Treatment of traumatic cervical myelopathy with surgery, prolonged positive-pressure ventilation, and physical therapy in a dog

Sean D. Smarick Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Helena Rylander Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Jamie M. Burkitt Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Nancy E. Scott Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Jacqueline S. Woelz Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Karl E. Jandrey Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Janet Aldrich Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Beverly K. Sturges Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Abstract

Case Description—A 9-year-old dog was evaluated for traumatic cervical myelopathy after a surgical attempt to realign and stabilize the C2 and C3 vertebrae.

Clinical Findings—The dog could not ventilate spontaneously and was tetraplegic; positive-pressure ventilation (PPV) was maintained. Myelography and computed tomography revealed spinal cord compression with subluxation of the C2 and C3 vertebrae and extrusion of the C2-3 intervertebral disk.

Treatment and Outcome—Surgically, the protruding disk material was removed and the vertebrae were realigned with screws and wire. For PPV, assist control ventilation in volume control mode and then in pressure control mode was used in the first 6 days; this was followed by synchronized intermittent mandatory ventilation until 33 days after the injury; then only continuous positive airway pressure was provided until the dog could breathe unassisted, 37 days after the injury. Physical therapy that included passive range of motion exercises, neuromuscular electrical stimulation, and functional weight-bearing positions was administered until the dog was discharged 46 days after injury; the dog was severely ataxic and tetraparetic but could walk. Therapy was continued at home, and 1 year later, the dog could run and had moderate ataxia and tetraparesis.

Clinical Relevance—Hypoventilation with tetraparesis in traumatic spinal cord injury can be successfully treated with PPV exceeding 30 days, surgery, and physical therapy.

Abstract

Case Description—A 9-year-old dog was evaluated for traumatic cervical myelopathy after a surgical attempt to realign and stabilize the C2 and C3 vertebrae.

Clinical Findings—The dog could not ventilate spontaneously and was tetraplegic; positive-pressure ventilation (PPV) was maintained. Myelography and computed tomography revealed spinal cord compression with subluxation of the C2 and C3 vertebrae and extrusion of the C2-3 intervertebral disk.

Treatment and Outcome—Surgically, the protruding disk material was removed and the vertebrae were realigned with screws and wire. For PPV, assist control ventilation in volume control mode and then in pressure control mode was used in the first 6 days; this was followed by synchronized intermittent mandatory ventilation until 33 days after the injury; then only continuous positive airway pressure was provided until the dog could breathe unassisted, 37 days after the injury. Physical therapy that included passive range of motion exercises, neuromuscular electrical stimulation, and functional weight-bearing positions was administered until the dog was discharged 46 days after injury; the dog was severely ataxic and tetraparetic but could walk. Therapy was continued at home, and 1 year later, the dog could run and had moderate ataxia and tetraparesis.

Clinical Relevance—Hypoventilation with tetraparesis in traumatic spinal cord injury can be successfully treated with PPV exceeding 30 days, surgery, and physical therapy.

A 9-year-old 22.7-kg (49.9-lb) spayed female Catahoula mixed-breed dog was referred to the Veterinary Medical Teaching Hospital, University of California, Davis, for continued care for a traumatic cervical myelopathy, 2 days after trauma. The dog had been given artificial respiration by use of a mouth-to-snout technique immediately after the trauma until it was brought to a local emergency hospital. Physical examination findings at that time included obtundation, nonresponsive dilated pupils, apnea, HR of 40 beats/min, and cyanotic mucous membranes. The dog was intubated and manually ventilated. Atropine (0.05 mg/kg [0.023 mg/lb], IV), dexamethasone sodium phosphate (1 mg/kg [0.45 mg/lb], IV), and maintenance fluids (IV) were administered. Abdominal radiography did not reveal any abnormalities. Survey thoracic radiography revealed subluxation of the second and third cervical vertebrae with dorsal displacement of the third cervical vertebra (Figure 1). Methylprednisolone sodium succinate (30 mg/kg [13.6 mg/lb], IV) was administered.

Figure 1—
Figure 1—

Lateral radiographic view of the cervical and thoracic regions of a dog with subluxation of C2 and C3 and dorsal displacement of C3.

