respiratory care in spinal cord injury with associated traumatic brain injury: bridging the gap in...

Neal Cook BScHons, MSc, PG CertSpecialist Practice,RN, Lecturer inNursing, SpecialistPractitioner CriticalCare Nursing,Department ofNursing, Universityof Ulster, MageeCampus, NorthlandRoad, Derry Co.,Derry, NorthernIreland BT48 7JL,UK. Tel: +44 (0) 28713 75463/+44 (0)7734 663894(mobile); E-mail:[email protected]

(Requests foroffprints to NC)

Manuscriptaccepted: 17/03/03

Original article

Respiratory care in spinal cordinjury with associatedtraumatic brain injury:bridging the gap in critical carenursing interventionsNeal Cook

Spinal cord injury (SCI) is a devastating and challenging condition. The events that lead toSCI, such as road traffic accidents, falls, sports and violence [Top. Spinal Cord Inj. Rehabil. 5(1999) 83], are also the common aetiologies of traumatic brain injury (TBI). It’s not surprisingthen, that 20–50% of those with cervical SCI have TBI [J. Trauma 46 (1999) 450]. Theliterature pertaining to the management of either injury in isolation is vast, but lackingwhere the two conditions are experienced together and require distinct adaptations tointerventions. Consequently, a gap in the literature exists. This paper focuses on thosepatients with SCI of the cervical spine with associated head injury, and pay particularattention to respiratory difficulties, and presents interventions required to minimise andtreat the effects of such pulmonary compromise.© 2003 Elsevier Science Ltd. All rights reserved.

KEYWORDS: Spinal cord injury; Brain injury; Trauma.

Introduction

Spinal cord injury (SCI) is a devastating andchallenging condition. The events that lead toSCI, such as road traffic accidents, falls, sportsand violence (Watanabe et al., 1999), are alsothe common aetiologies of traumatic braininjury (TBI). It’s not surprising then, that20–50% of those with cervical SCI have TBI(Iida et al., 1999). The literature pertaining tothe management of either injury in isolation isvast, but lacking where the two conditions areexperienced together and require distinctadaptations to interventions. Consequently, agap in the literature exists. This paper will

focus on those patients with SCI of the cervicalspine with associated head injury, and payparticular attention to respiratory difficulties.Adequate cerebral oxygenation has beenidentified as paramount in the prevention ofsecondary insult in those with TBI (Zafonteet al., 1999), and respiratory complications asthe leading cause of death in those with SCI(Mansel & Norman, 1990; Lucke, 1998).

The acute stage of illness will beapproached, as the first 72 hours are optimal inpreventing secondary neuronal damage(Chamberlain, 1998; Cunning & Houdek, 1998).Secondary neuronal damage is defined as “theprogressive cellular damage, which is as a

© 2003 E l sev i e r S c i ence L td . A l l r i gh t s re se r ved . Intensive and Critical Care Nursing (2003) 19, 143–153 143

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Intensive and Critical Care Nursing

result of degradative biochemical processesthat are set in motion at the time of injury”(Zafonte et al. 1999, p. 21). Comprehensive andfocused attention in these areas will help in theidentification of the three major complicationsof SCI, i.e. hypoxia, hypoxaemia, andhypoperfusion (Munro, 2000).

Spinal cord injury and respirationThe need for optimal respiratory function inthose with acute SCI alone has long been apriority in the nursing management of suchpatients (Wang et al., 1997). Those with acuteSCI, especially of the upper cervical spine, aretypically known to have chronic accumulationof pulmonary secretions, with an associatedhigh incidence of pneumonia, atelectasis, andrespiratory failure (Wang et al., 1997; Lucke,1998; Lanig & Peterson, 2000). Suchcomplications are brought about throughdisruption of muscle innervation by thephrenic nerve (Lucke, 1998) (see Table 1).Indeed, respiratory failure is the leading causeof death in patients with SCI (Lucke, 1998;Lanig & Peterson, 2000). Pulmonary hygieneto prevent such complications is therefore ofmajor clinical significance in reducingmortality and morbidity (Lanig & Peterson,2000), and in promoting better patientoutcomes and increasing quality of life.

