splint which correspond to the site of the resection at the time of making the splint. Then, a bolus of softened bolus material pressed against it extrudes through the holes, making the two into a single structure once the material cools.

After the defect is created, the splint, with its bolus heated and made malleable once again, is pressed hard into the defect. This gives a composite denture-splint which matches accurately the irregular contours of the post-resection surface. Fixed in this position, it holds the graft firmly against the defect. The methods used to fix the splint can be extra-oral or intra-oral.

Intra-oral fixation may be provided either by direct wiring to the upper alveolus or by wire suspension to the zygomatic arch. Direct wiring to the upper alveolus can be used when there is sufficient alveolus left after resection. Holes are drilled on the splint/ denture as planned and then, with the splint held in position, a curved bone awl is thrust through the upper alveolar bone corresponding to the site of the hole in the splint. A 0.4mm stainless steel wire is used to fix the splint/denture to the alveolar ridge. Zygomatic suspension is required when there is insufficient upper alveolus left after resection. For this method, cleats should be provided on the sides of the splint. With the splint in position, a wire is looped over each zygomatic arch and its ends brought into the oral cavity and fixed firmly to the splint. A splint wired intra-orally is tolerated well and is removed 7–10 days to allow inspection of the graft. Intra-oral fixation should be preferred whenever it is possible, as it is comfortable to the patient and convenient to the surgeon.

Extra-oral fixation is provided by attaching the splint to the skull through a system of universal rods or joints. For this, the splint/denture should be constructed with a metal plate inset in the midline on its anterior surface. Into this, the fixing rod may be screwed. The skull fixation is best provided by supra-orbital pins – rods with self-tapping screws attached to supra-orbital ridges on either side and attached to the intra-oral splint through a rigid connecting rod. Other alternatives, mostly of historical importance include the halo frame and plaster of Paris headcap.

When the patient has teeth, the making of dental splints is more complicated, and cap-splints are used. The teeth outside the line of the mucosal resection are cap-splinted. A screw attachment welded to the cap-splint carries an acrylic plate shaped to correspond roughly to the shape of the alveolar segment to be excised. A bolus of dental compound welded to this plate gives the final accurate splint needed to hold the graft in place. When cap-splints cannot be made or enough teeth are not present, a denture is made with holes to accommodate the remaining teeth. This can then be used as described for the edentulous patient.

The graft can be applied to the defect in two ways

  1. If the defect is markedly concave, the skin can be draped over the moulded dental compound so that when the splint is wired in position, it carries the graft with it. When this method is used, it is advisable to glue the graft (using skin glue) to the bolus to prevent it from slipping. The adhesion is lost over a few days, and so when the splint is removed at the first dressing, the two surfaces separate easily.
  2. When the defect is shallow, the graft can be sutured to the margins of the defect with the usual overlap. The dental splint with the bolus is then inserted and fixed in position.

Exposed grafting

The technical problem posed by exposed grafting inside the mouth is one of providing continuing contact and effective immobility for sufficiently long to allow vascularisation of the graft. This has been largely solved by the use of quilted grafting.

Quilted grafting

This method was described by McGregor in 1975. Quilted grafting is used in sites which are impossible to immobilise, and it finds its main application in defects of mobile parts of oral cavity, most frequently the side of the tongue. Its successful use has prompted many surgeons to make use of the technique in other intra-oral sites as well.

The split-skin graft is sutured with catgut to the margins of the defect with an overlap in the usual way, and multiple additional sutures are inserted through the graft and the underlying tongue muscle, anchoring them together, and giving the overall appearance of a ‘quilt’. Each quilting suture creates a point of immobile contact between the graft and the bed with a ‘mosaic of squares’, each sufficiently immobile to allow the graft to become vascularised.

As the blind insertion of the quilting sutures inevitably causes some bleeding beneath the graft, multiple slits should be made on its surface to allow for the escape of blood and oedema fluid.

The process of graft take

The graft initially adheres to its new bed by fibrin, and its immediate nutritional requirements are met by diffusion from plasma which exudes from the bed providing the so-called ‘plasmatic circulation’. This is quickly reinforced by the outgrowth of capillary buds from the recipient area to unite with those on the deep surface of the graft and re-establish a circulation of blood in the graft. This link-up is usually well advanced by the 3rd day.

Coinciding with the vascular link-up, the fibrin is infiltrated by fibroblasts which gradually convert the initial tenuous fibrin clot adhesion into a definitive attachment by fibrous tissue. The strength of this attachment increases quickly, providing an anchorage which allows the graft to be handled safely within 4 days. More slowly, a lymphatic link-up is added, and even more slowly, nerve supply is established although imperfectly and variably.

The processes most critical in graft take are revascularisation and fibrous tissue fixation. The speed and effectiveness of these processes are determined by the characteristics of the graft bed, the graft itself, and the conditions under which the graft is applied.

The graft bed

The bed on which the graft is laid must have a rich enough blood supply to vascularise the graft and also be capable of providing  the necessary initial fibrin anchorage.

Surfaces which show rapid and profuse outgrowth of capillary buds takes a graft readily. The capability of the surface to produce granulations is a good indicator of graft survival on that surface. The soft tissues of the face, muscle, fascia and fat are so vascular that they all accept grafts readily. Cartilage covered with perichondrium, bone covered with periosteum and tendon covered with paratendon takes skin grafts without difficulty. Bare cartilage and bare tendon cannot be relied upon to take a graft although if the area is too small, the vascularity of the surrounding tissue may be sufficiently profuse to allow the graft to bridge the area and cover it successfully. The bare cortical bone on the outer table of the skull and mandible lack sufficient vascularity to take a graft successfully. The hard palate, the surrounding maxillary bone, the walls of the orbit, the circum-orbital buttresses, and the bone of the diploë (after the outer table of skull is removed) all take up grafts readily. The dura mater, the mucoperiosteum and the mucoperichondrium are other surfaces which could be expected to take a skin graft successfully.

The influence of vascularity on graft take is best illustrated by the effect of radiation. A site with radiation injury is rarely capable of being successfully grafted, despite the fact that in the absence of such injury, it is routinely grafted without difficulty. Ideally, the excision should extent into the normal tissue beyond the radiation damage before the grafting is attempted but this is not always possible. A useful guide is provided by the amount of fibrosis and induration of the bed, and the amount of small vessel bleeding, compared at he time of excision with the amount expected if radiotherapy had not been given.

Any surface with sufficient vascular supply to support a graft has fibrinogen and the enzymes which convert it into fibrin in adequate quantities to provide the necessary adhesion, unless the surface is harbouring pathogens which destroy fibrin (e.g.- Strep. progenies and Ps. aeruginosa).

The graft

Skin grafts can vary both in their thickness and vascularity. These variables affect the revascularisation and consequently the ease of take of the graft. The number of cut capillary ends exposed when a thick skin graft is cut, is smaller than with a thin graft. Thus revascularisation is faster with thin grafts, and they tend to be taken easily. Nevertheless, the common head and neck donor sites have a rich blood supply, and even full thickness grafts from these sites compare favourably in their vascular characteristics with thin split skin grafts taken from elsewhere.

Conditions for take

Rapid vascularisation is the most important factor, and the distance to be travelled by the capillaries for the link-up needs to be as short as possible. The graft therefore has to be in the closest possible contact with the recipient bed. The most frequent causes of separation are bleeding from the bed resulting in haematoma, and tenting of the graft when used in concave sites.

The graft has also to lie immobile on the bed until it is firmly attached by fibrous tissue anchorage. The shearing strains which tend to make the graft slide to and fro and prevent capillary link-up are to be avoided.

The phenomenon of bridging

A graft may survive over bare cortical bone, tendon or cartilage, and even if separated from the bed by a clot, provided the area is small enough. In such circumstances, the graft survives solely by bridging, a phenomenon in which vascularisation takes place solely by capillary invasion from the graft bed. In most cases, bridging is strictly limited in area, and beyond this, the graft will not survive.

Healing of donor site

The cutting of a split skin graft leaves variable portions of the pilosebaceous apparatus and the sweat glands in the donor area and from these multiple foci, epithelium spreads until the area is resurfaced with skin. The pilosebaceous remnants are much more active as foci of epithelial regeneration than the sweat gland remnants. The donor site of a thin graft, with its full complement of cut pilosebaceous follicles, heals in approximately 7-9 days, while that of a thick graft, dependent virtually entirely on sweat gland remnants, may take 14 days or more. The quality of healed donor site skin derived solely from the sweat gland remnants is also poorer. Most grafts are of intermediate thickness and leave a percentage of pilosebaceous apparatus, and takes 9-14 days for donor site healing.

If the graft is so thick that no adnexal structures are left in the donor area, or infection in the area destroys any remnants which are left, the surface will granulate, and healing takes place by epithelial migration from the margins. This takes place very slowly and it is always advisable to split-skin graft such sites, particularly if fat is showing to any extent.

The skin of recently healed donor site looks more deeply coloured than normal, the colour slowly fading in time to leave the area paler than normal, often with areas of variation in pigmentation, indicative of the local minor variations in the thickness of the graft cut.

Donor site management

The management of the donor site is a very important, but mostly overlooked aspect of skin grafting. The problems are pain, the provision for an optimal local environment for the healing process, and removal of the dressings.

Pain usually settles in 3-4 days, and is often followed by itching. Although itching is a clinical indicator of satisfactory progress in healing, it causes more discomfort to the patient than pain and is more difficult to treat. Pain can be reduced by peri-operative application of topical local anaesthesia (in the form of jelly), or by impregnating the dressings with some liquid form of anaesthetic agent. Use of a long acting agent often gets the patient over the most painful period without the need to use potent analgesics.

The ideal donor site dressing would remain non-adherent during the healing phase, be absorbent, maintain a moist environment, and minimise the potential for bacterial contamination. Such an ideal dressing does not exist at present. Most cases are managed by dressing with Sofra tulle® (gauze impregnated with liquid paraffin and antibiotic), over which is laden absorbent gauze, the whole held in position with a crepe bandage. The dressing is removed after 10-14 days with care being taken not to disturb the graft.

Newly healed donor sites are often covered with a flaky keratinised layer, and the use of an emollient, non-irritant cream for 3-4 weeks is usually effective.

Mucosal grafts

Skin grafts have several disadvantages when used in oral cavity. They are

  1. Its colour and texture never match that of normal oral mucosa, although after several years the difference becomes less obvious.
  2. Unpleasant taste and smell in the absence of adequate hygiene, especially if adnexal structures are included in the graft.
  3. Poor adhesion of complete dentures when used in the maxilla.
  4. Scarring and discomfort of donor site.

In order to circumvent these minor drawbacks, mucosal grafts have been introduced to graft intra-oral sites. Mucosal grafts may be full-thickness grafts or split-mucosal grafts.

Full-thickness mucosal grafts

The concept of mucosal grafts was introduced by Peer (1955) who transplanted small areas of oral mucosa on to the conjunctiva. Lewis in 1963 deepened the anterior sublingual area using cheek mucosa, and Propper (1964) reported its application in periodontal surgery. Obwegesser (1965) and Steinhauser (1969) used cheek mucosa in maxillary vestibuloplasty. Robinson (1967) and Hall (1971) recommended keratinised masticatory palatal mucosa as the ideal tissue for denture support because of its similarity to attached gingiva, but the latter reported a troublesome ulceration beneath the denture in the healed donor site in the midline and recommended retaining the central palatine mucosa. Hall and O’Steen (1970) concluded that full-thickness palatal mucosa fulfilled the basic requirements of a skin graft by covering denuded soft tissue while the thick underlying connective tissue layer reduced contraction. The dissection of palatal mucosa was made by free hand between the lamina propria and submucous tissues, leaving the minor salivary glands, fat and neurovascular bundles intact. Guernsey (1973) also preferred palatal mucosa because of its resilience and toughness.

Dekker and Tideman (1973) showed that transplanted cheek mucosa tends to assume the appearance of normal mucosa of the edentulous alveolus. Tideman (1972) noted that taking full-thickness mucosa from the cheek caused post-operative trismus.

Split mucosal grafts

Steinhauser (1969) obtained a split mucosal graft using a mucotome developed from the dermatome (originally devised by Castroveijo in 1959). The advantages claimed for split mucosa included the rapid epithelialisation and scar-free healing of the donor area, the uniform thickness of the graft and reduced contraction at the recipient site. However, he concluded that because of its better stress-bearing capacity and because stability is more important than adhesion in lower jaw, skin is preferable to mucosa in lower labial vestibuloplasty.

Advances in skin grafting

Tissue-cultured skin graft

The development of epidermal culture systems has allowed skin grafting with sheets of cultured keratinocytes. This technique has recently been reviewed by Nanchahal and Ward (1992). It has been found to provide a high expansion factor in the management of burns (O’Connor et al –1981) and chronic ulcers (Leigh et al –1987). Allogenic cultured keratinocytes are rejected, and so autologous cells are necessary to provide permanent epidermal cover.

Application of cultured keratinocytes alone resulted in sloughing, blistering, scarring and wound contraction due to lack of dermal appendages. This led to the development of collagen substrate to support the keratinocytes for grafting. Now autologous keratinocytes are cultured with wide variety of dermal appendages like

  • Extruded collagen sheets.
  • Reconstituted collagen lattice
  • Fibroblast postulated collagen lattices
  • Collagen glycosaminoglycan substrates
  • Cadeveric dermis

In 1993, Kangesu et al used ‘kerato-dermal grafts’, prepared by combining autologous dermis with cultured keratinocytes, and reported significant improvement in the in vivo growth of the cells.

Donor site dressings

Though split skin graft donor sites have been traditionally dressed with non-occlusive dressings, recent evidence suggest that a moist wound provides a better healing environment. Dressings that provide wounds with a moist environment include semi-permeable films, semi-occlusive hydrogels and occlusive hydrocolloids.

Semi-permeable films are permeable to water vapour and gases including oxygen, but impermeable to water and bacteria. Semi-occlusive hydrogels, while having similar properties, possess an absorbent mechanism. The occlusive hydrocolloids are impermeable to gases, moisture and bacteria. According to Hutchinson (1989), the moist environment beneath these dressings do not encourage wound infection.

 

Skin graft as interposition material in TMJ ankylosis surgery

The use of skin grafts for arthroplasty dates back to Gluck in 1902. Skin grafts were first used in TMJ ankylosis surgery by Georgiade and Altany in 1957. In 1961, Franchebois and Souyris used a strip of de-epithelialised skin obtained from a full-thickness graft to cover the mandibular stump and obtained good results in 7 patients. In 1977, Popescu and Vasiliu described a full-thickness skin graft technique and reported a low rate of recurrence. Most failures were due either to insufficient availability of skin to cover the tip of the condyle or to the displacement of graft due to poor suturing. Recent studies by Meyer (1988), Kaban et al (1990), Clauser et al (1995) and Chossegros et al (1999) have reported around 90% success rate with inter-incisal width of more than 30 mm after one year follow-up. All these studies reported a low incidence of complications related to infection and inflammation.


Conclusion

Skin grafts have been used in a wide variety of clinical applications for a long time. The main indication is to provide a natural coverage to the raw areas left behind by surgical excisions, burns, ulcers etc.  A good clinical assessment and meticulous technique can provide an adequate coverage in such cases. Of late, the applications of skin grafting have grown into new arenas like pre-prosthetic surgery and TMJ ankylosis surgery. With the emergence of recent advances, one can now hope to provide the patient with a near-perfect natural wound cover.

References

  1. Fundamental techniques of Plastic Surgery and their surgical applications. 9th I.A. McGregor & A.D. McGregor. Churchill Livingstone 1995.
  2. Basic Principles of Oral and Maxillofacial Surgery. Vol. I. Peterson, Marciani, Indresano (eds.). Lippincott-Raven. 1997.
  3. Cancer of the Face and the Mouth: Pathology and Management for Surgeons. IA McGregor & FM McGregor. Churchill Livingstone 1986.
  4. Grabb and Smith’s Plastic Surgery. 5th S. J. Aston, R. W. Beasley, C. H. M. Thorne. Lippincott-Raven. 1991.
  5. Surgery of the Mouth and Jaws. J. R. Moore. Blackwell. 1985.
  6. Skin grafts. G. H. Branham, J. R. Thomas. In Facial Plastic Surgery. The Otolaryngologic Clinics of North America. Oct 1990. 23:5.

 

Posted in Trauma

Mandibular Fractures

 CLINICAL FEATURES AND MANAGEMENT

INTRODUCTION:

Fractures of the mandible are common in patients who sustain facial trauma.

Study conducted by Hang et al, showed the ratio of 6:2:1 of mandibular, zygomatic, maxillary fractures incidence respectively. Approximately 2/3rds of all facial fractures are the mandibular fractures.

The management of the mandibular fractures includes conservative and open reduction methods.

The management of mandibular fractures was proposed by various practitioners and authors are as follows:

Erich and Austin (1844) – Preantibiotic era, closed reduction.

Buck, (1847) – Transosseous silver wiring.

Gordon (1942) – Wire suturing, stainless intraosseous wiring + MMF.

Spiessl (1970) – AO / ASIF – compression plate.

Michelet (1973) – Non compression, monocortical screws with miniplate system.

Champy (1978) – Ideal osteosynthesis lines.

CLASSIFICATION

  1. Anatomical Location

Row and Killey’s classification

  1. Fractures not involving the basal bone – are termed as dentoalveolar fractures.
  2. Fractures involving the basal bone of the mandible.

Subdivided into following:

  1. Single unilateral.
  2. Double unilateral.

Dingman and Natvig’s classification by anatomic region:

  1. symphysis fracture (midline fracture).
  2. Canine region fracture.
  3. Body of the mandible between canine and angle.
  4. Ramus region – bounded by the superior aspect of the angle to two lines forming an apex at the sigmoid notch.
  5. Coronoid region.
  6. Condylar fractures.
  7. Dentoalveolar region.
  8. Relation of the Fracture to the Site of injury

 

  1. Direct fractures.
  2. Indirect (countercoup)fractures.
  3. Completeness

Complete and incomplete fractures.

  1. Depending on the mechanism
  2. Avulsion fracture.
  3. Bending fracture.
  • Burst fracture.
  1. Countercoup fracture.
  2. Torsional fracture.
  3. Number of Fragments:
  • Single, multiple, comminuted, etc.
  1. Involvement of the integument
  • Closed or open fracture.
  • Grades of severity I-V
  1. Shape or area of the Fracture
  • Transverse, oblique, butterfly, oblique surfaced.
  1. According to the Direction of Fracture and Favourability for treatment
  2. Horizontally favourable fracture.
  3. Horizontally unfavourable fracture.
  4. Vertically favourable fracture.
  5. Vertically unfavourable fracture.

This classification is aimed toward the angle fractures. Here, the direction of fracture line is important for resisting the muscle pull. When the muscle pull resists the displacement of the fragments then the fracture line is considered as favourable. If the muscle pull distracts the fragments away from each other, resulting in displacement, then the fracture line is considered as unfavourable.

