Cranial defects occur among all ages from a wide variety of causes. Trauma, infection, congenital malformations, pathology, and tumors and their surgical management can all lead to skull abnormalities and defects. Small defects that are covered in formidable soft tissue may not need repair. Other cranial defects can be immediately reconstructed when they are small or iatrogenically created for surgical access; most require secondary reconstruction.
Etiology
Cranial decompression has gained popularity in treating elevated intracranial pressure in traumatic brain injury. The mortality rate for this group of patients is high despite aggressive surgical and medical intervention. A full-thickness bone flap is removed and commonly stored in a freezer or subcutaneous abdominal pocket. The brain is often swollen and herniating out of the confines of the skull, and dural expansion is performed with autologous tissue or dural substitutes. After acute intracranial and neurosurgical issues are resolved, the autologous bone flap is normally replaced.
Complex or depressed skull fractures may require bone removal. If present, dural tears must be closed and elevated intracranial pressures treated. Current recommendations favor replacing the bone fragments at initial surgery. If the wound is contaminated, copious antibiotic irrigation should be used. The bone segments should also be soaked in antibiotic irrigation or betadine before reimplantation. Intravenous antibiotics are then continued for at least 48 hours. When the bone cannot be initially replaced, delayed skull reconstruction is indicated.
Skull osteomyelitis can arise from multiple sources, including extension of aerodigestive infection, progression of cutaneous wounds, and direct expansion of middle ear and mastoid disease. Each of these processes is associated with characteristic virulent organisms that can combine with patient susceptibility to produce a clinically significant infection. Although treatment with antibiotics is often successful, surgical drainage, debridement, and ultimately resection is sometimes necessary. Bone and tissue cultures should be taken to help guide length and type of antibiotic therapy. Unless frank osteomyelitis is noted at surgical drainage and debridement, the bone flap can be replaced, followed by placement of a subgaleal drain to eliminate fluid and infectious materials.
Encephaloceles are the most common congenital cause of cranial and skull base defects. Occipital lesions are normally diagnosed early in life because of their location. Midline, orbital, nasal, and skull base lesions may present in a delayed fashion as nasal obstruction, rhinorrhea, vision changes, recurrent meningitis, and facial deformity. Their treatment requires a combined neurosurgical and craniofacial approach for resection of redundant neurologic tissue, repair of dura, and separation of intracranial contents through reconstruction of the cranium and skull base.
Various other pathologic entities can lead to cranial defects that also require reconstruction. Extension of extracranial malignancies such as melanoma can necessitate skull removal as part of their surgical treatment. Osseous pathology such as fibrous dysplasia can also involve the cranium, and in severe cases may require contouring or resection of the affected area. Additionally, treatment of pathology with radiation and chemotherapy can lead to soft tissue fibrosis and atrophy and may require a soft tissue flap to cover the bony defect. Management of the primary pathology will dictate timing of the bony and soft tissue coverage.
Goals of treatment
The goal of secondary cranioplasty is restoration of permanent cerebral protection with both hard and soft tissue in a cosmetically acceptable fashion. Normalization of neurologic symptoms and cerebral physiology are also desired outcomes of successful reconstruction. Extreme examples of altered cerebral physiology that are associated with cranial defects are the syndrome of the trephined and paradoxically low intracranial pressure. Syndrome of the trephined involves the onset of new neurologic deficits from altered cerebral blood flow in brain parenchyma under the defect, whereas low intracranial pressure with herniation has been attributed to a negative pressure gradient between cranial and spinal compartments. Replacement of the bone flap can be curative in both conditions. Establishing a balance between waiting for resolution of intracranial pathology (eg, trauma, infection, bleeding, increased intracranial pressure, cerebrospinal fluid malabsorption) and the development of complications from the defect itself requires experience and good judgment.
Successful reconstruction necessitates the treatment and resolution of the cause. A healthy soft tissue envelope also must be present to accommodate an expanded cranial contour. Although numerous treatment protocols can be found in the literature, each patient requires a thorough physical examination and radiographic evaluation, including CT or MRI studies. The subsequent development of a thoughtful treatment plan must take into consideration the cause, timing, and resolution of the injury and intracranial sequelae, and the characteristics of the cranial defect.
