STANDARDS of CARE. Acute spinal cord injury (ASCI) is a common EMERGENCY AND CRITICAL CARE MEDICINE ACUTE SPINAL CORD INJURY

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1 Peer Reviewed AUGUST 2007 VOL 9.7 STANDARDS of CARE EMERGENCY AND CRITICAL CARE MEDICINE FROM THE PUBLISHER OF COMPENDIUM ACUTE SPINAL CORD INJURY Christina L. Vitale, DVM Resident, Veterinary Neurology/Neurosurgery Joan R. Coates, DVM, MS, DACVIM (Neurology) Associate Professor Veterinary Medicine and Surgery Veterinary Medical Teaching Hospital University of Missouri College of Veterinary Medicine Acute spinal cord injury (ASCI) is a common occurrence in dogs and cats, and it results in significant morbidity and mortality. The causes of ASCI are broadly classified as traumatic or vascular. Traumatic injuries may be from either internal or external causes. The most common cause of trauma-related ASCI in dogs is intervertebral disk disease (IVDD) with extrusion of the nucleus pulposus (Hansen type I). Vertebral fracture luxation or subluxation is often caused by vehicular trauma, and the thoracolumbar region is most frequently involved. Atlantoaxial instability may occur because of an underlying congenital anomaly or a traumatic incident. Fibrocartilaginous embolism (FCE) is a common ischemic insult to the spinal cord. Coagulopathy is a potential cause of intraspinal hemorrhage. Another categorization scheme for ASCI relates to the severity of injury. Complete spinal cord injury is characterized by physical or functional transection of the spinal cord, causing complete cessation of neurotransmission. In animals, this is clinically manifested as a loss of deep nociception. Incomplete injuries leave some functional axons with reduced or temporary loss of neurotransmission. The pathophysiology of ASCI includes primary and secondary injury processes. Types of primary spinal cord injury are concussion, compression, traction, laceration, and ischemia. Concussive injury occurs when external forces that vary in velocity are applied to the spinal cord tissue. Compressive injury from sustained pressure on the cord causes tissue deformation. Traction injury occurs with stretch of neural tissue. Laceration injury occurs when the nerve fibers or axons are severed. Ischemic injury results from blockage of blood flow to the spinal cord. Secondary axonal and myelin degeneration result from tissue ischemic necrosis. After the primary insult, secondary injury ensues. The primary injury causes direct damage of microvasculature, which begins the ischemic cascade. Release of excitatory neurotransmitters and vasoactive substances further damages the local vasculature and neuronal and glial cell membranes. Compromise of tissue perfusion and excessive neuronal excitation cause increased intracellular calcium and production of free radicals. Extracellular potassium concentrations also increase during secondary injury, resulting in loss of neurotransmission and membrane hyperpolarization. Release of vasoactive substances causes vasospasm. Normal spinal cord tissue has autoregulatory capabilities to allow for maintenance of perfusion despite changes in systemic blood pressure. Injured spinal cord tissue loses this autoregulatory capacity, thus exacerbating ischemia. Damaged lipid membranes release arachidonic acid, causing accumulation of leukotrienes and platelet-activating factor. Spinal cord grey matter is more susceptible to secondary injury because of the presence of motor neuron cell bodies, a higher metabolic demand, and increased vascularity. The end result of secondary spinal cord injury is local expansion of necrosis and apoptosis. Although most of the secondary injury occurs within the first 24 to 72 hours, apoptosis can continue for months after the injury. The prognosis for patients with ASCI varies depending on the rapidity and severity of injury. Veterinary practitioners need to be familiar with patient assess- Also in this issue: 9 Canine Brucellosis 1