Citation: Journal of the American Veterinary Medical Association 230, 3; 10.2460/javma.230.3.370

The dog was then referred to a surgical specialist and transported with manual ventilation. At the specialty hospital, ventilation was continued with a volume-controlled, time-cycled, pressure-limited anesthetic ventilator.a Methylprednisolone sodium succinate (10 mg/kg [4.5 mg/lb], IV) and mannitol (500 mg/kg [227 mg/lb], IV) were administered every 6 hours for 2 doses. A ventral surgical approach to the cervical portion of the vertebral column was performed to stabilize the vertebrae with cross pins and PMMA. Postoperative radiography revealed partial realignment of the vertebrae, but dorsal and ventral spinal cord compression with luxation of the right articulating process and subluxation of the left articulating process persisted. After recovery from anesthesia, the dog was unable to ventilate spontaneously. A tracheostomy tube was placed and PPV was continued. Neurologic examination revealed normal mentation but no respiratory effort or voluntary motor function in the limbs. Withdrawal and myotatic reflexes and deep pain sensation were unaffected.

Physical examination findings at the Veterinary Medical Teaching Hospital included absent spontaneous thoracic wall excursions and an HR of 42 beats/min. Neurologic examination revealed normal mentation, nonambulatory tetraplegia with superficial pain perception in all 4 limbs, and voluntary movement in the tail. Examination of all cranial nerves and spinal reflexes yielded normal results.

Positive-pressure ventilation was continued with a critical care ventilatorb with a Shiley size 4 cuffed tracheostomy tube in volume-control mode. The VT was initially 300 mL, respiratory rate was 20 breaths/min, and PEEP was 3 cm H2O; this resulted in a mean airway pressure of 6.7 cm H2O and PIP of 20 cm H2O. The minute volume was titrated to a PaCO2 of 40 ± 5 mm Hg by adjusting the rate, VT, or both. When the dog's condition was stable, end-tidal carbon dioxide concentrations and PvCO2 were monitored as surrogates of PaCO2 with intermittent validation by use of arterial samples. The FIO2 was adjusted to maintain PaO2 > 80 mm Hg, and after the dog's condition was stable, pulse oximetry readings were used to monitor oxygen saturation of hemoglobin. Tracheostomy tube care and recumbent patient care were provided according to a standard protocol.

Electrocardiographic monitoring revealed sinus bradycardia with occasional second-degree (type II) atrioventricular block, which was treated for 5 days with glycopyrrolate (0.01 mg/kg [0.005 mg/lb], IM, q 2 h as needed) to keep the HR > 60 beats/min. Twelve hours after admission, gastric distension was detected and treated with decompression via orogastric intubation. Abdominal radiography did not reveal any explanation for the gastric distension, such as compartmentalization or malposition of the stomach. Subsequent episodes occurred and were treated similarly.

The dog was anesthetized for neurologic diagnostic tests. Myelography revealed loss of the ventral contrast column and attenuation of the dorsal contrast column at the level of the C2-3 intervertebral disk space. There was also angulation of the vertebral canal with spinal cord compression from the cranial part of the body of C3. Computed tomography confirmed dorsal and ventral spinal cord compression at this site along with subluxation of C2 and C3 with the C3 luxated dorsally. A ventral surgical approach to the cervical portion of the vertebral column was made. The PMMA was removed, and the pins were left in place and shortened. A small ventral slot was made through the C2-3 disk. A moderate amount of protruding annulus fibrosus was removed from the spinal canal. The vertebrae were realigned by use of bone-holding forceps and secured with screws and wire. The PMMA was placed over the pins and screws to cover all metal implants. Postoperative radiography (Figure 2) revealed improved alignment of C2 and C3.

Figure 2—
Figure 2—

Lateral radiographic view of the cervical region of the dog in Figure 1, after orthopedic surgery.

