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NURSING STANDARD

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KeywordsXxxx; xxxxx

These keywords are based on the subject headings from the BritishNursing Index. This article has been subject to double-blind review.For author and research article guidelines visit the Nursing Standardhome page at nursingstandard.rcnpublishing.co.uk. For relatedarticles visit our online archive and search using the keywords.

Page 58Spinal cord injuriesmultiple choicequestionnaire

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Aims and intended learning outcomes

This article aims to provide an overview of someof the key components that practitioners shouldbe aware of when caring for a patient with aspinal cord injury (SCI), particularly during theacute period. After reading this article you shouldbe able to:

�Revise relevant anatomy and physiology inrelation to SCI.

�Differentiate between primary and secondarymechanisms of injury.

�Recognise the different types of SCI andrelevant syndromes.

� Identify how SCI may affect different systemsof the body.

�Outline an airway, breathing and circulation(ABC) approach to managing patients with SCIduring the acute phase of care.

Introduction

Injury to the spinal cord can affect many aspects ofcare and frequently requires a proactive approachto managing actual and potential complications toachieve the best possible rehabilitation outcomes.Effects of SCI are discussed in relation toappropriate management and interventions toensure effective, timely and appropriate care of thepatient with a SCI.

Anatomy

The spine (vertebral column) consists of 33 vertebrae descending from the cranium to thecoccyx. This includes seven cervical vertebrae, 12 thoracic vertebrae and five lumbar vertebrae,which are mobile segments; there are also five fusedbones that form the sacrum and four fused bonesthat form the coccyx. The spine has three maincurves – cervical lordosis, thoracic kyphosis andlumbar lordosis – which help to maintain balance inan upright position and absorb vertical shock fromactivities such as walking, which in turn protects thespinal column from fractures (Figure 1).

Between adjacent mobile vertebrae there areintervertebral discs, which consist of an outerrim of fibrocartilage (annulus fibrosus) and acentral core of soft, highly elastic material(nucleus pulposus). Under compression the

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NS498 Walker J (2009) Spinal cord injuries: acute care management and rehabilitation. Nursing Standard. 23, 42, 47-56. Date of acceptance: September 12 2008.

Spinal cord injuries:acute caremanagement and rehabilitation

SummarySpinal cord injury can have a devastating effect on patients andtheir families. An understanding of the mechanism of injury andhow this can relate to functional ability assists healthcareprofessionals to anticipate the care that is required and anydifficulties that the patient may encounter. Knowledge of spinalcord injury and the effects on the cardiorespiratory, gastrointestinaland genitourinary systems enables clinicians to provide effectivecare tailored to actual and potential complications, such as spinalshock and autonomic dysreflexia.

AuthorJennie Walker is clinical educator, Academic Division of Orthopaedicand Accident Surgery, Queen’s Medical Centre, Nottingham. Email: [email protected]

KeywordsAcute care; Paralysis; Rehabilitation; Spinal injury

These keywords are based on the subject headings from the BritishNursing Index. This article has been subject to double-blind review.For author and research article guidelines visit the Nursing Standardhome page at nursingstandard.rcnpublishing.co.uk. For relatedarticles visit our online archive and search using the keywords.

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thoracic region is limited by attachment of theribs to the sternum.

The vertebral foramen comprises two pediclesthat project backwards from the vertebral bodyand two laminae. At the point where the pediclesand laminae meet, the transverse processes projectlaterally; where the two laminae meet posteriorly,they form the spinous process (Figure 2). Thevertebral foramen has four articular surfaces, twoof which articulate with the surfaces above andtwo with the surfaces below. Collectively, thevertebral foramina form the vertebral canal,which provides strong bony protection for thespinal cord. Intervertebral foramina similarlyexist throughout the spinal column between eachpair of vertebrae, through which the spinal nerves,blood vessels and lymph nodes pass.