  1. When the fracture line passes from the alveolar margin, downward and forward, then upward displacement of the posterior fragment is prevented by physical obstruction caused by the body of the mandible. Hence, such a fracture line is termed horizontally favourable.
  2. If, on the other hand, the line of the fracture passes downward and backward, then the upward movement of the posterior fragment is unopposed. This type of fracture is termed horizontally unfavourable.
  3. The fracture line which passes from the outer or buccal plate obliquely backward and lingually, will tend to resist the muscle pull and is thus termed a vertically favourable type of fracture.
  4. When the fracture line pass from the inner or lingual plate obliquely backward and buccally, inward movement of the posterior fragment will take place as a result of the medial pterygoid muscle pull. This type of fracture is termed vertically unfavourable.

This classification is of clinical importance for the treatment planning and fixation, the amount of displacement can be judged and the type of fixation device can be chosen.

  1. According to Presence or Absence of Teeth in Relation to the Fracture line

It is very essential to note the presence or absence of teeth in relation to the fracture line, also the periodontal status as well as teeth size also matters for planning fixation method.

Kazanjian and converse classification

Class I when the teeth are present on both sides of the fracture line.

An adequate number of teeth of suitable shape and stability. Wiring – direct, continuous or multiple loop or interdental eyelet type, use of prefabricated arch bars.


Class II When the teeth are present only on one side of the fracture line.

  1. Short edentulous posterior fragment
  2. If favourable, immobilization of main fragment by interdental wiring or arch bars. Minor displacement can be accepted.
  3. If unfavourable – open reduction with direct fixation is a must.
  4. Long edentulous posterior fragment:
  5. Without displacement – conservative treatment.
  6. With vertical and medial displacement requires open surgical reduction and fixation.

Class III When both the fragments on each side of the fracture line are edentulous.

  1. Simple or compound fracture without much displacement in the body region. Simple Gunning type splints.
  2. Simple fractures which are unfavourable. Open reduction and fixation.
  • Compound fractures. Surgical intervention.
    • AO Classification (Relevant to Internal Fixation)
  1. F: Number of fracture or fragments.
  2. L: Location (site) of the fracture.
  3. O: Status of occlusion.
  4. S: Soft tissue involvement.
  5. A: Associated fractures of the facial skeleton

Such a classification is helpful in terms of:

  • Patient selection and treatment planning.
  • Evaluation of therapeutic results.
  • Comparison of different treatment methods.
  • Information and communication.

These criteria can be objectified clinically and radiographically:

  1. F: Number of fracture.

F0: Incomplete fracture.

F1: Single fracture.

F2: Multiple fracture.

F3: Comminuted fracture.

F4: Fracture with a bone defect.

  1. Categories of localization (site) L1-L8

L1: Precanine.

L2: Canine.

L3: Postcanine.

L4: Angle

L5: Supra-angular

L6: Condyle

L7: Coronoid.

L8: Alveolar process

 

  1. Category of occlusion – O0-O2

O0: No malocclusion.

O1: Malocclusion.

O2: Non existent occlusion – Edentulous mandible.

  1. Categories of soft tissue involvement – S0-S4

The risk of infection and healing depends on the condition of the soft tissues surrounding the fracture.

S0: Closed.

S1: Open intraorally.

S2: Open extraorally.

S3: Open intra and extraorally.

S4: Soft tissue defect.

  1. Categories of associated fractures A0-A6

A1: Fracture and / or loss of tooth.

A2: Nasal bone.

A3: Zygoma.

A4: LeFort I

A5: LeFort II

A6: LeFort III

Grades of severity – I-V

Grade I and II are closed fracture.

Grade III and IV – open fractures.

Grade V open fracture with a bony defect (gunshot).

Condylar Fractures:

According to the fracture level:

  1. Condylar head or intracapsular.
  2. Condylar neck.

Relationship of condylar fragment to the mandible:

  1. Displaced with medial overlap of the condylar fragment.
  2. Displaced with lateral overlap.
  3. Anterior and posterior overlap.
  4. Without contact between the fragments.

Relationship of condylar head to fossa:

  1. No displacement.

 

 

CLINICAL EXAMINATION

Examination of a patient with mandibular fracture is done in 3 stages:

  • Immediate assessment and treatment of life threatening conditions if any.
  • General clinical examination.
  • Local examination of the mandibular fracture.

The signs and symptoms of mandibular fractures are as follows:

  1. Change in occlusion:

This is highly suggestive of a mandibular fracture, and the bite will feel different. This may occur due to fractured teeth, alveolus mandible, or trauma to TMJ and muscles of mastication.

  • Anterior open bite may occur due to bilateral angle or condylar fractures or from maxillary fractures with inferior displacement of the posterior maxilla.
  • Posterior open bite can occur with fractures of the anterior alveolar process or parasymphyseal fractures.
  • Unilateral openbite – ipsilateral angle and parasymphyseal fractures.
  • Posterior crossbite-midline symphyseal or condylar fractures with splaying of the posterior mandibular segments.
  • Retrognathic occlusion – condylar/angle fractures and forwardly displaced maxillary fractures.
  • Prognathic occlusion – effusion of TMJ, protective forward positioning of the mandible, retropositioning of the maxilla.
  1. Anesthesia, paresthesia or dyesthesia of the lower lip:

Most pathognomonic sign of a fracture distal to the mandibular foramen, causing damage to the inferior alveolar nerve.

Conversely, most non displaced fractures of the body angle and symphysis are not characterized by anesthesia, so this is not a sole diagnostic feature in diagnosis.

  1. Abnormal mandibular movements:

Usually limited opening and trismus due to guarding of muscles of mastication are seen, but certain predictable abnormal movement are seen in certain cases, e.g. deviation to the same side on opening seen in condylar fractures, therefore lateral pterygoid of normal side is not counteracted by that of the fractured side.

  • Inability to open the jaw may be due to impingement of the coronoid on the zygomatic arch, either from fractures of the ramus and coronoid process, or from a depressed zygomatic arch fracture.
  • Inability to close the jaw due to fracture of alveolar process, angle, ramus, or symphysis causing premature dental contact.
  • Lateral mandibular movements may be inhibited by bilateral condylar fractures, and fracture ramus with bone displacement.
  1. Change in facial contour and mandibular arch form:
  • May be masked by swelling.
  • Flattened appearance of lateral aspect of face may be due to fracture body, angle or ramus.
  • Deficient mandibular angle – unfavourable angle fractures where proximal fragment rotates superiorly.
  • Retruded chin – bilateral parasymphyseal fractures.
  • Elongated facial appearance – bilateral subcondylar, angle or body fractures, which allows the anterior mandible to be displaced downwards.
  • Facial asymmetry.
  • Change in arch form.


  1. Lacerations, haematoma and echymosis:

Trauma significant enough to cause loss of skin or mucosal continuity or subcutaneous / submucosal bleeding certainly can cause trauma to the underlying mandible. The direction and type of fracture may be visualized directly through the laceration. The common practice of closing facial lacerations before treating underlying fractures should be discouraged.

Echymosis in the floor of the mouth indicates mandibular body or symphyseal fracture.

  1. Loose teeth and crepitation on palpation.

Multiple fractured teeth that are firm indicate that the jaws were clenched during the traumatic insult, thus lessening the effect on the supporting bone.

Crepitation will be felt in a fracture on palpation.

  1. Dolor, tumor, rubor, calor.

The signs of inflammation are excellent primary signs of trauma and can greatly increase the index of suspicion for mandibular fractures.

The 3 principles in the treatment of mandibular fracture are include Reduction, Fixation and Immobilization.

 

Champy’s Ideal Osteosynthesis Lines

Mandible has parabola shaped body. It consists of the outer and inner cortical plates with central spongiosa. The external cortex is strong and thicker in chin region. It is reinforced laterally by the external oblique line strong projection. In the chin region, there is a stronger cortex inferiorly at the lower border. By the virtue of its compact bone, it provides good anchorage for osteosynthesis screws. In the tooth bearing areas, alveolar proess is of variable thickness. Screw fixation in this area is not possible, due to the anatomy of the roots of the teeth and structure of the bone. The mandibular canal runs from lingula to the mental foramen on a concave course directed upward and forward. Traced from behind forward, the inferior alveolar nerve runs closer to the outer cortex and to the lower border (8 to 10mm from lower border). Distance between the nerve and the outer cortex ranges between 4 to 6mm. The mental foramen lies higher than the canine apices (no osteosynthesis).

In every mandibular fracture, the forces of mastication produce tension forces at the upper border and compression forces at the lower border. Therefore, distraction of the fractured fragments will be seen at the alveolar crest region. In the canine region, there are overlapping tensile and compressive loads in both the directions. Besides this torsional forces are also significant.

The experimental exercise on the model and on the fractured mandibles have confirmed the values calculated on the normal mandible is 60DaN (maximum) in molar region and 100DaN in the incisor region, allowing for the additional torsional forces. Taking into account these anatomical factors, the determination of these forces allows the establishment of ‘an ideal osteosynthesis lines’ for the mandibular body. It corresponds to the course of a line of tension at the base of the alveolar process. In this region a plate can be fixed with monocortical self tapping screws. Behind the mental foramen, a plate can be applied immediately below the dental roots and above the inferior alveolar nerve. At the angle of the jaw, the plate is most favourably placed on the broad surface of the external oblique line as high as possible. In the anterior region between the mental foramina, in addition to the subapical plate, another plate near the lower border of the mandible is necessary in order to neutralize torsional forces. Second plate is applied parallel to the first plate with a gap of 4.5mm between them.

Reduction:

Reduction of a fracture means the restoration of a functional alignment of the bone fragments.


Closed reduction:

Implies fracture reduction without opening skin or mucosa. It is a blind procedure relying on the fragments locking together. This is most likely if the periosteum is intact. E.g. I.M.F, M.M.F.

The reduction normally occurs without direct visualization of the fragments in final positions. The commonest method of closed reduction relies on correct positioning of teeth to control the reduction. The teeth are used to assist the reduction, check alignment of the fragments and assist in immobilization.

Advantages and disadvantages of closed reduction:

Advantages:

  • Only stainless steel wires needed (usually arch bars also).
  • Easy availability, convenient.
  • Short procedure, stable.
  • Gives occlusion some “leeway” to adjust itself.
  • Generally easy, no great operator skill needed.
  • Conservative, no need for surgical tissue damage.
  • No foreign object or material left in the body.
  • No operating room needed in most cases, outpatient treatment.
  • Callus formation (secondary bone healing) allows bridging of small bony gaps.

Disadvantages:

  • Cannot obtain absolute stability (contributing to nonunion and infection).
  • Non compliance from patient due to long period in IMF.
  • Difficult (liquid) nutrition.
  • Complete oral hygiene impossible.
  • Possible temperomandibular joint sequelae.
  • Muscular atrophy and stiffness.
  • Denervation of muscles alteration in fibre types.
  • Changes in temperomandibular joint cartilage.
  • Weight loss.
  • Irreversible loss of bite force.
  • Decrease range of motion of mandible.
  • Risks of wounds to operators manipulating wires.

Open reduction:

Open reduction involves exposure of the fracture through either the skin or mucosa and fracture segments are visualized and reduced.

Indications for open reduction:

  1. Displacement unfavourable fractures through the angle of mandible.
  • When proximal fragment is displaced superiorly, medially and cannot be maintained without intraosseous wires, screws or plating.
  1. Displaced unfavourable fractures of the body or the parasymphyseal region of the mandible.
  • When treated with closed reduction parasymphyseal fracture tend to open at the inferior border with the superior aspect of the mandibular segments rotating medially at the point of fixation.
  1. Multiple fracture of the facial bones.
  • In multiple fracture of the facial bones, open fixation of the mandibular segments provide a stable base for restoration.
  1. Midface fractures and displaced bilateral condylar fractures.
  • With midface frace and displaced bilateral condylar fracture, one of the condylar fractures should be opened to establish the vertical dimension of the face.
  1. Fractures of an edentulous mandible with severe displacement of the fracture segments.
  • Open reduction should be considered to reestablish continuity of the mandible.

Advantages and disadvantages of open reduction with rigid internal fixation.

Advantages:

  • Early return to normal jaw function.
  • Normal nutrition.
  • Normal oral hygiene after a few days.
  • Avoidance of airway problem.
  • Can get absolute stability, promotes primary bone healing.
  • Bone fragments re-approximated exactly by visualization.
  • Avoids IMF for patient with occupational benefits in avoiding mandible fixation e.g. Lawyers, teacher, sale people, seizure disorders.
  • Helpful in special nutrition requirements (diabetics, alcoholics, psychiatric disorders, pregnancy).
  • Easy oral access (for example in intensive care unit patients).
  • Decreased patient discomfort, greater patient satisfaction.
  • Less myoatrophy.
  • Decreased hospital time.
  • Substantial savings in overall cost of treatment.
  • Lower risk of major complications.
  • Lower infection rates, improved overall results.
  • Lower rate of malunion/nonunion?


Disadvantages:

  • Most obvious; need for an open procedure.
  • Significant operating room time.
  • Prolonged anaesthesia.
  • Expensive hardware.
  • Some risk to neuromuscular structure and teeth.
  • Need for secondary procedure to remove hardware.
  • “Unforgiving procedure”, the rigidity of the plate means no manipulation is permissible.
  • Need much operator skill, meticulous technique needed.
  • Higher frequency malocclusion.
  • Higher frequency facial nerve palsy.
  • Scarring (extraoral and intraoral).
  • No bridging of small bone defect (absence of callus)

Closed reduction and indirect skeletal fixation:

  1. Direct interdental wiring.
  2. Indirect interdental wiring (eyelet).
  3. Continuous or multiple loop wiring.
  4. Arch bars.
  5. Cap splints.
  6. Pin fixation.
  • Direct interdental wiring:

This method was introduced by Gilmer, this technique provides simple and rapid method of immobilization of jaws. But with this technique the wire tend to loosens and a broken direct wire cannot be replaced without first removing and then replacing all of the others.

A 15cm length of prestretched 0.35mm diameter soft stainless steel wire is passed around a tooth emerging through the interdental space with the wire around the neck of the tooth the two ends of the wire are tightened by twisting together to produce a 3cm tail.

For intermaxillary fixation the maxillary wire ends are twisted together with mandibular once. The cut ends should be bent in to the interdental space to avoid soft tissue trauma.

  • Indirect interdental wiring (eyelet or ivy loop):

Eyelet wiring is simple, quick, easyway and effective method of reduction and easy way of obtaining maxillomandibular fixation.

If immobilization of the jaws is required for a short period only, relatively few eyelets are necessary e.g. one or two in each quadrant.

 

 

Technique:

The loop is constructed of a 24 gauge wire and the wire is passed interproximal to two stable teeth. The ends of the wire are first brought around to the mesial and distal sides of the teeth. The distal end wire is then delivered under the loop and tightened to the mesial wire in apical direction. Then the cut ends of wire are adapted in the interproximal space.

Maxillomandibular fixation between eyelets can be achieved by passing a smaller gauge wire can be passed through the loops and tightened. The posterior tie wire should be tightened first to avoid excessive traction on the lower anterior teeth. The twist is to be made at the gingival margin and traction is applied to the wire in that direction to lessen the possibility of it breaking. The cut ends are bind tightly and should be intersected into the interdental space to avoid trauma.

Removal of eyelet wire: The normal period required for firm clinical union to take place in healthy adult is 6weeks with young patients and with minimally displaced fractures 3 to 4 weeks will allow adequate union.

 

 

  • Continuous or multiple loop wiring:

Stout (1943) described a technique which permits blocks of teeth in either jaw to be wired in such a manner that elastic traction can be used to reduce the fracture.

Technique:

A 30cm length of soft 0.5mm diameter stainless steel wire is used. One end of the wire is laid along the buccal surface of the teeth, while the other is passed around the most posterior teeth below its contact point to emerge through its anterior interdental space. The wire is passed around the buccal wire and back through the same interdental space. A pliable rod approximately 3mm diameter and 5cm in length is passed through the wire loop and laid along the buccal surface of the segment parallel to the buccal wire. The end of the wire on lingual or palatal aspect is then passed in sequence through the interdental space of remaining teeth around the rod and the buccal wire in a similar manner until the quadrant is closed. Then both the ends of the wire lie on buccal aspect, they are clipped pulled and twisted. Then the rod is withdrawn by a forward rotatory pull. First the posterior and each succeeding loop is twisted by an artery clip so that the loop lies horizontally.

 

ARCH BARS

Are the most versatile form of mandibular fixation.

There are two varieties of arch bars, those that are commercially produced and those which are individually made for a given patient.

Commercially:

  • Jelanko
  • German silver bars.

Indications for use:

  1. When insufficient teeth remain to allow efficient eyelet wiring.
  2. When teeth present are so disturbed that efficient intermaxillary fixation is otherwise impossible.
  3. In case of simple dentolaveolar fractures or where multiple tooth bearing fragments in either jaw require reduction into a arch form before intermaxillary fixation.
  4. As an integral part of internal skeletal suppression in the treatment of fractures involving the middle third of facial skeleton.
  5. To reduce the preoperative time which would otherwise be required for cap splint preparation.

Technique:

As the mandibular fragment are displaced owning to the fracture the bar is cut and adapted to maxillary arch. In practice it has been found that such a bar is quite satisfactory when applied to the lower arch as extreme accuracy is not required. It is advisable to wire one end to the posterior teeth of a principal fragment, then to secure the anterior section of arch bar in the incisor region and finally attach the other end. This permits adjustment of the length and contour before the intervening wires complete the attachment of the bar.

To be retentive the wires holding the bar must lie below the contact points.

They may be inserted as follows:

  1. Passed around the lingual or palatal aspect of tooth and tightened over the bar.
  2. Passed circumferentially around the entire tooth before being tightened over the bar.
  3. Both ends of wire loop are passed around the tooth one end passes over the bar and is inserted through the loop while the other end passes under the bar and remains fine of loop. The two ends are pulled to tighten the loop and the wires are twisted over the bar.

Once the fragments have been tightly secured to the arch bar, it is difficult to correct any errors in a vertical displacement of occlusion. It is advisable therefore not to tighten any ligature finally until all have been inserted any vertical displacement has been corrected by articulating the jaws.

PIN FIXATION

This technique was introduced during the second World War for use with compound, communited and frequently infected jaw fractures as a means of controlling the fragments remote from the affected area.

Indications:

  1. Pathologic fracture or gunshot injuries associated with gross bone loss.
  2. Osteomyelitis of an edentulous fracture site.
  3. Fractures associated with extreme atrophy of the edentulous jaw.
  4. Fractures of mandible associated with fractures of the middle third of facial skeleton.

Advantages of pins:

  1. Control of the edentulous fragments without involving the fracture lines.
  2. Can be applied under local analgesics if indicated.
  3. Reduction or avoidance of the need for surgery at the fracture site, thereby retaining the periosteal blood supply of the edentulous mandible.
  4. Elimination of laboratory facilities, with minimum operative time required.
  5. Simultaneous treatment of middle third and mandibular fractures by relatively simple combined techniques.
  6. Immobilization of the mandible may be less prolonged or even avoided.

