Techniques for achieving atlantoaxial fusion include posterior interspinous fusion with sublaminar cables and iliac crest bone graft ( ▶ Fig. 7.1), C1–2 transarticular screw fixation, and interlaminar clamp fixation. Although each of these methods has been used successfully to achieve atlantoaxial fusion, anatomical factors may exist in certain situations that preclude their use. Interspinous fusion at C1–2 with sublaminar cables or interlaminar clamps cannot be performed if the posterior elements of C1 or C2 are absent or disrupted. C1–2 transarticular screws cannot be placed successfully in the presence of a “high-riding” vertebral artery, irreducible subluxation, severe cervicothoracic kyphosis, or destruction of the C2 pars interarticularis. In these cases, constructs using C1 lateral mass screws may be used to achieve fixation. C1 lateral mass screws may be used to provide additional fixation points in occipitocervical constructs, thus increasing resistance to construct failure in the cervical spine without increasing the number of cervical levels fused. Additionally, C1 lateral mass screws may be used as a supplement to or substitute for other forms of atlantoaxial fixation.

Atul Goel and Jürgen Harms are the surgeons who popularized the use of C1 lateral mass screw fixation in combination with C2 screw fixation. We have successfully used this construct to create solid fusions in numerous patients.

7.2 Patient Selection

7.2.1 Indications for Posterior C1–2 Stabilization

Trauma is among the most frequent indications for posterior C1–2 stabilization. Traumatic injuries that are amenable to posterior C1–2 fixation include certain subsets of type II and type III odontoid fractures.

Although many type II odontoid fractures can be treated either with immobilization or anterior odontoid screw fixation, several subsets of this fracture pattern are not amenable to these treatment measures. These subsets include type II odontoid fractures associated with fractures of the atlantoaxial joint, type II odontoid fractures with oblique fractures in the frontal plane that preclude odontoid screw placement, type II odontoid fractures with significant displacement that may not heal in immobilization (and are too displaced to place an odontoid screw), type II odontoid fractures with an associated Jefferson fracture, and type II odontoid fractures in older, osteoporotic patients.

In addition, patients with a very large thoracic kyphosis or a very large barrel chest are not candidates for odontoid screw fixation because the surgeon cannot achieve the appropriate angle for anterior odontoid screw placement. These patients may be treated with a posterior C1 and C2 stabilization procedure.

Even when there is a type II odontoid fracture that might heal with immobilization, in certain cases, immobilization is not practical. Older patients in particular do not heal well with immobilization. They have a higher rate of nonunion as a result of osteoporosis and have increased respiratory morbidity when placed in halo vests.

In addition, all patients initially treated with immobilization who develop a pseudarthrosis are not good candidates for subsequent attempts at anterior odontoid screw fixation because of the pseudarthrotic material occupying the fracture line.

For patients for whom immobilization has failed and who are no longer considered good candidates for anterior odontoid screw fixation, posterior C1 and C2 fixation is the one remaining treatment option. Type III odontoid fractures with atlantoaxial joint fracture combinations and type III odontoid fractures with associated Jefferson fracture are also unstable and are often best treated with a posterior C1 and C2 stabilization procedure. Instability resulting from congenital malformations of C2 (i.e., os odontoideum and odontoid agenesis) is another indication for treatment with C1 and C2 fixation.

Degenerative diseases, inflammatory diseases, tumors, and infections can also result in instability of the atlantoaxial complex. Specifically, rheumatoid arthritis can often result in atlantoaxial subluxation or superior migration of the odontoid into the foramen magnum (with compression of the brainstem and upper cervical spinal cord), necessitating a posterior occipitocervical decompression and fusion (with or without transoral resection of the odontoid).

Patients with destructive tumors or infectious processes who require transoral decompression of their lesions typically require C1 and C2 fixation either during the anterior approach or with a subsequent posterior approach. Postsurgical instability relating to C1 and C2 laminectomies, with or without removal of adjoining facets, is another indication for posterior C1–2 fixation. We have performed posterior lateral approaches to remove retro-odontoid degenerative masses and also to remove tumors within the spinal canal that inherently destabilize the C1–2 complex and require posterior C1–2 fixation.

Patients with ligamentous laxity may have resultant C1 and C2 instability. Ligamentous instability of C1–2 is identified with measurements of the atlantodental interval on flexion and extension views. Normally this interval should not exceed 2 to 4 mm. When the atlantodental interval exceeds 5 mm (in patients without rheumatoid arthritis), there is instability of the C1–2 complex, and posterior C1–2 fixation is indicated.

Furthermore, atlantoaxial rotatory dislocations are also an indication for C1 and C2 fixation. This problem can be treated via a posterior reduction and fusion approach.