2 ment to make appropriate decisions for diagnostic procedures and treatment options. DIAGNOSTIC CRITERIA Historical Information Gender Predisposition There is no gender predisposition, but intact animals are more likely to roam and have increased exposure to potential causes of external trauma. Age Predisposition Type I IVDD usually occurs in dogs older than 3 years of age. Chondrodystrophoid dogs are more frequently affected between 4 and 6 years of age. Nonchondrodystrophoid dogs are frequently affected between 6 and 8 years of age. Although less frequent than in dogs, IVDD in cats occurs between 3 and 9 years of age. External trauma can affect animals of any age, but young animals are more likely to roam and be exposed to external trauma. FCE is prevalent in young to middle-aged dogs and cats. Breed Predisposition IVDD: Dachshunds are the most commonly affected breed. Other predisposed chondrodystrophoid breeds include beagles, bassett hounds, Pekingese, Pembroke and Cardigan Welsh corgis, Lhasa Apsos, and miniature poodles. Overall, IVDD is more frequent in small-breed dogs. Largebreed dogs that are commonly affected include Labrador retrievers and Doberman pinschers. There is no known breed predilection for IVDD in cats. External trauma: Any breed may be affected by external trauma. FCE occurs most frequently in nonchondrodystrophoid large-breed dogs. Breeds with a higher prevalence include miniature schnauzers, German shepherds, and Irish wolfhounds. FCE has not been widely reported in cats, but several recent reports have suggested that FCE may be more common in cats than previously thought. Owner Observations Clinical signs of ASCI vary with the extent, rapidity, and location of injury. Signs range from hyperesthesia to paraplegia and loss of nociception. Severe cervical spinal cord lesions may cause abnormal respiratory patterns and respiratory distress. The time of onset for ASCI is often peracute. An inciting event related to exercise such as jumping from furniture or vigorous play often occurs with IVDD and FCE. The dog may also vocalize from initial discomfort. History or suspicion of external trauma allows the clinician to give proper instructions to the owner with regard to safe transportation of the pet. If the history is unknown, similar transportation precautions should be taken. Animals that have suffered from IVDD may have a history of ataxia or weakness. KEY TO COSTS $ indicates relative costs of any diagnostic and treatment regimens listed. $ costs less than $250 $$ costs between $250 and $500 $$$ costs between $500 and $1,000 $$$$ costs more than $1,000 AUGUST 2007 VOL 9.7 STANDARDS of CARE EMERGENCY AND CRITICAL CARE MEDICINE Editorial Mission: To provide busy practitioners with concise, peer-reviewed recommendations on current treatment standards drawn from published veterinary medical literature. This publication acknowledges that standards may vary according to individual experience and practices or regional differences. The publisher is not responsible for author errors. Compendium s Standards of Care: Emergency and Critical Care Medicine is published 11 times yearly (January/February is a combined issue) by Veterinary Learning Systems, 780 Township Line Road, Yardley, PA The annual subscription rate is $83. For subscription information, call , fax , soc.vls@medimedia.com, or visit Copyright 2007, Veterinary Learning Systems. Editor-in-Chief Douglass K. Macintire, DVM, MS, DACVIM, DACVECC macindk@vetmed.auburn.edu Group Publisher Ray Lender rlender@vetlearn.com Editorial, Design, and Production Maureen McKinney, Editorial Director Danielle Shaw, Editor Michelle Taylor, Senior Art Director Bethany L. Wakeley, Studio Manager Whitney Etter, Editorial Assistant Editorial Review Board Mark Bohling, DVM University of Tennessee Harry W. Boothe, DVM, DACVS Auburn University Derek Burney, DVM, PhD, DACVIM Houston, TX Joan R. Coates, DVM, MS, DACVIM University of Missouri Curtis Dewey, DVM, DACVIM, DACVS Plainview, NY Nishi Dhupa, DVM, DACVECC Cornell University D. Michael Tillson, DVM, MS, DACVS Auburn University 2 A U G U S T V O L U M E 9. 7

3 TABLE 1 Lesion Localization Location Gait/Posture Postural Reactions Spinal Reflexes Cranial Nerves Bladder C1 5 Tetraparesis, tetraplegia, low head carriage Decreased to absent in all limbs Normal to increased in all limbs Normal, Horner s syndrome UMN C6 T2 Tetraparesis, tetraplegia, low head carriage Decreased to absent in all limbs Decreased to absent in thoracic limbs; normal to increased in pelvic limbs Normal, Horner s syndrome UMN T3 L3 Paraparesis, paraplegia Normal in thoracic limbs; decreased to absent in pelvic limbs Normal in thoracic limbs; normal to increased in pelvic limbs Normal UMN L4 S3 Paraparesis, paraplegia Decreased to absent in pelvic limbs Normal in thoracic limbs; decreased to absent in pelvic limbs; decreased anal tone Normal LMN Physical Examination Findings The respiratory and circulatory systems should be evaluated and supported in all suspected cases of trauma. It is important to be aware of injury to other areas such as the abdominal and thoracic cavities. An animal with a suspected spinal fracture or luxation