Disadvantages of pins:

  1. Conspicuous in daily life and uncomfortable while sleeping because of the projection of the pins which may easily be knocked.
  2. Difficult with washing and shaving.
  3. Soft tissue scars are caused by the pinholes and there is a constant, although slight, risk of infection.
  4. Readily accessible to an interfering, uncooperative or cerebrally irritated patient.

Technique:

Consist of inserting into each major bone fragment a pair of 3mm titanium or stainless steel about 7cm long which diverge from each other by means of universal joint. Self tapping pins such as moule or toller type are used, these being screwed into prepared holes in the bone of slightly diameter. After reduction of the fracture the pairs of pins are linked by attaching a connecting rod or rod to the centre of the cross bar by means of universal joints.

  • Pin fixation of this nature is not particularly rigid and supplementary intermaxillary fixation is usually required.

CAP SPLINTS

Silver cap splints were for many years the method of choice for the immobilization of all jaw fractures especially in U.K. during the second world war this technique was of great importance.

  • This technique is time consuming both clinically and in the laboratory and the results achieved are accomplished better and faster by other method.

 

 

Indications:

  1. Patients with extensive and advanced periodontal disease when a temporary retention of dentition is required during the period of fracture healing. A cap splint will splint all the loose teeth together and allow application of intermaxillary fixation.
  2. To provide prolonged fixation on the mandibular teeth in a patient with fractures of the tooth bearing segment and bilateral displaced fractures of the condylar neck. The cap splint will immobilize the body fracture and allow mobilization and if necessary, intermittent elastic traction for condylar fracture.
  3. Where a portion of the body of the mandible is missing together with substantial soft tissue loss.
  • Silver cap splints are usually cemented with black copper cement because this material will form a firm bond in the presence of a limited amount of moisture. It is also a useful abundant for retained teeth which have exposed and sensitive dentures.

Acrylic cap splints: are easily and more cheaply fabricated. They are particularly useful for the treatment of dislocated teeth and alveolar segmental fractures.

SURGICAL APPROACHES

Factors used to establish the location of incision include:

Fracture location                     Approaches :

Skin lines                                          Extraoral

Nerve position                                  Intraoral

Extraoral approaches

  1. Submandibular approach:

First described by Risdon in 1934, the skin incision is 4-5cm in length, 2cm below the angle of the mandible. Optimally the incision should be placed within a skin crease, so as to hide the scar.

  • Subcutaneous fat and superficial fascia are dissected to reach the platysma muscle.
  • The platysma is sharply dissected to reach the superficial layer of the deep cervical fascia. Marginal mandibular branch lies just deep to it.

The nerve passes above the inferior border of the mandible till the region where the facial artery crosses the inferior border, and then takes a downward course, upto 1cm below the inferior border. These branches below the inferior border distal to facial artery supply the platysma.

Dissection through the deep cervical fascia is done with the careful use of a nerve stimulator. The submandibular gland and its fascia then becomes evident, and the lower pole of the parotid may be seen. Dissection is then carried to the masseter taking care to retract the nerve fibers superiorly.

Once the muscle is encountered, it is sharply divided at the inferior border to expose the bone. The muscle, periosteum and soft tissues are retracted superiorly to expose the body ramus and fracture site.

Exposure can be increased and closure enhanced by dissecting the medial pterygoid and stylomandibular ligament from the inferior and posterior border. Further exposure can be obtained by distracting the angle and inferior border with a wire or bone forceps.

The capsules of parotid and submandibular glands should be avoided, or else disruption of gland parenchyma may lead to sialoceles or salivary fistulas.

  1. Retromandibular approach

Described by Hinds and Girotti in 1967. Basically a variation of the submandibular approach, except that the incision was 3cm above the submandibular incision.

The incision curves behind the angle of the mandible and the parotid, and massetric and deep cervical fascia are encountered. The dissection is then carried anterior to deep cervical fascia, and nerve stimulation is used. The incision to bone through the masseter is between the marginal mandibular and buccal branches of the facial nerve. The muscle and periosteum are incised over the angle. The soft tissues and nerve fibers are then retracted superiorly.

This incision gives superior access to the ramus and subcondylar region.

  1. Preexisting lacerations:

These lacerations may be made use of, if present, to gain access to the fracture site, if it is in direct relation to the fracture site.

Intraoral:

  1. Symphysis and parasymphysis:

Initially the region is infiltrated with LA and vasoconstrictor. The lip is then retracted, and a curvilinear incision is made perpendicular to mucosal surface. The incision is carried out into the lip so as to leave at least 1cm of attached gingiva.

The mentalis muscles now visible should be incised perpendicular to the bone, leaving a flap of muscle attached to the bone, for closure. The dissection is then carried sub periosteally to identify the mental neurovascular bundle.

The fracture site is then identified and reduced, and the surgical site is closed in layers. An adhesive bandage is then applied to the chin to support the mentalis muscle and thus prevent drooping.

  1. Body, angle and ramus

These regions can be approached through an extended wards incision.

Treatment by open reduction and dental skeletal fixation:

  1. Transosseous wiring (osteosynthesis).
  2. Intramedullary pinning.
  3. Titanium mesh.
  4. Circumferential straps.
  5. Bone clamps.
  6. Bone screws.


Transosseous wiring:

Is the direct skeletal fixation of two or more bone fragments with the aid of wire ligatures pulled through previously drilled holes.

  • Direct wiring keep the fragments in exact anatomic alignment after reduction, but additional fixation of the fracture mandible with splints and intermaxillary fixation is required to maintain stability.

Indications:

  1. For fractures of the ramus.
  2. For replacement of small fragments in grossly comminuted fractures.
  3. For functional stabilization of the fragments in plate and screw osteosynthesis.
  4. Edentulous mandibular fractures.

Contraindications:

  1. Fractures which are compound into the mouth should be treated with degree of reserve, as there is risk of infection from oral cavity tracking down the fracture line.


Technique:

The holes are drilled in the bone ends on either side of the fracture line 6mm distance after which a length of 0.45mm soft stainless steel wire is passed through the holes and across the fracture. After accurate reduction of the fracture the free ends of the wire are twisted tightly, cut off short and twisted ends tucked into the nearest drill hole.

Depending on type of fracture, various shapes of wire ligature are recommended:

  • Simple ligature is the most frequent form of ligature used but is only used to secure small bone fragments.
  • Most stable form of ligature is simple ligature combined with figure of eight and is recommended for stabilizing transverse as well as oblique fractures of the mandible at lower border.
  • Double ligature – also found to be static with respect to tension and bonding forces, one is placed below and the second above the mandibular nerve.
  • There is a risk of tooth root damage, so it is indicated in edentulous mandible.
  • The wiring osteosynthesis can be performed via either an intraoral or extraoral the extraoral provides a good overview of the fracture sites of the distal parts mandibular body including the angle.

Compression osteosynthesis:

The goal of a compression osteosynthesis is a condition called absolute stability in which no movements occurs at the area of interfragmentary contact or between the bone and the device.

Compression of the fractured bone segments enhances the likelihood of successful primary bone healing in two ways:

  • First is preload, the force generated across the fracture by fixation system.
  • Second component is the friction produced by compression of fracture bone segments.
  • The effect produced by interfragmentary compression help stabilize the fracture, minimizing complication such as osteomyelitis and non-union.
  • The maximum compressive force generated from compression plate is 300 kilopascals /cm2.
  • Ideally the favourable site for osteosynthesis is the region of maximal tension caused by muscular pull, which is the superior border of mandible. Because of the roots of the teeth and inferior alveolar canal, insertion of a plate in this locations is associated with unacceptable morbidity, so the plate only be inserted at the lower inferior border is capable of providing compression to the bone fragments, but fails to control the tensile forces at the alveolar process.

Dynamic compression plate:

The dynamic compression plate was originally designed for orthopedic surgery by the A.S.I.F. Lhur in 1972 adapted the principle of dynamic compression to the maxillofacial region for treatment of mandibular fractures. Spiessel et al was the first to apply the A.S.I.F. principles to the management of mandibular fractures.

  • Compression plates are available in thickness of 2.0mm, 2.7mm and 3.0mm and width of 6.5mm, 8.9mm. The indigenous design of compression plate is based on the screw head that when tightened slides down on inclined plane within the plate.

In dynamic compression plate one compression hole should be located in each fragment of fracture these holes are usually placed most proximal to the line of fracture. The screw movement produced from the inclined planes of there holes oppose each other, the fracture end will move toward one another relative to the plate.

The each compression hole will produce 0.8mm of bone movement and if compression is used on both sides a total of 1.6mm of bone movement may be achieved.

Technique: Before the plate is adapted to the bone, pretension across the fracture is achieved with the use of bone forceps. The use of bone forceps facilitate anatomic reduction.

Before the forces can be applied a hole must be drilled in the inferior aspect of the mandibular on each side of the fracture. These holes are ideally placed 1cm from fracture margin and screw is placed in each hole and the sleeves of the forceps are secured to these screws.

After reduction the plates are adapted and after proper adaptation of the plate the holes are made with appropriate size drill. The screws used are not self tapping and designed to engage both buccal and lingual cortices of mandible.

  • The drill is used through a drill guide toward the fracture. The guide has two numbers engraved on its surface 0.8mm and 0mm when the side marked 0.8mm towards the fracture line, any screw placed in this site will cause compression across the fracture. If portion labeled 0mm is located towards the fracture the screw will be placed in a passive position.
  • A depth gauge is used to establish the proper length screw. A screw of suitable length should be choosen so that when fully tightened it will project approximately 2mm through the lingual cortex.
  • When compression across the fracture is desired the compression holes should be drilled first. The first screw is tightened to hold the plate in position, but is not completely sealed, the second compression screw is placed on the either side of the fracture and is tightened initiating compression after 2nd screw is sealed the first screw is tightened fully maximizing compression. Then the remaining screws may be placed in passive position.

Eccentric Dynamic Compression Plate:

In 1973 Schomaker and Niederdellman developed a plate incorporating the principle of eccentric dynamic compression.

  • The design of the plate is similar to the D.C.P. In addition to the standard compression holes the plate also contains two oblique outer compression holes. The eccentric holes are aligned at an angle oblique to the long axis of the plate. The activation of these holes produce a rotational movements of the fracture segment. The rotational movement of the fracture segment establishes compression at the sup border of mandible.
  • When E.D.C.P. is applied an initial compressive force of 200N was observed at inferior border of mandible. As oblique screws are activated the compression at the base of mandible decrease to 150N, but compression of 150N was observed at the superior border of mandible. The superior compression also depends on the degree of oblique hole from the long axis of plate.

Technique:

A different bone reduction forceps is used and the sequence in which screws are inserted are also different. The reduction forceps incorporate pressure rollers that are located lateral to the holding screws once the holding screws have been engaged, anatomic reduction and precompression achieved, then the outer rollers are tightened which produces an occlusally directed forces on outer aspect of fracture, creating superior border compression.

  • Screws are placed in the holes closest to the fracture margin to achieve compression of fracture segment. After compression has been achieved at the inferior border screws are placed in the outer eccentric holes and tightened achieving compression at superior border.

Monocortical miniplate osteosynthesis:

The principle of miniplate technique is to identify the line of lesion within the mandible at the site of fracture. Then plate is applied across the fracture along this line without compression.

Champy studied examined the load at different parts of the mandible: Post to the canine the mylohyoid muscle pull medially whereas anerior to the canine, the digastric and genial muscle tend to pull posteriorly.

Taking into account the anatomy of the mandible, the location of the dental apices and the thickness of cortical layer chamy determined an ideal line of osteosynthesis which corresponds to the course of a line of tension at the base of alveolar process.

Behind the mental foramen only one plate should be applied below the roots and above the inferior alveolar canal. In front of the mental foramen in order to neutralize lighter tension forces at the canine another plate near the lower border of mandible is necessary in addition to the subapical plate.

The miniplates requires screw to be fixed only in the outer cortex of mandible.


Plates and screws:

The plates have a thickness of 1mm and are 6mm wide. The distance between the holes are standardized and the plates with more holes are available and those with intermediate plating are also available self tapping screws are used from 5 to 15 mm in length and diameter is 2mm, screw head are designed to allow insertion at a 30° slant with respect to the plate surface screws 7 or 5mm in length are normally used in mandible.

Advantages:

  1. Because of reduced size of miniplate, smaller incision and less soft tissue dissection are required for their placement.
  2. Miniplates can be placed intraorally thereby avoiding an external scar.
  3. Because of smaller size and thinner profile of the miniplates they are less likely to be palpable possibly reducing the need for subsequent plate removal.
  4. Because the screws are monocortical the plates may be placed in area of mandible adjacent to tooth roots with minimal risk of dental injury.
  5. Because of smaller size and the malleability of the materials, miniplates can be easily contoured in 3 dimensions.

Disadvantages:

  1. They are not rigid as standard mandibular fracture plates and decreased rigidity may lead to torsional movements of the fracture segments leading to infection or nonunion.
  2. Because of instability the use of miniplates fixation for comminuted fracture is limited.
  3. Because of reduced stability of miniplate fixation reduced function is recommended (soft diet).

Clinical application:

When miniplate is used for fixation of a mandibular angle fracture, placement should at the superolateral aspect of mandible extending onto the broad surface of the external oblique ridge.

In the region between two mental foramina two plates are recommended one in the subapical region of symphysis and the second at the inferior border.

In the body of mandible one plate is recommended just below the apices of the teeth but above the inferior alveolar nerve canal.

Bioresorbable plates:

Disadvantages associated with metallic plates:

  1. Plate, induced osteoporosis.
  2. Because the plate may become infected.
  3. Loosening and corrosion of the screws may occur overtime, leading to inflammation and pain.
  4. Long term retention of metallic plates in the facial skeleton include palpability of the plate, interferences with the fit of prosthetic appliances.

The bioresorbable material would avoid the problems associated with the use of metallic materials while maintaining the qualities necessary for successful rigid fixation.

Bioresorbable materials used include:

  1. Polyglycolic acid.
  2. Polyactic acid.

These materials are tolerated well by the body but their strength inadequate to provide clinically acceptable rigid fixation.

  • The self reinforced polyglycolic acid and self reinforcing polylactic acid. The self reinforcing technique increases the strength of the material by incorporating polymeric fibres having the same chemical composition as the binding matrix.
  • The major advantage of bioresorbable rigid fixation device is that initially they provide adequate fixation for direct bone healing but as the bone gains strength the plate is reabsorbed by the body.
  • The metabolism of P.G.A. is primarily by hydrolysis. The individual glycolic acid molecule are metabolized via the citric acid cycle and ultimately eliminated by respiration as carbon dioxide.
  • The resorption rate of these material is 5.3µm/day.

Lag screw fixation:

Lag screw fixation for mandibular fracture was introduced in 1970 by Brons and Boering.

A screw acts as a lag screw when it gains purchase in the cortex of the most distant osseous fragment while fitting passively in the cortex of the fragment adjacent to the screw head.

The true lag screw has the thread in the distal end and a smooth shank at the proximal end (i.e. adjacent to the screw heal). An oversized hole is drilled through the proximal cortex. The diameter of this hole must be as large as the thread diameter of the screw. The remainder of the hole in the distal segment must be smaller than the thread diameter and this is referred to as traction hole when the screw is tightened the distal fragment is pulled against the proximal fragment by the screw head.

It is possible to achieve 2000 to 4000 N of compressive force when using lag screws, compared with the 600N achieved with compression plates.

Indications:

  • A typical indication for lag screw fixation are fractures in the chin region. Where the mandible is constituted by a strong cortical bone which serves as a excellent buttress.
  • In fracture of angle the lag screw may be installed on the tension side of the fracture which is biodynamically advantages.
  • Long sagittal fracture in the body regions.
  • Lag screws are used to reduce condylar fracture
  • Lag screws are useful for fixture of inlay and onlay bone group.

Technique:

First the gliding hole in drilled in the near cortex with a diameter equal to the treat of the screw. The traction hole is then prepared with the aid of a centering guide, assuring that the two holes are prepared coaxially. This is performed with smaller drill sleeve.

The depth gauze is inserted prior to tapping the traction hole. The traction hole is then tapped to the final size.

Intra medullary pinning

Intramedullary pinning was first advocated by major in 1938 and was used by McDowell for maxillofacial fracture.

Kirscher wire are widely used for intra medullary pinning. Approx 2mm indiameter. In emergency situation these wire can be used to provide temporary stabilization of a fractured mandible. The fracture is held in a reduced position and one or more wires drilled through the fragments so that past of wire passes through undamaged bone on each side of fracture.

This method is versatile and can be applied with appropriate ingenuity to fracture in any part of the mandible.

Stability offered by this technique however was not adequate for fixation of mandibular fracture.

Bone clamps:

Bone clamps form of rigid internal fixation and was introduced around 1970. the device was clamped to the lingual and buccal cortices of mandible around the inferior border. The Brenthurst splint is the best known example of this system. Instead of pin screw into the bore the fragments each side of the fracture are secured by clamps attached to the lower border of mandible pins which project from the clamp are the connected by a system of external rods and universal joints in a similar manner to that employed with external pin fixation used in à oblique fracture.

Disadvantages is slippage of clamps.

Complications:

Infection:

The overall post operative infection rate has been reported to be between 3% and 27%. The most common cause is mobility of fracture segments.

Technical errors such as inadvertent placement of screws in the line of fracture, poor plate adaptation and inadequate cooling of bone during screw hole preparation increase the risk of post operative infection.

Fractures in the proximal part of the mandibular body or in the angle region have a higher propensity for infection because of decreased cross sectional surface area of bone.

The other factors implicated in an increased rate of infection include extraction of molar teeth from the line of fraction. The extraction of teeth is indicated when there is periapical pathology, fractured, or severely displaced or those that prevent fracture reduction.

Nerve Injury:

Iatrogenic injury to the sensory branches of the trigeminal nerve is known to occur following open reduction. The nerve injury is often the result of over retraction and also occurs following the application of rigid fixation.

Injury to branches of facial nerve occasionally occurs during repair of mandibular fracture, in case of submandibular incision and approach to condyle the marginal mandibular nerve and temporal branches are damaged respectively.

Malunion:

Mal union is the healing of bone segments in a non physiologic position secondary to either nontreatment or inadequate treatment of a displaced fractures malunion may occur as a result of plate bending, plate fracture, loosening of screw or poor intraoperative reduction. In dentate portion of maxilla and mandible this leads to a malocclusion.


Delayed union:

The time taken for a mandibular fracture to unite is unduly protracted it is referred to as a case of delayed union. If union is delayed beyond the expected time for that particular fracture it must be assumed that the healing process has been disturbed. This is the result of local factor such as infection or general factors such as osteoporosis or nutritional deficiency.

Nonunion:

Means that the fracture is not only not united but will not unite on its own.

Causes:

  • Infection
  • Inadequate immobilization
  • Unsatisfactory opposition of bone ends with interposition of soft tissue.
  • Inadequate blood supply
  • General disease, e.g. Osteoporosis, nutritional deficiencies.

Restriction of craniofacial growth:

The rigid fixation affect the growth potential of the growing craniofacial skeleton.

  • Secondary surgery to remove plates and screws may have a greater detrimental effect on growth than does the retention of plates.