Goals of treatment
The goal of secondary cranioplasty is restoration of permanent cerebral protection with both hard and soft tissue in a cosmetically acceptable fashion. Normalization of neurologic symptoms and cerebral physiology are also desired outcomes of successful reconstruction. Extreme examples of altered cerebral physiology that are associated with cranial defects are the syndrome of the trephined and paradoxically low intracranial pressure. Syndrome of the trephined involves the onset of new neurologic deficits from altered cerebral blood flow in brain parenchyma under the defect, whereas low intracranial pressure with herniation has been attributed to a negative pressure gradient between cranial and spinal compartments. Replacement of the bone flap can be curative in both conditions. Establishing a balance between waiting for resolution of intracranial pathology (eg, trauma, infection, bleeding, increased intracranial pressure, cerebrospinal fluid malabsorption) and the development of complications from the defect itself requires experience and good judgment.
Successful reconstruction necessitates the treatment and resolution of the cause. A healthy soft tissue envelope also must be present to accommodate an expanded cranial contour. Although numerous treatment protocols can be found in the literature, each patient requires a thorough physical examination and radiographic evaluation, including CT or MRI studies. The subsequent development of a thoughtful treatment plan must take into consideration the cause, timing, and resolution of the injury and intracranial sequelae, and the characteristics of the cranial defect.
Augmented treatment planning and custom implant fabrication
The availability of high-resolution imaging has combined with high-powered computer hardware, image manipulation software, and rapid prototyping to augment the reconstructive process. This process is facilitated by the use of stereolithographic biomodels, virtual surgical planning tools, and the production of custom fabricated craniomaxillofacial implants.
The evaluation of patients before cranioplasty includes CT imaging acquired at a maximum increment of 1.0-mm axial slices. Specific protocols are available from each implant or model manufacturer. These data are then converted to Digital Communications in Medicine (DICOM) standard files, which the radiology provider should make available on CD or DVD. The DICOM dataset can then, physically or electronically, be sent to companies that are approved by the US Food and Drug Administration to produce biomodels or custom craniomaxillofacial implants. If a model is desired, most manufacturers offer several different grades of material and levels of detail depending on the needs of the surgeon. These models can normally be fabricated and shipped within days. Surgical models are helpful for planning, and can also be used by the surgeon to locally fabricate or precontour implants.
Several manufacturers can facilitate surgeon-directed custom implant fabrication. This process involves DICOM data segmentation and the creation of a virtual skull model. Depending on the size, location, and complexity of the cranial defect, a virtual reconstruction can be performed to mirror or mimic normal anatomy. Subtracting the patient’s virtual skull from the reconstructed skull then creates a virtual implant. The treatment plan can then be reviewed and modified by the surgeon. If necessary, a biomodel and implant prototype can be printed for physical evaluation and approval. If autogenous bone will be used for the clinical reconstruction, the virtual implant can be printed and used as a surgical template. Otherwise, the implant is fabricated, sterilized, and shipped to the surgeon for use at surgery.
Overall, this process allows for improved visualization of the cranial defect and helps optimize the treatment plan by allowing for multiple iterations of reconstruction. The fabricated implants are highly accurate and lead to improved cosmetic outcomes, reduction in dead space, and reduced operative times. These benefits easily outweigh the increased costs associated with these techniques and materials that are commonly cited as a factor to justify exclusive use of traditional methods.
Skull Defect Reconstruction
Soft Tissue Preparation
The evaluation of the overlying soft tissue is a critical step before definitive cranial reconstruction. Consideration must be given to the health and thickness of the soft tissue, location of prior incisions, presence of scar tissue, anticipated expansion of the surface area, contour of the cranium after cranioplasty, and any history of radiation or infection. Depending on the size and nature of the soft tissue deficiency, staged soft tissue management may be required instead of simultaneous reconstruction. Regardless, placements of incisions away from the cranial defect, careful handling of tissues, and tension-free closure are all required.
