- •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
13.5 Subdural Hygroma |
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Raveh and Vuillemin (1988) found recurrent liquorrheainonly1.9%of374patientstreatedforcranio -facial fractures. The number of preoperative cerebrospinal fluid (CSF) rhinorrheas of patients operated on within the first 24 h, however, was unknown (Probst and Tomaschett 1990).
Sealing of dural lacerations has become more successful with the introduction of fibrin glue and the use of fascia-lata grafts (Raveh et al. 1984, 1988; Probst and Tomaschett 1990; Lädrach 2007) found postoperative CSF leakage in 2.3% of craniofacial traumas with skull base and dural injuries.
In our patient group, recurrent liquorrhea occurred in 2.8% of all operated patients. In the remaining patients, neither immediate postoperative nor late liquorrhea was found.
This proves that our surgical technique, which includes wide exposure, multi-layered dural and skull base repair and primary bony reconstruction provides reliable and stable results.
Our treatment concept for recurrent liquorrhea initially consists of waiting for 2-3 weeks with simultaneous antibiotics, 30° head inclination and lumbal drainage. If no spontaneous occlusion of the fistula occurs, localization of the leakage is performed with the use of CT/ Jotrolan - CT/MRI/Liquor Scintigraphy/Na-Fluorescein liquor marking.
dead space, an efficient separation between paranasal sinuses and intracranial space and the protection and support of neural structures and bone grafts (Eufinger et al. 1999; Stepnick 1999).
Flap techniques for skull base reconstruction
Local flaps
Temporal flap
Pericranial flap
Galea flap
Free flaps (fascio-cutaneous)
Lateral upper arm flap
Anterior lateral thigh flap
Rectus abdominis flap
Scapula/parascapular flap
Radialis forearm flap
Latissimus dorsi flap
DIEP flap
The selection of free flaps is based upon:
•Approach and possibility of integration
•Necessary volume
•Possible anastomoses
•Possibility of contouring
Control of the vitality of the inserted microvascular flaps and skin paddles is important, but difficult. In extreme situations angiographies or endoscopic controls may be necessary (Fig. 13.5).
Treatment concept for recurrent liquorrhea:
•Wait 2-3 weeks/antibiotics/30° head elevation/ lumbar drainage
•Clarify fistula localization
•(Coronal CT/Jotrolan-CT/MRI/liquor scintigraphy/Na fluorescein)
•Frontal skull base revision
Depending on the localization of recurrent liqor fistulas, either the transfrontal or the endonasal approach is performed. Occasionally a combined procedure is necessary.
In extreme cases with delayed liquorrhea and extensive bone loss, the skull base is either reconstructed with bone grafts or titanium mesh. The reconstructed skull base has to be covered with local flaps (pericranial flaps) or, alternatively, occluded by integrating microsurgically anatomized free flaps (fascio-cutane- ous flaps) (Seeger 1983; Bootz and Gawlowski 1995; Schmelzeisen and Schliephake 1998).
The advantages of microvascular free flaps are a secure watertight dural closure, the obliteration of any
13.4 Hematoma: Central Edema
In 2% of our patients, an epidural hematoma developed in the postoperative phase, which had to be evacuated according to the progression evident on computed tomography (CT). Meticulous intraoperative hemostasis, watertight dural occlusion, tack-up sutures and a subgaleatic suction drainage are important prophylactic measures.
Irreparable cerebral damage from central edema (2%) and severe cranio-cerebral trauma with extensive hemorrhage were responsible for the postoperative mortality in 4% of our patients.
13.5 Subdural Hygroma
Subdural effusions are an accumulation of fluid between the dura and arachnoid membrane. They occur as a result of cranio-cerebral injury and, rarely, as a postoperative complication of craniofacial injuries. Their treatment
244 |
13 Complications and Late Sequelae Following Craniofacial Reconstruction |
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a1 |
a2 |
a3 |
b1 |
b2 |
c1 |
c2 |
e |
d1 |
d2 |
d3 |
13.8 Meningitis |
245 |
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a
b1
b2
Fig. 13.5 Microvascular free flaps for coverage a traumatic liquor fistula 17 years after severe craniofacial trauma with extensive loss of bone in the anterior skull base. (a) Skull base exposure with large skull base defect (arrow) after bilateral craniotomy and frontal osteotomy. (b) Insertion and anastomosis of a microvascular DIEP flap before and after reintegration of the frontal segment and coverage of the lacerated and scarred dura with a parieto-occipital pericranial flap
corresponds with that of subdural hematomas with recraniotomy and hygroma removal as well as tack-up sutures and placement of an epidural suction drainage (Schmidek and Sweet 1988) (Fig. 13.6).