The control of respiration is a complexprocess, with automaticity and rhythmicitycontrolled by dorsal and ventral groups ofneurons in the medulla oblongata (Tortora &Grabowski, 2002), voluntary control by thecerebral cortex and the innervation ofrespiratory muscles by the peripheral nervesfrom the spinal cord (especially cervical andthoracic spinal nerves). Patients withadditional head injury may experience loss ofvoluntary control, as well as altered cognitiveabilities to comply with complex therapies

Table 1 Relationship between level of injury and effect on respiration mechanics (Lucke, 1998)

C1–C2 injury Diaphragm, accessory muscles, intercostal and abdominal muscles disrupted or paralysedC3–C5 injury Disrupts innervation of phrenic nerve—diaphragm or hemidiaphragm disrupted or paralysed

Disruption of scalenes, trapezius and clavicular portion of pectoral musclesT1–T6 injury Disrupts innervation of intercostal musclesT7–T12 injury Disruption of abdominal muscles which aid expiration

(Munro, 2000). This can lead tohypoventilation and hypoxaemia (Munro,2000). The level and completeness of injuryalso denotes the extent to which respiratorydynamics are affected (Borel & Guy, 1995). Inaddition, in the days following SCI, theappearance and nature of the injury canchange dramatically as a result of secondaryinjury (Dubendorf, 1999). The inflammatoryresponse that occurs begins immediately afterinjury (Dubendorf, 1999). In many instances,some secondary damage cannot be preventeddue to microcirculatory damage to the greymatter of the spinal cord, loss of autoregulationand vasospasm (Dubendorf, 1999). Nursinginterventions, however, can be tailored aroundreducing the effects of such complications.

The effects of acute SCI on respiratorymechanics are numerous and profound.Reduction or loss of diaphragmatic functionresults in a severe reduction in inspiratorycapacity, leading to hypoventilation (Lucke,1998). Paradoxical breathing in those with highcervical SCI, characterised by use of accessorymuscles, passive upward movement of thediaphragm and inversion of the abdomen, canresult from motor function loss, leading todecreased expiratory flow (Young & Shea,1998; Munro, 2000). Hypersecretion ofbronchial mucus leads to micro-atelectasis as aresult of inhibited elimination of suchsecretions (Munro, 2000). This can occur within1 hour after injury (Lanig & Peterson, 2000). Inaddition, failure to hyperinflate the alveoliresults in a significant reduction in the releaseof surfactant, which further contributes toincreased atelectasis (Lanig & Peterson, 2000).A marked decrease in the effectiveness ofcough and subsequent reduced expiratory flowis frequently observed (Linder, 1993; Bach &Valenza, 1996; Wang et al., 1997). Neurogenicpulmonary oedema may occur (particularly inthose with associated head injury), where

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Respiratory care in SCI with associated TBI

systemic and pulmonary vasoconstrictionoccurs, potentially causing left ventricularoverload, and reduced alveolar ventilation(Chen, 1995; Lucke, 1998; Lanig & Peterson,2000; Munro, 2000). This occurs as a result ofabnormal sympathetic nervous activity. Theloss of pulmonary reserve results in noresources to perform activities of daily living,and leaves patient vulnerable to hypoxia intimes of hypermetabolism (e.g. from stress, oracute illness, infection) (Lucke, 1998). Spinalshock, if it occurs, further results in abdominaland intercostal muscles being flaccid, with aloss of autonomic function (Lucke, 1998), andmore specifically sympathetic function. Thereis a high risk of aspiration pneumonitis as aresult of gastrointestinal paresis, whichpresents often with SCI (Borel & Guy, 1995).Gastric over-distension may also impedediaphragmatic function, as a result of such anileus (Lanig & Peterson, 2000). Breathlessnessis experienced by 13–18% of patients even 1year after SCI (Ayas et al., 1999), which leadsto respiratory fatigue (Lucke, 1998).

