Technician Update

Handling a basket case: complication After cervical spine stabilization

By Monique Cross, LVT

By Monique Cross, LVT

An 8-year-old Warmblood gelding used for high-level jumping was presented to Rood and Riddle Equine Hospital, in Lexington, Ky., for evaluation of right forelimb lameness and/or stiffness. Weight was 1,400 lb (636 kg). An extensive lameness examination, including nerve blocks, was performed, but it did not provide enough information for a diagnosis. A complete neurologic examination showed no neurologic deficits.

Stephen Reed, DVM, ACVIM, a neurologist at the hospital, suspected nerve compression along the spinal column and recommended a computed tomography (CT) scan and myelography with contrast to gather more information; the owners consented.

A few days later, the horse was sedated with xylazine, induced with ketamine and midazolam, and maintained with a triple-drip constant rate infusion of guaifenesin, ketamine and xylazine. He was placed in right lateral recumbency on a specialized myelography table, with his head elevated to 45°. His chin was flexed toward his chest, and a spinal needle was placed through the atlanto-occipital joint into the subarachnoid space by the veterinarian. A total of 35 mL of cerebrospinal fluid (CSF) was removed for testing, and iohexol contrast solution was administered. Radiographs of the neck in static, extended and flexed positions, extending through the C7-T1 joint, were obtained. The horse was then moved to CT, where the entire cervical spine was imaged. Recovery from anesthesia was uneventful.

Results of the CT scan and myelography showed the articular processes had overgrown on the right dorsolateral side at the C2-C3 joint, and there was suspected intervertebral disc material protruding into the ventral aspect of the spinal canal. A second site of compression was found at the C6-C7 joint with articular process overgrowth on both the medial and lateral aspects, and soft tissue material was again protruding into the ventral portion of the spinal canal.

This narrowing deformed the spinal cord at both locations. This articular overgrowth is often called Wobbler’s Syndrome. The enlarged articular processes of the vertebrae press into the spinal canal, causing deformation of the spinal cord and leading to neurologic or lameness symptoms (and occasionally both). This patient’s signs were mild and appeared more like a lameness or stiffness/weakness.

Wobbler’s Syndrome is congenital, and appears most commonly in larger-boned horses like Warmbloods and Thoroughbreds, although it can present in any breed. It is often diagnosed early, but occasionally, as with this patient, it is not diagnosed until they begin performing higher level work, such as Grand Prix dressage or high-level jumping. Although the C6-C7 joint is a common location for these lesions, the C2-C3 joint is not. The canal at this junction is quite spacious. Even if overgrowth occurs, there is enough room that it typically does not interfere with the spinal cord. When compression occurs at this location, it is usually due to a spinal misalignment rather than to large articular processes. The combination of an uncommon location and a second affected level made this case rare, but the surgical approach to repair is almost identical to that in common cases.

The findings were discussed with the owners, along with the recommendation of a double-level cervical stabilization surgery. The prognosis was described as guarded because of the unusual locations and necessity of 2 implants. After 5 months of conservative treatment, the owners agreed to the surgery.

The surgical procedure
In the early fall, the patient returned for surgery. Dr. Reed performed a follow-up neurologic examination; results showed the horse now had low-grade ataxia. Since the original examination was negative, it can be inferred that the horse had a gradual progression of disease.

A cervical stabilization procedure, also called a “basket surgery,” aims to fuse 2 adjacent vertebrae to prevent them from moving. Immediate benefit includes elimination of any symptoms caused by dynamic compression; however, the main goal of this procedure is long-term. Over the course of approximately 1 year, the articular processes should atrophy, and this reduction in size will give the spinal cord more room, hopefully eliminating any symptoms.

Once anesthetized, the horse was placed on the surgical table in dorsal recumbency, then clipped and aseptically prepared. Needles were placed superficially in the skin to serve as intraoperative radiographic markers.

On the morning of the surgery, the horse was given preoperative antibiotics, a tetanus toxoid injection, and a nonsteroidal antiinflammatory drug (NSAID). Results of bloodwork and a physical examination showed no abnormalities, so the patient was sedated with xylazine IV and induced with a combination of ketamine and midazolam IV. The horse dropped well with a head-rope assist. He was positioned carefully on the surgical table with a special wooden trough supporting the dorsal portion of the cervical spine to provide additional stability.

In anticipation of the potential for nasal edema due to recumbency, I placed an 18-mm, 16-inch nasal tube into the patient’s right nostril while he was being positioned. Anesthesia consisted of 3% isoflurane, which was reduced to 2% within the first 20 minutes. Due to the inability to access the head or neck during surgery, a proximal spot on the medial right hindlimb was clipped and aseptically prepped. A 14-gauge × 2-inch temporary catheter was placed in the caudal tibial vein for administration of lactated Ringer’s solution (LRS).

