- •Dedication
- •Citation
- •Preface
- •Contents
- •1 Anatomy of the Craniofacial Region
- •1.1 Anterior Skull Base
- •1.1.1 Cribriform Plate/Crista Galli
- •1.1.2 Fossa Olfactoria
- •1.1.3 Roof of the Orbit
- •1.1.4 Dura
- •1.1.5 Arterial Supply: Skull Base/Dura
- •1.2 Paranasal Sinuses
- •1.2.1 Frontal Sinus
- •1.2.2 Ethmoid
- •1.2.3 Sphenoid
- •1.3 Midface Skeleton
- •1.4 Subcranial and Midface Skeleton
- •References
- •2 Radiology of Craniofacial Fractures
- •2.1 Conventional X-Rays
- •2.2 Computed Tomography
- •2.3 Magnetic Resonance Imaging (MRI)
- •2.4 Ultrasonography
- •2.5 Diagnostic Algorithm
- •2.5.1 General Considerations
- •2.5.2 Craniocerebral Trauma
- •2.5.2.1 The Initial CT After Trauma
- •2.5.3 Skull Base Fractures
- •2.5.4 Midface Fractures
- •References
- •3 Classification of Craniofacial Fractures
- •3.1 Frontobasal: Frontofacial Fractures
- •3.1.1.1 Type 1
- •3.1.1.2 Type 2
- •3.1.1.3 Type 3
- •3.1.1.4 Type 4
- •3.2 Midface Fractures
- •3.2.1 Standard Classifications
- •3.2.2 Central Midface Fractures
- •3.2.3 Centrolateral Midface Fractures
- •3.2.4 Skull Base and Fracture Levels in the Region of the Septum
- •3.2.5 Lateral Midface Fractures
- •3.2.6 Midface: Combined Fractures
- •3.2.8 Cranio-Frontal Fractures
- •3.3. Craniofacial Fractures
- •3.3.1 Skull Base-Related Classification
- •3.3.2 Subcranial Facial Fractures
- •3.3.3 Craniofacial Fractures
- •3.3.4 Central Cranio-Frontal Fractures
- •3.3.5 Lateral Cranio-Orbital Fractures
- •References
- •4 Mechanisms of Craniofacial Fractures
- •4.1 Fractures of the Skull Base
- •4.1.1 Burst Fractures
- •4.1.2 Bending Fractures
- •4.2 Frontofacial: Frontobasal Fractures
- •4.2.1 Fracture Mechanism
- •4.3 Midfacial: Frontobasal Fractures
- •4.3.1 Trauma Factors
- •4.3.2 Impact Forces and Vectors
- •4.3.3.1 Degrees of Absorption
- •4.3.4 Impact Surface
- •4.3.4.1 Small Impact Surface
- •4.3.4.2 Large Impact Surface
- •4.3.5 Position of the Skull
- •4.3.5.1 Proclination
- •4.3.5.2 Reclination
- •References
- •5.1 Epidemiology
- •5.2.1 Frequency
- •5.2.2 Localization
- •5.3 Midface: Skull Base Fractures
- •5.3.2 Dural Injuries
- •5.3.2.1 Frequency
- •5.3.2.2 Localization
- •5.4 Cranio-Fronto-Ethmoidal Fractures
- •5.4.1 Frontal Sinus: Midface Fractures
- •5.5 Distribution According to Age
- •5.6 Distribution According to Gender
- •5.7 Associated Injuries
- •5.7.2 Eye Injuries
- •5.7.3 Facial Soft-Tissue Injuries
- •5.8 Special Fractures and Complications
- •5.8.1 Penetrating Injuries
- •5.8.3 Complicating Effects
- •5.8.3.1 Nose: Nasal Septum – Nasolacrimal Duct
- •5.8.3.2 Orbit
- •5.8.3.3 Ethmoid
- •References
- •6 Craniofacial Fracture Symptoms
- •6.1.1.1 Liquorrhea
- •Fistulas
- •Multiplicity
- •Time of Manifestation
- •Clinical Evidence of Liquorrhea
- •Chemical Liquor Diagnostic
- •Glucose-Protein Test
- •Immunological Liquor Diagnostic
- •Beta-2 Transferrin Determination
- •Beta-Trace Protein
- •Liquor Marking Methods
- •6.1.1.2 Pneumatocephalus
- •6.1.1.3 Meningitis
- •6.1.2.1 Lesions of the Cranial Nerves
- •Olfactory Nerves
- •Oculomotor Nerve
- •Trochlear Nerve
- •Abducent Nerve
- •Optic Nerve
- •Loss of Vision in Midface Fractures
- •Location of Optic Nerve Lesions
- •Clinical Appearance
- •Primary CT Signs
- •Secondary CT Signs
- •Additional Injuries
- •Operating Indications/Decompression
- •Decompression of the Orbital Cavity
- •Decompression of the Optic Canal
- •Therapy/Prognosis
- •6.1.2.2 Injuries at the Cranio-Orbital Junction
- •Frequency
- •Superior Orbital Fissure Syndrome (SOFS)
- •The Complete SOFS
- •Incomplete SOFS
- •Hemorrhagic Compression Syndrome (HCS)
- •Orbital Apex Syndrome (OAS)
- •Clivus Syndrome
- •6.1.2.3 Vascular Injuries in Skull Base Trauma
- •Cavernous Sinus Syndrome
- •Thrombosis of the Superior Ophthalmic Vein