Traumatic brain injury andrespirationIn those with TBI, the rise in intracranialpressure (ICP) as a result of alteredhomeostatic mechanisms requires optimalmanagement of respiratory mechanisms toprevent secondary neurological damage

Table 2 Complications of endotracheal suction

In traumatic brain injury In spinal cord injury

• Increases in ICP and reduction in CPP leading tocerebral ischaemia (Chamberlain, 1998)

• Hypoxia (Buglass, 1999)

• Hypoxia (Buglass, 1999) • Hypotension (Buglass, 1999)• Hypotension (Buglass, 1999) • Atelectasis (Buglass, 1999)• Atelectasis (Buglass, 1999) • Infection (Buglass, 1999)• Infection (Buglass, 1999) • Tracheal mucosal damage (Buglass, 1999)• Tracheal mucosal damage (Buglass, 1999) • Vagal nerve stimulation (Buglass, 1999)• Vagal nerve stimulation (Buglass, 1999) • Obstruction (Buglass, 1999)• Obstruction (Buglass, 1999) • Cardiac arrest (Buglass, 1999)• Cardiac arrest (Buglass, 1999) • Pulmonary haemorrhage (Raymond, 1995)• Death (Buglass, 1999) • Patient anxiety and fear (Raymond, 1995)• Cardiac dysrhythmias (Raymond, 1995) • Increased bronchial mucus production

(Raymond, 1995)• Broncho spasm (Raymond, 1995)• Inability to produce cough reflex impairsexpectoration of mucus

• Pulmonary haemorrhage (Raymond, 1995)• Patient anxiety and fear (Raymond, 1995)• Increased bronchial mucus production (Raymond, 1995)

caused by cerebral hypoxia, hypercarbia, andacidosis (Borel & Guy, 1995; Kamerling, 2000).In initial TBI, the injured brain is particularlyvulnerable to ischaemia as a result of impairedautoregulation (Chamberlain, 1998), with asubsequent local increase in cerebral blood flowthat pre-disposes the cerebral cortex to oedema(Cunning & Houdek, 1998). Maintainingadequate cerebral blood flow and oxygenationare the primary goals in preventing secondaryinjury (Price et al., 2000), which denotes theneed for managing respiratory elements toensure adequate oxygenation and maintainingpH within normal limits. It is essential toconsider cerebral perfusion pressure (CPP)with any interventions for those with TBI, asCPP is the pressure gradient that drivescerebral blood flow (Simmons, 1997).

Raised ICP impedes cough reflex,respiratory drive and airway reflexes, requiringthe need for adequate pulmonary hygiene.However, interventions such as endotrachealsuctioning can compromise neuronal viabilitythrough sudden rises in ICP, and subsequentfalls in CPP (Brucia & Rudy, 1996) (see Table 2).Cough induced by suctioning raises ICP byimpeding venous through raised intrathoracicpressure (Johnson, 1999). An awareness ofsuch patterns are essential, as a cycle of risingICP and falling CPP potentiates the occurrenceof cerebral oedema, ischaemia and death(Simmons, 1997). A drop in CPP to below 60 isknown to jeopardise the perfusion of the entire



brain (Chamberlain, 1998). It must further benoted that venous return is also impeded inthose with SCI as a result of loss of muscletone to abdominal musculature (Mansel &Norman, 1990). This leaves those with SCIand concomitant TBI at greater risk of raisedICP.

Respiratory assessmentIn-depth respiratory assessment is essential toidentify the patients dependence needs, toinitiate preventative and curative treatments totackle potential and existing pulmonarycomplications, and to identify factors likely topotentiate secondary neuronal damage(Cunning & Houdek, 1998). It must beacknowledged, however, that initialassessment in the acute stage must be followedup with further assessment, especially withinthe first 5–7 days after injury, as the nature oflesion to the spinal cord changes (Mansel &Norman, 1990; Lu et al., 2000). This is as aresult of progressive cord oedema,inflammation, calcium influx, excitotoxicamino acids and free radicals (Mahale et al.,1993; Lu et al., 2000). Such a pathophysiologicalprocess can result in respiratory failure inthose with no initial respiratory compromise(Lu et al., 2000). Delayed apnoea is one suchexample of this. Assessment must include thefollowing factors (see Appendix A):

• Alignment of the trachea to identifypresence of laryngeal injury or mediastinalshift (Munro, 2000).