Numerous local soft tissue rotation and advancement flaps are available for scalp resurfacing. Most designs involve local tissue excision and rearrangement with the use of back cuts and local undermining. These flaps can vary in size and range from simple to complex. If local tissue rearrangement is insufficient, regional or distant soft tissue recruitment requires careful consideration. The temporoparietal fasciocutaneous flap is the regional flap most commonly used in this area. It can be based on the anterior or posterior temporal arteries and has a great deal of flexibility in size and pedicle length. In some circumstances the skin flap overlying the cranial defect may be healthy but thin. Free fat grafting or the use of thin but well-vascularized fascial flaps, including the pericranium or temporoparietal fascia, may add additional bulk. If a significant amount of tissue is required or the area has a significant history of irradiation, microvascular free tissue transfer must be considered and may include either robust muscle flaps (ie, rectus abdominis, latissimus dorsi), which will atrophy to a more appropriate contour over time, or thinner tissues (ie, radial forearm, anterior lateral thigh) that are more consistent in appearance but provide less initial bulk.
Scalp expansion is an adjunctive technique that may be performed before hard tissue repair. Although specific protocols may vary, surgical implantation of tissue expanders is followed by serial hydraulic inflation. Resection of the damaged tissue occurs at skull reconstruction, with immediate coverage by the expanded scalp. The location of the expanders must be carefully chosen in areas with stable underlying cranium and healthy overlying hair-bearing scalp. Additional consideration must be given to the planned location of the incision for future exposure of the cranial defect, and the size of the planned scalp resection. Expanders are normally placed between the pericranium and galea, allowed to heal for 2 to 3 weeks, and then expanded on a weekly basis until the desired amount of expansion is achieved before final cranioplasty.
Neurosurgical Management
Outstanding neurosurgical issues can dictate success or failure of cranioplasty despite meticulous technique. Before skull reconstruction, imaging studies should be performed to assess brain pathology, rule out hydrocephalus or stroke, and ensure adequate brain relaxation to provide the optimum milieu for cranial repair. Many patients develop hydrocephalus after trauma or infection. If the cisterns around the brainstem and cervicomedullary area are patent, a lumbar drain or lumbar shunt can provide good cerebrospinal fluid (CSF) diversion. In most cases, however, a permanent ventriculoperitoneal shunt is needed. The risks of shunting include malfunction and infection (foreign body implant). Meticulous technique, thorough skin preparation (chlorhexidine or betadine), systemic antibiotics, and diligent postoperative wound care can minimize infection. If CSF leakage is present, it must be addressed through direct repair or diversion at or before cranial repair. Postoperative intracranial pressure should be maintained in the normal range (<20 mm Hg), because high or low pressures can contribute to bone resorption, poor healing, and other neurosurgical sequelae after cranioplasty.
General Surgical Technique
The patient is brought to the operating room and placed in a supine position for oral endotracheal intubation. The placement of ocular lubricant and tarsorrhaphy sutures is ideal. Depending on the location of the planned reconstruction, the patient is placed on a horseshoe Mayfield headrest in a supine or prone position. If prone, the globes must be checked to ensure they are free from pressure. The head and body must be positioned so that the C-spine is in a passive and neutral position.
The planned incision is ideally marked over healthy tissue away from the area of reconstruction and should take into account the need for wide exposure, management of the soft tissue as previously discussed, a hidden position of the final scar, and tension-free closure. Depending on the location, not all prior incisions should be reused, and often a posteriorly positioned postauricular curvilinear coronal incision is the most appropriate. If desired, a small area of hair surrounding the incision line may be trimmed with electric hair clippers but should not be shaved.
Preoperative antibiotics should be used to cover skin flora unless intradural or aerodigestive tract communication is present. This treatment is continued for 48 hours for autogenous reconstruction, and for an additional 72 hours for alloplastic reconstruction. Preoperative steroids should be used to assist with soft tissue edema and continued for 24 hours unless contraindicated. A solution of 1% lidocaine with 1:100,000 epinephrine is used to inject the incision line and into the subgaleal plane for hydrodissection. The cutaneous incision is opened in segments with a knife. Dissection in the subgaleal plane is then performed bluntly, leaving the pericranium in place. The incision is then retracted with opposing skin hooks and a needle tip cautery device used to cut and coagulate the deeper tissues. This technique virtually eliminates blood and minimizes damage to the hair follicles. Raney scalp clips may be counted and applied if desired once the incision is completely opened.