The vertebral bodies and intervertebral discsare supported by ligaments and paraspinalmuscles to maintain the stability of the spine.The four main ligamentous structures that helpto maintain stability are the anteriorlongitudinal ligament, the posterior longitudinalligament, the ligamenta flava and thesupraspinous ligament (Tortora and Derrickson2005) (Figure 3). These help create the threedistinct columns of support in the spinalcolumn; these are the anterior, middle andposterior columns (McLeod 2004a). If two ofthese columns are injured the vertebral columnmight be considered unstable and permitexcessive movement, which could result indamage to the spinal cord. The terms stable andunstable injury refer to the integrity of thevertebral column and the supporting ligaments.Disruption of these components necessitatesgreat care in maintaining the spine in correctalignment to avoid further neurological injury(Prendergast and Sullivan 2000).

The spinal cord originates at the caudal endof the medulla oblongata at the foramenmagnum and extends down to about L1-L2,where it tapers to a conical portion known as the conus medullaris. The remaining nerve rootsexit the spinal cord at this level and extendthrough the spinal canal. These nerve rootscollectively form the cauda equina. Nerve rootsexit at each vertebral level, with the anterior andposterior nerve roots combining to form thespinal nerves that pass through theintervertebral foramina. There are eightcervical, 12 thoracic, five lumbar, five sacral,and one coccygeal spinal nerve roots. Each ofthese nerves innervates a specific area of thebody (except C1). The area of skin specificallyinnervated by the nerves is known as adermatome.

The meninges that encircle the spinal cord andbrain are connective tissue coverings and areknown as the dura mater, arachnoid mater and

discs flatten and change shape, permittingmovement in the vertebral column. Suchmovement can be extensive, although it issomewhat limited between individualvertebrae. The greatest movement occurs in thecervical and lumbar regions as movement in the

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48 june 24 :: vol 23 no 42 :: 2009 NURSING STANDARD

FIGURE 1

Anterior Posterior

1st cervical vertebra (atlas)

2nd cervical vertebra (axis)

1st thoracic vertebra

Intervertebral disc

1st Lumbar vertebra

Cervical curvature (concave) C1 – C7

Thoracic curvature (convex) T1 – T12

Lumbar curvature (concave) L1 – L5

Sacrococcygealcurvature (convex)

Vertebral column

FIGURE 2

PosteriorSpinous process

Vertebral foramen

Spinal cord

Body

Pedicle

Superiorarticularprocess

Transverseprocess

Lamina

Anterior

Vertebral body

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pia mater. In the spinal cord there is grey matterthat contains: sensory cells (receive impulses fromthe periphery); cells of lower motor neurones(transmit impulses to the skeletal muscles); andcells of connector neurones (link sensory andmotor neurones at the same or different levels andform spinal reflex arcs). In the spinal cord there isalso white matter, which is arranged in tractsformed by ascending (sensory) tracts anddescending (motor) tracts. The key functions ofthe spinothalamic, dorsal column andcorticospinal tracts are outlined in Box 1.

Spinal injury

Injuries to the spine may involve the vertebralcolumn, spinal cord, spinal nerves or the bloodvessels that supply the spinal cord. The maincauses of SCI may be divided in to two categories:traumatic injury, for example road trafficaccidents, sporting injuries, recreational ordomestic accidents, self-harm, and criminalassault (Harrison 2000); and non-traumaticinjury, as a result of degenerative (spinal stenosis),infective (discitis) or oncogenic spinal lesions(primary or secondary tumours) (Sheerin 2005a).Other non-traumatic causes may include vascularabnormalities, post-surgical SCI and spinal cordischaemia and haemorrhage (spinal stroke).

The mechanism of injury might be the resultof flexion (rapid deceleration in a road trafficaccident), extension (falling forwards andhitting the forehead on a step), compression(diving into a shallow pool), penetration (stabwound or gunshot) or rotation. Fracture ordislocation of the vertebral bodies can alsocause direct trauma to the spinal cord or disruptthe blood supply to the spinal cord from thespinal and medullary arteries. Ischaemia of thespinal cord affects function and can result inmuscle weakness and paralysis (Moore andAgur 2002).