• Shape of thorax (Munro, 2000).• Symmetry of chest wall movement (Munro,

2000).• Patients pallor (Borel & Guy, 1995).• Respiratory rate, regularity and effort (Borel

& Guy, 1995; Lucke, 1998).• Careful analysis of arterial blood gases to

identify rise in CO2 and drop in O2, whilecarefully considering pH (Borel & Guy,1995).

• Past history of pulmonary complications(e.g. chronic obstructive pulmonary disease)(Lucke, 1998).

• Nutritional status requires assessment toensure adequate calories for use ofaccessory muscles (Lucke, 1998).

• Complete neurological assessment toidentify extent and level of cord injury andthus identification of muscle groupsaffected (Lucke, 1998).

• Careful auscultation of lung fields toidentify secretion retention (Lucke, 1998),and breath sounds to identify air entry andobstructed flow (Buglass, 1999).

• Swallow assessment to identify individuals’ability to handle secretions and subsequentrisk level for aspiration of same (Lucke, 1998).

• Assess patients’ ability to produce effectivecough (Lucke, 1998).

• Consultation with physiotherapists toidentify problems with pulmonarymechanics.

• Careful examination of chest X-rays,preferably taken in supine position toidentify upper lobe venous distension(Lucke, 1998).

• Careful monitoring of patients increasing ordecreasing ventilatory requirements (Lucke,1998).

• Cardiovascular assessment, i.e. ECGrhythm, haemoglobin count, peripheralperfusion, central venous pressure, andurinary output (to support circulating bloodvolume assessment) (Lucke, 1998).

Goals of careIn reference to respiratory management,interventions surrounding the care of patientswith SCI and concomitant TBI are focused on:

(a) Prevention of secondary neuronal damage.(b) Preventing hypoxaemia.(c) Preventing and treating atelectasis.(d) Maximising alveolar ventilation.(e) Maximising pulmonary hygiene for

impaired cough and secretion clearance(Lanig & Peterson, 2000).

InterventionsChamberlain (1998) states that the delivery ofexpert care involves the overlapping ofboundaries with other disciplines, and requirescareful analysis of therapeutic interventions,incorporation of preventative mechanisms andutilisation of specialist knowledge. Problemavoidance and resolution is a key role of the



specialist nurse, who is ideally positioned toevaluate the patient’s condition and who isequipped with the advanced thought processand knowledge to tailor dynamic care(McIlvoy et al., 2000). In essence, interventionsare what produce outcomes, and thus, aspecific focus of this paper will now approachthe interventions in respiratory managementof those with cervical SCI and TBI, with anemphasis on individual assessment of patients.

Endotracheal suctioningAs previously acknowledged, suctioning isessential in maintaining adequate pulmonaryhygiene and promoting optimal ventilationand oxygenation (Raymond, 1995), but is notwithout complications (Raymond, 1995).Contemporary literature has investigated thisnursing procedure, but has not yet led to aconsensus on its practice. While theknowledge base supporting the mechanism ofhow suctioning effects ICP so dramatically issparse, it is known that the insertion of asuction catheter alone can stimulate acute risesin ICP without suction being applied (Brucia &Rudy, 1996; Kerr et al., 1998). However, rises inMAP and CPP are also known to accompanysuch rises in ICP, compensating the potentialdrop in CPP (Brucia & Rudy, 1996). This doesnot occur with the application of negativesuction pressure, leading secondary insult verypossible (Brucia & Rudy, 1996). It must benoted, however, that in many with TBI, suchcompensatory responses may not be viabledue to alterations in autoregulation.Furthermore, abrupt rises in MAP maypromote cerebral oedema and neuronalhypoxia as a result of vasomotor paralysis(Brucia & Rudy, 1996). Return to baseline CPPand ICP may take up to 15minutes (Kerr et al.,1998). Consequently, any suction proceduremust be performed with extreme caution andonly after comprehensive patient assessment,and never as a routine nursing intervention(Drudling, 1997; McConnell, 2000). A review ofcontemporary, statically relevant research hasled the author to the following considerationsin the assessment for the need for suction:

• ICP less than 20mmHg and CPP greaterthan 70mmHg. In those with extreme raises

in ICP, CPP should be focused on moreand the presence of other indicators of theneed for suction (Johnson, 1999).Augmentation of CPP may be optimised byraising mean arterial pressure (MAP) withcrystalloids, colloids, or inotropes(Chamberlain, 1998).

• Suction should only be carried out when thepatients are unable to clear their ownsecretions, i.e. poor cough reflex or poorability to expectorate (Griggs, 1998).

• Presence of increased peak airway pressure,patient coughing, audible or visiblesecretions in the airway, deteriorating bloodgases, laboured breathing (Wood, 1998),lowered SaO2 levels, unrelieved coughing,diminished air entry, ‘feeling’ of secretionson chest, and patient restlessness (Place &Fell, 1998).

A review of contemporary statisticallysignificant literature yielded the followingconsiderations for integration into optimalimplementation of endotracheal suctioning:

• Aseptic procedure to be carried out, usingclean gloves, and handwashing before andafter (Buglass, 1999).

• A maximum of two passes at eachprocedure (Wainwright & Gould, 1996b).

• A maximum of 10 seconds for the suctionprocedure to prevent hypoxia andatelectasis (Buglass, 1999; Johnson, 1999).

• Suction pressure to be 100–120mmHg inadults, any higher will cause atelectasis,mucosal damage, or collapse of the suctioncatheter (Griggs, 1998; Buglass, 1999; Celik& Elbas, 2000). Higher pressures arethought not to remove any more secretionsthan the recommended negative pressure(Wood, 1998).

• Application of suction should only occur ascatheter is drawn out, to prevent adherenceand damage to tracheal mucosa (Griggs,1998; Buglass, 1999).

• Multi-eyed catheters should be used wherepossible as they produce less trachealmucosal trauma as a result of distributednegative pressure (Griggs, 1998).

• Catheter insertion should be one third of itslength, or about 15 cm into an adulttracheostomy tube (Griggs, 1998; Buglass,1999).



• Suction catheters should be half thediameter of the endotracheal/tracheostomytube (Odell et al., 1993; Buglass, 1999), so asto avoid mechanical stimulation of thecarina, and a subsequent rise in ICP (Garcia& Rudy 1996). Use of a close-suction systemwill prevent drops in O2 saturation, whilehelping to reduce infection (Wainwright &Gould, 1996a; Robb, 1997). Closed suctionsystems will reduce infection, maintainalveolar ventilation, and is associated with adecreased incidence of desaturation onsuctioning (Jesurum, 1997). Use of opensuction systems on patients requiringpositive end expiratory pressure (PEEP) oron continuous positive airway pressure(CPAP) means 30minutes will be requiredbefore the benefit of such therapies returns tothe pre-suction baseline (Steuer et al., 2000).While closed suction and open suction havenot yet been compared in patients with TBI,it should be acknowledged that the benefitsof closed suction systems highlighted byJesurum (1997) and Steuer et al. (2000) canonly benefit this group of patients.

• Avoid movement of the endotracheal tube,as such movement is a stimulant to raiseICP (Garcia & Rudy 1996).

• Hyperoxygenation for 1minute (O2 at100%) before and after suctioning isadvocated to counteract falls in oxygensaturation and cardiac dysrhythmias(Raymond, 1995; Wainwright & Gould,1996a; Wood, 1998; Tamburri, 2000).However, this must be administered withcaution and on an individually assessedbasis, especially in those with a ‘hypoxicdrive’ (Wainwright & Gould, 1996a). Asextent of brain injury cannot be fullydetermined at an acute stage, it still remainsnecessary to consider hypoxic drive in thosewith a relevant history of the same.

