- •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
6.3 Orbital Injuries |
105 |
|
|
6.3.4 Fracture Signs
6.3.4.1 Clinical Manifestations
Clinical signs of orbital wall fractures are emphysema, orbital hematoma, infraorbital nerve hypesthesia, altered position of the globe, disturbed eye motility, retraction syndrome and changes of the palpebral fissure (Neubauer 1987; Stassen et al. 2003; Dutton and Al Qurainy 1991).
Clinical manifestations in orbital wall fractures
•Change in globe position
•Disturbance of eye motility
•Pseudoptosis
•Orbital emphysema
•Hypesthesia of the infraorbital nerve
•Retraction syndrome
•Change in width of the palpebral fissure
6.3.4.2 Change in Globe Position
The position of the globe is determined by the volume of the orbital fatty tissue, the periocular muscle balance, tissue hydration and tension of the ligaments and septa (Manson et al. 1980).
Factors influencing the globe position
•Volume of periorbital fatty tissue
•Balance of ocular muscle tone
•Ligament integrity
•Atmospheric pressure
•Tissue hydration
Changes in globe position are either due to an increase/ decrease in osseous orbital volume or increase/ decrease in orbital/periorbital soft-tissue volume. An increase in orbital volume/deficit in periorbital tissues results in an enophthalmus, muscular imbalance and disturbed eye motility; a reduction in bony orbital volume/increase in periorbital soft tissue will result in exophthalmus, disturbed motility and change in the globe position (Parsons and Mathog 1988; Stassen et al 2003).
6.3.4.3 Enophthalmus
An anterior-posterior change in the globe position, an enophthalmus is caused by either a fracture-related size increase of the orbital cavity or a reduction in soft-tissue volume (Manson et al. 1986; Stassen et al 2003).
Enophthalmus
Reasons for a relative or absolute increase in orbital volume with changes in the position of the globe (anterior-posterior)
Increase in orbital volume |
Loss of support by orbital walls |
|
– fractures |
Reduction in fat volume |
Relative loss – herniation |
Loss of fatty tissue |
Irreversible loss – necrosis, fat |
|
liquefaction, fibrosis |
|
|
6.3.4.4 Exophthalmus
An exophthalmus results from an inward displacement of bony wall fragments or through a pathological increase in orbital soft-tissue volume.
Exophthalmus
Reasons for a relative or absolute volume reduction with changes in the position of the globe (anteriorposterior)
•Inward dislocation of orbital wall fragments (blow-in fracture)
•Reduction of osseous orbital volume
•Retrobulbar – intraconal hematoma
•Edema – emphysema
•Subperiosteal hematoma
6.3.4.5 Vertical Displacement of the Globe
Vertical changes in the position of the globe are based on either a dislocated orbital floor fracture with antral soft-tissue prolapse or on an orbital roof fracture of the blow-in type.
Reasons for vertical globe displacement
Orbital floor fracture |
Globe elevation – hematoma |
|
Globe depression – floor defect |
Orbital roof fracture |
Globe depression |
|
Hematoma, emphysema |
|
Fragment displacement (blow-in |
|
fracture) |
|
|