Traumatic injury to the vertebral column most commonly occurs at the lower cervical andthoracolumbar junctions as these areas are themost mobile and therefore more vulnerable toinjury (Prendergast and Sullivan 2000). Damageto the spinal cord and spinal nerves is largely theresult of direct mechanical insult to the spinalcord at the time of injury. This is known as theprimary injury (Karlet 2001). Following trauma,a cascade of local biochemical andhaemodynamic processes cause additional cellnecrosis; this is termed secondary injury (Karlet2001). Traumatic SCI therefore may be viewed asa sequence of primary and secondary events.

Primary injury is caused by trauma, whichresults in haemorrhagic changes that lead toischaemia and necrosis (Hickey 2002). Secondaryinjury unfolds during the following hours to days

and involves varying degrees of vascularcompromise, inflammatory changes and cellulardysfunction, and may be exacerbated by hypoxia,hypoperfusion and further mechanical injury tothe spinal cord (Greaves et al 2001).

In the first few minutes to hours of the primaryinsult, there is a release of vasoactive agents andcellular enzymes, which cause changes to

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FIGURE 3

Anterior longitudinal ligament

Nucleus pulposus

Annulusfibrosus

Posterior longitudinalligament

Ligamentumflavum

Intraspinousligament

Supraspinous ligament

Spinal ligaments

BOX 1

Spinothalamic tracts (ascending/sensory)Convey impulses for sensing:

� Pain.� Temperature.� Deep pressure.� Crude touch.

Dorsal column tracts (ascending/sensory) Convey nerve impulses to sense:

� Proprioception (the body’s ability to sense spatialposition and muscular activity).

� Discriminative touch.� Two-point discrimination (the ability to

differentiate touch stimuli at two nearby points on the body at the same time).

� Pressure.� Vibration.

Corticospinal tracts (descending/motor)Convey nerve impulses destined to cause precise andvoluntary movements of skeletal muscles. They help to:

� Co-ordinate body movements with visual stimuli.

� Maintain skeletal muscle tone.

� Regulate muscle tone in response to head movements and maintain equilibrium.

(Tortora and Derrickson 2005)

Key functions of the spinothalamic, dorsal column and corticospinal tracts

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type of function retained depends on which areasof the spinal cord have been affected. While eachSCI is unique, there are four types of spinal cordsyndromes that are differentiated by the type offunction retained.Central cord syndrome This usually occurs inolder patients with cervical spondylosisfollowing hyperextension injury to the neck(Kirschblum and Donovan 2002). Haemorrhageand oedema occurring in the central part of thecord results in bilateral weakness of the upperlimbs (Prendergast and Sullivan 2000). In thelower limbs, strength and sensation is preserved.Spondylosis and hyperextention injuries causecompression of the spinal cord with inwardbulging of the ligamentum flavum (Hickey2002); this in turn places pressure on the cells inthe anterior horn (Sheerin 2005a). Thispredisposes the individual to developing oedemaand haemorrhage in the central cord region. The cervical fibres are located medially to thethoracic, lumbar and sacral fibres. Because ofthis arrangement, central pressure is exerted onthe thoracic and cervical fibres, resulting ingreater motor loss in the upper limbs (Sheerin2005a).Anterior cord syndrome This may occurfollowing damage to the anterior two thirds of thespinal cord, for example as a result of a highimpact/velocity incident such as a road trafficaccident (Sheerin 2005a). The syndrome affectsthe corticospinal and the spinothalamic tractsand results in variable motor function below thelevel of injury, with impairments to pinprick(pain) and temperature sensation below the levelof injury (Hayes et al 2000). Sensation of lighttouch, deep pressure, proprioception andvibration often remain intact.Brown-Séquard’s syndrome This involves ahemisection of the spinal cord and can occurfollowing injuries that partially transect the cord,such as stab and gunshot wounds. It may also beevident when one side of the spinal cord hassustained more damage than the other side. Thereis a loss of voluntary motor function, vibration andproprioception ipsilateral (same side) to the injury,with contra lateral (opposite side) loss of pain andtemperature sensation below the level of injury(Prendergast and Sullivan 2000). The motor nervesin the corticospinal tracts cross over at the level ofthe medulla oblongata. Therefore, injury to thecorticospinal tracts results in functional loss ofcontrolled voluntary movements on the same sideas the injury (Hudak et al 1998). Posterior cord syndrome This affects the posteriorsegment of the spinal cord and can occur withposterior impact injury or hyperextension injury of the neck affecting the dorsal columns. Thisresults in the loss of proprioception, vibration,light touch and deep pressure (Hughes 2003).