Citation: Journal of the American Veterinary Medical Association 230, 3; 10.2460/javma.230.3.370

The dog was unable to trigger spontaneous breaths with the ventilator inspiratory trigger set at 0.5 L/min, and PPV was continued in pressure assist–control mode with a PEEP of 3 cm H2O, PIP of 15 cm H20, respiratory rate of 18 breaths/min, and FIO2 of 0.25, which resulted in a VT of 250 to 300 mL and PaO2 > 80 mm Hg. Midazolam (0.1 to 0.2 mg/kg/h [0.05 to 0.90 mg/lb/h]) and fentanyl (0.1 to 0.4 μg/kg/min [0.05 to 0.18 μg/lb/min]) were administered IV for analgesia and sedation for 1 week. The dog remained tetraplegic and was unable to lift its head, but could move it from side to side and rotate the head along the long axis of the neck.

Because of the recurrent gastric distension, a 24-F gastrostomy tube was surgically placed and gastropexy was performed. Nutritional support was started with 59 mL of a 2:1 mixture of rice and low-fat cottage cheese every 4 hours. Metoclopramide (0.02 mg/kg/h [0.01 mg/lb/h], constant rate infusion, IV) was given to control vomition. The vomiting continued, so the tube feedings were discontinued after 2 days and partial parenteral nutrition was instituted with a mixture of lipids, amino acids, dextrose, and B vitamins. Gastric distension continued to recur and appeared to be related to episodes of agitation. Approximately 2 to 2.5 L and up to 6 L of air were aspirated each day via the gastrostomy tube during most of the hospital stay.

On day 8 following the injury, PPV was continued but in synchronized intermittent mandatory ventilation mode with the inspiratory trigger set at −0.6 cm H2O; PS of the spontaneous breaths was provided. The number of breaths initiated by the dog progressively increased overall but varied throughout the day. Pressure support was set between 4 and 7 cm H2O to maintain end-tidal carbon dioxide concentration < 50 mm Hg.

Over the next 2 weeks, there was a 7.5-kg (16.5-lb) loss in body weight despite reinstituting enteral nutrition via the gastrotomy tube, first with low-fat cottage cheese and rice and then with a low-fat canine maintenance diet slurry.c Because the hydration needs were being met via the gastrotomy tube, IV administration of fluids was discontinued.

Initially, nursing treatment and rehabilitation focused on prevention of secondary complications caused by immobility via pressure relief, turning body position every 4 hours, and passive range-of-motion exercises. Sixteen days after surgery, a physical therapist was consulted and treatment techniques were suggested to promote active movement. The rehabilitation treatments were continued on a twice-daily basis by the attending neurology clinicians and veterinary student on the basis of the physical therapist's reevaluations and recommendations.

Manual therapy techniques were introduced to stimulate reflexive and voluntary motor responses of the thoracic and pelvic limbs. Neuromuscular electrical stimulation was used to elicit muscle contractions of the thoracic limbs. Functional weight-bearing positions were gradually introduced to promote proximal muscle strength for postural control and eventual coordinated movement. It was not necessary for the dog to completely master a functional task prior to advancing to the next level of challenge. The duration of each therapy session was determined by the dog's strength, endurance, and quality of posture or movement.

In lateral recumbency, passive range-of-motion exercise was performed in all planes of movement for each joint. Neuromuscular electrical stimulation was applied to the triceps.d Strengthening for pelvic limbs included manually facilitated active range-of-motion exercises, hip abduction isometric holds, and use of the resisted withdrawal reflex. Body massage techniques included skin rolling, stroking, and kneading. The first functional weight-bearing position introduced was sternal recumbency. Because the dog required support to hold its head up, cervical muscle strengthening consisted of short-duration isometric holds.

Weight-bearing positions were used progressively on the basis of strength of the proximal musculature and the return of muscle tone and voluntary motor control of the limbs. The sternal position was advanced to sternal with pelvic limb weight bearing over the edge of the table, on a lower surface, and with hip joints in neutral position and stifle joints extended. Manually supported sitting on a raised surface was used to introduce thoracic limb weight bearing. Supported standing over an inflatable rolle was used to advance weight bearing to all limbs.