- •6.1.3.2 Hemorrhage in the Skull Base Region
- •Basal Mucosal Hemorrhage
- •Hemorrhage in Frontal Skull Base Fractures
- •6.3.1.1 Emphysema
- •Orbital Emphysema
- •6.2 Midface Injuries (Clinical Signs)
- •6.2.1 Central Midface Fractures without Abnormal Occlusion (NOE Fractures)
- •6.2.2 Central Midface Fractures with Abnormal Occlusion (Le Fort I and II)
- •6.2.4 Lateral Midface Fractures
- •6.3 Orbital Injuries
- •6.3.1 Orbital Soft-Tissue Injuries
- •6.3.1.1 Minor Eye Injury
- •6.3.1.2 Nonperforating Injury of the Globe
- •6.3.1.3 Perforating Injury of the Globe (2%)
- •6.3.2 Orbital Wall Fractures
- •6.3.2.1 Fracture Frequency
- •6.3.3 Fracture Localization
- •6.3.3.1 Orbital Floor Fractures
- •6.3.3.2 Medial Orbital Wall Fractures
- •6.3.3.4 Multiple Wall Fractures
- •6.3.4 Fracture Signs
- •6.3.4.1 Clinical Manifestations
- •6.3.4.2 Change in Globe Position
- •6.3.4.3 Enophthalmus
- •6.3.4.4 Exophthalmus
- •6.3.4.5 Vertical Displacement of the Globe
- •6.3.4.7 Retraction Syndrome
- •6.3.4.8 Disturbances of Eye Motility
- •References
- •7.1 Intracranial Injuries
- •7.2 Management of Skull Base and Dural Injury
- •7.2.1 Skullbase Fractures with CSF Leakage
- •7.2.2 Skullbase Fractures with CSF Leak without Severe TBI
- •7.2.3 Skullbase Fractures with CSF Leak with Severe TBI
- •7.2.4.1 Skullbase Fractures with Spontaneously Ceased CSF Leakage
- •References
- •8 Surgical Repair of Craniofacial Fractures
- •8.1 Indications for Surgery
- •8.1.2 Semi-Elective Surgery for Frontobasal and Midface Fractures
- •8.1.3 No Surgical Indication
- •8.2 Surgical Timing
- •8.2.1 Evaluation
- •8.2.1.1 Neurosurgical Aspects
- •8.2.1.2 Maxillofacial Surgical Aspects
- •8.2.2 Surgical Timing
- •8.2.2.3 Elective Primary Treatment
- •8.2.2.4 Delayed Primary Treatment
- •8.2.2.5 Secondary Treatment
- •8.3 Surgical Approaches
- •8.3.1 Strategy for Interdisciplinary Approach (Decision Criteria)
- •8.3.1.2 Approach Strategy: Transfacial-Frontoorbital or Transfrontal-Subcranial
- •8.4.1 Indications
- •8.4.2.1 Coronal Approach
- •8.4.2.2 Osteoplastic Craniotomy
- •8.4.2.3 Skull Base Exposition
- •Technical Aspects
- •Technical Aspects
- •8.5 Transfrontal-Subcranial Approach
- •8.5.1 Indications
- •8.5.2 Surgical Principle
- •8.5.3 Subcranial Surgical Technique
- •8.6 Transfacial Approach
- •8.6.1 Indications
- •8.6.2 Surgical Principle
- •8.6.4.1 Frontal Sinus
- •8.6.4.2 Ethmoid/Cribriform Plate
- •8.6.4.3 Sphenoid
- •8.7 Endonasal-Endoscopical Approach
- •8.7.2 Sphenoid Fractures
- •References
- •9.1 Principles of Dural Reconstruction
- •9.2 Dural Substitutes
- •9.2.1 Autogenous Grafts
- •9.2.2 Allogeneic Transplants
- •9.2.2.1 Lyophilized Dura
- •9.2.2.2 Collagenous Compounds
- •9.3 Principles of Skull Base Reconstruction
- •9.3.1 Debridement of the Ethmoid Cells
- •9.3.3 Skull Base Repair
- •9.3.3.1 Extradural Skull Base Repair
- •9.3.3.2 Intradural Skull Base Occlusion
- •9.4 Skull Base Treatment/Own Statistics
- •References
- •10 Bone Grafts
- •10.1 Indications
- •10.1.1 Midface
- •10.2 Autogenous Bone Grafts
- •10.2.1 Split Calvarial Grafts
- •10.2.2 Bone Dust/Bone Chips
- •10.2.3 Autogenous Grafts from the Iliac Crest
- •References
- •11 Osteosynthesis of Craniofacial Fractures
- •11.1 Biomechanics: Facial Skeleton
- •11.3 Osteosynthesis of the Midface
- •11.3.1 Plating Systems
- •11.3.2 Miniplates: Microplates
- •11.3.3 Screw Systems
- •11.4 Surgical Procedure: Osteosynthesis of the Midface
- •11.4.1 Different Plate Sizes: Indication
- •11.4.2 Fracture-Related Osteosynthesis
- •11.4.2.1 Surgical Approaches
- •11.4.2.2 Lateral Midface Fractures
- •11.4.2.4 Complex Midfacial Fractures
- •11.5.1 Mesh-Systems
- •11.5.2 Indications and Advantages
- •References
- •References
- •12.1 Craniofacial Fractures