microvessels in the grey matter and multifocalhaemorrhages (Sapru 2002). The injury site is theninfiltrated by neutrophils and macrophages,resulting in post-capillary venule distention(Sheerin 2005a). An increase in intracellularcalcium levels may also cause damage to thevascular endothelium, as with leakage oferythrocytes into interstitial spaces (Sapru 2002).The resultant interstitial and intracellular oedemamay inhibit perfusion of the spinal cord and causefurther deterioration of neurological status(Mcleod 2004a). There is also an increase inextracellular potassium levels and consequentialdepolarisation of cells, which results in aconduction block of nerve impulses. Between fourto eight hours, hypoxia-induced catecholaminerelease may cause further haemorrhage andnecrosis of the spinal cord. Continuation ofelevated calcium levels may also result in theappearance of aneurysms and vessel rupture in thelateral columns of the spinal cord (Sapru 2002).

Clinical assessment of spinal injuries shouldfollow an ABC approach (Stevens et al 2003).Practitioners should also be vigilant for otherinjuries as 20-60% of patients can present withadditional injuries, most commonly involving thehead, chest or abdomen (Sekhon and Fehlings2001). All patients admitted to hospital followingsignificant trauma or head injury should beassumed to have a potentially unstable spinalfracture until proven otherwise (Brooks andWillett 2001). It is essential that extreme cautionis taken when moving a patient with a known orsuspected spinal injury to ensure that spinalalignment is maintained at all times to preventfurther neurological damage (Prendergast andSullivan 2000, Hickey 2002).

If a spinal injury has been sustained, appropriatetesting of movements (power) and sensationshould be carried out using an assessment tool(Figure 4) (Mcleod 2004a). The lowestdermatome at which sensation is felt determinesthe level of injury in relation to the spinal cord(Greaves et al 2001).

Complete SCI is the permanent loss of allvoluntary movement and sensation below thelevel of injury (Hughes 2003). With incompleteinjury some function is retained, however the



Time out 1Discuss with a moving and handling adviser about how to log roll and transfer patients with spinal injuries appropriately.

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FIGURE 4

Standard neurological classification of spinal cord injury

Spinal shock

Spinal shock is a specific term that relates to theloss of all neurological activity below the level of injury, including loss of motor, sensory, reflex and autonomic function (Karlet 2001). Spinalshock is a temporary physiologic disorganisationof spinal cord function that may start 30-60minutes following injury (Boss 1998), and can last up to six weeks post injury (Sheerin 2005a).

One theory suggests that the sudden loss ofconduction in the spinal cord occurs as a result of the migration of potassium ions from theintracellular to extracellular spaces (Sheerin2005a). This is associated with a transient loss of somatic and automatic reflex activity belowthe level of neurological damage. The spinal cord

reflex arcs that are immediately above the injurymay also be severely disrupted (Bravo et al 2004).

Spinal shock results in flaccid paralysis,areflexia and anesthesia below the level of injury(Karlet 2001). The return of the reflexes indicatesthe end of spinal shock. Assessment of theresolution of spinal shock is based on the returnof reflexes, with the bulbocavernosus reflextypically being the first to return (Hickey 2002).However, some clinicians may classify the end ofspinal shock as the return of deep tendon reflexesor the return of reflexive detrusor function, whichmay be months after injury (Ditunno et al 2004).

SCI at T6 and above results in the disruption of the autonomic nervous system because of theinterruption of the sympathetic outflow at T6(Sheerin 2005a). The sympathetic andparasympathetic divisions of the autonomicnervous system usually work to maintainequilibrium of smooth muscle function, cardiac


Time out 2Consider how each of the four types of SCI syndrome can affect an individual’s ability to perform activities of daily living. Discuss with multidisciplinary team members about how this will affect thepatient’s rehabilitation.

Time out 3Revise the principles of the sympathetic and parasympathetic nervous system and how each affects different parts of the body.