Voluntary movements in the limbs and tail were seen 6 days after the injury. On the 25th day, the dog attempted stepping movements with the left thoracic limb and attempted to climb over the inflatable roll with the pelvic limbs. By day 32, the dog was able to independently roll from right lateral recumbency to sternal recumbency and propelled itself with the pelvic limbs to the front edge of the treatment table. Manual resistance was added to active movement of the pelvic limbs, and functional weight-bearing challenges were advanced to longer duration with less assistance.

Rehabilitation sessions were increased to 3 times/d. The dog consistently had increased motivation and functional movement during the owners' visits. The dog was able to hold its head up for several hours and had limb advancement during gait training, with all but the right thoracic limb. During body weight–supported gait training over 3 m, the thoracic region was supported with a harnessf and gentle joint compression was applied manually to each limb, during the stance phase to facilitate antigravity muscle recruitment and increased contralateral limb flexor activity.

During this time, progression was made until nearly all breaths were patient-initiated and the PS ranged from 3 to 6 cm H2O. However, from immediately after to 6 hours after physical therapy sessions, hypoventilation and decreased patient-initiated breathing required an increased need for PS. Aminophylline was administered (15 mg/kg [6.8 mg/lb], q 12 h) via the gastrostomy tube in an attempt to increase the strength of diaphragm contractions. On the 33rd day of ventilation, only CPAP (2 cm H2O) was provided. This was discontinued by day 35 except during physical therapy sessions, during which a PS of 4 to 6 cm H20 was provided. The ventilatory support was fully discontinued 37 days after the injury.

Thirty-nine days after the injury, the dog was able to take a few steps with support, placing all limbs but dragging the right thoracic limb. Food was offered PO. Forty-one days after the injury, the tube feeding was discontinued and all food was given orally. The aerophagia diminished, and the feeding tube was removed 43 days after the injury. The dog was discharged to the owner 46 days after the injury. At the time of discharge, the dog was severely ataxic and tetraparetic. The dog was able to walk with minimal support, with the right thoracic limb knuckling more often than the other limbs. The pelvic limbs were less paretic than the thoracic limbs. Upon discharge, a comprehensive home rehabilitation program was demonstrated and recorded on video for the family's reference.

At the 1-year follow-up examination, the dog was able to run (with some ataxia) and catch a thrown toy. On neurologic examination, the dog was ambulatory with moderate generalized ataxia and tetraparesis. There was occasional dragging of the right thoracic limb toes during running. Conscious proprioception was absent in all limbs. Spinal reflexes were within normal limits. Approximately 1.5 years after the accident, the dog was euthanized for complications from hemangiosarcoma.

Discussion

Traumatic cervical spinal cord lesions in dogs have been described.1 Of 56 dogs with cervical spinal cord injury, severity of the neurologic deficits and the extent of delay between the time of injury and referral were associated with a poor outcome.1 Seven of the dogs were euthanized in the first 24 hours, 11 were treated surgically, and the remainder were treated nonsurgically. There was a 36% perioperative mortality rate, which is consistent with previous reports and was attributed to cardiopulmonary dysfunction; however, of the dogs that survived the perioperative period, 100% achieved a functional recovery. Another report2 indicated that among 14 dogs with cervical spinal cord lesions, lesions between C2 and C4 and treatment by means of a dorsal decompressive laminectomy were associated with a substantially increased risk of perioperative hypoventilation.

Spinal cord injury results in neurologic deficits related to the affected spinal cord segment1,3–5 In addition to the motor deficits resulting in tetraparesis or tetraplegia with cervical spinal cord injury, ventilatory function may also be compromised. Experimentally in dogs, spinal paralysis caudal to and including the fourth thoracic spinal nerve roots results in substantial decreases of respiratory frequency and tidal volume attributable to loss of function of the intercostal muscles. Lesions cranial to the C5 also will cause more hypoventilation because of the additional loss of motor function of the diaphragm because it is innervated by the phrenic nerve, which originates from the third to fifth cervical spinal segments. Immediate ventilatory support is needed to avoid hypoxemia and respiratory acidosis.6 Hypoventilation with cervical spinal cord injury has been reported in dogs.1-3,7

The dog described in the present report received early clinical recognition and intervention after the traumatic episode, support during transport, appropriate referral to specialty centers, and rehabilitation; these factors are described in emergency medical systems as the chain of survival.8 Ventilatory support has been described in dogs with cervical spinal cord disease and hypoventilation.1-3,7 In those studies and others9–15 regarding PPV in dogs, no dogs were ventilated for > 14 days. However, similar to previous reports2,13–14 of dogs with hypoventilation, the dog reported here was mostly ventilated in a synchronized intermittent mandatory ventilation mode and had similar PIP and VT.

