| Correction of dentofacial deformities with orthognathic surgery: Outcome of treatment with special reference to costs, benefits and risks | ||
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Nerve injuries in orthognathic surgery can be caused by indirect trauma, such as compression by surgical edema, or direct trauma, such as compression, tear or cut with surgical instruments or stretching during manipulation of the osteotomized bone segments (Ylikontiola 2002). Seddon (1943) classified neurosensory and motor deficits into three categories to characterize the morphophysiologic types of mechanical nerve injuries: neuropraxia, axonotmesis and neurotmesis.
Neuropraxia is the mildest form of injury, and it is described as slight localized myelin sheath damage without continuity defect. The majority of inferior alveolar nerve (IAN) injuries following bilateral sagittal split osteotomy of the mandible (BSSO) are neuropraxias and may be due to nerve manipulation, traction or compression. Normal sensation or function is usually recovered within two months.
Axonotmesis is characterized by disruption and damage to axons and the myelin sheath without disruption of the perineurium or epineurium. This is due to greater or more prolonged injurious forces, and a longer and more profound neurosensory deficit follows than in neuropraxia.
Neurotmesis is a severe disruption of the nerve trunk, which may cause a profound and possibly permanent neurosensory deficit.
The incidence of neurosensory deficits in IAN after BSSO has been reported to vary from 0% to 85%. This wide range of incidence may reflect the variation in the number of subjects in the study groups, the follow-up times and the sensibility testing methods. (Westermark 1999). Several factors have been proposed to predispose neurosensory injury to IAN: the patient´s age; the surgeon´s skills; the magnitude of mandibular movement; additional genioplasty; and the degree of manipulation of the IAN (Westermark 1999, Ylikontiola 2002, Van Sickels et al. 2002). Even after perfectly performed sagittal splitting, there may sometimes occur sensibility disturbances, which have been proposed to be caused by manipulation of the IAN during the soft tissue dissection in the initial phase of BSSO (Jones & Wolford 1990, Jääskeläinen et al. 1995, Westermark 1999). Due to the common use of BSSO, further studies to develop the dissection techniques are indicated.
Reports on lingual nerve (LN) sensory deficits are fewer than reports on IAN sensory disturbances. The initial postoperative incidence has varied from 1% to 19% (Schendel & Epker 1980, Jacks et al. 1998), but according to most reports, the sensory deficit of LN tends to resolve over time. The proposed mechanism of injury to the LN appears to be associated with the fixation methods, either bone screws or wires, or with medial side tissue retraction.
Facial nerve injuries in orthognathic surgery are rare, but the consequences of such injuries may be devastating to the patient. Damage to the marginal mandibular branch of the facial nerve is a well-known complication of extraoral approaches to the mandibular ramus or angulus, but these approaches in current orthognathic surgery are rare. The facial nerve has been reported to be damaged in intraoral vertical subcondylar osteotomy and in BSSO setback procedures with an incidence of less than 1%. The presumed trauma mechanisms have been compression caused by retractors behind the posterior ramus, fracture of the styloid process and direct pressure as a result of distal segment setback. Prognosis is good in incomplete loss of function, but poor if the loss of function is immediate and complete. (Jones & Van Sickels 1991).
Neurosensory impairment in the greater palatine and infraorbital nerves may be encountered after maxillary osteotomies. The incidence of prolonged sensitivity disturbances has been reported to be less than 4%, and they do not seem to bother the patients (De Jongh et al. 1986, Karas et al. 1990, De Mol van Otterloo et al. 1991).
TMJ fibrous ankylosis or hypomobility following orthognathic surgery has been proposed to be caused by several factors: immobilization of the TMJ by intermaxillary fixation (IMF) (Ellis & Hinton 1991), iatrogenic displacement of the condyle posteriorly and intra-articular hematoma (Nitzan & Dolwick 1989) or excessive stripping of the periosteum and muscle attachments in the ascending ramus, resulting in scar contraction and myofibrotic tissue formation (Storum & Bell 1984). Fibrillation and erosion of condylar cartilage may be consequences of these factors, resulting in hypomobility or even condylar resorption.
Idiopathic progressive condylar resorption is a rare condition that has been considered to be caused by factors that diminish the normal functional remodeling capacity (age, systemic illnesses, hormones) or increase the biomechanical stress on the TMJ (occlusal therapy, internal derangement, parafunction, macrotrauma, unstable occlusion). As a consequence of these, a decreased condylar head volume, ramus height, growth rate (juvenile), progressive mandibular retrusion or apertognathia and a limited mandibular range of motion may occur. (Arnett et al. 1996a). The incidence of idiopathic condylar resorption is unknown. Arnett and Tamborello (1990) found 10 cases (1.2%) of condylar resorption in a population of approximately 800 dentofacial deformities examined over a 10-year period.