(American Spinal Injury Association 2002)

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consciousness are present, endotracheal intubationmay be required to protect the patient’s airway.

The function of the respiratory system dependslargely on the level of SCI and nerve involvement(Table 1). The increase of secretions as a result ofunopposed parasympathetic activities in cervicalinjuries is complicated by the inability toexpectorate because of the loss of abdominalmuscular innervation and paralysis of theintercostal muscles (Cook 2003, Urdaneta andLayon 2003).

In the patient with a cervical SCI, changes inbreathing patterns need to be anticipated (March2005). Respiratory assessment should beperformed frequently during the acute phase ofSCI, including:

� Observing for general signs of respiratoryinsufficiency, for example respiratory distressand central cyanosis.

� Monitoring respiratory rate, depth, rhythm,and checking that chest movement is equal oneach side.

� Measuring oxygen saturation levels with apulse oximeter.

� Listening to breath sounds; rattling noises mayindicate the presence of secretions in theairway whereas stridor or wheeze suggestspartial airway obstruction.

� Listening to the chest with a stethoscope.

Signs such as excessive accessory muscle use,exaggerated abdominal movements, reducedbreath sounds and limited ability to expectorate are features that may be observed in patients withrespiratory fatigue (March 2005). Lucke (1998)described the paradoxical inward chest movementsthat occur as a result of intercostal muscle paralysis.

muscle and glands. The parasympathetic outflowremains undisrupted in injuries T6 and above and therefore continues with unopposedparasympathetic activity. The loss of thesympathetic outflow causes an imbalance, whichpresents as hypotension and reduced cardiac output(as a result of dilation of blood vessels), andconsequently a reduced stroke volume. Bradycardiasimilarly results from unopposed vagal stimulationof the heart (Sheerin 2005a). Poikilothermia (loss of thermoregulation) is caused by passive dilationof the dermal blood vessels, resulting in an inabilityto maintain body heat. The loss of sweat glandactivity below the level of injury and the ability toshiver also affects the ability to thermoregulate.

Airway and breathing

Maintaining the patient’s airway remains a prioritythroughout the acute phase of care (Sheerin2005b). The airway may become obstructed withblood or vomit, or as a result of craniofacialtrauma (Prendergast and Sullivan 2000). The jaw-thrust technique may be initially used to open theairway with little spinal hyperextention. If apnoea,respiratory distress or depressed levels of



Time out 4Write a list of the factors that may affect a patient with poikilothermia, and actions that may be taken to ensure that the patient’s temperature is maintained in an acceptable range.

Effects of spinal cord injury on the body

Level of injury Effect of injury Effect on respiratory function

Injuries above C3 Diaphragm paralysed. Loss of inspiratory and expiratory capacity.Accessory muscles may be weakened or No cough effort.paralysed. Mechanical ventilation required.Intercostal and abdominal muscles paralysed.

C3-C5 Diaphragm may be weakened and/or paralysed. Decreased tidal volume and vital capacity.Intercostal and abdominal muscles paralysed. Limited inspiratory and expiratory capacity.

Ineffective cough.

C5-C8 Diaphragmatic function intact. Decreased total lung capacity.Intercostal and abdominal muscles paralysed. Ineffective cough.

T1-T6 Weakened and/or paralysed intercostals. Limited expiratory capacity.Paralysis of abdominal muscles. Weak cough.

T7-T12 Abdominal muscles weakened and/or paralysed. Reduced expiratory capacity.Variable cough effort.

(Adapted from Lucke 1998, March 2005)

TABLE 1

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Ventilatory function in cervical SCI typicallyworsens in the initial two to five days followinginjury and then, with optimal care, progressivelyimproves without ever returning to pre-injurycapacity (Stevens et al 2003). Injuries below C5are associated with lesser degrees of ventilatoryimpairment; however, patients still remain at riskof respiratory complications such as atelectasis,pneumonia, pulmonary oedema, pleuraleffusions and pulmonary embolisms. (Stevens etal 2003). Respiratory complications may alsoresult from direct trauma, for examplepneumothorax, haemothorax, flail chest andpulmonary contusions.