Patients requiring PPV who do not have pulmonary disease generally require less aggressive ventilator settings than patients with pulmonary disease.16,17 The dog reported here was successfully ventilated with mouth-tosnout breathing, hand bagging, and a ventilator designed for surgical anesthesia in the initial days of treatment. This reinforces that patients with hypoventilation caused by cervical myelopathies can be initially ventilated in most veterinary settings and during transport; however, long-term ventilation should be performed with a critical care ventilator.

Compared with hand bagging and anesthesia ventilators, a critical care ventilator offers the advantages of an adjustable FIO2, a humidification system, different ventilatory modes, and the availability of respiratory mechanics information that allows for better ventilatory management and weaning. Ventilating with FIO2 > 0.6 runs the risk of oxygen toxicosis, which causes respiratory failure. Oxygen toxicosis is related to the time, atmospheric pressure, and FIO2 to which the patient is exposed. In dogs, FIO2 < 0.6 at atmospheric pressure is not associated with the development of oxygen toxicosis, and although there are variations among individuals, an FIO2 of 1.0 is tolerated for at least 24 hours. Patients with hypoventilation without pulmonary disease require ventilation but not oxygen supplementation; however, recumbency can result in atelectasis that may require some oxygen supplementation. Long-term ventilation without humidification can increase the risk of infection and increase the viscosity of secretions, leading to undesirable complications such as ventilator-associated pneumonia or airway obstruction. Pressuresupport ventilation and CPAP are modes of ventilation in which the patient is spontaneously breathing but the ventilator is providing positive pressure during inspiration or throughout inspiration and expiration. These modes decrease the work of breathing by partially unloading the inspiratory muscles and, during CPAP, also prevent atelectasis similar to PEEP. They are useful in providing incremental support and the weaning of a patient from PPV.17,18

The dog in this report was ventilated through a tracheostomy tube. It has been suggested that ventilating through a tracheostomy tube permits better neurologic evaluation and weaning of patients with neurologic disease because minimal or no sedation is usually needed.2,16 In this report, once the dog's anxiety and pain were treated, sedation was discontinued. In humans with spinal cord injuries requiring long-term ventilation, earlier weaning and decreased duration of hospitalization in an intensive care unit have been achieved in part by use of a tracheostomy tube.19

Injuries to the cervical spinal cord have the potential to involve the autonomic nervous system. Potentially life-threatening bradyarrhythmias have been reported in dogs undergoing cervical spinal surgery.1,3 Bradycardia in the dog reported here was likely a direct result of the injury to the cervical spinal cord. The bradyarrhythmia responded to anticholinergic administration, which suggested either decreased sympathetic or increased vagal tone as a cause of the bradycardia.20

The dog received high-dose corticosteroids within 8 hours of the injury. The use of corticosteroids in acute spinal injury remains controversial. Results of initial experimental studies suggested that high doses of methylprednisolone could alter outcome when used within 8 hours of the initial injury. This led to large-scale human studies that appear increasingly not to support use of that drug. A few experimental studies have been performed in dogs, without resultant clinical recommendations; however, the risk of gastrointestinal ulceration has been well documented, and medications such as H2 antagonists, prostaglandin E1 analogs, and gastrointestinal protectants will not prevent their occurrence despite widespread recommendations of their use.21–25

Physical therapists play a leading role in the rehabilitation of spinal cord–injured human patients. Treatment strategies include preventing the secondary complications of immobility to promoting optimal locomotor and functional recovery. Recently, the benefits of physical rehabilitation for canine patients with neurologic conditions have been recognized.26,27 Neurorehabilitation should progress to facilitation of active muscle contractions as soon as possible because there is no measurable neural adaptation or prevention of muscle atrophy with passive movements. Adding manual resistance to the active movement recruits more motor units than active movement alone and can be applied to a withdrawal reflex early in rehabilitation. At the time of discharge, carefully outlined rehabilitation home programs are essential to ensure optimal functional outcome. The outcome of the case reported here indicated that hypoventilation with tetraparesis in traumatic spinal cord injury can successfully be treated with PPV exceeding 30 days, appropriate surgical intervention, and directed physical therapy.

