Pharmacological management of a spinal cord injury patient

Case Scenario

Mr SK is a 32-year-old male involved in an unfortunate diving accident while holidaying on Stradbroke Island at the beginning of the year. Mr SK was air-lifted to the nearest hospital for emergency surgery. He was diagnosed with an injury to the C4 vertebra. Prior to the injury, Mr SK was fit, healthy, with no co-morbidities and was taking no regular medications. He did not smoke and consumed 1–2 units of alcohol each week. Once stabilised in ICU, Mr SK was transferred to the orthopaedic ward and then subsequently the spinal injury rehabilitation unit. His injury was categorised as ASIA C.

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Introduction

Approximately 20,800 Australians are living with a spinal cord injury (SCI), with the majority of cases resulting from trauma. A third of this cohort are classified as having a severe injury, resulting in no functionality of the affected limb.¹ The incidence of SCI in males is significantly higher than females, representing 70% of all new cases.² Incidence of SCI in young males <35 years of age represents approximately 25% of all cases. For patients <65 years of age, 81% of all SCI injury cases are due to trauma (e.g. road accidents, sports injuries and falls), while in the >65 years of age cohort approximately 71% of cases are due to non-traumatic events (e.g. degenerative disorders and tumours).^1,2 See Figure 1 for a breakdown of traumatic SCI causes.

Classification, injury level and assessment

The patient’s extent of SCI is assessed as per the International standards for neurological classification of spinal cord injury (ISNCSCI) created by the American Spinal Injury Association (ASIA).³ This universal classification tool includes the ASIA Impairment scale, which is used to grade a patient’s degree of motor and sensory impairment post injury.⁴
The ASIA Impairment Scale⁴:

● A = Complete. No sensory or motor function is preserved in the sacralsegments S4–S5
● B = Sensory Incomplete. Sensory but no motor function preserved below the neurological level of injury
● C = Motor Incomplete. Motor function is preserved below the neurological level of injury, but more than half of the key muscles are unable to move against gravity
● D = Motor Incomplete. Motor incomplete with at least half or more of key muscle functions below the neurological level of injury being able to move against gravity
● E = Normal sensory and motor function.

A complete spinal cord injury occurs when the spinal cord has been completely severed.⁵

An incomplete injury refers to reduced motor and sensory function remaining below the level of injury and is classified into syndromes including central cord, Brown-Séquard, anterior cord or posterior cord syndrome.⁵ The patient’s neurological level of injury is classified based on the location of the spinal segment injured including cervical, thoracic, or lumbosacral region.

Tetraplegia, also known as quadriplegia, refers to loss of motor and/or sensory function in the cervical spinal segments, and is considered the most severe form of paralysis.⁴ Paraplegia refers to an injury located within the thoracic, lumbar or sacral regions. Typically, patients with an injury sustained above the conus medullaris located at T12/L1 will experience an upper motor neuron lesion (UMN) whilst injury below T12 results in a lower motor neuron lesion (LMN). To confirm the type of lesion, a physician must perform a rectal examination to assess sphincter tone and presence of reflexes. Patients with an UMN lesion often suffer from spasticity, hypertonicity, and hyperreflexia, whilst LMN lesions result in hyporeflexia, hypotonicity, and flaccid muscles.³

Once the patient’s injury has been assessed, rehabilitation goals can be set to match the patient’s abilities and potential for improvement.

Complications from spinal cord injury and their management

SCI significantly impacts the patient’s quality of life with complications including respiratory insufficiency, loss of bladder and bowel control, immobility, reduced independency, post-traumatic stress disorder, depression, spasticity, neuropathic pain, and chronic pain. Such complications can result in significant lifetime costs for the patient and Australian government, currently costing approximately $3.7 billion annually.²

Presently there is no cure for SCI, consequently pharmacological interventions are required to manage patients’ multisystem impairments. Pharmacists in both the inpatient rehabilitation setting and community setting (post-discharge) play a pivotal role in managing the care of SCI patients. Due to the broad nature of topics affecting this population, this article will focus on the pharmacological management of autonomic dysreflexia, bowel and bladder management, and spasticity.