The aim of respiratory management is toprevent respiratory complications, promoteoxygenation and optimise spinal cord perfusionto reduce the incidence of further secondarydamage to the spinal cord (Stevens et al 2003).Respiratory interventions may improve air entryand control, resulting in more effective breathingand tissue perfusion, thus minimising the risk ofrespiratory complications.

The unstable nature of many patients withacute SCI may restrict the positioning of thepatient. The individual often requires flat bed restand log rolling techniques, where the patient isturned maintaining correct anatomical alignmentwithout twisting or bending the spine, orinterventions such as traction (March 2005).Regular repositioning of patients usesgravitational effects to aid the redistribution ofventilation and perfusion throughout the lungs,thus preventing one area of the lung fromdeteriorating (Field 2000). Altering the chestposition also aids the mobilisation of chestsecretions from affected areas of the lung byencouraging mucus from smaller airways to moveinto larger areas under the influence of gravity,potentially preventing chest infections andatelectasis (Harrison 2000, March 2005).However, Field (2000) noted that repositioningcan potentially increase oxygen demands, and close monitoring of respiratory rates andrespiratory effort is required to ensure thatrespiratory distress does not develop during or following position changes.

The use of chest physiotherapy is essentialin patients with acute SCI. It aims to improvegaseous exchange and prevent atelectasis andconsolidation, which may occur as a result of

mucosal plugging. Two commonly usedphysiotherapy techniques include percussion andvibration. Percussion involves manually clappingthe chest over the affected area (Stiller 2000). Thisis effective in removing sputum from the proximalairways, although it is insufficient in isolation toprevent consolidation of lower airways (March2005). Vibration may be used by applying avibrating or shaking motion to the patient’s chestduring expiration. This is beneficial in patientswhere coughing is problematic. Other techniquesthat may promote respiratory function includeusing assisted coughing techniques. These involvethe application of pressure to either the chest orabdominal wall in co-ordination with the patient’sforced expiration to promote an increase in thevelocity of exhaled air, thus aiding the movementof secretions in the larger airways (March 2005).The use of an inspirometer also promotes deepbreathing, strengthens respiratory muscles andencourages mobilisation of chest secretions.

Cardiovascular function

While hypotension can be attributed to neurogenicshock in uncomplicated cases of acute SCI,haemorrhage should be excluded. Blood pressureshould be measured regularly to ensure that a meanarterial pressure is maintained above 85mmHg topromote adequate perfusion of the spinal cord(Sheerin 2005b). Care should be taken not to over-infuse patients with hypotension as this maybe caused by the loss of sympathetic tone ratherthan hypovolaemia (McLeod 2004b). Overperfusion can lead to pulmonary oedema and mayfurther compromise respiratory efforts (Sheerin2005b). Using an arterial catheter can assist withassessment of intravascular volume andmanagement (Stevens et al 2003). Severehypotension may require treatment with avasopressor such as dopamine (Guin 2001).

Bradycardia can also result from interruptionof the sympathetic nervous system. Patients withsevere bradycardia might require the use ofinotropes to ensure adequate perfusion of vitalorgans. Procedures, such as tracheal suctioning orrepositioning of the patient, may also causeworsening bradycardia as a result of stimulationof the vagal nerve. Therefore, cardiac monitoringmight be advised where available during suchprocedures (Sheerin 2005b).

Deep vein thrombosis after SCI is common,hence it is advisable that prophylactic measures,such as the use of anti-embolic stockings or lowmolecular weight heparin, are taken during theacute phase (Prendergast and Sullivan 2000). As sensory loss deprives the patient of the abilityto detect tenderness or warmth of theextremities, these should be checked regularlyfor redness, swelling and warmth.


Time out 5Discuss with a resuscitation officer the principles of assessing and managing an airway in a patient with an actual or potential injury to the spine.

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Bowel function is also commonly alteredfollowing SCI and therefore needs to be assessedand appropriately managed from the point ofadmission. Defecation is a complex co-ordinatedprocess that involves reflex and voluntary action(Ash 2005). Injuries above T12 typically result ina reflex neurogenic bowel function in whichreflex functions are preserved, but sensation andvoluntary functions are absent. This results in thepatient having little or no awareness of bowelfullness; neither will the individual be able toinitiate or inhibit defecation.