7.3 Preoperative Preparation: C1 Lateral Mass Screws with C2 Pars or Pedicle Screw Fixation

7.3.1 Radiographic Studies

All of our patients are imaged using reconstructed computed tomographic (CT) images of the upper cervical spine to assess the exact location of the transverse foramen. We have found that CT is an excellent method to assess for variations in the normal anatomical course of the vertebral artery at C2, which may preclude transarticular screws or even C2 pars screws. In addition, we often also obtain a cervical magnetic resonance imaging scan to check the integrity of the transverse ligament and to assess the potential need for spinal canal decompression.

7.3.2 Medications

We recommend that patients be taken off of nonsteroidal anti-inflammatory drugs (NSAIDs) and anticoagulants 1 week before surgery to avoid platelet dysfunction. In addition, we ask patients to avoid NSAIDs for 3 months after surgery because these medications may inhibit bone fusion.

Preoperatively, patients are given 1 to 2 g of cefazolin for antibiotic prophylaxis. We typically also give patients 10 mg of dexamethasone at the start of the case.

7.3.3 Anesthetic Agents and Neuromonitoring

In patients without myelopathy, we typically do not use neuromonitoring. In these cases, we typically induce anesthesia with propofol and then maintain anesthesia with an inhalational anesthetic such as sevoflurane [1 to 2 minimal anesthetic concentrations (MAC)]. We use a short-acting paralytic to create temporary muscular relaxation for these patients to facilitate the dissection of the posterior cervical musculature easier.

Motor evoked (MEPs) and somatosensory evoked potentials (SEPs) may be used to ensure the integrity of the spinal cord during posterior cervical fixation in patients with cervical myelopathy. We caution, however, that SEP monitoring is not always accurate, and there have been cases where changes in evoked potentials have not been accompanied by changes in the neurologic status of the patient. In some cases, a neurologic injury has occurred without accompanying changes in the evoked potentials.

The choice of anesthetic agents is critical when evoked potentials are used. Paralytics cannot be used in these cases because they blunt the MEPs. Nitrous oxide cannot be used because it blunts SEPs. One MAC of vapor (inhalation agent) can also blunt evoked potentials. Consequently, we prefer to induce patients with propofol (2 to 3 mg/kg), and we maintain a propofol infusion throughout the case. After induction, we prefer to use one-half MAC of vapor (i.e., isoflurane) and remifentanil (0.1 to 0.25 mcg/kg per minute) as a narcotic infusion. This combination is least likely to affect the evoked potentials.

It is important to obtain baseline readings of the evoked potentials once general anesthesia has been induced. Because changes in the anesthetic regimen can cause changes in the evoked potentials, we try not to change the anesthetics or the doses throughout the case.

Furthermore, we also obtain baseline readings of the evoked potentials for severely myelopathic patients while the patient is supine. We then repeat the readings after positioning the patient prone to ensure that the change to the prone position has not created a stenotic situation with reduced potentials.

In addition, ensuring spinal cord perfusion throughout the case is important. We check the patient’s mean arterial pressure (MAP) before intubation. We maintain a MAP of greater than 90 mm Hg throughout the case. We do not hesitate to use transfusions and pressors (phenylephrine) as needed throughout the case to maintain this MAP parameter.

7.4 Operative Procedure

The patient is positioned prone on chest rolls, the arms are tucked at the sides, and the bed is placed in a moderate reverse Trendelenburg position (30 degrees up). The head is typically fixated using a Mayfield head holder (OMI, Inc., Cincinnati, Ohio). The neck is kept neutral and the head is placed in the military tuck position. The arms are tucked at the sides. The shoulders are retracted caudally using tape. The anatomical C1–2 realignment is then confirmed by lateral fluoroscopy before starting the operation. A midline incision is made extending from the suboccipital area to the spinous process of C3. The C2–3 facet joints are exposed, and the dorsal arch of C1 is exposed laterally, exposing the vertebral artery in the vertebral groove on the C1 arch. The C2 nerve root is identified and mobilized inferiorly ( ▶ Fig. 7.2). Bipolar cautery and hemostatic agents such as Gelfoam (Pfizer, Inc., New York, New York) are used to control bleeding from the venous plexus surrounding the C2 nerve root and also surrounding the vertebral artery. The lateral mass of C1 inferior to the C1 arch is exposed after the C2 nerve root has been mobilized inferiorly. The medial wall of the C1 lateral mass is identified using the forward-angle curet to palpate the medial limit of screw placement. The medial aspect of the transverse foramen at C1 and C2 can also be identified and serve as a lateral limit for screw placement.

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