Autonomic dysreflexia

Autonomic dysreflexia (AD) is a common complication in SCI patients with a level of injury (LOI) T6 and above and is predominantly the result of nociceptive stimuli below the LOI.⁶ An episode of AD is the result of excessive reflex activity of the sympathetic nervous system that stimulates constriction of blood vessels leading to uncontrolled blood pressure. Stimulated aortic and carotid baroreceptors trigger parasympathetic activity that leads to vasodilation and bradycardia above the LOI. Subsequently actions of parasympathetic activity prove insufficient to compensate for elevated blood pressure.^6,7

AD signs and symptoms can vary considerably between patients, with some patients experiencing multiple signs of an impending episode. It is important to note that an average blood pressure in this cohort could range from 90/60 mmHg to 100/60 mmHg while the patient is supine and even lower averages when a patient is sitting. A blood pressure reading of 130/90 mmHg represents a high blood pressure reading.⁶

Without appropriate intervention, autonomic dysreflexia is a medical emergency that can result in myocardial ischaemia, seizures, stroke, or death.⁶

Patients should be made aware that after an acute AD episode they are at an increased risk of further episodes in the following 48–72 hours due to excess circulating catecholamines. Attacks may be triggered by events that would notnormally cause an attack for the patient such as stretching or performing routine bowel care, and therefore close monitoring is required.⁶

Educating the patient and carer on the signs, symptoms, causes and management strategies of AD leads to improved outcomes and quality of life.^6,7

Common symptoms of autonomic dysreflexia include:

● blurred vision
● flushing/blotching of the skin (on skin above LOI)
● chills without fever
● pounding headache
● hypertension
● bradycardia
● profuse sweating
● anxiety/shortness of breath

Glyceryl trinitrate (GTN) is the first-line medication treatment for AD. Options for GTN include tablet, patch, and spray. GTN spray and patches are readily available, have reduced shelf life after first use. GTN is contraindicated in patients who have recently taken a phosphodiesterase-5- inhibitor; GTN can be given if it has been greater than 24 hours since sildenafil was taken or greater than 48 hours since tadalafil was taken, though longer intervals may be required. 12 AD medication treatment options are detailed in Table 1.

Table 1 – AD medication treatment options

* Ensure medication has been primed prior to use i.e. 5 sprays before first use, 1 spray if not used within 7 days, and 5 sprays if not used for >4 months. Ensure that the canister is held upright, and spray administered sublingually, not inhaled. Reference: MSHPrescribe⁸

Table 2 – Bowel management treatment plans

Reference: Pryor et al¹⁰

Bowel management

Most patients will suffer from a malfunctioning bowel post SCI with severity of symptoms depending on the neurological level and completeness of injury.⁹ Neurogenic bowel dysfunction results from autonomic dysfunction, impaired gastrocolic reflex, delayed colonic transit time, and immobility.^9,10 An individualised bowel program should be degree of immobility, diet, lifestyle, and ability to participate in bowel care.⁹ A rectal examination is performed by a physician assessing anal tone, anocutaneous reflex and bulbocavernosus reflex to ascertain whether the patient has a flaccid or reflex bowel.⁹ Typically, patients with an injury T12 and above will have a reflex bowel and medication regimes are tailored to stimulate activity within the gastrointestinal tract. For patients with a flaccid bowel, medication regimes are tailored to target fibre intake and daily manual evacuation. Bowel management plans are generally dependant on the patient’s level of injury and are detailed in Table 2. This regime is then adjusted to the patient’s individual response and preferences aiming to create a predictable, painless bowel routine performed at the same time each day, reducing the risk of constipation or faecal incontinence.⁹

Bladder management

Most SCI patients will also suffer from a malfunctioning ‘neurogenic’ bladder post injury.¹¹ Appropriate bladder care is essential as SCI patients are prone to complications including recurrent urinary tract infections, strictures, nephrolithiasis, and renal failure. ^7,11 An UMN lesion results in detrusor muscle overactivity, urinary sphincter spasms and an elevated voiding pressure.¹¹ Often the neurogenic bladder will empty automatically but not completely or at an inappropriate time. A LMN lesion results in a flaccid bladder and patients will experience reduced detrusor muscle contractions, decreased voiding pressure and urinary retention. Bladder management often involves the use of catheters for both overactive and flaccid bladders. Depending on the patient’s level of injury and hand dexterity, they may learn to use intermittent self-catheters, require long-term indwelling urethral catheters or need placement of a supra-pubic catheter.