Condylar resorption has been associated with orthognathic surgery. Several risk factors have been proposed. Preoperative morphological or functional factors include radiological signs of osteoarthrosis, TMJ dysfunction, condyles with a posterior inclination, a high mandibular plane angle and a low posterior-to-anterior facial height ratio (Kerstens et al. 1990, Moore et al. 1991, Merkx & van Damme 1994, Bouwman et al. 1994, Arnett et al. 1996a,b, Hoppenreijs et al. 1998, Hwang et al. 2000). Contributing surgical factors include major mandibular advancement, counterclockwise rotation of the mandibular proximal fragment, IMF, rigid internal fixation, bimaxillary osteotomies and avascular necrosis of the condyle (Schellas et al. 1989, Kerstens et al. 1990, Moore et al. 1991, Merkx & van Damme 1994, Bouwman et al. 1994, Cutbirth et al. 1998, Hoppenreijs et al. 1998). Young females (15–30) have a higher risk for condylar resorption than males and older females (Kerstens et al. 1990, Moore et al. 1991, Merkx & van Damme 1994, Arnett et al. 1996a,b, Hoppenreijs et al. 1998). The incidence of postoperative condylar resorption has been reported to vary from 1% to 31%. This is probably partly due to the great variation in the study populations (Kerstens et al. 1990, Moore et al. 1991, Bouwman et al. 1994, De Clercq et al. 1994).
Uncontrolled hemorrhage in the jaws may result from either a mechanical disruption of blood vessels or congenital or acquired coagulopathy (Christiansen & Soudah 1993). The most common cause of hemorrhage in association with orthognathic surgery is a lack of surgical hemostasis (Lanigan et al. 1990a, 1991a). Variations in the bony or vascular anatomy or inadvertant handling of tissues with normal anatomy, hypotensive anesthesia or infection may be causes of immediate or secondary hemorrhages. If major hemorrhage can be avoided, recovery is quicker (Neuwirth et al. 1992).
Maxillary osteotomies, especially LeFort I and II osteotomies, have the potential for the most serious bleeding sequelae in orthognathic surgery. These complications may present as immediate intraoperative bleeding or as postoperative swelling or epistaxis. The most common sources of hemorrhage are the terminal branches of the internal maxillary artery, especially the descending palatine or sphenopalatine arteries. Bleeding from these may be caused by a curved osteotome, drilling, an oscillating saw or downfracture of the maxilla. The downfracture may even damage the internal carotid artery, if a basal skull fracture ensues that involves areas such as the foramen lacerum and the carotid canal. Even arterio-venous fistulas are possible. (Lanigan 1988, Lanigan et al. 1990a, 1991b, Mehra et al. 1999).
Most bleeding associated with mandibular osteotomies tends to be intraoperative and occurs rarely compared to maxillary osteotomies (Lanigan et al. 1991a). If the soft tissues are retracted properly to allow the operation to be done completely in a periosteal envelope, the risk for significant hemorrhage is small.
Severe, prolonged disturbances in blood circulation may lead to avascular tissue necrosis, which may cause tooth devitalization, periodontal defects or even loss of major bone segments. Due to the dense network of anastomoses in the face, this is a rare event, but may manifest both in the maxilla and in the mandible, especially in association with segmental osteotomies. The anterior part of the maxilla is a special risk zone. (Epker 1984, Lanigan et al. 1990b, Lanigan & West 1990, Lanigan 1995). Although, in animal studies, preservation of the descending palatine artery was not found to be critical for maintaining blood flow to the downfractured maxilla (Bell et al. 1975, 1995), Lanigan et al. (1990b) recommended that the artery should be preserved whenever possible and the segmentalization of the maxilla should be minimized. A wide, intact soft tissue pedicle is important for the circulation of the downfractured maxilla. In the mandible, avascular necrosis can be largely avoided by minimal stripping of the mucoperiosteum and muscle attachments (Bell & Schendel 1977).
Relapse is an unpredictable risk of orthognathic surgery. Many of the studies reporting relapse have limitations of sample size or the duration of follow-up, involve different surgical techniques being applied in the same sample or suffer from limitations in the application of cephalometric measurements. Relapse may be dental or skeletal or both.
In general, mandibular advancement appears to be stable, if rigid internal fixation is used (Van Sickels & Richardson 1996, Dolce et al. 2000, 2002) and if anterior facial height is maintained or increased (Proffit et al. 1996). Several factors may affect relapse in mandibular advancements: the surgeon´s skills; proximal segment control, including condylar positioning and prevention of proximal segment rotation; prevention of counterclockwise rotation of the distal segment in cases with a high mandibular plane angle; the degree of mandibular advancement; and stretching of the perimandibular tissues, including skin, connective tissues, muscles and periosteum. (Will et al. 1984, Smith et al. 1985, Phillips et al. 1989, Moenning et al. 1990).