Scar:

Mandibular fractures have associated soft tissue injuries which leads to scar formation.

  • Open reduction with internal fixation often requires the use of extraoral incision.
  • When possible incision should be placed in existing skin creates a usually parallel to resting tension lines.
  • Prophylactic treatment for the patient a risk consist of local application of steroid tape and intratensional infection of 0.1ml of triamcinolone 40mg/ml at 2 to 3 weeks interval.

Injury to tooth roots:

There is always the possibility of trauma to the dental structures when placing screws in the dentate region of maxilla and mandible. This is more commonly seen with D.C.P.

Limitation of opening:

Prolonged immobilization of the mandible in intermaxillary fixation will result in weakening of the muscles of mastication. Excess haemorrhage within the muscles, considerable amount of organizing traumatoma and early scar tissue because limitation of opening and reduced mandibular excursion simple jaw exercise and mechanical exercise may be employed.

Fractures in Edentulous & Atrophic Mandible:

Following resorption of the alveolar process, the vertical depth of the subsequent denture-bearing area is reduced by approximately one-half and in some cases by considerably more. The resistance of the bone to trauma is further reduced.

The ageing process is also associated with significant changes in the vascular architecture. The endosteal blood supply from the inferior dental vessels begins to disappear and the bone becomes increasingly dependent on the periosteal network of vessels.

The denture-bearing area of the edentulous mandible is therefore not only more easily fractured, but also less well disposed to rapid and uneventful healing. If the fracture is simple with little or no displacement it will heal satisfactorily.

Reduction:

For the reasons already stated, precise anatomical reduction is not necessary in fractures of the denture-bearing area. This is fortunate because reduction is frequently difficult when there is over-riding of the bone ends. Reduction and subsequent fixation become more difficult as the mandible atrophies.

However, operative open reduction involves further disruption of the periosteal attachment which interferes significantly with postoperative repair of bone.

Methods of immobilization:

Direct osteosynthesis:

  1. Bone plates.
  2. Transosseous wiring.
  3. Circumferential wiring or straps.
  4. Transfixation with Kirschner wires.
  5. Fixation using cortico-cancellous bone graft.

Indirect skeletal fixation:

  1. Pain fixation.
  2. Bone clamps.

Intermaxillary fixation using Gunning-type splints.

  1. Used alone.
  2. Combined with other methods.

 

Special features associated with jaw features in children

The reparative process in children is rapid due to the increased metabolic rate and the high osteogenic potential of the periosteum. This results in early union, usually within 2-3 weeks, and delay in treatment for any reason is, therefore, a more serious problem than in the adult. Non-union or fibrous union is almost unknown and excellent remodeling occurs under the influence of masticatory stresses, even when there is imperfect apposition of the bone surfaces.

Due to its inherent elasticity, the developing bone predisposes to the characteristic ‘greenstick’ type of fracture. Fracture of the body of the mandible frequently show a considerable degree of displacement and the fracture lines tend to be long and oblique, extending downwards and forwards from the upper border of the mandible. This obliquity of the fracture line is quite different from that observed in the adult where the direction of the fracture line is usually downwards and backwards. Fractures of the neck of the condyle are usually of the ‘greenstick’ variety.

Before eruption, the developing permanent teeth occupy most of the maxilla and the body of the mandible. Eruption may be delayed and the involved teeth may subsequentlyh exhibit varying degrees of damage. Miniplates or transosseous wiring are used; the fixation must be placed near the lower border of the mandible.

Condylar fractures and injuries should always be viewed with concern in the growing child because of the possibility of impaired facial growth attributable to the injury.

FRACTURES OF THE MANDIBLE

An undisplaced crack fracture at the angle of the mandible or through the body may be treated without immobilization, but careful judgement is indicated in such cases.

Unless there is mechanical interference with mandibular movement, there is no indication for open reduction and derangement, both unilateral and bilateral condylar fractures or fracture dislocations respond well to muscle training exercises where the child is encouraged to close the mouth with the teeth in their correct occlusal relationship. If severe pain precludes such active treatment, a day or so of rest using a headcap and chinstrap may be necessary prior to the commencement of exercises. A unilateral fracture with occlusal derangement or a bilateral fracture that exhibits posterior displacement of the mandible and an anterior open-bite deformity will benefit from immobilization in centric relationship until stability of the occlusion is achieved; in practice this takes 2-3 weeks, after which active exercises are encouraged.

Care should be exercised in the placement of such plates in order to avoid damage to developing teeth.

When considering methods of immobilization of fractured jaws, Rowe (1969) found it convenient to subdivide patients into four groups based upon the state of the dentition at the time of injury.

Age in years Dental development
0-2 Eruption of the deciduous dentition is incomplete
2-4 Before the roots of the deciduous incisors show marked resorption, although many of the permanent teeth are partly formed.
5-8 Before resorption of the deciduous molars is advanced or the roots of the permanent incisors adequately developed
9-11 After adequate formation of the roots of the permanent incisors and first molar teeth, but before eruption of the premolars. Development of the paranasal air sinuses may predispose to fractures of the middle third of the facial skeleton

Infancy to 2 years old

Two categories of injury. The first is where the fracture is in the tooth-bearing part of the mandible and in practice this usually occurs in the region of the symphysis. The fracture should be treated essentially as an edentulous problem and the technique described by MacLennen (1956) is excellent. A prefabricated acrylic ‘Gunning-type’ lower splint with a thick lining of softened gutta-percha is pressed down over the lower teeth and alveolus following manual disimpaction and reduction of any displacement. The splint is retained in place by two circumferential wires placed one on either side of the fracture line.

Two to three weeks is generally sufficient to ensure union and any discrepancy in alignment is automatically adjusted by later bone growth.

The second type of fracture that has occurred proximal to the tooth-bearing area, i.e. through the angle, and it will be necessary to immobilize. In order to immobilize the mandible, the acrylic splint described above is modified to incorporate blocks in the molar region and these are hollowed out to accommodate soft gutta-percha on the alveolus, thus stabilizing the bite. Immobilization of the mandible may be effected by nasomandibular fixation as described by Thoma (1943) in which wires from the margins of the piriform aperture of the nose pass beneath the circumferential wires that secure the lower splint to the mandible.

When latoratory facilities and bone-plating systems are not available, open reduction and fixation of the fracture with a carefully placed transosseous wire may be carried out.

2-4 years old

Interdental eyelet wiring can be used. If there are gaps in the dentition an arch bar may be used. If there are gaps in the dentition an arch bar may be required or, if facilities are available, cap splints can be used. The latter are best avoided, since the cementing on of the splints and their subsequent removal and cleaning of the teeth necessitates considerable cooperation between operator and child.

If the fracture is within the tooth –bearing area of the mandible, a single one-piece lower cap splint, despite its other shortcomings, may often be the best method since immobilization of the lower jaw is avoided. If there is any doubt about the security of the cement fixation, this can be reinforced with the aid of two circumferential wires.

5-8 years old

It is between these ages that the greatest problems arise with regard to fixation of the mandible.

The anterior teeth are of littie or no use because the roots are either resorbed in the case of the deciduous teeth or incompletely formed in the permanent teeth.

These difficulties can generally be overcome by constructing partial maxillary and mandibular ‘Gunning-type’ splints with occlusal blocks, the exact construction being dependent on the precise location of the tooth loss.

The mandibular splint is secured by circumferential wires.

9-11 years old

In patients in this age group the development of the roots of the permanent incisor and first molar teeth has proceeded to the point where they can safely be employed for fixation, either by means of cap splints or arch bars.

Plating or transosseous wiring, particularly in the externally compound fracture, is also useful.

Clinical features

The clinical features of condylar fractures in children are similar to those in the adult.


Management

The primary aims of treatment of condylar fractures in children include the restoration of undisturbed joint function, a normal occlusion and avoidance of subsequent growth disturbance.

In children there is overwhelming evidence to support the conservative management of condylar fractures.

Rowe (1969) summarized the situation succinctly when he declared.

‘It is time to state unequivocally that there is no indication for the open reduction in the case of condylar fractures in children unless there is mechanical interference with mandibular movement.

In children fractures of the condylar neck are often the ‘greenstick’ variety.

When the fractured condyle is displaced, it usually undergoes remodeling under the influence of the physiological stresses and strains imparted by masticatory function.

The angular deformity of the neck of the condylar process is corrected and the reconstituted condyle frequently appears to be relocated in the glenoid fossa, even when there has been bilateral fracture dislocation.

Minor disturbance in occlusion will be rapidly corrected by further eruption of existing teeth and alveolar remodeling.

An unacceptable occlusal disharmony may occasionally be seen in unilateral condylar fractures and these can often be managed by means of a training flange or interarch elastic traction. If this management fails, a short period of immobilization is necessary.

Severe disturbances of the occlusion are most commonly encountered after bilateral fracture dislocation, with open bite and possible retro-positioning of the mandible.

Treatment in these instances should, as in the case of the adult, be by a conservative immobilization regime.

 

TREATMENT OF CONDYLAR FRACTURES

3 main schools of treatment have been evolved.

CONSERVATIVE:

Relies on used of rest and immobilization by IMF for a period of 7-10 days – to allow muscle spasm and telescoping to settle down in unilateral fracture dislocation.

IMF for 4 weeks – bilateral fracture dislocation with anterior open bite.

FUNCTIONAL

Emphasis is on Active Movement – it is important on fractures which one at risk causing Ankylosis therefore movement can prevent bony union traction. Devices can be attached to mandible to remedy Distoocclusion combined with active movements.

SURGICAL

Consist of exploring condylar fragment reducing it to normal anatomic relationship and then fixing it in that position.

CONSERVATIVE AND FUNCTIONAL TREATMENT

The goal of treatment is to allow bony UNION to occur when there is no significant displacement of condyle or in case of fracture dislocation, to produce an acceptable FUNCTIONAL PSEUDOARTHROSIS by reeducation of neuromuscular pathways.

Conservative management can be as simple as observation and soft diet:

Variable period of immobilization followed by intense physiotherapy.

If patient is able to establish and maintain normal occlusion with minimal amount of discomfort – no active treatment is required.

Patient encouraged to adhere to soft diet and close supervision is mandatory for any signs of occlusal instability deviation with opening increasing pain.

Any one of the signs indicate the conversion of non displaced fracture to displaced one requiring active treatment.

Active treatment is:

IMMOBILIZATION  involving:

IMF; arch bars, cycht wires, or splints.

Period of immobilization should be long enough to allow initial union of fracture segments.

Should be short enough to avoid complications such as muscular atrophy, joint hypomobility and ankylosis.

Currently, period of immobilization ranges 7-21 days. It can be increased / decreased depending on:

Age of patient, Level of fracture, Degree of displacement, Presence of additional fractures.

Crucial aspect of post immobilization treatment:

Consist of intense active physical therapy which allows for return of mandibular range of motion, functional movements that were hindered by injury and assists in neuromuscular system in adapting to alterations in occlusion, joint position or morphology.

Following the release of IMF guiding elastics used to direct mandible to maximal intercuspation.

Guiding elastics are placed lightly during day to promote increased mobility and more lightly at night to maintain occlusion.

Once occlusion remains stable, elastics discontinued and arch bars removed.


Studies which support conservative  management:

  1. 1947 Chalmer J. Lyons published their data on 140 cases of condylar fractures with average followup range of 5 years incidence of functional disturbance was 5.8%.
  2. 1952 McLENAN followed 180 condylar fracture for 14-37 months with a complication rate of 20%.
  3. Functional disturbances such as limitation of lateral excursions. Deviation of jaw to affected side on opening clicking of joint on fractured side.

INDICATIONS FOR CONSERVATIVE MANAGEMENT OF CONDYLAR FRACTURES

Young patients with maximum remodelling potential:

  1. In young patients under the age of 12 years. Bony union and adaptive remodelling will produce a functional condyle with its head restored to glenoid fossa even in cases of severe fracture distraction. In view of excellent remodelling potential and increased hazard to 7th cranial nerve surgery is usually contraindicated.
  2. Adult dentate patients with unilateral fracture soft diet for 2-3 weeks. 4 weeks of immobilization.
  3. Intracapsular fractures : Immobilization for 7-10 days and active movement should be encouraged as soon as possible.
  4. Adult dentate patients with bilateral fracture.
  5. Edentulous patients.

SURGICAL MANAGEMENT OF CONDYLAR FRACTURES

Objective is to reposition fractured condyle on near to its anatomical location as possible.

ZIDE and KENT (1983) have outlined the indication for open reduction.

ABSOLUTE INDICATIONS FOR BOTH CHILDREN AND ADULTS

  1. Displacement of condyle into middle cranial fossa.
  2. Impossibility of restoring occlusion by closed reduction.
  3. Lateral extracapsular displacement of condyle.
  4. Invasion by foreign body (Gun Shot wounds).

RELATIVE INDICATIONS

  1. Bilateral condylar fractures associated with comminuted mid facial fractures. Mandible is treated first by ORIF to provide a stable platform on which remaining midfacial fractures are repaired.
  2. Bilateral condylar fractures associated with gnathologic problems such as retrognathia, prognathism open bite deformity.
  3. Bilateral condylar fractures in edentulous patients where splinting is impossible because of severe alveolar bone atrophy.
  4. When IMF is contraindicated for medical reasons:
  • Seizure disorders, Psychiatric problems, Alcoholism.
  • Refractory behaviour / mental retardation secondary to neurologic injury. COPD upper airway resistance from IMF.

VARIOUS APPROACHES FOR TEMPORO MANDIBULAR JOINT

1) Preauricular.   2)Endaural   3) Postauricular.  4)Alkayat and Bramley. 5) Submandibular.   6) Rhytidectomal.  7) Intraoral.

Prime determinants in selection of approach are:

  • Location of fracture, Degree of displacement.

If fracture is intracapsular

High on condylar neck – Preauricular / Endauricular approach preferred.

Advantages:

  • Better access, Greater visibility of fracture site, Ease of placement of fixation devices, Ease of manipulation of soft tissues within joint.

Disadvantages:

  • Possibility of damage to facial N, Presence of facial scar.

Fracture subcondylar – Submandibular approach. Possible damage to marginal mandibular nerve with weakness of dedpressor muscles of lower lip.

Intraoral approach:

Advantages:

  • Visualization of fracture reduction and occlusion simultaneously.
  • Minimal risk of damage to facial N.
  • Avoidance of unesthetic facial scar.

Disadvantages:

  • Limited access in highly subcondylar and condylar neck fractures.
  • Difficulty in placing certain fixation devices.

REDUCTION OF FRACTURE SEGMENT:

In case of minimal- Displacement à Reduction accomplished by manipulating proximal segment into position with hemostat.

Condylar segment is –  More severely displaced à Reduction becomes difficult because of the pull of lateral pterygoid.

Distraction of mandible on inferior direction via clamp, towel clip, or S.S. wires placed at angle aids in visualizing and manipulating condylar segment. Condylar segment is then grasped and reduced into proper location atop mandibular ramus.

Stewart ad Bowerman (1991) suggested inserting a Moule pin into condyle to assist in positioning this small fragment.

Once the fragment is reduced and secured, pin removed prior to wound closure.

METHODS OF IMMOBILIZING CONDYLE:

  1. GLENOID FOSSA-CONDYLE SUTURE

Wassmund (1935) described drilling or small hole through lateral edge of glenoid fossa and related edge of condylar articulating surface. A chonric categut future was looped through and tied.

  1. TRANSOSSEOUS WIRING

Described by Thoma (1945); Messer (1972).

  1. BONE PINS

Thoma (1945) placed pins in condylar neck and zygomatic bone which were connected with external bar and universal joint.

Archer (1975) Insertion of pins into condylar head and neck.

  1. KIRSCHNER-WIRE (K-WIRE)

Stephenson and Graham (1952) drilled vertically from main mandibular fragment avoiding inferior alveolar bundle to that it enters fracture interface and further inserted into condyle.

  1. INTRAMEDULLARY PINS

PETZEL (1982) à Use of intramedullary screw transfixing distal and proximal segments.

KITAYAMA (1989) à

  1. BONE PLATING

Robinson and Yoon (1960) à 2-hole plate.

Koberg and Momma (1978) à 4-hole plate.

Currently majority of open reduction are secured using RIGID FIXATION involving miniature bone plating and monocortical screws.

SPECIFIC TREATMENT OF CONDYLAR FRACTURES

  • Young patients with maximum remodeling potential:
  • In patients under the age of 12 years Bony union and Adaptive Remodelling will restore a functional condyle regardless of treatment.
  • Surgical reduction is contraindicated in children because of excellent remodelling potential and increased hazard to 7th cranial nerve.
  • Treatment consist of IMF for 7-10 days followed by active movement of the joint to reduce the formation of scar tissue and prevent ankylosis.
  • Ankylosis prevents anterior and inferior distraction of mandible by its soft tissue envelope. The opposite condyle deposits appositional bone along its posterior and superior aspects. This process results in shortened ramus on ipsilateral side and normal / elongated ramus on contralateral side.
    • ADULT DENTATE PATIENTS WITH UNILATERAL FRACTURE

If patient able to attain normal centric occlusion in unilateral fracture / fracture dislocation, treatment protocol consists of:

  1. Advocating soft diet for a period of 2-3 weeks.
  2. Put the patients on NSAIDS.
  • Advising patient to take care to avoid impact to another area.

If this regime is accompanied by excessive pain / if the patient not able to attain normal occlusion then IMF for 7-10 days advised.

If there is any tendency of minimally displaced fracture to be converted to fracture dislocation or if there is real risk of further trauma to the area.

Then IMF for 4 weeks should be given to ensure union in already existing good position.

  • Sometimes it is feasible to delay IMF for 48 hours during this time spasm of pterygomassetric shrig will often settle and allow a minor occlusal discrepancy to remedy itself.
  • It should be remembered that teenage patients have greater propensity or adaptive remodelling to restore a functional condyle than adult patients. This persuades operator towards more conservative regime.

Surgical reduction and fixation by bone plating for unilateral fractures is absolutely indicated in following circumstances:

  • Impossibility of obtaining adequate occlusion by closed reduction due to locking of condylar fragment / in true lateral fracture dislocation.
  • Fracture dislocation of condyle into middle cranial fossa.
    • ADULT DENTATE PATIENTS WITH BILATERAL FRACTURES
      1. If occlusion is normal then institute IMF for 3-4 weeks as the risk of converting deviated/displaced fracture to dislocation is significantly greater with bilateral fracture than with unilateral fractures.
      2. If anterior open bite is present institute 4 weeks of IMF. After this period patient taken out of fixation and carefully watch while still maintaining the means of fixation (arch bar). If relapse is found to occur then further 2 weeks of IMF instituted.
  • If degree of anterior open bite is severe at the outset of treatment / fracture has been delayed then posterior distraction by gagging open the molar regions should be considered. This overdistraction tends to stretch any developing scar tissue and reach the tendency to relapse.

Overdistraction of molars can be achieved by one of the following methods:

  1. Thickening of molar regions of cap splints.
  2. small gutta percha blocks placed between post molar teeth in combination with arch bars.

If there is tendency towards recurrence of anterior open bite after adequate period of immobilization then.