A stepwise approach to treating a neurogenic bladder may include ^11,12:

1. Trial anticholinergics (e.g. oxybutynin, which targets muscarinic receptors inhibiting involuntary bladder contractions)

● If the patient is unable to tolerate oral oxybutynin switch to transdermal oxybutynin or an alternative anticholinergic (e.g. solifenacin)

2. If symptoms continue add an alpha- adrenergic receptor antagonist (e.g. prazosin, which inhibits contraction of the external urethral sphincter)

● If urinary retention occurs consider switching the anticholinergic to a beta-3-agonist (e.g. mirabegron, which elicits detrusor relaxation)

Overall, goals for bladder management are to allow regular and complete emptying of the bladder to avoid complications such as incontinence or over-distension which can lead to AD.

Table 3 – Anti-spasticity medications

References: MSHPrescribe,⁸ AMH,¹² Cabahug¹⁵

Spasticity management

Despite numerous clinical and physiological definitions for spasticity, the most referenced remains Lance’s definition: ‘spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the UMN syndrome’.¹³ Normally, neuronal signalling from the brain sends descending inhibition to muscle groups. For SCI patients, descending inhibitory reflexes cannot pass the injured segment of the spinal cord, resulting in uncoordinated and uncontrolled reflexes (e.g., erratic and jerky limb movements). Spasticity is common in 65–80% of SCI patients, and represents a major cause of disability.¹⁴

Individuals experiencing spasticity report pain, reduced skin integrity, bladder problems, poor sleep, contractures, difficulty sitting or lying, difficulty transferring, and inability to perform daily activities. While significant impact on quality of life is observed, spasticity may provide unexpected advantages such as increased stability while sitting and standing, improvement in venous return (preventing deep vein thrombosis) and improvement of some activities of daily living (ADLs).¹⁴

Using a patient-centred approach, the team must assess requirements for physical rehabilitation and/or pharmacological intervention. For SCI patients, spasticity generally affects multiple muscle groups resulting in physicians’ preference for regional or systemic pharmacotherapies. Anti-spasticity medications are summarised in Table 3. Patients are commonly prescribed combinations of anti-spasticity medications to achieve symptom improvement.

Knowledge to practice

Pharmacists play an important role in the long-term management of patients with SCI by being able to provide advice on medicines and treatment, lifestyle advice and dose administration aids when hand dexterity issues are present.

Pharmacists should provide counselling and lifestyle tips such as:

● dietary guidance e.g. limiting fatty foods, alcohol and caffeine which may cause diarrhoea
● providing strategies for managing constipation e.g. advising to increase the dose of softeners or stimulants
● regularly assessing the patient’s medications for adverse effects e.g. anticholinergics causing urinary retention, or opioids increasing the risk of constipation
● discuss urinary tract infection prevention strategies e.g. cranberry supplements
● discuss autonomic dysreflexia symptoms and appropriate medication management in an emergency.

Case scenario continued Medications charted during Mr SK’s admission at the spinal injury rehabilitation unit: Aspirin 100 mg 1 m (vertebral artery dissection) Baclofen 10 mg tds cc (spasticity) Dalteparin 5000 units nocte (venous thromboembolism prophylaxis) Gabapentin 300 mg 2 tds (neuropathic pain) Pantoprazole 40mg 1 n (stress ulcer prophylaxis) Glyceryl trinitrate 400 mcg sublingually prn (autonomic dysreflexia) Paracetamol 1 g qds prn (pain) Bowel management medications (neurogenic bowel): Docusate 50 mg 2 bd – regularly Senna 15 mg n – regularly Sodium citrate-sodium lauryl sulfoacetate-sorbitol enema 1 m – regularly PLUS 1 prn Macrogol 3350 with electrolytes 2 bd prn  After a 3-month stay in the spinal injury rehabilitation unit Mr SK is ready for discharge as he has progressed well in therapy and all home modifications have now been completed. The patient’s medications can now be managed by his local pharmacy which can provide a medication administration aid such as a Webster pack. Mr SK will be reviewed by the spinal injury medical team on a yearly basis to ensure he is provided with appropriate ongoing care.