An area over the lateral side of the right distal limb was clipped and aseptically prepared for the placement of a 20-g × 1.5-inch temporary catheter in the metatarsal artery for invasive blood pressure monitoring. Initial mean arterial pressure (MAP) was 62 mm Hg; dobutamine via constant rate infusion (CRI) was started and titrated to effect. MAP increased to 72 mm Hg within 5 minutes, and it remained between 78 mm Hg and 91 mm Hg for the duration of the anesthetic event.

Analgesics, including an IM injection of detomidine in the right pectoral muscle and ketamine and lidocaine via CRI, were administered prior to the first incision. Within the first hour of anesthesia, calcium gluconate was added to the LRS to support cardiovascular function and potentially enhance neuromuscular strength during the recovery period.

To monitor his respiratory status, 3 arterial blood gas (ABG) samples were collected during the approximately 3-hour procedure. The first sample was taken at 68 minutes and showed mild hypercapnia (partial pressure of carbon dioxide [paCO2],
55.6 mm Hg), which was corrected by increasing the tidal volume (TV) from 8.5 L/breath to 9.5 L/breath. A second sample was taken 30 minutes later and showed mild hypoxia (partial pressure of oxygen [paO2],
91.6 mm Hg), which was quickly treated with administration of 12 puffs of albuterol for bronchodilation. A third sample was taken 20 minutes after the second, and showed a marked increase in hypoxia ([paO2],
62.5 mm Hg).

At that point, the surgeon was nearing the end of the surgical procedure, so the horse was treated with an additional 12 puffs of albuterol, and an alveolar recruitment maneuver was initiated. The horse’s positive end-expiratory pressure (PEEP) was increased to 5 cm H2O for 3 minutes, and then titrated as follows:

• Increased to 10 cm H2O for 3 minutes
• Increased to 15 cm H2O for 3 minutes
• Decreased to 10 cm H2O for 3 minutes
• Decreased to 5 cm H2O for 3 minutes
• Decreased to 0 cm H2O

Within minutes of completing the maneuver, the horse was taken to the recovery stall; a fourth ABG was not collected.

The horse was positioned in the recovery stall in right lateral recumbency with the recumbent limb pulled forward to prevent radial nerve paralysis. The nasal tube was secured to his halter with a quick-release knot, and 2 puffs of phenylephrine hydrochloride were administered into his left nostril to reduce any edema; 5 minutes of blow-by oxygen was provided using a demand valve.

A urinary catheter was placed to drain the bladder, reduce discomfort, and prevent early attempts to stand. After 5 L of urine was drained from the bladder, the catheter was removed. Once the patient was breathing spontaneously, he received IV xylazine. At the time of extubation, IV xylazine was again administered.

During recovery, 3 L of lactated Ringer’s solution with calcium gluconate was administered. In total, the patient received general anesthesia for 172 minutes, with a total downtime (including recovery) of 247 minutes. He received a total of 25 L of LRS (22 L intraoperatively and 3 L in recovery).

Post-anesthesia recovery complications
Initial recovery proceeded normally. The patient was able to swallow 20 minutes after arrival at the recovery stall and was extubated; he remained quiet for another 10 minutes. The anesthesia technician then noticed increased airway noise and entered the stall to adjust the nasopharyngeal tube. The surgeon and anesthesiologist were contacted and were on their way to evaluate.

Within approximately 2 minutes, the airway noises abruptly ceased, and the horse panicked—he began thrashing all limbs and demonstrated paradoxical respiratory movements (eg, rib cage rising while abdomen retracted). The anesthetist was no longer able to feel airflow from the horse’s nostril or from the end of the nasal tube. Within seconds, the mucous membranes began to darken and became cyanotic.

The anesthetist decided to attempt reintubation at this point; the nasal tube was removed, and an 18 mm endotracheal (ET) tube was placed in the same nostril. As soon as it passed the larynx, the horse took several large breaths and settled quickly. The surgeon and anesthesiologist had arrived and observed the above proceedings. A decision was made to have the anesthetist administer IV furosemide and 10 minutes of blow-by oxygen to offset potential pulmonary edema.

The ET cuff was left deflated, and the tube was secured to the halter to allow the horse to stand without accidental extubation. Approximately 30 minutes after blow-by oxygen was discontinued, the patient stood up unassisted in one strong, successful movement. Once standing, he coughed several times and produced thick, pale-pink foam from his mouth, nostrils, and ET tube, but he did not appear overtly distressed. Due to evidence of pulmonary edema, the surgeon and anesthetist administered 1 L of hypertonic saline to draw excess fluid from the interstitial (pulmonary) space into the vascular space, and 7.5 mL (30 mg) of IV dexamethasone sodium phosphate to decrease inflammation.

