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Management tips for the postoperative neurosurgical case (Proceedings)
Postoperative care of the neurosurgical patient is contingent upon a team approach that begins with patient evaluation, pain management, bladder assessment and supportive care.
Postoperative care of the neurosurgical patient is contingent upon a team approach that begins with patient evaluation, pain management, bladder assessment and supportive care. The veterinary practitioner and technician work with the pet owner to tailor the appropriate care that enables the animal to return to activity. Recently, increased numbers of dedicated facilities specific for animal rehabilitation have become an important part of the postoperative care process.
An effective treatment plan for pain management provides acceptable analgesia with few side effects. In veterinary medicine, this may include clinical interventions and pharmacologic and rehabilitative approaches singly or in combination. Goals are to reduce pain and improve function as much as possible. Efficacy, tolerability, cost and safety need consideration with any type of pharmacologic therapy. Routes of administration may factor into effective pain control. Considerations should also be given for short-term and long-term therapeutic regimens. Recognition of different pain types assist with development of a pain management protocol.
Inflammatory pain is associated with tissue damage either of visceral or somatic origin (Kitchell 1987). Pain relates to ongoing activation of primary sensory pathways of somatic and visceral end organs and arises from increased tissue swelling and tension from fluid accumulation, and presence of inflammatory mediators. These mediators facilitate perception and transmission in cutaneous areas and in the dorsal horn of the spinal cord. Pain-sensitive structures include bone, soft tissue, muscle, nerve, viscera and blood vessels.
Neuropathic pain results from disease and dysfunction of the nervous system that transmits pain (Truini 2006). Neuropathic pain can be generated at the site of injury or referred. Neuropathic pain occurs with injury to neural tissue and represents abnormalities in transmission and somatosensory processing in the peripheral or central nervous system. Some disease processes encompass both nociceptive (pain perception)/inflammatory and neuropathic pain mechanisms. Cancers can infiltrate, and compress neural tissue and pain-sensitive structures or cause unlocalizable pain through paraneoplastic effects. Pain associated with chemotherapy and radiation may result from induced axonal injury and vascular compromise.
Common causes include nerve transection and compression of neural tissue. The spine and nerve roots (radicular pain) are common sites affected by mechanical and inflammatory disorders. Anatomic structures of the spinal column that are pain sensitive include the dura, nerve roots, outer annular fibers of the disk, periosteum and cancellous layers of bone, facet aspect of joints, joint capsule and paraspinal ligaments, muscles and aponeuroses. Nerve roots lack appreciable epineurium and perineurium and thus, a well developed intraneural blood-nerve barrier that cause them to be more susceptible to compression injury.
Identification of mechanisms underlying signal transduction and transmission and processing of painful stimuli has led to the development of drugs that target chemical mediators of pain (Muir 2001). Steroidal and nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for inflammation; opioids, alpha-2 agonists modulate excitatory and inhibitory neuronal activity; and local anesthetics suppress electrical impulses. Nonopioid drugs act at the nociceptor level and alter transduction processes of pain. Opioids alter transmission and perception of pain in the CNS. Various pharmacologic regimens most often are based on complementary mechanisms of action that need to be combined in a rational fashion. For chronic pain, combination therapy or multimodality therapies may be more effective than a single agent. NSAIDs appear to have synergistic effects with opioids and may allow for lower dosage of both (Muir 2001; Willis 1987).
Opioid analgesics are classified into various groups based on their pharmacologic activity, potency and clinical use. Type and dosage of opioid selection varies upon severity of pain. Opioid analgesics modify pain perception and behavioral reactions, and relieve anxiety and distress. Effectiveness of pharmacologic opiates may vary with route of administration: parenteral, epidural, rectal, oral, and transdermal drug delivery (fentanyl patch). Direct delivery of opioids to the spinal cord (epidural anesthesia) is used to produce effective anesthesia for surgical procedures. Opioids are more effective for postsurgical and traumatic pain and considered less effective for neuropathic pain (Muir 2001). Opioids that are pure agonists may provide more effective pain control than agonist-antagonist opioids. Tolerance to opiate effects may develop during repeated and chronic administration. Side effects may include altered consciousness, including dysphoria and respiratory depression.