Mild traction by bands put in place for a further period of 2-4 weeks.

Absolute indication for surgical reduction are.

If there is associated comminuted midface fracture, then it is necessary to reconstitute a mandibular platform.

EDENTULOUS PATIENTS:

  • In unilateral fractures / there is reduced need for treatment on there is slight discrepancy in bite which can be compensated by prosthetic means.
  • In bilateral cases:
    • Gunning splints employed for establishing vertical dimension.
    • Patients own dentures may be modified to be used as splints by provision of cleats some means of attaching denture to underlying skeletal bases.

Splints are secured by either piriform aperture wiring / circumzygomatic wiring.

Indication for surgical reduction in bilateral edentulous condylar fractures:

  • Splint is unavailable.
  • When denture are lost.
  • When condition is too painful for prosthetic manipulation.

COMPOUND FRACTURES

  • There is risk of postoperative infection, and development of fibrous ankylosis.
  • Any lacerations in condylar area should be carefully explored, subjected to lavage and site drained, if there is a dead space to prevent hematoma formation prophylactic antibiotics are indicated.
  • If there is comminution of condylar bone, removal of non viable bone fragments indicated at the time of exploration and closure. This may even necessitate condylectomy in grossly contaminated and comminuted cases.
  • After condylectomy there is premature posterior contact on that side so short period of IMF for 10 days necessary to allow spasm of pterygomassetric sling to settle.

 

 

Posted in Trauma

Fractures of Zygomatic complex and Orbit

Fractures of Zygomatic complex and Orbit

Introduction

Zygomatic bone forming the lateral wall of the orbit and giving prominence to the cheek is commonly involved in facial injuries, representing either the most common facial fracture or the second in frequency after nasal fractures. All zygomatic complex fractures involve the orbital floor and therefore understanding of the anatomy of the orbit is essential for management of these fractures.

The orbital skeleton represents an important anatomic crossroads because of its intimate relationship to the central nervous system, the nose, the paranasal sinuses, the face and the structures related to the support and function of the eye. Maxillofacial injuries of the middle third of face commonly destroys the integrity of the orbital skeleton ranging from blow out to complex comminution. These type of injuries often leads to orbital dysfunction and incapacitating visual dysfunction. The fractures of the orbit are to be approached with caution and it requires precise knowledge of its anatomy.

Since the gross shape of the face is influenced by largely by the underlying bone, the zygoma plays an important role in facial contour. Its disruption also has great functional significance because it creates impairment of ocular and mandibular function. Therefore for both cosmetic and functional reasons, it is imperative to diagnose and adequately treat zygomatic complex fractures.

 

Frequency

The fracture of this region is of higher incidence. The incidence, aetiology, age and sex predilection varies depending on the region studied due to social, economic, political factors. Male to female ratio is of 4:1. The peak incidence is during 2nd and 3rd decade.

Orbital fractures are present in all midface fractures with the exception to le fort I, the alveolar process fracture, the isolated Zygomatic arch fracture and the simple nasal bone fracture.      Orbital fractures are present in approximately in 90% of all midface fractures either as separate or combined injuries.

 

Aetiology

The etiological factors road traffic accidents and interpersonal violence. If the fracture is due to domestic violence, left zygoma is commonly involved due to greater incidence of right handed persons. In road traffic accidents both sides were equally involved. Bilateral fractures were uncommon and it usually results from road traffic accidents.

Factors contributing to the high incidence of these fractures include

(i)      Zygoma being a prominent position relative to the rest of the facial skeleton.

(ii)     A force of only 50 to 80gm is enough to create a fracture in this region of the face.

(ii      As  society become more mobile and  urbanised,  motor  vehicles accident has
increased  in incidence of zygomatic and orbital injuries.

Surgical anatomy

Anatomy of the zygomatic complex.

The Zygoma is a strong bone that gives the prominence of the cheek. It forms the lateral wall and floor of the orbit. It also forms the boundary for temporal and infratemporal fosssae. It is roughly equivalent to four sides of a pyramid with four processes – the temporal, orbital, maxillary and frontal. It articulates with the maxilla, sphenoid, frontal and temporal bones. These articulating bones play a significant role in preventing extensive injury to the zygoma and the face.  The zygomatic process of the temporal bone acts as a buttress for the Zygoma against posteriorly directed forces.  The Zygomatic process of the frontal bone and the greater wing of the sphenoid bone provide resistance to vertically directed forces upon the zygoma.

The lateral surface is convex and temporal surface is concave. The orbital surface together with greater wing of sphenoid and orbital surface of maxilla form the lateral wall of orbit and floor of the orbit. The temporal process is a narrow, relatively thin projection that articulates with the zygomatic process of the temporal bone to form the zygomatic arch.

Zygomatico frontal and Zygomatico temporal nerves, branches of the trigeminal nerve, exit from the body of the zygoma to provide sensation to the cheek and anterior temporal region.  The lateral surface gives origin to zygomaticus muscles and levator labii superioris muscle.

The infra orbital nerve, also a branch of fifth nerve passes through the floor of the orbit, lying in the infraorbital groove, and exit through the infraorbital foramen, which is located in the anterior wall of the maxilla 5 to10 mm below the infraorbital rim. Orbito zygomatic fractures occur in close proximity to these nerves, and injuries in this region of the face may disrupt the sensation provided by these nerves. Masseter muscle attaches to the concave temporal surface of the zygoma and the arch. The temporalis fascia is attached to the frontal process of the zygoma and the zygomatic arch. This fascia produces resistance to inferior displacement of a fractured segment. The coronoid process of the mandible is medial to the zygomatic arch, so any medial displacement of the arch results in mechanical interference and the ensuing trismus.

Anatomy of the orbit

The orbit consists of the bony framework with periocular soft tissues, globe and the protective soft tissue apparatus.

Bony Orbit

The orbit is a unique bony structure that has the primary purpose of housing and protecting the globe. By 5yrs 85% of the growth of the orbit is completed and growth is completed between 7yrs and puberty. The orbit is a four-sided pyramid with its apex at the optic foramen and base formed by orbital rim.

The bony orbit is formed by union of seven bones: frontal, ethmoid, Sphenoid, maxilla, Zygoma, lacrimal and palatine bones.  The orbital rim is very solid and it protects the eye from many injuries. The rim comprises of the frontal bone superiorly, laterally and medially, the zygomatic bone laterally and inferiorly, the maxillary bone inferiorly and medially.

The orbital wall consists of a roof, medial and lateral walls, and a floor. The orbital walls vary in thickness and strength. Fractures of the anterior and middle third of the orbit are common, with the maxillary sinus and ethmoidal air cells acting as shock absorbers and acute volume expansion compartments. Posterior third fracture of the orbit is rare and this commonly results in blindness.

The roof of the orbit is triangular and is formed by the orbital plate of the frontal bone, and the lesser wing of sphenoid.  The posterior extent of the roof ends at the optic canal. The roof of the orbit is thin and it separates it from anterior cranial fossa. In the elderly, the orbital roof may become resorbed, resulting in the periorbita becoming fused to the overlying duramater. Anterolaterally is a smooth, broad fossa for the lacrimal gland. Medially 4 mm behind the orbital rim lies the trochlear fovea, where the cartilaginous pulley inserts for the superior oblique muscle tendon. Supraorbital notch is present at the junction of the lateral 2/3rd and medial 1/3rd through which supraorbital nerves & vessels pass.

The lateral wall of the orbit is composed of the greater wing of the sphenoid bone and the frontal process of the zygoma. This is the strongest wall and it might fracture along the thinnest portion along the suture line. This wall is angled at 45o to the medial wall and 90o to the other side lateral wall. This wall is separated at the apex from the roof and the sphenoid by superior orbital fissure. Whitnall’s tubercle is located internally 5mm behind the lateral orbital rim and approximately 1cm below the frontozygomatic suture. This gives attachment to the lateral horn of the levator aponeurosis, lateral canthal tendon of the eyelid, lockwood’s suspensory ligament of the globe and check ligaments of the lateral rectus.

The floor is formed by the orbital surface of maxilla, zygoma and a small portion of palatine bone. The floor is delineated posteriorly by sphenomaxillary fissure. The infraorbital groove originates from the middle of the inferior orbital fissure about 2.5 to 3 cm from the inferior orbital rim. This is converted into a canal halfway anteriorly. It exists via infraorbital foramen 5mm below the lower orbital rim. It transmits the infraorbital nerve and vessels. The floor of the orbit is usually 0.5 mm thick and the thinnest portion is medial to the infraorbital groove and canal.

The medial wall of the orbit is more complex and it is about half the height of the lateral wall as the floor is inclined upwards at 45o to meet the medial wall. The medial wall is made up of the orbital plate of the ethmoid bone (lamina papyracea), the angular process of the frontal bone antero-superiorly, the lacrimal bone antero-inferiorly and lesser wing of sphenoid posteriorly. The orbital surface of ethmoid is extremely thin (0.2 to 0.4 mm) forms the largest section of the medial wall.  The medial wall is frequently involved in orbito-zygomatic fractures, primarily in the area of the thin lamina papyracea.  Posteriorly and superiorly the optic canal is located within the strong lesser wing of sphenoid. At the junction of the medial wall and roof about the level of optic canal two or three foramina are present which transmit branches of ethmoidal vessels and nerves. The lacrimal sac is tucked into the medial rim between the lacrimal and maxillary bones. This is lined anteriorly and posteriorly by lacrimal crests which gives attachment to the medial canthal ligament, Lockwood’s suspensory ligament. The medial wall is aligned parallel to the anteroposterior axis or median plane of the skull and is extremely fragile because of the presence of the adjacent ethmoidal air cells.

Rontal et al 1979 studied various skulls and gave the mean distance of locating the vital structures in relationship to identifiable fine bone margins.

  1. Infraorbital foramen to the midpoint of the inferior orbital fissure is 24mm.
  2. Anterior lacrimal crest to anterior ethmoidal foramen is 24 mm.
  3. Anterior lacrimal crest to medial aspect of the optic canal is 42 mm.
  4. Frontozygomatic suture to the superior orbital fissure is 35 mm.
  5. Supraorbital notch to the superior orbital fissure is 40 mm.
  6. Supraorbital notch to the superior aspect of the optic canal is 40 mm.

Thus it is safer to commence the exploration from the lateral wall of the orbit. The maximum safe distance of safe exploration is 25 mm from the inferior orbital margin and frontozygomatic suture.

Orbital apex

The confluence of the bony walls forms the orbital apex, which is more complex due to the presence of superior and inferior orbital fissure and the optic foramen.

The anterior border of the inferior orbital fissure is approximately 20 mm from the infra orbital rim, so orbital floor exploration should not proceed beyond 20 mm. Structures passing through the inferior orbital fissure include zygomatic nerve, inferior orbital vein to pterygoid venous plexus and some parasympathetic from sphenopalatine ganglion.

The superior orbital fissure runs between the greater and lesser wing of sphenoid. The lacrimal, frontal, nasociliary nerve branches of trigeminal nerve, oculomotor nerve, abducent nerve, trochlear nerve, superior and inferior ophthalmic veins pass through this fissure. These groups of neurovascular structures pass immediately from the cavernous sinus to the superior orbital fissure. This accounts for the optahalmoplegia when injury occurring to this space.

The optic foramen is just medial to the superior orbital fissure and transmits the optic nerve and ophthalmic artery. This is about 45 mm posterior to the supraorbital notch. The muscular cone surrounds the posterior globe and inserts into the orbital apex forming a tendonous ring. The ring surrounds the optic foramen and part of superior orbital fissure including the oculomotor and abducens. Trochlear nerve runs outside this cone and is more thus increasing the risk of superior oblique muscle palsy.

The soft tissue of the orbit

The structures within the orbit can be viewed as a globe surrounded by a muscular cone, in turn surrounded by protective fat and attachments to bony system by suspensory ligaments and attachments.

Lining of the bony orbit is a layer of periosteum known as the periorbita, which becomes the orbital septum superiorly and inferiorly at the orbital rim as it extends into the eyelids.

Interior to the periosteum is a layer of periorbital fat. The fat contains many fibrous septae, which can become trapped in blow out fracture. The fat and the periosteum outside the globe and the extraocular muscles are called the extraconal space.  The intraconal space is formed by the extraocular muscle cone and the fascia lining the extraocular muscles. It contains the optic nerve and the intraconal fat.

The eye is protected within the orbit by complex arrangements of fascia and ligaments. Lockwood’s suspensory ligament supports the globe vertically and it has medial and lateral attachments. Medial it is attached to the anterior and posterior lacrimal crest while laterally it is attached to the whitnal’s tubercle. A fascial sheath called Tenon’s capsule surrounds the globe posterior to the cornea and invests around the extraocular muscles. Lateral and medial folds of the Tenon’s capsule form the lateral and medial check ligaments, which resist the posterior pull of the extraocular muscle. Some part of this fascia fuses with the fascia surrounding the inferior rectus and the inferior oblique muscles to form the suspensory ligament. The suspensory ligament prevents the dropping of the globe in case of fracture of the orbital floor.

The six extraocular muscles that form the muscle cone and move the globe are medial, lateral, superior and inferior rectii muscles, superior and inferior oblique. The eyes normally has the capability of moving along a vertical axis, horizontal axis, both axes simultaneously (oblique motion) and rotational axis (torsion). The seventh extraocular muscle Levator palpebrae superioris runs immediately above the muscular cone and it does not move the globe. It invests in the upper eyelid and aids in its retraction. All the extraocular muscles originate from the orbital apex region as a musculo tendinous ring except for the inferior oblique muscle, which originates from medial part of inferior orbital rim. All extraocular muscles are supplied by oculomotor nerve except for superior oblique and lateral rectus. Superior oblique muscle is supplied by trochlear and lateral rectus is supplied by abducens. For normal vision both the eyes requires co-ordinated action. Losses of co-ordination as a result of nerve damage, muscle entrapment or oedema results in diplopia.

The Globe

The eye is the organ of visual perception and much of the functional anatomy and physiology of the midface is designed to protect and service the globe.

The eye is more or less round and it projects about 3 mm anterior to the inferior and lateral orbital rims. A very thin layer of conjunctival membrane coats the inner lid surfaces and the visible part of the eye up to the cornea which is covered by bulbar conjunctiva. The eyeball is about 2.5 cm in length and is surrounded by three layers: the fibrous layer, vascular layer and the inner retinal layer.

The sclera makes up the posterior five sixths of the tough fibrous layer. The anterior portion is made up of the clear cornea. The cornea is vulnerable to injury and drying out and it should be protected during maxillofacial procedures.

The middle layer is vascular and pigmented. It is composed of the choroid posteriorly and the ciliary body and iris anteriorly. The ciliary body secretes the aqueous humor. Its obstruction results in glaucoma. The pigmented iris is a diaphragm that projects form the ciliary body. The central aperture of the iris is the pupil. Inflammation of the iris and ciliary body as a result of trauma results in traumatic mydriasis (dilation). The lens is positioned posterior to the iris by suspensory ligaments attached to the ciliary process. The lens is biconcave, avascular and transparent. Posterior to the lens is the vitreous humor which comprises four fifth of the eye. It is a clear gel. The inner coat of the eye is the retina, which contains the pigmented cells and outer neural cells. The blood supply to the retina is through the central retinal artery, which travels with optic nerve.

Anatomy of the lid

Eyelid anatomy is necessary for clinical assessment and for various surgical approaches. The lids and adnexa serve to protect the eye and as well as lubricate and clean the corneal surface.

The eyelids are composed of three layers: the outer skin, the middle orbicularis layer and the innermost is the tarsal plate, which is lined by vascular palpebral conjunctiva.  The tarsal plate is semilunar and forms the skeleton of the eyelids. At the lid margin posterior to the eyelashes is the grey line junction of the skin and conjunctiva. The upper eyelid has levator muscle attached to the tarsal plate. The orbital septum continuation of the periorbita is attached to the tarsal plate. The eyelids are attached to the bony orbit medial and laterally by medial and lateral canthal tendon. The preservation of the general contour and the integrity of the lid margins are of greatest importance both aesthetically and functionally and the maintenance of the canthal attachments in correct anteroposterior and horizontal planes is essential for normal outline of the palpebral fissure.

 

BIOMECHANICS OF ORBITO ZYGOMATIC FRACTURES

The fracture patterns of any bone depends on several factors like the areas of weakness and the direction and magnitude of the force. Fracture lines thus created passes through the areas of greatest weakness of a bone or between bones. Thus any forcible blow coming in contact with the prominent and sturdy zygoma, is transmitted to its four weaker articulating surfaces, the fronto- zygomatic, Zygomatico-maxillary, Zygomatico-Sphenoid, and zygomatico-temporal sutures as well as to the adjacent weaker bones that articulate with the zygoma.  Because of the sturdier nature of the Zygoma and thin bones surrounding it, it is rare to find a fracture of the body of the zygoma itself.

Ellis mentioned, inferior orbital fissure is the key to knowing the location of fracture lines occurring during zygomatic complex fracture. Three lines of fracture extend anteromedially, superolaterally and inferior direction from the inferior orbital fissure.

1.) One fracture line extends antromedially along the orbital floor through the orbital process of the maxilla, towards the infraorbital rim, frequently passing through the infraorbital rim onto the anterior maxilla superior or medial to the infraorbital foramen, as well as extending laterally and inferiorly on the maxilla under the Zygomatic buttress of the maxilla.

2.) A second fracture line from the inferior orbital fissure runs inferiorly through the infra temporal aspect of the maxilla and joints the fracture line from the anterior aspect under the zygomatic buttress.

3.) The third fracture line extends superiorly from the inferior orbital fissure along the lateral orbital wall posterior to the rim usually separating the zygomatico-sphenoid suture and frequently extending superiorly, laterally and anteriorly creating a fracture in the area of the frontozygomatic suture at the lateral orbital rim.

An additional fracture line classically occurs at the zygomatic arch, usually 1.5mm posterior to the zygomatico temporal suture line (middle of the zygomatic arch).  The fracture lines that extend from the inferior orbital fissure are frequently comminuted, except for the fracture in the area of the fronto zygomatic suture, which is usually a linear fracture.

Orbital blow out fracture, are fractures of the orbital floor in which the orbital rim remains intact. The mechanism involved is a sudden increase in intraorbital pressure from a force.  This sudden increase in intraorbital pressure generally causes the weakest portion of the orbital floor to fracture, thus preventing orbit from rupturing. This usually fractures medial to the infra orbital groove about 2 cm posterior to the inferior orbital margin. As with injuries to the zygomatic complex, each injury to the bony orbit should be evaluated for variation from the classic location of fractures to the orbito zygomatic region, and a complete ophthalmologic examination should be performed.

In the pathogenesis of the orbito-zygomatic fracture, the pull of masseter and temporalis muscle must be over come at the fracture site for optimal stabilisation and bony healing. There will rotation of the zygomatic complex fracture about the vertical axis and horizontal axis, which will interfere with adequate reduction.