Dissection is continued until the margins of the entire defect are delineated in a supraperiosteal plane. Further dissection of the scalp overlying the cranial defect may be difficult. It is best completed with a combination of sharp and blunt instrumentation with the goal of leaving a healthy overlying skin flap without violating the dura. The pericranium can then be incised around the margin of the defect, and pericranial flaps can be developed that are extremely versatile and may be used for dural patching, soft tissue bulk, and separation of the aerodigestive tract. Subperiosteal dissection is then performed and any bleeding from the cranium controlled with gelfoam and thrombin. The use of bone wax is minimized unless significant osseous bleeding occurs.
In the anterior region, the supraorbital neurovascular bundles should be identified and protected within the soft tissue flap. Laterally, the temporalis musculature should be left in place to minimize potential muscle atrophy and temporal hollowing. If temporal exposure is necessary, the temporalis can be taken up with the scalp flap or incised, leaving a small cranial margin of muscle to help with reapproximation, and then elevated as an independent muscle flap. If the zygomas or lateral orbits are to be exposed, dissection must be performed in a plane deep to the temporal branch of the facial nerve.
If dural repair is necessary, pedicled or free pericranium should be used over synthetic materials. This technique provides watertight coverage to prevent CSF leakage and brain herniation, and the pericranium itself has osteoinductive properties. Intracranial dead space is often left untreated to allow for any brain swelling that may occur. It is also reasonable to obliterate the space with epidural tacking sutures to prevent air or fluid accumulation and possible mass effect. Ventricular or lumbar shunt management is important because both can create negative intracranial pressure that can exacerbate intracranial dead space. Trapped air usually resolves on its own, but air under tension can be treated with high flow oxygen supplementation or, in extreme cases, aspiration.
The frontal and ethmoidal sinuses are often in continuity with the area requiring reconstruction. If a communication is encountered, any respiratory epithelium must be completely removed. The nasofrontal or ethmoidal recess should be packed with autologous bone, fat, muscle, dermis, or fascia, and pericranial tissue can then be brought down to provide an additional barrier between dura and aerodigestive tract. Consideration should be given to delaying further reconstruction until healing has occurred.
After wide exposure and management of the underlying dura, brain, and aerodigestive tract communication, the boney margins of the defect should be clearly delineated. Rotary instruments or rongeurs should be used to freshen the bone edges back to healthy bleeding bone with defined margins. If an autogenous bone graft is to be used for reconstruction, a template can be fashioned at this time, or a prefabricated template may be brought to the field and verified. The donor site is chosen and exposed, and the bone graft is harvested as outlined later. After the donor site is reconstructed, the graft should be adjusted to match the defect with minimal gaps or overlaps. Bone grafts may be bent, scored, or segmented to provide the best fit and contour. Large block grafts may be fixated in one piece, whereas larger defects may require sequential reconstruction and fixation.
If a prefabricated implant is used, it should be soaked in antibiotic laden irrigation. After placement over the defect, it should be evaluated for bulk, contour, margin thickness, and position. Significant modifications are more readily made at a separate sterile table. Minor modifications may be completed in situ before or after application of fixation. The use of lag screws is ideal but require enough implant overlap and thickness to prevent material fracture. Otherwise, fixation should be applied with the fewest number of low-profile titanium plates and screws necessary for rigid stability.
In all cases the soft tissues should be redraped and the contour of the reconstructed skull evaluated for further irregularities. Over or under contour deformities may be corrected through repositioning of the principle bone graft or implant, additional onlay bone grafting, placement of bone cement, or ostectomy with rotary or hand instruments.
Once the reconstruction is complete, available pericranial flaps can be used to cover the implant edges and fixation hardware. If the temporalis muscles have been elevated, they must be reapproximated to the temporal line with permanent tacking sutures. If the dissection has included the zygomas or periorbital regions, the lateral canthi and supporting fascia of the face must also be resuspended using permanent tacking sutures to the skull, pericranium, or temporal fascia. Copious antibiotic laden irrigation should be used to ensure the wound is free of debris. Raney clips should be removed and counted. Closure is then performed in layers using Vicryl to close the underlying galea and subcutaneous tissue. The skin should be closed with permanent sutures to be removed in 7 to 14 days. Drains are not normally used, but meticulous attention must be given to hemostasis and layered closure to minimize the risk of hematoma and seroma. After closure, the head should be irrigated, cleaned, and covered with antibiotic ointment, fluff dressings, and a loose stocking.
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