The plethora of different NSAIDs available for use in dogs and cats provides the practitioner with a choice for the most appropriate NSAID which will best complement pain management while minimizing patient side effects (Curry 2005). Response to a specific NSAID may vary with each individual patient and the type of pain (Mathews 2002). If one NSAID does not appear to remedy the pain, an alternative NSAID or adjunctive use of a different class of analgesic needs consideration. Concurrent use of other NSAIDs or glucocorticoids should be avoided. A "washout" period (48 to 72 hours) should be allowed before administering a different NSAID.
Inflammatory pain also can be alleviated through anti-inflammatory actions of glucocorticoids. Specific neurologic disease processes vary widely in optimal corticosteroid usage (Platt 2005). It is important to obtain a confirmatory diagnosis before glucocorticoid usage. Initial rapid improvements without a differential diagnosis can be misleading. Moreover, chronic use of corticosteroids without monitoring can lead to deleterious side effects (Behrend 1997). For compressive spinal cord disease, dexamethasone and prednisone have been administered at anti-inflammatory doses to control inflammatory response and pain and to reduce spinal cord edema. Concurrently, strict cage rest is important to prevent excessive activity in animals with spinal disease. Only short-term anti-inflammatory regimen of prednisone is recommended.
The anticonvulsant, gabapentin has been extensively investigated and proven to be effective for a variety of neuropathic pains. The mechanism of action is unclear. Gabapentin is an analog of GABA, the major inhibitory neurotransmitter in the CNS. Gabapentin may alter voltage-sensitive ion channels. Unlike many analgesics, gabapentin is minimally metabolized by the liver and eliminated by renal clearance. In veterinary patients, gabapentin has been used empirically for management of refractory neuropathic pain. Dosage is 3 to 10 mg/kg q8 to q 24 h. Muscle relaxants (e.g. diazepam, methocarbamol) can be administered for musculoskeletal pains that cause muscle spasm.
Until proven otherwise, it should be assumed that animals with spinal cord disease may be unable to voluntarily urinate or complete the micturition process. Associated risks with urine retention include developing urinary tract infection (UTI), bladder overdistention and damage to the kidneys. Dogs with neurogenic related urine retention, and had intermittent and in dwelling urinary catheters have potential risks for UTI (Stiffler 2006, Sequin 2003). A prospective study determined the prevalence of UTIs in dogs with thoracolumbar lumbar IVDD was 30% with higher incidence in dogs that were female and had lower intraoperative body temperatures (Stiffler 2006).
The most common cause of voiding problems in the neurosurgical patient is urinary retention secondary to the underlying neurologic disease. Upper motor neuron (UMN) dysfunction occurs with lesions between the pons of the brain stem and L7 spinal cord segment. UMN bladder dysfunction is a common sequela to T3 to L3 myelopathies. With an UMN bladder both the motor and sensory pathways of the detrusor reflex are affected. The bladder becomes large and firm and the urethral sphincter tone is increased. The bladder is difficult to express manually. Secondary overflow incontinence occurs when bladder pressure exceeds urethral pressure. Lower motor neuron (LMN) bladder dysfunction occurs in a lesion within the sacral spinal cord and nerve roots, and the pelvic plexus. A lesion in this area will abolish the detrusor reflex. The detrusor muscle becomes flaccid (detrusor atony) as a result of over-distension secondary to absent detrusor contraction and external sphincter tone is lost. The internal sphincter is innervated by the hypogastric nerve and remains intact. This may actually make bladder expression difficult. Animals with LMN bladder dysfunction also will lose their perineal reflex and sensation. Trauma is the most common cause for this type of dysfunction. Bladder atony from over-distension can result from non-neurogenic or neurogenic causes. Non-neurogenic bladder atony is secondary to urinary obstruction and disruption of the tight junctions of the detrusor myofibers. Over-distention also can result from pelvic fractures and recumbency, itself.