• Hyperinflation is not recommended as itmay cause hypotension (Wood, 1998), whichwould result in a marked drop in CPP.

• Where possible, and especially whereextremes of raised ICP is being experienced,administration of neuro-muscular blockingagents should be utilised to counteractreactive intracranial hypertension fromcatheter insertion and negative suctionpressure (Kerr et al., 1998).

To gain access to the left mainstembronchus, a curved tip catheter is useful, whileturning the patients head to the right (Lucke,1998). However, this is considered impracticalin those with cervical SCI and raised ICP dueto the obstruction of venous return to the heartand manipulation of the cervical spine.

Instillation of normal salinepre-suctionThe common practice of normal salineinstillation (NSI), mainly by nurses andphysiotherapists, in the perceived assistance ofaiding the mobilisation and removal ofpulmonary secretions has been long debatedwithin the literature. From a review of theliterature, no single article or piece of researchidentified any beneficial aspect in usingnormal saline to remove or mobilise secretions(Ackerman et al., 1996; Drudling, 1997;Blackwood, 1999; Sievers & Adams, 2000).Therefore, in accordance with the NMC(Nursing and Midwifery Council) code ofprofessional practice, no therapy should beperformed which has no proven benefit topatients, especially when hazards to its use arewell-published (Drudling, 1997; NMC, 2002).No scientific basis exists to support its use(Raymond, 1995). Normal saline is immisciblewith secretions, and on suctioning, mostlysaline is aspirated back (Raymond, 1995;Drudling, 1997). The saline solution does notactually reach the peripheries of the lungs toloosen secretions (even if it could), even after30minutes (Raymond, 1995). While someargue that stimulating a cough from NSImobilises secretions, this is considered aninvalid rationale for its use, as a suctioncatheter alone while avoiding thecomplications of NSI may stimulate a cough(Gray et al., 1990; Raymond, 1995). This isespecially so when a neuro-muscular blockingagent is being administered, whereby nostimulation of a cough is possible. Suchcomplications are identified as:

• Greater falls in oxygen saturation thanwhen suction without NSI is used(Ackerman et al., 1996), which may lead tosudden hypotension and cardiacdysrhythmias (Kinloch, 2000).



• NSI has an adverse effect on mixed venousoxygenation (Kinloch, 1999; Sievers &Adams, 2000), dropping to a level of 38%(less than 53% pre-disposes to tissue oxygendeprivation) in one study (Kinloch, 1999).

A further argument often used to advocateits use is that it reduces the build up of driedsecretions on the inner lumen of theendotracheal/tracheostomy lumen (Ackermanet al., 1996). However, this can be avoidedwith proper use of heated humidification(Ackerman et al., 1996). It is concluded that theprevention of the production of thin andtenacious secretions should be the focus of care,rather than their removal as a result of poorpatient care (Blackwood, 1999). Blackwood(1999), further emphasises that this wouldfurther avoid the excessive anxiety caused topatients when NSI is utilised, an aspect ofcritical illness which must not go unrecognised.This is especially so where intubation hasrendered the patient helpless in voicing theirfears and concerns, and where body image islikely to be distorted (Serra, 2000).

Humidification and hydrationIt is not uncommon for patients with TBI andSCI to be self-ventilating, depending on theextent and severity of their illness. Frequently,unventilated critically ill patients are treatedwith dry oxygen through face/trache masks orT-pieces. With endotracheal and tracheostomytubes bypassing the upper airway, naturalmechanisms for humidifying and warminginspired air is lost (Buglass, 1999).Consequently, unless inspired gases arehumidified and warmed, the action of thetracheal cilia are inhibited, secretions dry andencrust and there is a greater risk of tubeblockage and infection (Griggs, 1998; Buglass,1999). Consequently, the use of heated oxygenhumidifiers is recommended (Hopper, 1996;Blackwood, 1999; Tamburri, 2000).Humidification will also reduce the perceivedneed for NSI. In addition to this, patients whoare kept well hydrated systemically willproduce looser secretions as those who aredehydrate tend to have dried mucosalmembranes which produce thick secretions(Buglass, 1999; Blackwood, 1999; Serra, 2000).