should be immobilized and manipulation minimized to prevent further injury to the spinal cord. The neurologic examination should be limited to only tests needed to determine the neuroanatomic localization and presence of nociception. Neurologic examination findings (Table 1) reflect the location of injury. Neurologic Features for Causes of ASCI Paraspinal hyperesthesia occurs with compressive and concussive injuries to pain-sensitive structures such as the muscles, meninges, periosteum, nerve roots, and intervertebral disks. The spinal cord is not innervated by pain fibers. Specific injury to the spinal cord tissue, such as FCE, usually does not incite pain. FCE often causes acute-onset, asymmetric neurologic deficits. Soft tissue wounds may be observed with external trauma. Neurologic Syndromes of ASCI Spinal shock is manifested as flaccidity and hyporeflexia in the limbs caudal to the lesion (despite no injury along the reflex pathway). One should be aware of this phenomenon because it may result in incorrect neuroanatomic localization and adversely affect accurate prognostication. These signs typically last for 12 hours or less in animals but longer in humans; withdrawal may last longer. The Schiff-Sherrington posture is observed with acute and severe lesions in the thoracolumbar spinal cord. The thoracic limbs are in spastic extension but have normal neurologic function. The extensor muscles in the thoracic limbs are disinhibited because of damage to border cells and their ascending inhibitory pathways. This condition does not impact prognosis. Central cord syndrome is more frequently recognized after injury of the grey matter in the cervicothoracic intumescence. Neurologic deficits are more severe in the thoracic limbs than the pelvic limbs and are more common with acute than external trauma. Tether effect occurs after traction injury. This is more commonly recognized after tail avulsions or sacrococcygeal fracture or luxation, especially in cats. (Tethering cord injury is more common in cats.) Traction of neural tissue in the lumbosacral intumescence occurs secondary to avulsion of nerve roots that compose the cauda equina. Signs include paralysis and sensory loss in the tail, urinary and fecal incontinence, and sciatic nerve injury. Similarly, animals with brachial plexus avulsions have upper motor neuron (UMN) signs to the pelvic limbs from traction of descending tracts. Neuroanatomic Localization Proper neuroanatomic localization (Table 1) is crucial in determining the differential diagnosis, prognosis, and treatment options. It is important to be aware of the order of neurologic dysfunction with progressive severity of injury. The order of function loss is reflective of fiber diameter and location within the spinal cord. Large, heavily myelinated fibers associated with proprioception STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 3

4 are more superficially located within the spinal cord and are more predisposed to compressive injury than the deeply located motor and pain fibers. Thus, proprioception is lost first, followed by voluntary motor function and finally nociception. Loss of micturition occurs along with loss of voluntary motor function. The examiner should discern voluntary motor function from reflex movements. Determining the presence or absence of nociception is a crucial part of diagnosis. When testing superficial (cutaneous) and deep (periosteal or bone) nociception, a positive response is characterized by conscious awareness of the stimulus. A withdrawal reflex observed upon application of a noxious stimulus only implies an intact reflex arc, not conscious perception of the stimulus. When deep nociception is absent, it is important to test the lateral and medial aspects of the affected limbs and tail. Respiratory distress can occur in animals with cervical and thoracic spinal cord lesions. Respiratory distress manifests as short, shallow breaths and increased abdominal effort. Loss of descending UMN pathways from the medullary respiratory center prevents facilitative input to the intercostal nerves. Loss of deep nociception is not typically recognized in animals with severe cervical spinal cord injury because respiratory failure often leads to death with this degree of cervical cord damage. Bradycardia and hypotension also can occur with cervicothoracic lesions because of the loss of descending UMN sympathetic pathways and unopposed vagal tone. Lateralized lesions in the cervical (C6 T2) or lumbar (L4 S3) intumescences cause nerve root signature or radicular pain. Affected patients