Anesthetic Considerations in a 21-Year-Old Female Undergoing High-Grade L4–S1 Spondylolisthesis Decompression and Fusion

A 21-year-old female (BMI 18) presented for high-grade L4–S1 spondylolisthesis decompression and fusion under general anesthesia. The airway was secured in the supine position with a 6.5 mm North Pole nasal RAE tube inserted via the left nostril to minimize oral tube–related soft tissue trauma. Following intubation, the patient was positioned prone with hip extension to optimize surgical exposure and restoration of lumbar lordosis. Neuromonitoring included somatosensory evoked potentials (SSEPs), motor evoked potentials (MEPs), and anal sphincter electromyography (EMG) to preserve sacral nerve integrity. The surgery was performed on a Jackson table with free-abdominal suspension.

1. Respiratory Concerns

Anatomical Basis

Respiratory mechanics are driven by the diaphragm, intercostal muscles, and posterior paraspinal musculature. In the prone position, especially with hip extension, abdominal viscera are displaced cranially, compressing the diaphragm and reducing its caudal excursion. Chest supports limit rib cage expansion, altering thoracic compliance.

Pathophysiology

Prone positioning increases intra-abdominal pressure (IAP), which is transmitted to the thoracic cavity and reduces overall lung compliance by 20–35% under general anesthesia. Functional residual capacity (FRC) decreases approximately 1–1.5% for each mmHg rise in IAP. Dependent alveoli collapse, reducing transpulmonary pressure gradients, increasing intrapulmonary shunt fraction, and predisposing to hypoxemia.

Molecular Basis

Compression of alveoli reduces surfactant activity, leading to microatelectasis. Hypoxia activates hypoxic pulmonary vasoconstriction (HPV) through inhibition of oxygen-sensitive potassium channels in pulmonary arterial smooth muscle cells. This results in calcium influx, vasoconstriction, and a rise in pulmonary vascular resistance.

Risks

Patients may develop reduced FRC, increased peak inspiratory pressure, alveolar collapse, hypoxemia, and ventilator-induced lung injury if airway pressures exceed 25 cmH₂O. Prone positioning also increases the risk of endotracheal tube kinking, migration, and elevated cuff pressures.

Mitigation Strategies

Pressure-controlled ventilation with tidal volumes of 6–8 mL/kg ideal body weight and positive end-expiratory pressure (PEEP) of 5–10 cmH₂O should be used. Recruitment maneuvers every 30–60 minutes are recommended. FiO₂ should be kept below 0.8 to avoid absorption atelectasis. The nasal RAE tube must be secured, and cuff pressure monitored regularly.

2. Cardiovascular Concerns

Anatomical Basis

The inferior vena cava (IVC), lying retroperitoneally anterior to the vertebral bodies, is susceptible to compression during hip extension and abdominal pressure, particularly at the L4–L5 level near the aortic bifurcation.

Pathophysiology

An IAP greater than 12 mmHg reduces venous return and stroke volume by up to 25%. General anesthesia compounds this effect through vasodilation and blunting of baroreceptor reflexes via central depression of the nucleus tractus solitarius. Positive-pressure ventilation further diminishes preload.

Molecular Basis

Reduced preload decreases myocardial stretch, impairing stroke volume generation via the Frank–Starling mechanism. At the cellular level, diminished sarcomere stretch reduces the calcium sensitivity of troponin C, impairing cross-bridge cycling and contractile force.

Risks

Hypotension is observed in 20–40% of prone cases under general anesthesia. Low-BMI patients, such as this case, are especially vulnerable to organ hypoperfusion.

Mitigation Strategies

Preload should be optimized with judicious fluid administration. Phenylephrine infusion serves as the first-line vasopressor. Free-abdominal positioning on the Jackson table reduces IAP and improves venous return.

3. Neurological and Positioning-Related Injuries

Anatomical Basis

Peripheral nerves at risk during prone positioning include the brachial plexus, from excessive arm abduction; the ulnar nerve, from compression at the cubital tunnel; and the lumbosacral nerve roots, from traction during spinal correction. Sacral nerve roots (S2–S4) innervating the external anal sphincter are of special concern, necessitating intraoperative EMG monitoring.

Pathophysiology

Stretch and compression impair intraneural blood flow, producing ischemia. Sustained ischemia compromises Na⁺/K⁺-ATPase function, causing axonal swelling and predisposing to Wallerian degeneration.

Molecular Basis

Ischemia induces glutamate excitotoxicity through NMDA receptor activation, leading to calcium overload, mitochondrial dysfunction, and neuronal injury.

Risks

Nerve injury occurs in 1–5% of prone spine surgeries. Rarely, compartment syndrome may occur.

Mitigation Strategies

Adequate padding, neutral joint alignment, and vigilant neuromonitoring are essential.

4. Ocular Complications

Anatomical Basis

The optic nerve, encased in cerebrospinal fluid within the subarachnoid space, drains venously through the ophthalmic veins into the cavernous sinus. Prone positioning increases venous pressure, compromising outflow.

Pathophysiology

A rise in intraocular pressure (IOP) coupled with a fall in mean arterial pressure (MAP) reduces ocular perfusion pressure (OPP = MAP − IOP). Prolonged reduction in OPP leads to ischemic optic neuropathy.

Molecular Basis

Ischemia of the optic nerve results in mitochondrial dysfunction of retinal ganglion cells, triggering cytochrome c release and caspase-mediated apoptosis.

Risks

Perioperative visual loss occurs in 0.03–0.2% of prone spinal surgeries.

Mitigation Strategies

Head position should remain neutral or slightly elevated. Adequate perfusion should be maintained with MAP >65 mmHg and hemoglobin >9 g/dL. Direct ocular pressure must be avoided at all times.

5. Airway and Oropharyngeal Concerns

Anatomical Basis

The nasal RAE tube traverses the nasal cavity, nasopharynx, and oropharynx into the trachea. In the prone position, neck flexion or extension alters tracheal length and tube positioning.

Pathophysiology

Neck flexion shortens the trachea, risking mainstem bronchial intubation. Prone positioning increases venous engorgement, raising cuff pressure and predisposing to mucosal ischemia.

Molecular Basis

When cuff pressure exceeds 30 cmH₂O, mucosal capillary perfusion is compromised. This leads to hypoxia-induced upregulation of inflammatory mediators such as interleukin-1β and tumor necrosis factor-α, contributing to ulceration and potential airway injury.

Risks

Endotracheal tube dislodgement occurs in 1–3% of prone cases. Macroglossia and vocal cord injury are additional risks.

Mitigation Strategies

ETT placement should be reconfirmed after positioning using capnography and, if necessary, fiberoptic bronchoscopy. Continuous cuff pressure monitoring is advised throughout the procedure.