Administration of frequent saline nebuliserswill further aid adequate pulmonaryhydration (Odell et al., 1993). Adequatehumidification and hydration will also preventblockage of the patients airway (Serra, 2000).However, care must be taken to ensure thatwhile patients require adequate hydration,those who are critically ill may tolerate lessintravascular volumes of fluid, and renal andcardiac function must be monitored closely.

Ventilatory management forintubated patientsWhile many patients require ventilatorymanagement as a result of level ofconsciousness and impaired airway control,ventilation in itself can raise ICP andpre-dispose to secondary injury if incorrectlymanaged (Borel & Guy, 1995). The use of highPEEP, and positive pressure ventilation initself, raises intrathoracic pressure and thusimpedes venous return to the right atrium(Borel & Guy, 1995; Romand & Donald, 1995;Ashurst, 1997). This venous congestionimpedes cerebral blood flow, raising ICP.CPAP, although rarely used in severe TBI withconcomitant SCI, of 12 cmH2O has beendemonstrated to produce a 3–5 cm increase incerebrospinal fluid pressure (Romand &Donald, 1995). Therefore, PEEP levels as highas 10 and 12 cm H2O should be avoided (Borel& Guy, 1995). This applies for those on CPAPcircuits also. To maximise the use of PEEP, aclosed suction system should be utilised tomaintain alveolar inflation. In addition, it isrecommended that tidal volume and PEEPvalues are significant enough to hyperinflatealveoli so as to maintain surfactant release, andthus help prevent atelectasis (Lanig & Peterson,2000). Those who are not generating sufficienttidal volumes spontaneously may requireintermittent positive pressure ventilation.

The traditional use of hyperventilation toreduce ICP through a reduction in CO2, whichresults in cerebral vasoconstriction and asubsequent reduction in cerebral blood flow, isno longer recommended due to highincidences of ischaemia in those withintracranial hypertension (Geraci & Geraci,1996; Kerr et al., 1997; Chamberlain, 1998;Cunning & Houdek, 1998). Despite these



studies not always looking at homogenousgroups of patients with neurological disorders,the trend across these studies support thisassertion. Even under strict control trials,ischaemia and hypoxic episodes occur, and ithas subsequently been felt that outside ofcontrol trials such events are more likely tooccur, with detriment to the patient (Geraci &Geraci, 1996). In addition, no study hasdemonstrated any benefit of hyperventilationfor patients (Geraci & Geraci, 1996). It is thusrecommended that patient’s ventilatoryparameters should be individually tailored tonormal physiological limits so as to notcompromise cerebral blood flow (Chamberlain,1998), and that prophylactic treatment withhyperventilation be avoided with nodemonstrated benefit to patients (Zafonteet al., 1999). It must be noted that hypercapniaor hypoxia will result in intense cerebralvasodilation and a subsequent rise in ICP andthus should be avoided (Ma et al., 2000).

Patient positioningPatient positioning has been demonstrated tohave the ability to improve respiratorymechanics, and thus essential in those with SCI(Simmons, 1997). Patients with SCI who havehigh oxygenation saturation while supine maybecome dyspnoeic when sitting up and dropsuch saturation (Borel & Guy, 1995; Lucke,1998). This is as a result of the hemidiaphragmbeing inhibited in achieving maximal tensionin such a position (Borel & Guy, 1995).Postural drainage and percussion have beenshown to reduce pulmonary complicationsthrough clearing the proximal airways, butwith turning and prone positioning shown toreduce such complications further (Fishburn,1990; Lucke, 1998). Therapies should befocused on draining the left lower lobe, asstudies have demonstrated a high incidence ofatelectasis, consolidation and pneumonia inthis region (Lucke, 1998). This is thought to bedue to the angle of the left mainstem bronchusoff the trachea, lending suction to the rightmainstem bronchus more probable. Oscillatingbed therapy has also been found tosignificantly reduce mortality from pulmonarycomplications also (Harris & Reines, 1987),however, such research is outdated and

requires to be carried out in contemporaryunits.