Key points

● A spinal cord injury results from damage to any part of the spinal cord often causing permanent damage.
● Over 20,000 Australians are living with a spinal cord injury with males outnumbering females by over 4:1 for traumatic causes.
● This article has focused on medicines used for SCI-associated complications such as AD, bowel management, neurogenic bladder and spasticity.
● Many support groups are available to assist patients and families including:
● Spinal Life – support sites based in QLD & Western Australia
● Spinal Cord Injuries Australia (SCIA) – support sites based in all states and territories (excluding Tasmania)
● Spire – support sites based in Tasmania and Victoria.

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1. Spinal Cure Australia and Insurance and Care NSW, Spinal Cord Injury Australia: – The Case For Investigating In New Treatments. 2020. p. 37.
2. Harrison J, O.B.D., Pointer S, Spinal cord injury, Australia, 2017–18 Injury research and statistics. Australian Institute of Health and Welfare Canberra (AIHW), 2021(Series no. 136 Cat. no. INJCAT 219. Canberra: AIHW): p. 56.
3. The 2019 revision of the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI)-What’s new? Spinal Cord, 2019. 57(10): p. 815-817.
4. Tovell, A., Spinal cord injury, Australia, 2013–14. Injury research and statistics. AIHW, 2018(107. Cat. no. INJCAT 183. Canberra: AIHW).
5. Ge, L.A., K. Ikpeze, T. et al, Traumatic and Nontraumatic Spinal Cord Injuries. World Neurosurg, 2018. 111: p. e142-e148.
6. Middleton, J.R., K. Cameron, I, Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal Cord Injuries. 2014.
7. Middleton, J.W., G. Leong, and L. Mann, Management of spinal cord injury in general practice – part 1. Aust Fam Physician, 2008. 37(4): p. 229-33.
8. Committee, M.M.M. Metro South Health Prescribe. 2021  [cited 2021 01/07/2021]; Available from: https://mshprescribe.com/.
9. Johns, J., et al., Management of Neurogenic Bowel Dysfunction in Adults after Spinal Cord Injury: Clinical Practice Guideline for Health Care Providers. Topics in Spinal Cord Injury Rehabilitation, 2021. 27(2): p. 75-151.
10. Julie Pryor, M.F., Dr James Middleton, ACI Management of the Neurogenic Bowel for Adults with Spinal Cord Injuries. NSW AGENCY FOR CLINICAL INNOVATION 2014.
11. Middleton, J.R., K, Ian Cameron, ACI Management of the Neurogenic Bladder for Adults with Spinal Cord Injuries. NSW AGENCY FOR CLINICAL INNOVATION 2014  2014.
12. Australian Medicines Handbook, Australian Medicines Handbook, in Australian Medicines Handbook. 2021.
13. Adams, M.M. and A.L. Hicks, Spasticity after spinal cord injury. Spinal Cord, 2005. 43(10): p. 577-586.
14. Elbasiouny, S.M., et al., Management of spasticity after spinal cord injury: current techniques and future directions. Neurorehabil Neural Repair, 2010. 24(1): p. 23-33.
15. Cabahug, P., et al., A Primary Care Provider’s Guide to Spasticity Management in Spinal Cord Injury. Topics in Spinal Cord Injury Rehabilitation, 2020. 26(3): p. 157-165.
16. 2021, G.V.C.I.C., Tizanidine. In: In Depth Answers [database on the Internet]. MIcromedex.

SCOTT MITCHELL B Pharm, BBioMedSc, GradCertClinPharm, AdvPractII is Team Leader, Ambulatory Services & Rehabilitation, Princess Alexandra Hospital, Queensland. He is passionate about ensuring health care system sustainability, development of future leadership capability and optimisation of patient care.

NATALIE MURRAY B Pharm, BHlthInfoMgt is Senior Brain Injury Rehabilitation Pharmacist, Princess Alexandra Hospital, Queensland. She has a passion for assisting patients through their rehabilitation journey, previously working for the Spinal Injuries Unit, and is currently working in the Brain Injuries Unit at the PAH.