have pain and are lame or nonambulatory in the affected limb. Monoparesis or plegia can be a functional sequela. Brachial plexus avulsions result in monoparesis to plegia and frequently sensory loss in the affected thoracic limb. This can occur concurrently in animals with spinal fractures and traumatic injury. The cutaneous trunci reflex is elicited by pinching the skin over the dorsum of the trunk and observing bilateral contraction of the cutaneous trunci muscle of the thoracic and lumbar regions. This reflex may be absent caudal to the affected spinal cord segment. Micturition dysfunction often occurs in animals that lose voluntary motor function. Neurogenic micturition dysfunction is classified based on UMN (suprasacral) or lower motor neuron (LMN; sacral) localizations. In UMN disease, the detrusor muscle is firm and the bladder difficult to express. In LMN disease, the detrusor muscle is flaccid, and the bladder is large and difficult to completely express. The internal urethral sphincter remains intact from sympathetic input from the hypogastric nerve. Neglect of voiding patterns results in serious consequences of detrusor muscle atony and urinary tract infections (UTIs). The severity of micturition dysfunction also has prognostic implications. The owners may not be able to manage a pet with micturition dysfunction. Fecal incontinence is another clinical manifestation of spinal cord dysfunction and is unacceptable to some pet owners. Laboratory Findings Complete blood count, serum biochemical profile, and urinalysis are unremarkable but should be performed if there is suspicion of concurrent disease. $ Cerebrospinal fluid analysis may be normal or may show a mild mononuclear pleocytosis or increased protein concentration suggestive of central nervous system pathology. $ Other Diagnostic Findings Spinal Radiography $ Radiographic assessment of the spine is performed after the animal has been stabilized. It is important to minimize manipulation of the spine. Radiographic assessment is based on lateral and ventrodorsal orthogonal views. The ventrodorsal view can be obtained using a horizontal beam technique to minimize spinal motion. Spinal radiography enables lesion localization and assessment for malalignment and instability. Radiography of the entire spine is important because fractures and luxations have been reported at more than one site in 20% of patients with external spinal trauma. Radiographic evidence of spinal instability uses the three-compartment scheme: The dorsal compartment includes the spinous process and associated interspinous ligaments, articular process, lamina, and pedicle. The middle compartment includes the dorsal longitudinal ligament, dorsal third of the vertebral body, and annulus fibrosus. The ventral compartment includes the ventral two-thirds of the vertebral body and annulus fibrosus, nucleus pulposus, and ventral longitudinal ligament. Injury involving more than one compartment suggests spinal instability. Radiographic findings in intervertebral disk extrusion include narrowing of the affected intervertebral disk space and intervertebral foramen, presence of mineralized disk material in the vertebral canal, and wedging of the disk interspace. Recent evidence suggests that spinal radiography 4 A U G U S T V O L U M E 9. 7

5 combined with computed tomography (CT) is more sensitive than radiography alone for identifying spinal fractures and luxations and the extent of compartment injury. Thoracic and Abdominal Radiography $ Assessment of injury to other organs influences prognosis and financial considerations. Myelography $$$ Myelography is useful for assessing spinal cord compression (extradural, intradural extramedullary, and intramedullary). Attenuation of the contrast flow within the subarachnoid space occurs at sites of compression. In cases of fracture or luxation, myelography is indicated if the lesion localization does not correlate with spinal radiography findings. Intramedullary swelling may cause extensive longitudinal subarachnoid contrast attenuation. Myelomalacia is suspected when intramedullary contrast is detected. Computed Tomography $$$ CT is an excellent technique for determining the extent of vertebral fracture and evidence of fracture fragments within the vertebral canal. The extent of intervertebral disk extrusion is visualized as mineral density within the vertebral canal. Magnetic Resonance Imaging (MRI) $$$ MRI is the most sensitive modality available for evaluating the spinal cord parenchyma. MRI detects intramedullary and extramedullary lesions. Spinal