- •12.1.1 Concept of Reconstruction
- •12.1.5 Own Procedure: Statistics
- •12.2 NOE Fractures
- •12.3.1 Concept of Reconstruction
- •12.4 Zygomatico-Orbito-Cranial Fractures
- •12.5 Craniofrontal Fractures (CCF)
- •12.5.1 Concept of Reconstruction
- •12.5.6 Fractures of the Frontal Sinus with Comminution of the Infundibulum
- •12.6 Own Statistics
- •13.1 Infections and Abscesses
- •13.2 Osteomyelitis
- •13.3 Recurrent Liquorrhea
- •13.4 Hematoma: Central Edema
- •13.5 Subdural Hygroma
- •13.6 Frontal Sinus: Complications
- •13.7 Functional Neurological Deficits
- •13.8 Meningitis
- •13.9 Facial Contour Irregularities
- •13.10 Conclusion
- •References
- •14.1.1 Autogenous Grafts
- •14.1.1.1 Split Calvarial Grafts
- •14.1.1.2 Cartilage Grafts
- •14.1.3.1 Synthetic Calcium Phosphates
- •14.1.3.2 Synthetic Polymers
- •14.1.4 Titanium-Mesh
- •References
- •15.1 Overall Objective
- •15.2 Patient-Related Conditions
- •15.2.1 Size and Location of the Defect
- •15.2.1.1 Examples
- •15.2.2 General Health Status
- •15.2.3 Neurological Status
- •15.2.4 Patient’s Wish
- •15.2.5 Treatment Plan
- •15.2.6 Technical Aspects
- •15.3 New Developments
- •15.3 1.1 The SLM process
- •15.3.2 PEEK-Implants
- •15.3.3 Outlook
- •References
- •Index
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9 Methods of Dural and Skull Base Treatment |
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distinct tendency to shrink and must, therefore, be of sufficient size on insertion (Probst 1986). The grafts are fixed with fibrin glue and sutures.
There is a tremendous amount of clinical and experimental knowledge about autogenous fascia transplantation. All results indicate that free autogenous fascial tissue grafts (fascia lata, temporalis fascia) remain vital (Probst 1971, 1986). Blood supply is assured by direct spontaneous anastomosis between the vessels of the graft and those of the local tissues.
9.2.1.2 Autogenous Muscle Grafts
(Probst 1986; Stoll 1993)
In contrast to fascia grafts, autogenous muscle grafts taken from the frontalis, temporalis, or quadriceps femoris muscles share the disadvantageous tendency to shrink and cicatrize and are afflicted with the problems of other free transplants. Similar to autogenous bone grafts, autogenous muscle grafts must be surrounded by vital tissue in order to heal (Stoll 1993) (Fig. 9.1).
9.2.1.3 Pericranium Flap/Graft (Kessel et al. 1971; Jackson et al. 1986; Imhof 2000)
The vital and vasularized pericranial flap is available in a variety of sizes and because of its adaptability and vitality has become standard in skull base reconstruction.
Adjacent sections of pericranium may be used as nonvascularized tissue patches (Price et al. 1988).
9.2.2 Allogeneic Transplants
9.2.2.1 Lyophilized Dura
Freeze-dried lyophilized human dura, which was frequently used in the past, is only rarely used today due to the risk of slow virus infection [Jakob-Creutzfeld disease, bovine spongiform encephalopathy (MartinezLage et al. 1993; Lane et al. 1994; Christmann 2003)].
9.2.2.2 Collagenous Compounds
Today there is an increased availability of products based on collagen structural proteins. These compounds are derived from both humans and animals. Chemical processing can alter the connective tissue structures to such an extent that a mere acellular and antigen-free collagen frame remains (Chaplin et al. 1999). As a result, membranes exist which are exclusively composed of collagen fibrils or collagen-laminated substrates — e.g., polyglactin — without bearing the relatively high infectious risks of nontreated alloor xenogenic transplants (San-Galli et al. 1992).
Fig. 9.1 Harvesting of temporal muscle patches. (a) Reflected temporal fascia, muscle patch incised. (b) Muscle patch harvested prior to closure of temporal fascia