After approximately 20 minutes, most of the patient’s postanesthetic ataxia had faded, and the surgeon performed an endoscopic evaluation of the larynx via the left nostril. The nasotracheal tube was removed, and evaluation of the larynx post-extubation revealed an immobile left arytenoid and only slight movement of the right arytenoid on inspiration.

The horse appeared content and quiet, so he was carefully moved to his stall. He was observed closely, and after 45 minutes, the surgeon passed the endoscope again. The right arytenoid had regained most of its mobility, but the left arytenoid remained completely immobile. A tracheostomy kit was hung on the stall, and his respiratory rate and effort were monitored closely by the nursing team until the following morning. He remained comfortable and calm, with no further incidents, until his discharge from the hospital 5 days later. He was moved to a rehabilitation facility and recovered fully with no airway concerns.

Due to the anesthetist’s attentiveness to the patient in recovery and the speed of reintubation, the total time that the patient remained obstructed was minimal. The rapid administration of IV diuretics and anti-inflammatories allowed a quick resolution of the pulmonary edema, which was mild. The edema did not affect his recovery from surgery, and his retraining progressed as well as could be expected. At 1-year follow-up, the patient no longer displayed any sign of stiffness, lameness, or neurologic deficits, and he was in full work, preparing for his next show. MeV

WEAVING THE BASKET
In a basket surgery, the attending surgeon makes a ventral midline incision above the affected joint (or joints), bluntly dissects down to the trachea, and retracts it and the neighboring structures to gain access to the ventral aspect of the cervical spine. The surgeon then uses an array of drill guides, pins, and intraoperative radiographs to ensure the implant is in the correct location. A series of drill heads is then used to create a spot in the vertebral joint where the implant will be placed. This specialized implant, called a kerf-cut cylinder, is the “basket” in “basket surgery.” The implant is carefully placed and then packed with the bone pulp collected during the drilling process. Finally, the incision is closed in layers, and the horse is taken to recovery.

TEACHING POINTS
After independent research and discussion with the anesthesiologist and the surgeon, the following is what I think happened based on the evidence.

When I think of pulmonary edema, I think of fluid overload. Therefore, I first investigated the amount of fluid. According to protocols at Rood and Riddle Equine Hospital, the maintenance fluid rate for a healthy horse under general anesthesia is 11 mL/kg/hr. If I calculate based on only general anesthesia time, the horse received 11.53 mL/kg/hr. If I calculate based on total downtime, the horse received 9.8 mL/kg/hr. I do not think this was enough extra fluid to cause a problem in this case.

The other possible cause could be the upper airway obstruction event.

Since we know the arytenoids were not functioning properly, it is likely that, as he regained consciousness, he took deeper breaths, which increased airflow and caused the arytenoids to close together, resulting in laryngeal collapse and obstruction. His inability to breathe naturally caused panic, which lead him to attempt to take larger breaths. The large movement of the rib cage without the ability to move air caused negative pressure to build up inside the lungs. This large pressure gradient increased the permeability of the pleural membranes, allowing excess fluid to move into the alveoli. Ultimately, his problem was negative pressure-induced pulmonary edema.

The only question that remains, then, is why he became obstructed in the first place. The left-sided laryngeal paralysis was likely pre-existing. According to Auer & Stick (Equine Surgery, 4th edition. Elsevier Saunders; 2012), it is estimated that 2.5% to 8.0% of performance racehorses have laryngeal hemiplegia; however, the population investigated was Thoroughbreds. The incidence of laryngeal hemiplegia in heavy Draft horses is estimated to be closer to 35%.

This condition is typically chronic and would not have improved with time. The right-sided arytenoid weakness was likely a temporary partial paralysis caused by slight irritation of the vagosympathetic nerve trunk. During the procedure, the carotid artery and vagosympathetic nerve trunk are bluntly dissected away from the trachea and retracted to allow access to the surgical site. Though these delicate structures are retracted carefully and handled with deliberate gentleness, irritation or compression of the nerve trunk is still possible and is rare enough to be considered an acceptable risk of the procedure.

Even slight compression or irritation of this nerve trunk would cause, at the minimum, weakness of the right arytenoid cartilage that would improve with time—exactly as we observed in this case. I think that the chronic, complete paralysis of the left arytenoid and the temporary, partial paralysis of the right arytenoid, in addition to the increased airflow during the anesthetic recovery, caused laryngeal collapse and total upper airway obstruction.