13.6 Frontal Sinus: Complications
If there is remaining mucosa following cranialization of the frontal sinus, this may lead to formation of mucoceles, pyoceles, and epidural abscesses (Lädrach 2007: 2%). We observed mucocele formation at a frequency of 3.3% in the region of the frontal sinus (Neidhardt 2002).
These patients were re-craniotomized, the mucocele removed and the residual dead space filled either with a pericranial flap or cancellous bone grafts (Baker et al. 2003) (Figs. 13.7, 13.8 and 13.9).
13.7 Functional Neurological Deficits
Nearly 7% of our patients had persisting anesthesia of the supraorbital nerve. In 3%, permanent weakness of the frontal branch of the facial nerve was found, and in 4% there was a traumatic injury of the optic nerve with loss of vision. In 2% of the patients, posttraumatic epilepsy occurred as a result of the primary trauma. Olfactory dysfunction (hypor anosmia) as a result of the surgical intervention (transfrontal-intracranial) was found in 8% (Neidhardt 2002).
13.8 Meningitis
Meningitis following skull base revision is always a sign of persisting, mostly occult liquorrhea. Every suspicion of liquorrhea must, therefore, be examined until finally proven otherwise. There was no occurrence of meningitis in our patient group, whereas Lädrach (2007) observed postoperative meningitis in 2.1%.
Fig. 13.4 Frontal osteomyelitis. Reconstruction of the craniofrontal region with titanium mesh (a1–a3). Depressed cranio- naso-orbito-maxillary fracture. (b1–b2) Primary reconstruction of the frontocranial and naso-ethmoidal region. (c1) Chronic infection with cutaneous fistula formation (5 weeks after primary
reconstruction). (c2) Revision with removal of all infected bone fragments and the osteosynthesis material and reconstruction with titanium mesh. (d1–d3) Postoperative X-ray control. (e) Integrated titanium mesh 12 months postoperatively. No signs of infection
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13 Complications and Late Sequelae Following Craniofacial Reconstruction |
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a |
b |
Fig. 13.6 Subdural hygroma following caniofacial reconstruction. (a) CT: enlargement of the subdural space over both frontal lobes with fluid collection of varying density, partly also fresh blood following hemorrhage. (b) Bilateral opening of the dura demonstrating enlargement of the subdural space
a
b1
b2 |
b3 |
Fig. 13.7 Posttraumatic mucocele of the frontal sinus. (a) Depression of the orbital roof and caudal dislocation of the left globe by the expanding mucocele. (b) MRI demonstrating the expanding mucocele in the frontal sinus. Downward displacement of the left globe and atrophy of the orbital roof. The high T1 signal indicates high protein content
13.8 Meningitis |
247 |
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a1 |
a2 |
b1 |
b2 |
c |
d |
Fig. 13.8 Expanding mucocele following craniofacial treatment (8 years postoperatively). (a) Preoperative caudal dislocation of the left globe. (b) Bone resorption as a result of expansion of the mucocele. (c) Contour reconstruction with frontal bone fragments following exstirpation of the mucocele. (d) Filling of the defect with cancellous bone grafts. (e) Reconstruction with titanium mesh. (f) Correct postoperative contour normal position of the globe
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13 Complications and Late Sequelae Following Craniofacial Reconstruction |
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e1 |
e2 |
Fig. 13.8 (continued)
a |
b |
c
Fig. 13.9 Expanding mucocele of the frontal sinus. (a) Mucocele of the frontal sinus. (b) Extirpation of the mucocele. (c) Sinus obliteration with homogenized cancellous bone grafts and coverage with stabilizing titanium mesh