cord edema is evident as hyperintensity on T2-weighted and fluid-attenuated inversion recovery images. The appearance of hemorrhage can vary with regard to intensity depending on the length of time since injury based on the ferric state of hemosiderin. Summary of Diagnostic Criteria Paraspinal hyperesthesia denotes involvement of pain-sensitive structures. Loss of deep nociception is the most important prognostic indicator. Patient immobilization is important until vertebral fracture or luxation has been ruled out. Imaging assists with lesion localization and assessment of spinal instability. Diagnostic Differentials IVDD The index of suspicion is increased in chondrodystrophoid breeds. ON THE NEWS FRONT A myriad of treatments have been proposed and evaluated for use in ASCI for both human and veterinary patients. Drugs that work at numerous levels of the secondary injury cascade have been evaluated. These have been shown to: Decrease excitotoxicity: N-methyl-Daspartate antagonists (thienylphencyclidine, MK801, NBQX) block the effects of excitatory neurotransmission. Calcium antagonists (nimodipine, diltiazem, nifedipine, flunarizine) dampen the effects of excitatory neurotransmission. Progesterone also decreases excitotoxicity. Inhibit lipid peroxidation or free radical damage: MPSS, 21-aminosteroids (tirilazad mesylate, adenosine), and free radical scavengers (vitamins A, C, and E; selenium; coenzyme Q; dimethyl sulfoxide) Support or replace cell membranes: Polyethylene glycol seals damaged membranes. Gangliosides are cell membrane components that facilitate axonal sprouting and decrease excitatory neurotransmission. Improve spinal cord blood flow: Opiate receptor antagonists (naloxone, thyrotropinreleasing hormone) result in endorphin release and increases in spinal cord blood flow. (Thyrotropin-releasing hormone may also inhibit leukotrienes and plateletactivating factor.) Enhance neuronal and axonal repair: Oscillating field stimulation uses alternating electrical currents across the site of injury to stimulate continued signaling down damaged axons. Restore intracellular and extracellular potassium concentrations: Potassium channel blockers. Modulate the inflammatory response: Interleukin antagonists decrease the effects of microglial products. Lipopolysaccharides stimulate growth factors and decrease associated cytotoxic cytokine effects. Decrease metabolic activity: Hyperthermia of the spinal cord decreases the injury response after ASCI. STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 5

6 History may be acute and progressive. Paraspinal hyperesthesia is often evident. Advanced imaging detects spinal cord compression associated with the disk interspace. FCE The history is acute in onset. Clinical signs remain static or improve. Paraspinal hyperesthesia is usually absent after the peracute phase. Asymmetry of neurologic deficits is common. Clinical suspicion and the use of imaging modalities to rule out other causes of ASCI can provide a solid presumptive diagnosis. MRI of the spinal cord may reveal focal areas of hyperintensity. Trauma Clinical signs often remain static, but neurologic deterioration can occur with destabilization. Trauma is suspected based on history and physical examination findings. Spinal radiography may be sufficient for diagnosis. CT can further assess the extent of fractures. Nonmyelopathic Differentials Acute-onset LMN tetraparesis: This condition is caused by disease of the motor unit. Affected patients have decreased reflexes in all limbs. Cranial nerve signs are evident with some disease processes. Common differentials include tick paralysis, acute fulminant myasthenia gravis, polyradiculoneuritis, and botulism. Arterial thromboembolism (especially in cats): A heart murmur or history of previously diagnosed cardiomyopathy may be present. The affected limb(s) is cool to the touch, and nail beds of the affected limb(s) may be discolored. Muscle palpation of the affected limb(s) is painful. Bilateral pelvic limb dysfunction is the most common presentation (because of aortic thromboembolism), but thromboembolism of the subclavian artery may result in thoracic limb signs. Creatine kinase is increased in these patients. Acute bilateral cranial cruciate ligament rupture: The patient shows the cranial drawer sign or tibial thrust. Proprioception and voluntary motor function remain intact, but other postural reactions that require weight bearing may be reduced. Severe abdominal pain: The neurologic examination is normal. Abdominal radiography or ultrasonography can further