Bony resorption, is a major long-term complication of fracture management. In the case of orbito zygomatic fractures, maintenance of orbital volume is critical.  It has been demonstrated that one of most common cause of posttraumatic enophthalmos is displacement and resorption at the fracture site. A critical assessment of the clinical studies on orbito zygomatic fracture shows that

1) A small subset of orbito zygomatic fractures that can be treated with reduction only.  This includes only low velocity, non comminuted fractures that are stable post reduction.  Close follow up is needed to detect delayed displacement and deformity.

2) High velocity injuries with communication and displacement, mandate open reduction and internal rigid fixation…

3) Miniplate or microplate fixation is the best tolerated and provides optimal rigid stabilisation, with the lowest rate of attendant complication.

Classification

Many classifications have been proposed. These include Mclndoe (1941), Moore and ward (1949), Rowe (1960), Knight and North (1961), Rowe and Killey (1968), Himmelfarh (1968), and Spiessl & Schroll (1972). The classification systems were based on the location and the type of displacement seen. Classifications were also based on the amount of stability after reduction and the need for fixation.

Classification of Zygomatic complex fractures     Knight & North 1961

Based on direction of displacement in waters view radiograph.

Group I       Nondisplaced fractures – cases in which there is no clinical or radiographic evidence of displacement; no treatment required.

Group II     Arch fractures – A pure fracture of the zygomatic arch. The classical three fracture lines produce a ‘V’ shaped deformity.

Group III    Unrotated body fractures – Caused by a direct blow to the zygomatic prominence. Zygoma is driven posteriorly and medially, producing a flattening of the cheek. Water’s view shows a displaced infra orbital rim inferiorly and medially at the buttress.

Group IV    Medially rotated body fractures – Caused by a blow from above the horizontal axis of the zygoma. Bone is driven medially, inferiorly and posteriorly with rotation. The X rays shows displacement inferiorly at the infraorbital rim and either outward at the malar buttress or inward at the frontozygomatic suture.

Group V     Laterally rotated body fractures – Caused by a blow below the horizontal axis of the bone. Zygoma is displaced medially and posteriorly with lateral rotation. The radiograph indicates upward displacement at the infraorbital rim and lateral displacement at the frontozygomatic suture.

Group VI    Complex fractures – these have additional fractures across the body of zygoma.

Classification of Zygomatic complex fractures      Rowe & Kiley     1968

Modified North & Knight classification by giving consideration to the periosteal envelope of the bone and adequacy of the bony apposition at the fracture interface.

Classification of Zygomatic complex fractures      Yanagisawa        1973

Group I       Nondisplaced fractures – no treatment required.

Group II     Arch fractures – A pure fracture of the zygomatic arch.

Group III    Medial or lateral rotation around a vertical axis.

Group IV    Medial or lateral rotation around a longitudinal axis.

Group V     Medial or lateral displacement without rotation.

Group VI    Isolated rim fracture.

Group VII   All Complex fractures.

Classification of malar fractures          Spiessl & Schroll 1972

Type I                       Zygomatic arch fracture

Type II                      Zygomatic complex fracture – – no significant displacement

Type III                     Zygomatic complex fracture – – partial medial displacement (kinking at the FZ suture)

Type IV                     Zygomatic complex fracture – – total medial displacement. (Complete ≠ of FZ suture).

Type  V                     Zygomatic complex fracture – – dorsal displacement. (2 ≠ sites in zygomatic arch).

Type VI                     Zygomatic complex fracture – – inferior displacement.

Type VII                   Zygomatic complex fracture – – Comminuted fracture

 

Classification of Zygomatic complex fractures      Larsen & Thompson   1978

Group I       Nondisplaced fractures requiring no treatment – During the initial evaluation, if there is any doubt about stability, revaluation should occur 1 week after injury.

Group II     All fractures requiring treatment –  This is further subdivided into fractures that are stable and fractures that are unstable after reduction.

Classification of malar fractures          Eberhard Krüger 1986

  1. Fractures of Zygoma
  2.   No significant displacement
  3.   Partial medial displacement
  4.   Total medial displacement
  5.   Dorsal displacement
  6.   Inferior displacement
  7.   Comminuted fractures
  8. Fractures of Zygomatic arch
  9. Complex fractures
  10.   Centrolateral midface fractures
  11.   Zygomatico-maxillary fractures
  12.   Zygomatico-mandibular fractures.

 


Classification of Orbital fractures        Rowe & Williams        1985

Zygomatic complex fractures

  1. Fractures stable after elevation
  2.   Arch only (medially displaced).
  3.   Rotation around vertical axis
  4. i) Medially
  5. ii) Laterally
  6. Fractures unstable after elevation
  7.   Arch only (inferiorly displaced).
  8.   Rotation around horizontal axis
  9. i) Medially
  10. ii) Laterally
  11.   Dislocation en bloc
  12. i)  Inferiorly
  13. ii) Medially

                                    iii) Postero-laterally

  1.   Comminuted fractures

Isolated fractures of the orbital rim

  1. Superior rim
  2.   Lateral third (lacrimal recess)
  3.   Central third (supraorbital nerve)
  4.   Medial third (frontal sinus)
  5. Inferior rim
  6.   Central third (infraorbital nerve)
  7.   Medial third (inferior oblique margin)
  8. Medial rim
  9.   Medial canthal ligament
  10.   Lacrimal passage
  11. Lateral rim
  12.   Lateral canthal ligament
  13.   Suspensory ligament

Isolated fractures of the orbital wall

  1. Roof
  2.   Anterior fossa
  3.   Levator palpebrae superioris / superior rectus
  4.   Frontal sinus
  5. Floor
  6.   Antrum
  7.   Infraorbital nerve & vessels
  8.   Inferior rectus / inferior oblique
  9. Medial wall
  10.   Lacrimal sac & nasolacrimal canal
  11.   Ethmoidal sinus
  12.   Medial rectus
  13.   Suspensory ligament
  14. Lateral wall

                        Superior orbital fissure & related structures.

Complex comminuted fracture

 

Classification of zygomatic fractures   Zingg et al 1992.

Type A                 Incomplete fractures

Isolated lateral orbital rim

Isolated inferior orbital rim

Type B                 Monofragment malar or classic tetrapod fractures

Type C                 Multifragmented fractures

The various types of fractures are differentiated principally according to the type of fracture dislocation.

Clinical features

Several signs and symptoms accompany zygomatic fractures. The presence and magnitude depends on the extent and type of zygomatic injury. The signs and symptoms accompany zygomatic fractures:

Periorbital ecchymosis and oedema, Flattening of the malar prominence, flattening over the zygomatic arch, pain, ecchymosis over the maxillary buccal sulcus, deformity of zygomatic buttress of the maxilla, deformity of the orbital margin, trismus, abnormal nerve sensibility, epistaxis, subconjunctival ecchymosis, crepitation from air emphysema, displacement of palpebral fissure, proptosis, unequal pupillary levels, diplopia, and enopthalmus.

In total medial displacement, the orbital rim is completely severed at the fronto zygomatic suture.  The Zygoma is depressed in the orbital region as well, leading to reduction in size of the orbit.  This can lead to exophthalmos, which may be aggravated by further haematoma.  On the other hand with a defect of the floor of the orbit, orbital tissue may prolapse into the maxillary sinus so that enophthalmos would result due to medial displacement.  The telescoping intrusion of the Zygoma into the orbit and maxillary sinus can lead to incarceration and injury of orbital fatty – tissue and musculature causing diplopia as a result of disturbances of mobility.  As the medial fracture lines is always in the region of the infra orbital nerve, that nerve is pinched or torn in medial displacement fractures.

Duker and scheduble (1974) found loss of sensation in 92% of isolated fractures of the Zygoma.  Narrowing of the maxillary sinuses and orbit are seen in radiographs of the paranasal sinuses in this type of fracture.

When forces impact frontally, the zygoma can be displaced dorsally.  This leads to compression of the Zygomatic arch, which fractures at two points.  The resulting enlargements of the orbit in the dorsal direction and the possibility of prolapse of the orbital tissue into the maxillary sinus can lead to enophthalmos and double vision.

Inferior displacement arises when force impinges on the body of the Zygoma obliquely from above. Temporal fascia prevents inferior displacement of the zygoma by its broad attachment.  The frontal process of the Zygomatic bone may be titled dorsally or forward, In this type of displacement, the orbital cavity is enlarged.  This leads to exophthalmos with the eye lowered and double vision.  Sagging of the lateral wall of the orbit leads to displacement of the palpebral fissure in the lateral region in a caudal direction (antimongoloid).

The total medial fracture dislocation can lead to restriction of mouth opening as a result of impingement of the coronoid process on the zygoma.

Management algorithm for zygomatic complex fracture

Assessment: –

History: –

The mechanism of injury is of primary importance to aid in the location of fracture. High velocity injury is more likely to have displaced comminuted fractures than with low velocity injuries.

In the presence of high velocity facial trauma, the index of suspicion should be higher for associated injuries like occular injuries or possible cervical spine damage.

A direct lateral blow would often result in isolated arch fracture or an inferiorly displaced zygomatic complex fracture. A frontal blow usually is associated with posteriorly and inferiorly displaced fracture.

The patient might usually complaints of pain, periorbital oedema, and ecchymosis. There might be paresthesia or anaesthesia over the area supplied by infra orbital nerve. Patients might complaint of restricted mouth opening when the arch is displaced medially. There is frequently epistaxis and diplopia may result from the entrapment of muscles and displacement of the globe. This becomes obvious within 2 to 3 days.

Physical Examination:

Ecchymosis and oedema are the most common early clinical signs present. Flattening of the cheek is seen in depression of the malar eminence. Downward displacement of the zygoma produces an antimongoloid slant to the lateral canthus, enophthalmos and accentuation of the supra tarsal fold.

Palpation is the hallmark in the diagnosis of fracture displacement. The zygoma, zygomatic arch and the entire rim of the orbit is palpated for tenderness, step defect or separation of the sutures. The zygomatic buttress is also palpated.

The mandibular movements are evaluated to rule out the impingement of the zygomatic arch over the coronoid process.

A complete ophthalmological examination is critical.  This includes an examination of visual acuity, pupillary response to light, occular movements, globe position and a fundoscopic examination for evidence of hyphema or retinal detachment.

Deficits in facial sensation, particularly within the distribution of the infra orbital nerve are identified.

Radiographic Studies:-

History and physical examination usually establish the diagnosis of the zygomatic fracture. Radiographs are helpful in confirming, medicolegal documentation and in some cases to establish the extent of bony damage.

Useful plain facial radiographs include the submento vertex view, waters’view, Caldwell view, lateral views, tomograms and computed tomography.

Waters’ view is the best radiograph for evaluation of zygomatic complex fractures. It is posteroanterior projection with head positioned at 27o to the vertical plane. This projects the inferior orbital rim, the maxillary sinuses and the lateral orbits. This also aids in diagnosing the orbital blow fractures.

The Caldwell view most accurately assesses the zygomaticofrontal suture.

Submentovertex “jug handle” view is helpful in visualising the fractures of the zygomatic arch and malar projection.

Continued suspicion of an orbito zygomatic fracture based on the radiographic data mandates thin slice CT Scanning in the axial and coronal planes.  This is critical in determining degree of displacement as well as associated orbital fractures.

ZYGOMATIC COMPLEX FRACTURES – MANAGEMENT

Since Duverney 1751 used closed reduction for medially displaced zygoma fracture various treatment modalities have been advocated. The schemes of treatment for zygomatic complex fracture range from

  1. Observation (No treatment).
  2. Indirect reduction with
  3. No fixation
  4. Temporary support
  5. Direct fixation
  6. Indirect fixation
  7. Direct reduction and fixation
  8. Immediate reconstruction by bone grafting for orbital floor fractures
  9. Delayed reconstruction by osteotomy and grafting
  10. Late restoration of contour by onlay grafts.

The optimal time for surgery

This should give consideration to the following factors

  1. Presence of ophthalmic injuries
  2. Progressive proptosis.
  3. Deterioration in visual acuity.
  4. Visual integrity of the unaffected side.
  5. Necessity for immediate operation in relation to other facial and general condition.
  6. The medical condition of the patient

Any manipulation of the bones of the orbit is contraindicated when there is any risk of injury to the eyeball or to its contents or from aggravating existing haemorrhage either from an intraocular or retrobulbar source.

Progressive proptosis following trauma is indicative of retrobulbar haemorrhage, usually of the intraconal variety, and may be accompanied by changes in the pupillary reflex and visual acuity.

In conditions of pre-existing blindness in the other eye, or vision has been lost in the other eye as a result of the trauma, an extremely conservative approach is to be adopted. Surgical procedures may be deferred or avoided.

Orbital injuries as a result of fall precipitated by general medical conditions as coronary thrombosis, cerberovascular disaster or severe anaemia contraindicate an early surgical intervention.

If general anaesthesia is to be administered for other injuries surgical intervention can be taken up for management of zygomatic complex along with other maxillofacial injuries.

If the above conditions do not apply, it will be ideal to defer the surgical procedure for 5 – 7 days, particularly in the case of complex orbital floor fracture. This period will aid in resolution of the gross oedema and permit a more detailed examination of the eye, assessment of diplopia and provides an improved radiograph, as the antrum would not be filled with blood. The surgical procedures are not to be delayed beyond 10 days, as the development of fibrosis will increase difficulty. After 3 – 4 weeks fractures would have clinically firmly united.

Treatment of the zygomatic complex fractures

No treatment

Appreciable number of cases of zygomatic complex requires no treatment. Apart from medical contraindications, cases of undisplaced zygomatic complex and cases of stable, minimally displaced fractures which following union would not result in cosmetic or functional deformity does not require any treatment. Patients are to be observed longitudinally for signs of displacement, extraocular muscle dysfunction and enophthalmus after swelling resolves. Care is necessary in interpretation of radiographs. An absence of significant displacement at frontozygomatic suture and infra orbital rim does not exclude an unacceptable displacement at the prominence of the zygomatic bone since a rotation around these points, and the middle of the zygomatic arch, may have taken place resulting in impaction into the antral cavity.

Indirect reduction

This involves procedures that disimpact and reduce the fracture by direct application of instruments deep to the temporal surface of the zygomatic bone through an indirect approach remote from the fracture line. Fractures that are stable after reduction does not require fixation, while unstable fractures  are fixed temporarily or permanently.

There are many techniques that have been employed for this operative approach.

  1. Temporal fossa approach (Gillies).
  2. Upper buccal sulcus approach (Keen).
  3. The Cheek approach (percutaneous)
  4. The nose (transantral).
Temporal fossa approach

This method was introduced by Gillies et al 1927 for elevation of zygomatic arch and the zygomatic complex.

The rationale for this procedure is the fact that temporal fascia is attached to the outer aspect of the zygomatic bone and superior aspect of the arch. Deep to temporal fascia there is a potential space or tissue plane above the temporalis muscle, along which long instrument can be introduced to engage the temporal surface of the zygoma and medial surface of the zygomatic arch.

The technique involves shaving of the hair from the temple region  (around the area of bifurcation of temporal artery). An incision of 2.5 cm long is made above and parallel to the anterior branch of temporal artery. Dissection is carried down to the temporal fascia. The fascia is incised and a Howarth periosteal elevator is introduced in a downward and forward direction as far as the temporal aspect of the zygomatic bone. The periosteal elevator is withdrawn and then Bristow’s orthopaedic elevator or Rowe’s modification of Bristow’s elevator is introduced to engage the zygoma. Rowe’s elevator has a blade and an handle similar to the Bristow’s elevator, but it also incorporates a lifting handle which is attached by a strong hinge with a positive stop at the origin of the handle. The external or lifting handle is of the length of the blade and aids in orienting the blade accurately and giving a parallel force on the blade when force is applied. The reduction is often accompanied by an audible click. The fracture reduction is verified by palpating for the persistence of step defect. The temporal fascia is closed with interrupted absorbable sutures and skin edges approximated. Postoperatively, care is taken to avoid pressure over the fractured site until union is complete at the end of approximately 3 weeks.

Upper buccal sulcus approach (Keen)

This technique was introduced by Keen in the early 20th centuary. The major advantages of this approach are:

  1. It is an intraoral approach and spares a skin incision.
  2. The approach is more direct.
  3. Less dissection is required.
  4. Reduction vector is more ideal
  5. No major vessels are encountered

An approximately 1.5 cm incision is made in the buccal sulcus inferior to the zygomatic buttress. A periosteal elevator is introduced upwards supraperiostealy to contact the deep or infra temporal surface of the zygomatic bone thus enabling upward, forward and outward pressure to be applied. For elevation various elevators can be used like Bristow’s, Rowe’s, Taylor Monks etc.

Quinn 1977 has described a modification of the method, which is of particular value in the case of medially displaced fractures of the zygomatic arch. This employs a lateral coronoid approach through an incision situated over the anterior border of the ramus. The incision is deepened by blunt dissection in a supraperiosteal plane lateral to the coronoid process until the zygomatic arch is reached. An elevator is used to raise the fractured segment.

Percutaneous approaach

This method consist of inserting a hook through the skin below and behind the prominence of the zygomatic bone so that it engages the deep aspect and allows reduction by strong outward traction of the handle of the instrument. This technique is also useful in case of isolated fracture of the zygomatic arch. Poswillo gave the exact location of the initial stab incision at the intersection of a perpendicular line dropped from the lateral canthus and a horizontal line extended posteriorly from the alar margin of the nostril.

Instead of using a hook, insertion of Carroll-Girard screw into the body of zygoma have been advocated for percutaneous approach.

Intranasal transantral approach.

This technique is employed by certain otorlinolarygologists but not used commonly. An opening is made into the antrum below the inferior meatus at the same location for intranasal antrostomy. A curved instrument like Urethral sound is used to manipulate the fractured bone.

Fixation following indirect reduction.

Fixation following fracture reduction is required in case of unstable fracture after reduction. Lack of stability of a reduced zygomatic complex can lead to displacement with subsequent functional and aesthetic deformities.  These include facial deformity, occular dysfunction, masticatory impairment, nerve dysfunction, and combination thereof.

Elements that contribute to unstable fracture fixation include:

  1. Muscular forces across the fracture lines.
  2. Type of fracture.
  3. Bone loss at the fracture site.
  4. Displacement of fracture with disruption of the enveloping periosteum or temporalis fascia.
  5. Lack of bone thickness at the infra orbital rim and residual fibrosis and resorption of the fracture line when treatment is delayed.

Stability of zygomatic fractures depends upon the type of fracture than the type of fixation used. Rowe reported the factors for instability as:

  1. Those fractures that are rotated around the horizontal axis (Medially or laterally).
  2. Fractures that are dislocated enbloc, and
  3. Comminuted fractures, such as many fractures of the infra orbital rim and maxillary buttress, are unstable.

Also, fractures with bone loss at fracture site are inherently unstable. In additions severely displaced fractures are often unstable because the enveloping periosteum or temporalis fascia has been disrupted.

The longer the time period prior to reduction and fixation of a zygomatic fracture the less chance that the fracture will be stable owing to the development of fibrosis and eburnation of the fractured bony ends.

The Need for Fracture Fixation

If a fracture is not stable after reduction or cannot withstand digital pressure on the malar eminence, then fixation is required.