ABBREVIATIONS

HR

Heart rate

PMMA

Polymethylmethacrylate

PPV

Positive-pressure ventilation

VT

Tidal volume

PEEP

Positive end-expiratory pressure

PIP

Peak inspiratory pressure

FIO2

Fraction of inspired oxygen

PS

Pressure support

CPAP

Continuous positive airway pressure

a.

SAV 2500, Surgivet, Waukesha, Wis.

b.

Esprit ventilator, Respironics, Carlsbad, Calif.

c.

Waltham Low Fat, Royal Canin USA Inc, St Charles, Mo.

d.

JACE TriStim, Jace Systems, Cherryhill, NJ.

e.

40-cm Physio-roll, Sportime, Norcross, Ga.

f.

Walkabout Harnesses, Santa Cruz, Calif.

References

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  • Figure 1—

    Lateral radiographic view of the cervical and thoracic regions of a dog with subluxation of C2 and C3 and dorsal displacement of C3.

  • Figure 2—

    Lateral radiographic view of the cervical region of the dog in Figure 1, after orthopedic surgery.

  • 1

    Hawthorne JC, Blevins WE, Wallace LJ, et al. Cervical vertebral fractures in 56 dogs: a retrospective study. J Am Anim Hosp Assoc 1999;35:135146.

    • Search Google Scholar
    • Export Citation
  • 2

    Beal MW, Paglia DT, Griffin GM, et al. Ventilatory failure, ventilator management, and outcome in dogs with cervical spinal disorders: 14 cases (1991–1999). J Am Vet Med Assoc 2001;218:15981602.

    • Search Google Scholar
    • Export Citation
  • 3

    Clark DM. An analysis of intraoperative and early postoperative mortality associated with cervical spinal decompressive surgery in the dog. J Am Anim Hosp Assoc 1986;22:739744.

    • Search Google Scholar
    • Export Citation
  • 4

    Jeffery ND, Blakemore WF. Spinal cord injury in small animals 2. Current and future options for therapy. Vet Rec 1999;145:183190.

  • 5

    Rosenfeld JF, Vaccaro AR, Albert TJ, et al. The benefits of early decompression in cervical spinal cord injury. Am J Orthop 1998;27:2328.

    • Search Google Scholar
    • Export Citation
  • 6

    Skjodt NM, Farran RP, Hawes HG, et al. Simulation of acute spinal cord injury: effects on respiration. Respir Physiol 2001;127:311.

  • 7

    Olby N, Munana K, De RL, et al. Cervical injury following a horse kick to the head in two dogs. J Am Anim Hosp Assoc 2002;38:321326.

  • 8

    American Red Cross. Emergency response. Philadelphia: Mosby Lifeline, 1997;56.

  • 9

    Beal MW, Poppenga RH, Birdsall WJ, et al. Respiratory failure attributable to moxidectin intoxication in a dog. J Am Vet Med Assoc 1999;215:18131817.

    • Search Google Scholar
    • Export Citation
  • 10

    Campbell VL, King LG. Pulmonary function, ventilator management, and outcome of dogs with thoracic trauma and pulmonary contusions: 10 cases (1994–1998). J Am Vet Med Assoc 2000;217:15051509.

    • Search Google Scholar
    • Export Citation
  • 11

    King LG, Hendricks JC. Use of positive-pressure ventilation in dogs and cats: 41 cases (1990–1992). J Am Vet Med Assoc 1994;204:10451052.

    • Search Google Scholar
    • Export Citation
  • 12

    Parent C, King LG, Van Winkle TJ, et al. Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985–1993). J Am Vet Med Assoc 1996;208:14281433.

    • Search Google Scholar
    • Export Citation
  • 13

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