localize the source of pain. TREATMENT RECOMMENDATIONS Initial Treatment If present, injuries to other body systems should be treated as indicated. Medical treatment is aimed at treating the primary injury as well as minimizing the secondary spinal cord injury. Few specific treatments prevent secondary injury. The primary goal is to support perfusion and prevent further ischemia. Systemic blood pressure support is crucial to maintain spinal cord perfusion and reverse loss of autoregulation. $ Blood pressure is measured at regular intervals with the goal of maintaining normotension (systolic blood pressure, mm Hg; mean, mm Hg). Hypotension accentuates ischemic injury to the spinal cord. Crystalloid fluids are administered at 1.5 times maintenance rates or as needed to maintain normotension. Aggressive fluid therapy is avoided in patients with known or suspected cardiovascular disease and in hypothermic cats. Pulse oximetry and blood gas analysis assist with monitoring tissue oxygenation. Supplemental oxygen should be administered via intranasal catheter, oxygen tent, or face mask, if needed. Tissue hyperoxygenation may lessen further injury. $ Methylprednisolone sodium succinate (MPSS) has been shown to be beneficial in humans with complete spinal cord injury only when administered according to a specific protocol and only if it has been less than 8 hours since the injury; however, these results have been questioned. Evidence-based research is lacking to show therapeutic efficacy for high-dose MPSS treatment in veterinary medicine and is generally considered ineffective. $ The proposed benefits of MPSS are because of its free radical scavenging properties, not its antiinflammatory effects. Glucocorticoids other than MPSS have not shown therapeutic efficacy. MPSS is contraindicated if administered after 8 hours from the time of injury and in patients that have not lost deep nociception. The potential side effects of high-dose steroids (infection, delayed wound healing, and gastrointestinal ulceration) are well recognized. Recommended protocols for dogs and cats are outlined below. (Other protocols are available; these are examples.) In dogs, an initial bolus of 30 mg/kg IV followed by a continuous-rate infusion (CRI) of 5.4 mg/kg/hr IV. This is continued for 24 hours if therapy was started within 3 hours of the injury and 48 hours if it was started between 3 and 8 hours after the injury. In cats, an initial bolus of 30 mg/kg is given IV followed by 15.0 mg/kg IV at 2 and 6 hours after the initial bolus. Then a CRI of 2.5 mg/kg/hr is given for 42 hours. 6 A U G U S T V O L U M E 9. 7

7 Analgesics are often indicated for management of spinal pain. Opioids have minimal adverse effects on the circulatory system. Nonsteroidal antiinflammatory drugs (NSAIDs), such as carprofen, deracoxib, meloxicam, and firocoxib, relieve pain and inflammation. Aspirin alters platelet function and should be avoided. $ External coaptation $$ $$$ Nondisplaced fractures and mild subluxations may be amenable to immobilization with external coaptation. External coaptation is also an option for pet owners with financial constraints that preclude surgery. Materials for rigid splints include fiberglass cast material, metallic rods, and rigid collar-type supports. These materials are incorporated into a soft bandage. The bandage should extend cranial and caudal to the fracture site to prevent excessive mobility. Adequate padding must be placed over bony prominences to prevent decubital ulcers. These patients require strict cage confinement as well as diligent nursing and bandage care (and changes as needed) to prevent ulcers and urine scald. If the patient s neurologic status worsens despite other modes of therapy, adjunctive short-term prednisone may be given at an antiinflammatory dosage (0.5 mg/kg/day for dogs and 1.0 mg/kg/day for cats) to reduce spinal cord edema. Surgical Management Surgery is indicated if the animal has severe and declining neurologic deficits, spinal cord compression, or spinal instability. $$$$ IVDD Surgery is indicated in patients that have lost superficial or deep nociception or have rapidly deteriorating neurologic status. Common decompressive procedures include hemilaminectomy, dorsal laminectomy, and ventral slot. The type of decompressive procedure indicated depends on the location of the disk herniation. Vertebral Fracture, Luxation, or Subluxation If more than one compartment is damaged, instability is suspected, indicating the need for surgical stabilization. Compressive spinal cord injury may necessitate