The fixation is applied only when indicated, if there is any question regarding the stability of a reduced zygomatic fracture, it is prudent to apply fixation.

Methods of Fracture Fixation

The Zygomatic complex is a tetrapod with four buttresses at the frontozygomatic region, infra orbital rim, maxillary buttress and zygomatic arch.  Fracture fixation is most often applied at these buttresses.

The location of fixation is important.  The frontozygomatic region is the strongest pillar of the zygoma therefore it is the most important point of fixation.  The maxillary buttress is the best site for fixation to oppose the direction and force of the masseter muscle.  The infra orbital rim is a poorer choice for the site of fixation due to lack of bone thickness.

Fixation can be by temporary, direct or indirect fixation. Temporary fixation is by means of antral packing. Direct fixation after fracture reduction is done by means of wire osteosynthesis or by use miniplate at the fractured site. Indirect fixation is achieved by means of Kirsehner wires and external pin fixation techniques.

Temporary support

Antral Packing

A number of materials have been placed in the maxillary sinus in an attempt to support the fractured zygoma or orbital floor.  These include balloons, penrose drain materials, plastic cubes, penrose drain stuffed with gauze and strip gauze.  The strip gauze is impregnated with iodoform or antibiotic ointments or white head’s Varnish. Antral packing is left in place for 14 days after initial placement.  Antral packing is indicated when the zygomatic complex is unstable following reduction, when gross comminution of the zygomatic complex has occurred and when comminution of the orbital floor without bone loss is present.  For the antral packing to be effective, there must be total stability of other bones that comprise the maxillary sinus and other process of the zygomatic complex, or they may be displaced.

Antral packing considered only in situation in which severely comminuted zygoma fracture is there and the application of rigid fixation is not possible.

Indirect fixation

This implies that the zygomatic bone will be rigidly secured to some point elsewhere on the facial skeleton until the union has occurred, after which the connecting apparatus is removed.

This is achieved by the use of

  1. Internal medullary pins or wires
  2. External pins and rods that are attached by universal joints

The osteosynthesis effected by transosseous wires alone will provide considerable amount of stability, but lacks absolute rigidity. This has been overcome with the use of miniplates, so the use has indirect technique has largely been reduced. This technique of providing fixation is indicated when there is gross loss of of bone in the region of the Fronto-zygoamtic suture and inferior orbital rim. The indirect fixation is done to other stable structures such as zygomatic bone, frontal bone, maxilla etc as in

  1. Zygomatic-zygomatic
  2. Naso-zygomatic
  3. Zygomatic-palatal
  4. Maxillo-zygomatic
  5. Fronto-zygomatic
  6. Cranio-zygomatic

In Zygomatic-zygomatic (transmaxillary) fixation the opposite sound zygoma and nasal structures are used for cantilever support of the reduced zygomatic bone.

In Naso-zygomatic fixation a transnasal Kirschner is used to stabilise the zygoma from contralateral frontal process of the maxilla to the natral surface of the zygoma.

In zygomatico-palatal fixation is by use of wires obliquely towards the contalateral palatal process at its junction with the lateral wall of the nose.

Maxillo-zygomatic fixation is by use of external pins and joints stabilised to the maxillary teeth by means cemented cap splint.

Fronto-zygomatic fixation is by use of pins and joint to the zygoma and the zygomatic process of the frontal bone. This is also done by fixing the reduced zygoma to halo frame.

Indirect Fixation by Kirschner wires

Use of the internal K wire fixation has been shown to be reliable, safe and stable.

Three different placement techniques are there.

  1. The transfacial approach, in which the pin is inserted through the stable  zygoma and nasal cavity and into the fractured Zygoma.
  2. The trans nasal approach – in which the K wire is inserted through the fractured Zygomas and nasal cavity into the maxilla.
  3. The trans palatal approach where in the K wire is passed from the fractured zygoma to engage the palatal process of the contrallateral maxilla at the lateral wall of the nose.

The wires are removed 3 to 6 weeks after placement.

Advantages:-

–    A minimal amount of equipment is necessary and usually readily
available.

  • The technique is fast and easy
  • Minimal scaring
  • Fixation is stable to some extent
Disadvantage:

–   Zygoma must be properly reduced prior to insertion.

–   Second procedure is needed to remove the pin.

–   The orbital contents or naso endotracheal tube could be impinged by the pin.

  • These techniques are ineffective when there is comminuted fracture.
  • The rigidity is less when compared to miniplate fixation.
Indirect fixation by External pins:

External fixation of the Zygoma following reduction, via a hook extension and a plaster head cap, rests on extension efforts of stenzol (1902) and on the apparatus proposed for extension of the mandible by Wassmund (1927) and Rehrmann (1935).

Following percutaneous reduction and removal of single tined hook, a rentention hook is placed through the puncture channel.  This hook is connected to a plaster head cap elastically with a rubber band or by use of the spring force of the bar to which it is connected.  External fixation may be undertaken on a haloframe, or to another pin placed in the zygomatic process of the frontal or to the maxillary teeth by means of cap splint. The apparatus removed after 8 to 14 days.

The disadvantage is that the apparatus is protruding out and produces discomfort to the patient.

Direct fixation

This is indicated when there is lack of stability to the reduced fracture segment of zygoma. This is done by means of

  1. Intraosseous wiring
  2. Rigid fixation by means of miniplate fixation and lag screws.
Surgical approaches for zygoma and orbital floor

Various approaches are used to access the zygoma and orbital floor for direct fixation and for exploring the orbit. The approaches used for direct fixations of zygoma uses incisions placed around the orbit, coronal approach and intraoral approach in the zygomatic buttress region. The orbital region exploration is approached by placing incisions in and around the orbit.

The surgical approach used for direct fixation of  zygoma are

  1. Lateral eyebrow approach
  2. Subciliary approach
  3. Infraorbital approach
  4. Subconjunctival approach
  5. Bitemporal / Bicoronal approach
  6. Buccal sulcus approach

As a rule, placement of single intraoseous wire at the frontozygomatic suture and on the lower orbital margin suffice.

The Supra Orbital Eyelid Incision

(Dingman and Natvig 1964, Kruger 1964, Rowe and Killey 1968, Spiessel and Schroll 1972)

Thin incision serves to expose the lateral orbital margin.  Following separation of the muscle fibers and periosteum, the fracture site is exposed at the frontozygomatic sutures.  This lies deeper than the end of the incision, should be lengthened laterally downward not further than the level of the palpebral fissure, because a longer incision is cosmetically undesirable and because the lid fibers of the facial nerve could be damaged in the process.  When necessary, the incision may be lengthened medially along the eyebrow to permit treatment of a typical fracture lines at the Supraorbital margin.

Approaches to orbital floor

There are various ways to gain access to the lower orbital margin. These include.

  1. Infra orbital approach
  2. Subciliary approach
  3. Trans conjunctival approach
  4. Lower eye lid incision

The infra orbital incision

(Thoma 1958), Kazanjian and Converse 1959), Kruger 1964, Rowe and killey 1968, Luhr 1971, Spiessl and Schroll, 1972, Albright and Mefarland 1972).

This incision lies directly above the lower orbital margin.  After incision of the skin and the orbital part of the orbicularis oris muscle, the infra orbital margin is exposed at the fracture site.

Advantages of the incision: –

–   Short path to the infra orbital margin.

–   Avoidance of the orbital septum.

–   Clear line of vision.

–   The possibility of lateral extension of the incision.

Disadvantages:- (Becker and Austerman 1977)

–   Post traumatic cicatrical distortion of the skin

–   Lid edema.

The lower Eye lid Incision

It is a step shape was described by converse et al (1961).

The orbicularis muscle is divided more deeply than the skin.

Disadvantage – Lateral repositioning of the orbicularis occuli muscle is not always ideal and distortion of lower lid may arise (Georgiade 1972, Becker and Autermann 1977)

Subciliary Skin Incision

( by Rankow and Mignogna 1975)

Deeper divisions of orbicularis occuli.

Disadvantage:-  The separated think lid skin does not adapt well to be musculature.

Albright and mefarland (1972), Becker and Austermann (1977) and Luhr (1971) therefore prefer the mid lower eyelid incision without step deformation.

The Trans Conjunctival Approach

(Bourquet 1923), Tenzel and miller 1971, Tassier 1973.

Here the incision is in the region of the conjunctiva, eliminating the external scar.  Good experience with this technique reported by kazanjian and converts (1974) Lynchetal (1974) and Schule and Weiman (1975). This is by two types preseptal and retroseptal approach.

After atropinization of the lower lid, the palpebral conjunctiva is incised below the tarsus, and the anteriorly placed orbital septum is divided as well.  Dissection is than continued in front of the orbital septum to the infraorbital margin.

Retroseptal Approach

This is another way of approaching the orbital floor by trans conjunctival approach.

Disadvantage – View is not clear.  Occasional it might result in  scar distortions of the lower lid which are difficult to correct.

The approaches described are sufficient, as a rule, for transosseous fixation of the Zygoma.  After elevation of periosteum at the orbital margin on its external surface, the fracture sites are exposed.  Then the periosteum of the orbit is carefully elevated with an elevator.  With reduction complete, holes are drilled at both sided of the fracture site at the orbital margin for the transosseous wires.  Contents of the orbit protected during the procedure by an elevator.  Before the ligatures are tied securely, the correct positioning of Zygoma is checked.  When the ligatures have been tightened and the zygoma in proper position, the incision may be sutured.  Strains avoided postoperatively, soft diet given.

Transosseous wiring

Transosseous wiring fixation on the orbital margin can be ascribed to Gill (1934) other description provided by Adams (1942) Thoma (1958) Kazanjain and Converse (1959, 74) etc.

The indication for open reduction with direct transosseous wiring at the fracture sites at the lower and lateral orbital margins are provided when an orbital exploration is required simultaneously, when a comminuted fracture is present and when a percutaneous reduction has failed.

Internal fixation of zygomatic fractures by means of miniplates and lag screws

The  best method of providing stable fixation to an unstable zygomatic fracture is to rigidly secure it internally with bone  plates.

Advantages :-       Three dimensional stability,

Faster bone healing (Primary bone healing).

Disadvantages:    larger incision

More extensive periosteal stripping of bone

Extreme retraction of wound edges.

Need for technical expertise and cost.

A bone thickness of 2mm is adequate to allow stable fracture fixation with plates and screws.

So rigid internal fixation can be placed at fronto-zygomatic region, maxillary buttress, infra orbital rim and at the zygomatic arch.

Four point fixation with plates at the fronto-zygomatic region, infraorbital rim, maxillary buttress and zygomatic arch is stable.  This technique is usually performed on communited zygomatic complex fractures or fractures associated with extensive midfacial trauma.

Three-point fixation with bone plates at the frontozygomatic region, infraorbital rim, maxillary buttress or zygomatic arch has also been shown to be stable.

Rudderman & Mullen 1992, have shown that single point fixation at one of the buttress fractures would result in instability due to translations and rotational forces. Two-point fixation would also result in instability. For best form stability requires fixation at all the three buttresses.

Bone plates and screws with a thinner profile and smaller overall size have been advocated for rigid internal fixation of zygomatic complex fractures.

The added advantage of these fixation devices include a decreased bulk and palpability in the area of fixation within overlying skin and the implantation of less total metal.

Armamentarium

In the regional of the midface special ASIF miniplates and 2mm screws.  The mini DCP that makes compression osteosynthesis possible has screw holes designed according to the spherical gliding principle.

For making the drill holes, a 1.5mm twist drill bit and a small air powered drill are necessary.  For drilling at the orbital margin, there is a special orbital drill guide.  One can also use a drill and tap sleeve or an eccentric drill guide and protect the orbital contents with an angled elevator passed around the orbital margin.  A depth gauge, a 2mm tap, and a screwdriver also belong to the armamentarium.

For lag screw osteosynthesis, miniscrews with a screw diameter of 1.5mm are used, the 1.1mm twist drill bit for the thread hole corresponding to the core diameter of the screws.  For the gliding hole, 1.5mm twist drill bit is needed.  The drill guide and tap have an outer diameter of 1.5mm.  The depth gauge is same as for the 2mm screws.

Direct reduction and fixation

Here the fracture is approached directly and fixed directly by means of intraosseous wires or miniplate fixation.

ORBITAL FRACTURES AND MANAGEMENT

Fractures of the walls of the orbit are seen along with fractures of zygomatic complex, nasoethmoid complex, midface fractures, frontal bone fractures or as an isolated fractures of orbital floor.

Fracture patterns

Fractures involving the orbit can be classified as

  1. Zygomatic complex fractures
  2. Naso-orbito ethmoidal complex fractures
  3. Internal orbital fractures

Zygomatic complex

Zygomatic complex fractures are the most commonly involved fractures of the face secondary to nasal fractures. These fractures are also the most common occuring fractures of the orbit. Zygomatic complex fractures are often displaced in an inferior, posterior and medial direction and the complex fulcrums about the frontozygomatic suture. Various classification system have been proposed but the one by Jackson is notable

Type I         Nondisplaced

Type II        Segmental fracture of orbital rim

Type III      Tripod fracture

Type IV      Fragmented

Naso-Orbito-Ethmoid complex

Naso-Orbito-Ethmoid complex fractures often occur following blunt trauma to the midface. These fractures primarily result in cosmetic deformity such as flatenning of the nasal dorsum and widening of the intercanthal distance. This can occur as a result of disruption of one or both of the medial canthal ligaments. The fracture ranges from minimal displacement of a large segment of the medial orbital rim to severe comminution with complete avulsion of the canthal ligament from the bone.

Internal orbital fractures

Internal orbital fractures can occur in numerous patterns. Thay are often described by their location and size of the defect. Three patterns of internal orbital fractures are seen

  1. Linear
  2. Blow-out
  3. Complex

Linear fractures maintain periosteal attachments and therefore do not result in a defect, however they can result in a significant enlargement of the orbit.

Blow-out fractures are the most commonly occurring injury and are limited to one wall, with a defect less than 2 cm in diameter. Blow-out fractures most commonly occur in the anterior and middle part of the floor. They can also occur in the medial and superior walls, where they present as blow-in type of fracture.

Complex fractures consist of extensive fractures that affect two or more orbital walls, may involve the posterior orbit and also the optic canal. This type of fracture is associated with fractures of the facial skeleton such as Le Fort II, III and also frontal bone fractures.

Diagnosis of orbital injuries in midfacial fractures

The diagnosis of the orbital fractures is by clinical examination, radiological examination and evaluation of vision and orbit. The goal of clinical and radiological diagnosis is to help make the decision between conservative management and operative exploration.

The clinical examination involves

  1. A brief history of the mechanism of injury and direction of the force should be ascertained. The clinical examinations involve a systematic approach for assessing the orbits, which will further define the functional and anatomic defects associated with orbital injuries.
  2. The initial ophthalmologic evaluation should include periorbital examination, visual acuity, ocular motility, pupillary responses, visual fields and fundoscopic examinations.
  3. The eyelids and periorbital area should be inspected for oedema, ecchymosis, lacerations, ptosis, asymmetric lid drape, canalicular injury and canthal tendon disrutption.
  4. Extraocular movements are evaluated to rule out mechanical entrapment or paresis.
  5. Any diplopia in any field of gaze is noted.
  6. Forced duction test is carried out to determine the mechanical entrapment if any and to differentiate between the mechanical and neurological origin of the limitation of extraocular. Absence of restriction of movement has a number of implication based on the time elapsed since injury. Resistance to free movement is seen in mechanical obstruction, which is likely to be related to
  7. Herniation of the periobital fat.
  8. Incarceration and entrapment of the extrtaocular muscles.
  • Impingement of bone fragments upon fat and muscle
  1. Fibrous tissue formation and adhesions
  2. Depression of the orbital roof.
  3. Pupillary size, shape symmetry and reaction to light are to be noted.
  4. The globe is evaluated for acute enopthalmus or proptosis.
  5. Visual fields are tested and fundoscopic examination is done to rule out internal eye injury (retinal, lens etc.).
  6. Tonometry measurements are made to note the intraocular pressure. Normal range is 10 to 20 mm of mercury.
  7. Slit lamp test is done to rule out corneal abrasion.
  8. Additional investigation of radiographs, CT scans and MRI scan are useful. MRI is useful in identifying the incarceration of the orbital fat into the antrum. CT and MRI are useful in identifying the amount of bone loss and also the amount of bone intact left behind for reconstructing. Orbitography with the use of radiopaque contrast medium is helpful in revealing the orbital floor defect.

Some of the early features of the injury to the integrity of the orbital floor are

  1. The history of the injury
  2. Presence of gross periorbital ecchymosis and edema
  3. The presence of immediate limitation of elevation of the eye.
  4. The existence of limited elevation of eye with intact orbital margin and paresthesia of infraorbital nerve.
  5. Alteration of the ocular level. Initially there is slight elevation owing to haematoma. In large defect of the orbital floor and the hematoma small there is lowering of the orbital level.
  6. Hanging drop appearance of the roof of the antral cavity as seen by Water’s view (PNS view) or by CT scan.
  7. The presence of relatively denser fragmentation of the segments of the orbital floor within the general opacification of the antrum as seen in the PNS views.
  8. Propotosis due to effusion of blood into and arround the extraocular muscles (associated with upward displacement of the globe). As this blood becomes absorbed and the oedema subsides, the late signs and symptoms become evident.

After an interval of 7 to 10 days the following changes may be observed.

  1. Restriction in movement of the eye especially in the vertical direction.
  2. The concomitant development of diplopia usually most evident when looking upwards and inwards.
  3. A slight lowering of the ocular level.
  4. Enopthalmus
  5. Deepening of the supratarsal fold
  6. Retraction of the globe upon attempted elevation and in some cases of depression
  7. Narrowing of the palpebral fissure.

ISOLATED FRACTURE OF THE ORBITAL FLOOR (BLOW OUT FRACTURES)

The consequences of isolated fractures of the orbital floor were described very early on by ophthalmologists, among them lang (1989) Beer (1892) and Lederer (1902).

The sudden increase in hydraulic pressure in the orbit is the cause of this type of fracture. Reny and stricker 1969, Fujino 1974, Says forces that affect the strong bony components can lead to isolated fractures within the orbit by transmission; without the outer bony frame being fractured.

Diagnostic difficulties in blowout fractures exist.  No steps defects on palpation or displacement of the bony orbital rim can be felt and routine radiograph generally does not show fractures of the thin bony lamellae of the orbital floor.

Occasionally, opacification of the maxillary or ethmoidal sinuses, or an opacity on the roof of the maxillary sinus cavity may suggest the presence of a fracture.  If diplopia and impaired mobility of the globe are present, tomography is absolutely indicated.  Even in the absence of opthalmologic symptoms when swelling and haematoma of the eyelids, as well as the kind of trauma, indicate the possibility of such an isolated fracture of the orbit.  Only by CT can the isolated orbital fracture be diagnosed for certain and the localisation and extent of the bony injury be determined.

TREATMENT OF FRACTURES OF THE ORBIT

A classification of fractures of the orbit based on treatment is appropriate.  This gives some basic guidance with regard to the indication for surgery in those injuries of the orbit, which are combined with midface fractures.  In addition to possible ophthalmologic symptoms, this classification takes into consideration the  type and extent of tomographic finding and the mechanism of fracture.

