- •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
6.1 Combined Skull Base and Midface Fractures |
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Fig. 6.21 Orbital apex syndrom with internal ophthalmoplegia and amaurosis and complete iridoplegia following zygomaticoorbital fracture on the right
Symptoms
•Loss of function of cranial nerves III, IV, VI
•Damage of the optic nerve (N. II) with loss of visual acuity
Clivus Syndrome
Intracranial bleeding can lead to a compression and interruption of the oculomotor nerve at the clivus prior to its point of entrance into the superior orbital fissure. The clinical consequence is a mydriasis on the affected side.
6.1.2.3 Vascular Injuries in Skull Base Trauma
Particularly endangered in frontal skull base injuries are the cavernous sinus and the sagittal sinus. There is potential injury to the internal carotid artery by fractures in the sphenoid region, especially in the pyramidal apex. Carotid-cavernous sinus fistulas are more common than isolated injuries to the internal carotid artery.
Cavernous Sinus Syndrome
In severe craniofacial trauma with fractures of the sphenoid and/or petrous bone, there may also be an injury to the internal carotid artery on its course through the cavernous sinus (Takenoshita et al. 1990). As a consequence of arterial damage, arterial blood flow into the venous circulatory system occurs (cavernous arterio-venous fistula), producing a back-flow in the orbital veins (superior ophthalmic vein) (Hasso et al. 1979; Harris et al. 1984).
Clinically, this results in a massive unilateral (occasionally bilateral and seldomly contralateral) pulsating, progressive exophthalmus (exophthalmus pulsans)
and leads to an extreme conjunctival reddening through intense dilatation and congestion of the conjunctival and episcleral veins. There is additional chemosis and lid swelling.
This results in a pulse synchronic sound above the eye and beside the temple and cerebral nerve damage (abducent nerve, oculomotor nerve, trochlear nerve, first, and second trigeminal branches) due to their course within the cavernous sinus wall as well as reduction in visual acuity and visual field. Further risks arise from raised intraocular pressure.
The reduction of vision may end in a complete amaurosis. Vascular fistulas can be detected by MRI examination as well as by angiography (Schaller 2002) (Fig. 6.22).
Symptoms
•Internal ophthalmoplegia
•Exophthalmus (pulsating)
•Ptosis
•Conjunctival injections
•Pulse synchronic sound
Thrombosis of the Superior Ophthalmic Vein
Fractures in the region of the orbital roof can lead to a thrombosis of the superior ophthalmic vein, resulting in a mild exophthalmus and damage to the external branch of the oculomotor nerve. Ptosis and reduced motility are clinical signs.
Craniofacial injuries can also lead to disruptions of the ophthalmic and the anterior cerebral arteries as well as the anterior and posterior ethmoidal arteries. In frontal skull base injuries the cavernous sinus and the sagittal sinus are particularly susceptible to lacerations. Thrombi, hemorrhage, and air embolism are possible consequences (Fig. 6.23).