decompression. Successful surgical fixation requires knowledge of biomechanical forces of the fracture. Appropriate fixation devices are chosen based on fracture type and anatomy. The goals are spinal decompression, alignment, and stabilization. Alternative/Optional Treatments/Therapy If financial constraints preclude surgery, medical therapies as described above can be instituted. The owner should be educated regarding prognosis and recovery. Supportive Treatment Supportive care is similar in patients treated with medical and surgical modalities. Strict cage confinement is enforced for 6 to 8 weeks. Spinal radiographs are taken after 6 weeks to evaluate bone healing and implant placement in cases of fracture or luxation. Bladder management: Bladder emptying is important in animals with loss of voluntary micturition. The bladder should be expressed or catheterized every 6 hours to prevent detrusor atony, urine retention, and UTI. Long-term bladder management consists of prevention of UTIs. Pharmacologic management facilitates urethral relaxation and bladder emptying. Intact sympathetic tone results in increased urethral sphincter tone. $ Prazosin relaxes the internal urethral sphincter muscle by blockage of α 1 -adrenergic receptors. The dosage is 1.0 mg/15 kg PO q12 24h for dogs and mg/kg PO q12 24h for cats. Phenoxybenzamine relaxes the internal urethral sphincter muscle by nonspecifically blocking α 1 -adrenergic receptors. The dosage is mg/kg PO q12 24h for dogs and or mg/kg PO q12 24h for cats. Either prazosin or phenoxybenzamine may be used. They should not be used simultaneously because hypotension may result. Diazepam is a centrally acting skeletal muscle relaxant with effects on the external urethral sphincter. The dosage is mg PO or IV q6 8h for dogs and mg PO or IV q8h for cats. Bethanechol stimulates detrusor muscle contraction via cholinergic stimulation. The dosage is mg PO q8h for dogs and mg PO q8 12h for cats. This should not be used if there is significant urethral sphincter tone because the detrusor muscle will be contracting against a closed sphincter. The low end of the dosage range is used at first, and the patient is monitored for signs of cholinergic crisis. Physical therapy exercises assist with improvement in range of motion and muscle strength. Passive range of motion entails flexion and extension of the limbs to the point of mild resistance. STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 7

8 8 Standing exercises encourage patients to support as much of their weight as possible. Hydrotherapy is useful for regaining muscle strength and limb flexibility during recovery. Veterinary physical therapy and rehabilitation facilities can also be used. $$ $$$$ Physical supports: Patients with severe ataxia or motor function deficits should be assisted to walk using commercially available supports, towels, or blankets. $ Wheelchairs designed specifically for pets are available for animals in which maximal return to function precludes ambulation. $$ $$$ Prevention of decubital ulcers: Nonambulatory patients should be kept on well-padded surfaces and turned frequently (every 4 to 6 hours). Ulcers or urine scald should be treated appropriately. It is important to keep recumbent patients clean and dry. Patient Monitoring Serial neurologic examinations are important to assess improvement or worsening neurologic status. $ Regular urinalyses and cultures are important to monitor for UTI. Animals with spinal cord dysfunction are prone to urine stasis and incomplete bladder emptying. $ Home Management Owners should be counseled about the importance of diligent physical therapy, bladder management, and prevention of decubital ulcers, as described above. Milestones/Recovery Time Frames The rate and degree of improvement vary depending on the cause and type of treatment pursued. In a recent study, 78% of dogs lacking deep nociception that underwent surgical decompression for IVDD and recovered nociception did so within 2 weeks after surgery. The mean time for recovery of voluntary motor function was 7.5 weeks. The same study also showed dogs that made no improvement within 1 month after surgery were less likely to show improvement of neurologic status thereafter. Voluntary tail wag is often the first sign of returning motor function in dogs. A U G U S T V O L U M E 9. 