Mandibular setback is not always stable, and the inclination of the ramus at surgery appears to have an important inluence on stability (Proffit et al. 1996)
The stability of maxillary osteotomies is affected by the magnitude of the anterior movement and the magnitude of the inferior repositioning of the maxilla, the adequacy of mobilization of the downfractured maxilla at surgery, the extent of bone contact in the newly established position of the maxilla and the type of fixation (Proffit et al. 1991a,b, 1996, Baker et al. 1992). Louis et al. (1993), on the other hand, did not find any correlation between relapse and the magnitude of maxillary advancement. The most stable maxillary procedure is superior repositioning, and forward movement is also reasonably stable. Inferior repositioning is less stable, especially if it causes downward rotation of the mandible and stretching of the elevator muscles of the jaw. The least stable orthognathic procedure is transverse expansion of the maxilla. (Proffit et al. 1996).
Infection after orthognathic surgery may be acute or chronic, local or general. Most postoperative infections are caused by endogenous bacteria, most likely aerobic streptococci (Peterson 1990). Infection is initiated if the equilibrium between the host’s defence system and bacterial virulence is lost. Factors contributing to this in orthognathic surgery populations may be the usage of steroids, the duration of the surgical procedure, the patient’s age, interference with the blood supply to the bony segments, dehydration of the wounds, presence of foreign bodies or sequestrum, hospitalization in large wards, nutrition, hematomas and smoking. The surgeon’s experience, a good aseptic technique and gentle tissue handling are also relevant factors. (Peterson 1990).
In the classical wound cleanness classification, normal orthognathic surgery wounds fall into the Class II category (Clean Contaminated Wound). An infection rate of 10% to 15% can be expected without use of antibiotics, in comparison to Class III with an expected infection rate of 20% to 30%. In a Clean Wound (Class I), the probability of infection is approximately 2%. (Peterson 1990).
Studies dealing with infection after mandibular osteotomies report infection rates ranging from 0% to 18% (White et al. 1969, Guernsey & DeChamplain 1971, Willmar et al. 1979, Martis & Karabouta 1984, Buckley et al. 1989). In maxillary osteotomies, infection rates lower than 6% are mostly reported (Kufner 1971, Perko 1972, Kahnberg & Enström 1987), but in the study of Zijderveld et al. (1999), a 52.6 % infection rate was found in a placebo medication group with bimaxillary surgery.
There is some controversy concerning the need for prophylactic antibiotics (Peterson 1990, Martis & Karabouta 1984, Zijderveld et al. 1999), and many different practices exist. The operator must assess dosage, timing, duration of therapy and side-effects when considering antibiotic prophylaxis. Peterson (1990) has outlined the following principles for rational use of antibiotic prophylaxis in orthognathic surgery: (1) the surgical procedure should involve a significant risk for infection. Wound Cleanness Class II includes an increased risk for infection (10–15%), as do bone grafts; (2) correct antibiotics should be selected; (3) the antibiotic level should be high; (4) the antibiotic must be administered in a correct time sequence; (5) the shortest effective antibiotic exposure should be used.
Fractures of the osteotomized segments in BSSO, i.e. bad splits, have been reported to occur in 3% to 23% of cases (Van Merkesteyn et al. 1987, Ylikontiola 2002). Ophthalmic complications are rare sequels of maxillary osteotomies. They include decreased visual acuity, extraocular muscle dysfunction, neuroparalytic keratitis and nasolacrimal problems (Lanigan et al. 1993). These injuries appear to be caused by indirect trauma to the neurovascular structures during the pterygo-maxillary dysjunction or fractures extending to the base of the skull.
Other anecdotal problems, such as endotracheal tube damage (Thyne et al. 1992), tympanometric changes (Baddour et al. 1981) and prolonged dysphagia (Nagler et al. 1996), have been reported. Even life-threatening events may occur (Edwards et al. 1986).
Periodontal problems and tooth damage may be encountered, especially in segmental osteotomies. Problems are probably mostly caused by errors in the surgical technique. The design of the soft tissue incisions is critical: vertical incisions in the area of osteotomy will predictably create periodontal problems. Trauma to the palatal mucoperiosteum is a risk. Excessive heat generation with oscillating or rotating instruments, soft tissue injury or excessive interdental bone removal may result in compromised vascular supply to the area, as does also marked repositioning of the segment. Poor oral hygiene plays some role in periodontal problems. Many of the surgical problems can be minimized if an interdental space is created preoperatively by orthodontic means. (Wolford 1998).