Decisions for urinary bladder emptying involve use of manual expression that can be facilitated using pharmacologic therapies and use of catheters (intermittent, indwelling). Basic principles need to be followed to prevent bladder over distension in animals with urinary retention. Urinalysis and urine culture should be periodically performed to monitor for UTI. Manual expression is indicated if the bladder is easily expressed, but residual urine should be periodically monitored by ultrasound or urinary catheterization. Urinary bladder expression can be difficult in dogs with UMN disease or obesity and is considered a painful procedure in dogs that have recently had spinal surgery. Residual urine after expression is a potential source of infection and can lead to overflow incontinence and detrusor atony. Intermittent urinary catheterization often is indicated and has lower risk of inducing a urinary tract infection over indwelling closed-system urinary catheterization techniques (Bebenik 2007; Barsanti 1985). If an indwelling system is selected, minimizing the duration is important. (Bebenik 2007) Pharmacologic therapies for urine retention include drugs that improve bladder contraction and relax the urethral sphincters. (Table 1)
Table 1: Drug therapies that assist with urinary bladder emptying in dogs
Supportive care to involve the psychological and physical well being is especially important in the recumbent patient. Bedding should be supportive enough to evenly distribute the patient's weight especially over boney prominences to prevent decubitus ulcers (Swaim 1995). Absorbent materials (lamb's wool, diaper pads) need to overlay supportive materials (air, foam mattresses). The patient will need to be rotated on a frequent basis (q 4 h). Cleanliness is critical to prevent fecal and urine scalding. Cryotherapy of the surgical incision is applied for several days until the incision is no longer warm to touch. An ice pack covered with a towel to protect the skin is applied for 10 to 20 minutes 3 times daily to lessen edema and for pain management. Hydrotherapy also can play role in increasing circulation of the limb vasculature and prevention of decubitus ulcers. Having the pet owner and technicians intimately involved with the postoperative care is important in the patients overall well being and quality of life.
Physical rehabilitation is integral in management of neurologic diseases and enhancement of neuro-regenerative processes (Olby 2005, Millis 2008). Disuse and immobilization can cause loss of muscle mass and debilitating joint contracture. Physical rehabilitation during recovery from neurologic disorders not only is important for strengthening and increasing flexibility but also for pain reduction and improvement in quality of life (Sherman 2004). Rehabilitation in immediate post-operative and recumbent patients begins with massage and passive range-of-motion (ROM). Joints of limbs are extended and flexed through normal ROM 5 to 10 minutes several times a day. Active ROM includes swimming and standing exercises. Water buoyancy aids in rehabilitation of weak muscles and painful joints by minimizing amount of weight-bearing on joint while generating the gait cycle. The goal is to have the limbs in normal position which bearing only a portion of the body weight. Superficial and deep heat therapy also can be instituted to reduce muscle spasm and improve circulation (Steiss 2005). Neuromuscular stimulation is applied to selected muscle groups that undergo atrophy and assists with preservation of muscle strength (Steiss 2005).
As the patient begins to ambulate without assistance, therapeutic exercising includes standing and more dynamic ambulation activities which serve to enhance ROM, muscle strength, balance and overall daily function. Static and mechanical forms of stretching techniques are performed in conjunction with ROM exercises to prevent fibrosis and contracture of joints and muscles. Gait training exercises encourages more ambulation to affected limbs. This process can be initiated with carts and hydrotherapy. Proprioceptive neuromuscular training improves the awareness and use of limbs at rest and in motion.
Other modalities of physical therapy and supplemental therapies that complement mobility therapies include thermal, electrical stimulation, massage, ultrasonographic, acupuncture and weight loss (Steiss 2005). Rehabilitation protocols are individually tailored to meet patient's needs during the recovery process.
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16. Also presented at the 145th AVMA Annual Convention, New Orleans, LA. July 19-22, 2008.