7 TABLE 2 P rognosis for Recovery in Dogs with IVDD Medical Medical and Treatment Surgical Neurologic Status Only (%) Treatment (%) Pain only Ataxia or paraparesis only Paraplegia (superficial nociception intact) Paraplegia (superficial nociception absent; deep nociception intact) Paraplegia (deep nociception absent) Data from Coates JR: Paraparesis, in SR Platt, NJ Olby (eds): BSAVA Manual of Canine and Feline Neurology. Gloucester, British Small Animal Veterinary Association, 2004, p 245. Treatment Contraindications Dexamethasone and dexamethasone sodium phosphate have not been shown to provide any benefit in patients with ASCI, and they have numerous potential side effects. One study examining dogs that underwent surgery for intervertebral disk extrusion demonstrated that 41% of dogs that received dexamethasone perioperatively suffered from gastrointestinal hemorrhage and 2% of those died as a result of this complication. Concurrent use of glucocorticoids and NSAIDs is contraindicated. A washout period of approximately 5 days should be allowed between administrations of these agents. PROGNOSIS The presence of deep nociception is a positive prognostic indicator in patients with ASCI. Physical therapy instituted early appears to be associated with a shorter time from injury to recovery and may also result in a better outcome overall. Physical therapy lessens secondary complications of muscle atrophy and reduced range of motion. Loss of deep nociception is associated with a grave prognosis for return to function in most cases of spinal fracture or luxation. Loss of deep nociception associated with IVDD may have a better prognosis if the patient undergoes prompt surgical decompression (Table 2). IVDD Longer time between loss of deep nociception and surgical decompression in dogs with intervertebral disk extrusion is associated with poorer outcome. Prompt referral for surgery is important in patients that have lost deep nociception. A longer recovery period is associated with increased patient age and weight. (continues on page 11)

9 ACUTE SPINAL CORD INJURY (continued from page 8) External Trauma In dogs with loss of deep nociception and with vertebral displacement or subluxation, prognosis for return to function (even with surgery) is less than 5%. Prognosis for dogs with loss of deep nociception and no vertebral displacement is less than 25% with surgery. FCE Dogs affected with FCE appear to have a good prognosis. One study of 75 dogs showed that more than 90% of dogs that were not euthanized recovered. More than 65% of all dogs in the study population recovered. Prognosis was improved in dogs that demonstrated some degree of recovery within 2 weeks from onset. Dogs with asymmetric deficits have better outcomes. Data are lacking for dogs affected with FCE and loss of nociception. Several studies have shown FCE and an intumescence localization have a poorer prognosis than those with lesions in other spinal segments. This may be because of the greater sensitivity of grey matter to ischemic injury. The grey matter of an intumescence contains cell bodies for motor neurons of the limb muscles and is more vascularized, which may intensify an ischemic insult. RECOMMENDED READING Bergman R, Lanz O, Shell L: Acute spinal cord trauma: Mechanisms and clinical syndromes. Vet Med 95: , Bergman R, Lanz O, Shell L: A review of experimental and clinical treatments for acute spinal cord injury. Vet Med 95: , Bracken MB, Holford TR: Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long-tract neurological function in NASCIS 2. J Neurosurg 79(4): , Bracken MB, Shepard MJ, Collins WF Jr, et al: Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the second National Acute Spinal Cord Injury Study. J Neurosurg 76(1):23 31, Coates J: Paraparesis, in SR Platt, NJ Olby (eds): BSAVA Manual of Canine and Feline Neurology. Gloucester, British Small Animal Veterinary Association, 2004, pp Fehlings MG, Baptiste DC: Current status of clinical trials for acute spinal cord injury. Injury 36(suppl 2):B113 B122, Gandini G, Cizinauskas S, Lang J, et al: Fibrocartilaginous embolism in 75 dogs: Clinical findings and factors influencing the recovery rate. J Small Anim Pract 44:76 80, Meintjes E, Hosgood G, Daniloff J: Pharmaceutic treatment of acute spinal cord trauma. Compend Contin Educ Pract Vet 18: , Olby NJ: Current concepts in management of acute spinal cord injury. J Vet Intern Med 13: , Olby NJ, Levine J, Harris T, et al: Long-term functional outcome of dogs with severe injuries of the thoracolumbar spinal cord: 87 cases ( ). JAVMA 222: , Platt SR, Olby NJ: Neurological emergencies, in SR Platt, NJ Olby (eds): BSAVA Manual of Canine and Feline Neurology. Gloucester, British Small Animal Veterinary Association, 2004, pp STANDARDS of CARE: EMERGENCY AND CRITICAL CARE MEDICINE 11