Classification of Orbital Fractures Based on Treatment

(1)   Simple or linear fractures of the bony orbit as accompanying injuries in typical fractures.

Treatment:-

Surgical reduction  and fixation of midface fractures.  The bony segments extending into the orbit are thus reduced.  In the absence of ophthalmologic symptoms no surgical exploration of the orbit itself.

(2)  A  Comminuted fracture of the orbit (mostly) orbital floor) in  conjunction   with  midface fractures.

Treatment.

  1. Surgical reduction and fixatrion of midface fractures
  2. Surgical  exploration of orbital fractures  . Also in absence of  ophthalnological early symptoms.

(2) B.  Comminuted  fractures of the Orbit –  in  conjunction with  atypical periorbital fractures.

For eg. Periorbital comminuted fractures, frontal bane fractures with fracture of the orbital roof, or  circumscribed detachment of part of the inferior orbital margin.

Treatment-

In conjunction with surgical reduction and fixation of periorbital fractures.  The neighbouring section of the orbital wall can be included and treated as well.

(3)   Isolated Orbital Floor  Fractures (Blow out  Fracture)

(If  isolated the thin  bony  lamellae of the medial or lateral walls are fractured)

Treatment:

The management of orbital floor fractures depend upon the severity and nature of fracture.

Surgical exploration depending

  • On C.T. finding as for the presence of an isolated  comminuted defect fracture of the orbital  wall
  • If there persistent diplopia.

The objectives of surgical exploration are to

  1. Repositioning of the displaced orbital tissues.
  2. Reductions of fractures
  3. Stabilisation of the fragments.
  4. Restoration of the orbito antral partition
  5. Elimination of the interference with ocular movements.
  6. Preservations of orbital volume and periorbital fat.

The above surgical goal can be achieved by various surgical approaches in orbital floor injury. This is by

  1. Antral approach by use of packs as support and also by use of graft with antral pack.
  2. Reconstructing the orbital floor with autogenous or allogenous or alloplastic materials through various infraorbital approaches.

Reconstruction of the Orbit floor

This is done by the use of autogenous and allogenous transplants and also by use of alloplasts.

If  injuries to the orbital walls are present   as a  secondary injury in midfacial fractures,  and if they require exploration, the midface fractures are reduced  first and fixed by osteosynthesis at the beginning of the operation.

In many midface fractures plate osteosynthesis is the procedure of choice, especially when periorbital fractures are present.  Thin vitallium minicompression plate (Luhr 1979) which, because of the highly corrosion resistant cobalt, chromium, molybdenum alloy may remain in situ, So that removal is not needed.  By the eccentric gliding hole principle (Luhr 1968) the plates may be kept so thin that remains inconspicuous even in difficult region with thin covering skin (Naso orbital rim, infraorbital rim).

After restoration of the orbital margin, the fractures of the orbital wall are displayed by strictly subperiosteal dissection.  The prolapsed orbital soft tissue in the maxillary sinus are removed from the fracture margin with a fine periosteal elavator.  Isolated bone fragments, stock in the soft tissue are removed.

In most cases a bony defect exists in fractures in the paper thin section of the orbital floor of the medial wall.  For the reconstruction of the orbital wall, that is for the bridging of the such defects, many procedures have been suggested.  Various alloplastic materials have been used for eg. polyethylene (Rubin 1951, Browing and Walker 1965) Teflon (Freeman 1962), Poly vinyl sponge (Henderson 1963) Silastic (Lerman and Cramer 1964 ) Dacron urethane (Leake etal 1980) aluminium oxide ceramic (Niederdell mann etal 1976) Tantalum gauze (prowler 1965) Autologus bone grants eg. iliac bone graft used by converse and smith (1970, 1977) and Maillard 1977) thin transplants from the wall of the antrum by converse and smith (1960) and by Obwegeser and Chause (1970).

Homologus transplants have found a further application today in primary reconstruction of the  orbital floorlyophilized dura (Luhr 1969, 71 ) Cialit – preserved dura (Schmelzle 1978), lyophilized cargilage (obwegeser and chaused 1975) Sailer, 1974), Cialit preserved cartilage (Schmelz 1974).

Lyophilized dura is good in primary treatment of fractures of the orbital floor.   It causes no increase in volum in the orbit by virtue of its minimal thickness and it heals without complication.  Lyophilized dura is superior to alloplastic materials, since it is completely organized within a few weeks and reconstituted into an endogenous connective tissue layer capable of load bearing.

In small to medium defects (2cm in diameter) bridging of the defect with lyophilised dura alone is sufficient.  The transplant is cut in such a way that it is applied to the intact bony surface of the orbital floor with 6-7mm overlap at the edge of the defect of all sides.  The pressure of the repositioned orbital soft tissue holds the transplant in situ.  Fixation with fibrin adhesive on the bony substratum may be undertaken.

In very large defects – particularly when they extend deeply into the orbital funnel – to reinforce the dural transplant, supplementary packing of the antrum is done.  Though a window in its antero lateral wall the sinus is tightly packed from below to the exact level of the margin of the defect.  The free end of the pack is lied out of the inferior meatus via an intra nasal antrostomy.  The pack should remain in place for 14 days.

Replacing the prolapsed soft tissue in the depth of the orbital funnel through the infraorbital incision alone is unsatisfactory because of limited visibility and damage the optic nerve.  Replacement in the dorsal region of the orbit is more safely achieved transantrally with the palpating finger.  In further exploration of fracture of the medial orbital wall, the killian incision at the lateral bridge of the nose is preferred.  After removal of the ethmoid bone cells the optic nerve can be displayed well and possible bone fragments removed.

COMPLICATION FOLLOWING ORBITO ZYGOMATIC FRACTURES

Complication of Zygomatic complex and arch fractures are uncommon.  The complications consist of

  1. Oculocardiac reflex
  2. Ophthalmic complication
  3. Malunion

The most serious complication involves the eye and surrounding structures. The early systemic complication is occurrence of Oculocardiac reflex where there is reflex bradycardia. Malunion of fracture is a late complication resulting in asymmetric appearance.

Oculocardiac reflex

The oculocardiac reflex is bradycardia following significant compression of the eye (Ascher 1908). Bradycardia caused by this reflex has already been reported following fracture of zygoma (Bainton & Lizi 1987), blowout orbit (Habal et al 1972) and maxilla (Precious & Sulsky 1990, Sorenson & Gilmore 1956).

Sinus dysfunction are caused by Cardiac abnormalities (as Hypert4ension, Myocardial infarction and Arteriosclerosis), Infection (Rheumatic fever), Congenital anomalies of the conducting system, Drugs (Digitalis), Electrolyte abnormalities, Respiratory abnormalities (anaesthesia & Suffocation) and Ageing.

The oculocardiac reflex is known as phenomenon that is associated with the facial area during cardiac abnormalities. This mechanism is thought to be inhibition of the heart rate by reflex excitation of the vagus nerve following stimulation of the trigeminal nerve by compression of the eye.

Clinically Aschner 1908 used it for eye compression test and Bailey 1935, Dewar & Wishart 1976, Kato & Hara 1978, Störtebecker 1953 used this as treatment for tachycardia. Barré 1921 observed development of bradycardia after experimental application of 500g or more pressure to the eye. This reverted to normal within 20s after release of the compression. Bradycardia have been reported following contusion of the eye (Habal et al 1972, Störtebecker 1953), operation for strabismus (Alexander 1975, Dewar & Wishart 1976, Sorenson & Gilmore 1956), compression after eneculeation (Bailey 1935) and orbital hematomas (, Sorenson & Gilmore 1956).

Bradycardia similar to Oculocardiac reflex have been reported following maxillofacial surgery.

Bainton & Lizi 1987 reported a case of bradycardia following reduction of zygoma through Gillies’ approach. The bradycardia was managed with intravenous atropine.

Robideaux 1978 noted bradycardia for 20s after reduction of maxillary fracture using Rowe’s disimpaction forceps.

Percious & Skulsky 1990 observed development of bradycardia and their recovery after 1 –2 min in six patients treated by Le Fort I Osteotomy and two patients treated for ankylosis.

Percious & Skulsky 1990 suggested the following mechanism for the development of the oculocardiac reflex induced by osteotomy of the midfacial bones. Sensation of the cheek is controlled by terminal branches of trigeminal nerve (Zygomatic branch and temporal branch). Following fracture/ fracture reduction / osteotomy of the zygomatic or maxillary area afferent impulses are conducted from peripheral sensory branches via maxillary and mandibular nerves to the nucleus of the trigeminal nerve. When excessive pressure impulses are transmitted, the efferent pathway of the vagus running along side is stimulated. This increases the tonus in the parasympathetic nerve resulting in bradycardia.  Hamlin & Smith 1968 demonstrated the termination of vagus nerve in SA and AV nodes, suggesting the induction of bradycardia such as AV block by Vagus stimulation.

The bradycardia can be managed by means of intravenous atropine.

Eye Complications

Corneal Abrasion

May occur as a result of the initial injury, operative trauma of corneal or conjunctival designation.  The Patient complains of scratchy feeling.  If corneal abrasion is identified, instil topical antibiotics and apply eye patch and consult an ophthalmologist.

This consist of early orbital injuries which consist of loss of vision as a result of optic nerve compression, central retinal artery occlusion, retrobulbar haemorrhage, superior orbital fissure syndrome, orbital apex syndrome, cavernous sinus syndrome.

The late orbital complications include late development of enopthalmus and diplopia, ectropion, entropion, medial canthal and lacrimal apparatus injury, lateral canthus injury and eyelid injury.

Retrobulbar Haemorrhage

Disruption of the retinal circulation may lead to irreversible ischaemia and permanent blindness.  The patient may complain of visual changes or increased pressure in the eye.

Ord in a review of 1450 zygomatic complex fractures, reported 0.3% incidence of postoperative retrobulbar haemorrhage with visual cells.  An emergency ophthalmology consultation is necessary.

Superior Orbital fissure syndrome and orbital apex syndrome

This rare complication is the result of compression of the structures within the superior orbital fissure.  Trauma and neoplasm are two most common causes.  Ophthalmoplegia is due to palsy of cranial nerves III, IV and VII.  Pupillary light reflexes may be abnormal and the first division of trigeminal nerve may be affected, producing decreased sensation of the forehead and loss of corneal reflex.  Neurological and ophthalmological consultation are necessary.  Treatment is generally by observation, and the problems may take up to one year to resolve.

Traumatic Hyphema

Trauma to the eye may lead to bleeding into the anterior chamber, the area between the clear cornea and the coloured iris.  In ophthalmologist should be consulted.  Initial treatment consists of a combination of bed rest, use of cylloplegic agent and eye shield protection.

Other eye injuries like lens dislocation, ruptured globe, retinal detachment and canalicular injuries can also occur.

Neurosensry Deficiencies

The incidence of sensory alteration of the infraorbital nerve following zygomatic trauma ranges from 18 to 56 %.  Entrapment of nerve or perineural fibrosis is responsible for persistent defects.

Exploration of the orbital floor through an extra oral approach should be done to remove any bone spicules or to decompress the nerve.

Enophthalmos

May be a noticeable and debilitating consequence of Zygoma fractures.  Treatment is difficult and the results are poor.  As many as 80% of treated patients have persistence of exophthalmos.  Better results are achieved with early reduction of fractures of the orbit and zygomatic complex.

Ectropion

This is seen as a result of scarring of the subciliary region of the eye following surgical treatment to repair the orbital floor region. This results in increased visibility of the sclera. This can be reduced by putting a stepped incision in the subciliary region.

Entropion

This is a complication associated with trans-conjunctival approach to the orbital floor. This is also as a result of scarring.

Diplopia

Binocular diplopia is one of the common complications of zygomatic complex fractures and in fractures involving the orbital wall. A minor degree of alteration in the visual axis can be compensated by an addittional input of neurovascular activity but beyond a certain point, this will be ineffective in correcting the visual axis of the affected eye.

Putterman et al in 1974 postulated the limited ocular mobility that follows a blow out fracture as due to

  1. Oedema
  2. Hemorrhage
  3. Fat entrapment as opposed to muscle entrapment

The three basic mechanism of persistent binocular diplopia following trauma are

  1. Muscle / fat entrapment in a fracture line.
  2. Bony displacement resulting in alteration of origin of the muscle
  3. Creations of adhesions between periosteal muscle or fat and the fractured bony margin.

Orbital oedema and hematoma are common and often result in diplopia, particularly in peripheral fields of gaze, which usually resolves in 7 to 10 days.

Diplopia is present when there is displaced fracture zygoma above the level of the frontozygomatic suture. A displaced fracture below the level of the whitnall’s tubercle does not predictably result in diplopia unless the supensory ligaments are disrupted.

Herniation of the orbital fat into the maxillary sinus can cause restriction of the affected globe in the primary upward and lateral gaze, resulting in diplopia in that quadrant.

Causes of diplopia following trauma are due to

  1. Physical interference
  2. Physiological interference
  3. Neurological deficit

The physiological deficit might be due to

  1. Extravasation of blood into and around the extraocular muscles.
  2. Impingement of extraocular muscles by bone fragments.
  3. Displacement of the bony origin of the muscle.
  4. Avulsion from the bony origin including displacement of the pulley of the superior oblique muscle.
  5. Entrapment of the muscle within the fracture line.
  6. Formation of the fibrous adhesions between the muscle sheath, periorbital fat and the margins of the defect.

Physiological imbalance

This is due to muscles acting at a mechanical disadvantage following displacement of the globe.

Neurological deficit

This might be due to

  1. Supra-nuclear lesions
  2. Nuclear lesions
  3. Infra nuclear and intra cranial lesions
  4. Cavernous sinus compression
  5. Superior orbital fissure syndrome
  6. Intra orbital damage to cranial nerves.

Treatment of Long Term effects of Orbital Fractures

The late sequel of orbital fractures include depression of the globe, immobility of the globe, diplopia, and enophthalmos. Such problems can arise if an orbital fracture is overlooked as in polytraumatized patients with life threatening injuries.  Considerable deformity of the bony orbit and globe results in functional and esthetic handicaps.

The displacement of the globe has serious consequences, such as diplopia in the principal direction of gaze and can lead to total disablement.

Reconstruction plastic procedure to correct such displacement may involve the use of autologus, homologus and alloplastic materials in the form of grafts or implants to elevate the globe, that is to compensate for the defects by placing some space occupying body within the orbit.

Aichmair and Fries (1971) reported good results in the correction of enophthalmos by cartilage implants with measurements of the volume of the transplant (1mm enophthalmos requires 0.5ml transplant volume).  For successful correction of displacement of the globe, the shape and the placement of the transplant in the orbit are additional decisive factors that can not be calculated exactly (Luhr 1977).

Definitive correction with autologus rib cartilage or several layers of lyophilised dura are used in cases where slight depression of the globe up to 5mm and with no significant lateral displacement of the visual axis.

In very marked global depression (in excess of 3mm) with considerable deviation of the visual access and diplopia usually a two-stage correction is done. This type of defect is seen in comminuated fractures of the orbit with loss of substance of the malunited fragments and extensive scar tissue formation within the orbit. For the first operation, an assortment of acrylic implants of various sizes and shapes are used.  These ready made acrylic inserts are placed in the orbit after removal  of soft tissue until a satisfactory globe position is obtained.  Later the implant is exchanged for a cartilage implant, usually after 3 months or more.

The two stage operation has also become an established procedure for the late correction of the misplaced globe occuring in conjunction with asymmetries and profile disorders of the neighbouring periorbital parts of the facial skeleton, resulting from severe comminuted fractures.  In the first operation, the displaced globe is corrected by temporary acrylic implants, in the second operation, the periorbita, the nose and the lateral midface region are reconstructed with cartilage grafts together with the replacement of the orbital  implant by a definitive cartilage graft.

In a large number of patients followed up after autologus cartilage transplantation, the results show minimal tendency to resorption with long term maintenance of the volume of the transplants (Luhr 1976, Luhr and Neutrodt 1979).  Fresh homologus grafts also are suitable (Kruger 1964) Schweuzer and Schwelzle 1976) have report good results with homologus cartilage preserved in Cisplatin. Sailer (1976, 79) used lyophilised homologus cartilage with similar success.  Gibson and Davis 1953, Kole 1962 report considerable reportion with preserved grafts.  According to current knowledge the long term results that is the degree of resorption – depends on the method of preservation.

As an alternative method to augmentation procedures, osteotomy (refracturing) and repositioning of the displaced parts of the skelelton have been recommended (Ding mann and Harding 1951, Gillies 1967, Converse and smith 1970, Rowe 1967) An osteotomy as a sole corrective procedure is successful only when a large part of the skeleton was originally displaced with clean fracture lines.


CONCLUSION

Great progress has been made in both the basic science and the clinical knowledge base used in orbito zygomatic fracture management and reconstruction.  With this increasing complex orbital reconstructive problem are better managed.  The diagnosis, treatment plan and the reconstruction  have evolved to a higher level.

Several areas of progress are of note the greater appreciation of the intimate relation between the bony orbits shape and the position of the globe, application of computer technology in orbital injuries, effect of rigid internal fixation on autogenous and alloplastic graft and the use of advanced bio compatible synthetic materials in orbital reconstruction.  Although this progress has great impact on treatment of orbital injuries, there are many unanswered challenges to be solved with further research in the treatment of the fragile frame of the window to the human soul.

 


References

  1. Zygomatic complex fractures. Daniel lew & John Bribe. Trauma. Robert D. Marciani & Barry H. Hendler. Oral & maxillofacial surgery. Vol. III. Raymond J. Fonseca. 2000. 149 – 204. W B Saunders.
  2. Orbital Trauma. Mark W Ochs & Francis R John. Trauma. Robert D. Marciani & Barry H. Hendler. Oral & maxillofacial surgery. Vol. III. Raymond J. Fonseca. 2000. 205 – 244. W B Saunders.
  3. Management of Zygomatic complex fractures. David H Perrot & Leonard B Kaban. Principles of Oral & Maxillofacial surgery. Vol. I. Larry J Peterson, Steven M Roser, Robert D Marciani & A Thomas Indresano. 1997. 489 – 508.
  4. Management of Ocular & Orbital trauma. Michael S Hauser. Principles of Oral & Maxillofacial surgery. Vol. I. Larry J Peterson, Steven M Roser, Robert D Marciani & A Thomas Indresano. 1997. 509 – 546.
  5. Fractures of the zygomatic complex and Arch. Edward Ellis III. Oral & Maxillofacial Trauma. I. 2nd Edition. Raymond J Fonseca & Robert V Walker. 1997. 571 – 652.
  6. Fractures of the zygomatic complex and Orbit. N L Rowe & J Ll Williams. Rowe and Williams’ Maxillofacial Injuries. Vol. I. 2nd J Ll Williams. 1994. 475 – 590. Churchill Livingstone.
  7. Orbital trauma. Stephen A Shendel. Oral and maxillofacial surgery clinics of North America. August 1993: Vol. 5: No. 3.

 

 

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