Complete SCI below T12 characteristicallyresult in a flaccid neurogenic bowel dysfunctionbecause of the disruption of the reflex pathways(Ash 2005). This results in the bowel notresponding to chemical (laxatives,suppositories, microenema) or mechanical(digital) stimulation and therefore requires theuse of digital removal of faeces (Coggrave2004). As there are no active reflexes to bestimulated in the patient with a flaccid bowelthere is no basis for the administration of rectalstimulants (Ash 2005).

Integumentary effects

Patients with SCIs are particularly vulnerable todeveloping pressure ulcers as a result of impairedcirculation and muscular disuse, combined withthe possibility of sensory dysfunction. Pressureulcer prevention is a fundamental aspect of careand should be assessed and the risks managed fromthe time of the accident, through the acute periodand for the duration of the person’s life. Patientswith SCIs may be unable to relieve pressureindependently, not only because of physicalinability, but also as a result of sensory loss, whichmay inhibit the ability to feel pain in these areas(McLeod 2004b). Meticulous pressure areamanagement, and patient and family education,are essential to prevent such complications.

An inspection of the skin should be carried out during each log rolling procedure to check the integrity of the skin. Pressure relief may beobtained by regular position changes every twohours (McKinley et al 2002). Where possible,resting the patient on an area of discoloured skinshould be avoided. Using techniques such as the30° tilt – where the patient is placed on their side at30° supported by pillows to relieve the pressureover bony prominences – or the use of pillows

Gastrointestinal function

A paralytic ileus may be present in the early stagesof SCI, but typically resolves between 48-72 hours. A paralytic ileus can be managed by insertion of a nasogastric tube (left on freedrainage) to decompress the stomach and preventit splinting the diaphragm, which couldconsequentially exacerbate respiratorycompromise (Hughes 2003). A nil-by-mouthregimen should also be maintained until thereturn of bowel sounds (Karlet 2001).

Gastritis and peptic ulcer disease are commonlyassociated with cervical spine injuries, possiblybecause of unopposed parasympathetic activity(Hickey 2002). The risk of gastric ulceration as a result of vagal stimulation may be reducedthrough the use of histamine receptor agonists,for example ranitidine, or protein pumpinhibitors, such as omeprazole (Sheerin 2005b).

Continence

During spinal shock it is unlikely that the bladderwill empty through reflex activity. It is thereforeimportant that patients are catheterised on arrivalin the emergency department to avoid urinaryretention and over expansion of the bladder.Because of sympathetic inactivity, oliguria(diminished capacity to form and pass urine) maybe evident during the acute period following SCI.It is essential that practitioners are aware that alow urine output in this period does notnecessitate vast fluid resuscitation as this canresult in pulmonary oedema. Unlike in traumaticshock, oliguria in spinal shock is not related tocirculatory volume. Following acute injury, an indwelling catheter may not necessarily berequired. For those requiring assistance withbladder emptying, options might include the useof self-catheterisation or an external urinarycollection device such as a conveen. Assessmentof long-term continence needs should be carriedout once patients are transferred to specialistrehabilitation centres (Ash 2005).



Time out 6Talk to a continence adviser about different methods of bladder management that may be used in patients with SCIs. Consider the advantages and disadvantages for each method and how acceptable these may be to patients.

Time out 7Consider the effects of bowel management on a patient, including physical relationships, employment, education and social life.

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under heels to relieve pressure, may assist inmanaging the effects of pressure. Contributoryfactors should be assessed and addressedappropriately to help minimise the risk of pressureulcers developing, for example maintainingadequate nutrition and hydration and cleaningpatients as soon as possible after soiling orexcessive perspiration.

Joints should be passively moved through afull range of movement to prevent contractures.Hand splints can be useful in maintaining thehand in a functional position; similarly ankleorthoses may avoid the development of footdrop(inability to dorsiflex the foot) and shortening ofthe Achilles tendon (Grundy and Swain 2002).The presence of such contractures greatly affectsthe potential for rehabilitation and can reducesignificantly the level of independence that maybe achieved during rehabilitation.

Autonomic dysreflexia

Autonomic dysreflexia is a life-threateningsyndrome that potentially affects all patients withan SCI at T6 or above (McLeod 2004b).Autonomic dysreflexia is caused by spinal reflexmechanisms that remain intact despite the injury(Blackmer 2003).

Noxious (painful) stimuli below the level ofinjury produces an afferent impulse. However, as complete SCI results in the disruption of theneural pathways between the central andperipheral nervous system, the signal is unable to pass the level of injury. The noxious stimulusgenerates a generalised sympathetic response and results in vasoconstriction. Baroreceptors inthe carotid sinus and aortic body respond to thevasoconstriction and consequent hypertension,resulting in vasodilation and sweating above thelevel of injury. As the efferent impulse is unable topass the injury there is vasodilation above the levelof injury and vasoconstriction below.

A patient with an SCI may have a restingblood pressure of 90/60mmHg, hence readingsof 120/80mmHg might represent a considerableelevation in blood pressure. Excessivehypertension during autonomic dysreflexia maylead to seizures, intracranial haemorrhage and in severe cases, coma or death (Essat 2003,Krassioukov et al 2003). However, as thedetrusor reflexes are disrupted in spinal shock,autonomic dysreflexia is not common in earlySCI, and if it does occur, it is usually the result ofa huge noxious stimuli (Silver 2000).Subjectively, patients may complain of anxiety,apprehension or acute distress and may alsopresent with:

� Severe headaches (most common symptom).

�Nasal congestion.

� Sweating above the level of the injury withpallor below the level of the injury.

�Blurred vision.

�Palpitations.

Early recognition of autonomic dysreflexia isessential so that appropriate treatment can beinitiated immediately. If not contraindicated, the patient should be placed in an uprightposition to induce postural hypotension. If this iscontraindicated, tilting the head of the bed mightinduce some degree of orthostatic hypotension tohelp combat the increasing hypertensive effects.Other actions that may be taken duringautonomic dysreflexia include:

�Loosening tight clothing and checking forcommon causes of autonomic dysreflexia (Box 2).

�Monitoring blood pressure every five minutes.

�Removing noxious stimuli, for example recatheterisation if caused by a blockedcatheter, or manual evacuation if faecalimpaction is the cause.

�Administering antihypertensive agents orglyceryl trinitrate to control hypertensive effects.

Conclusion

There are diverse manifestations of SCI and it isuseful to relate the mechanism of injury to actualor potential injury. There are a number ofcausative factors that influence and determine theextent of the injury sustained. Although the effectof the primary injury cannot be altered, the degreeof secondary injury can be minimised bymanaging factors that create the cellular changesand underlying pathophysiology. The goal inacute care remains to prevent deterioration of the


BOX 2

Common causes of autonomic dysreflexia

� Distended bladder, for example a blocked catheter.

� Distended bowel, for example faecal impaction.

� Urinary tract infection and/or renal calculi.

� Ingrown toenail, visceral pain and/or visceral trauma.

� Pressure ulcers.

� Fracture and/or trauma below level of spinal cordinjury.

� Severe anxiety and emotional distress.

� Pregnancy and childbirth.

� Erection and ejaculation.

(Harrison 2000)

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practitioners to anticipate and manage elementsof care effectively.

SCI requires a multidisciplinary approach tocaring for patients and their families through theacute and rehabilitation phases, and requires good communication with all members of themultidisciplinary team to ensure that goals can beachieved. Psychosocial factors are also importantbut are not within the scope of this article NS


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References


current condition while optimising rehabilitationpotential through the multidisciplinary team.

Effective use of anticipation and planning is essential when caring for patients during theacute phase of SCI, particularly focusing onairway, breathing and circulation. Successfulmanagement of pressure areas and limbpositioning similarly enables patients to begintheir rehabilitative phase.

In the early stages of SCI nursing,management is multifaceted, primarily becauseof the presence of spinal shock. Understandingthe principles of acute care management helps

Time out 8Now that you have completed the article you might like to write a practice profile. Guidelines to help you are on page 60.

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