With 50–75% of patients with TBI estimatedto have raised ICP (Simmons, 1997), it isessential to appreciate how turning to improverespiratory dynamics effects those with raisedICP. No research on positioning for those withSCI takes into consideration concomitant TBIand effect on ICP or CPP (and vice versa).Positioning patients with head up, and inneutral position is recommended by Borel andGuy (1995). This would be consideredstandard practice in many units, however, it issuggested that positioning should be based ona more individualised basis (Simmons, 1997).Turning itself can raise ICP, and it has beenidentified that rises in ICP with patientspositioned with the head rotated, or with hipsor arms extremely flexed may occur due toimpeded venous return (Simmons, 1997),however, the evidence base to support this isweak, but still requires consideration. Previousstudies have observed positioning in terms ofeffect in ICP, and recent authors recommendthat CPP should be considered more closely indetermining whether position is beneficial ordetrimental (Johnson, 1999). It would thereforeseem more appropriate to assess eachindividual’s tolerance to various positions,with the head kept in neutral alignment on thebasis of CPP being maintained above 70, andwithout excess rises in ICP (Chamberlain,1998). Any intervention that maintains CPPabove 70mmHg is regarded beneficial(Simmons, 1997). Those with higher degrees ofraised ICP are less likely to tolerate their headbeing raised due to the relative lack of venousblood available for displacement (Rosner &Daughton, 1990; Simmons, 1997). It must beacknowledged, however, that Rosner andDaughton’s (1990) research was not exclusiveto those with TBI, but included those withhydrocephalus, and cerebral tumours. Theconsensus appears to support the opinion thatraising the bed does, more often than not, raiseICP (Davenport et al., 1990), but in some casesdoes not lower CPP (Feldman et al., 1992).

Further considerations, rarelyacknowledged, are whether the patient’scervical collar (if present) is impeding venousreturn, or whether the presence of a HaloBrace can enable adequate positioning. Rigid



cervical spine collars have been demonstratedto raise ICP through impeding venous return(Davis et al., 1996; Hunt et al., 2001).Furthermore, those with unstable cervical SCIwill not be able to be sat up, with strictalignment being maintained. The preventionof pressure sores also bears consideration, withoccipital pressure sores being highly prevalentin those with SCI (Powers, 1997), highlightingthe importance of regular position change. Inthose able to be sat up, the patients responseshould be gauged at gradually increasingheight (i.e. initially 15◦ and then 30◦), and theiroptimal position determined and charted.

CoughAs cough production is significantly impairedby SCI (Bach & Valenza, 1996; Wang et al.,1997), cough production is a major part ofnursing intervention in those not requiringintermittent positive pressure ventilation, butwho remain critically ill (Lanig & Peterson,2000). Furthermore, those who have atracheostomy are significantly impaired inproducing a cough due to their inability toraise intrathoracic pressure (Tamburri, 2000).Manually assisted cough, through abdominalsupport and thrusts, have been shown to bethe most effective (Jaeger, 1993; Linder, 1993).Such intervention is rarely seen in practiceoutside spinal injury units, and can be usedeven in those who are cognitively impaired.Where assisted cough is being utilised, the useof bronchodilators and mucolytics arebeneficial in mobilising secretions to gainmaximum benefit from the cough (Lanig &Peterson, 2000). Another area being currentlyexplored is the use of functional electricalstimulation to innervate the phrenic nerve andaid in producing effective cough (Bach & Alba,1990; Linder, 1993).

NutritionIt is essential that the patient’s nutritionalstatus is maintained or restored to ensuresufficient calorific intake for the additionalworkload on breathing (Robb, 1997). For thosewith poor swallow function,nasogastric/nasojejunal feeding is required,providing no gastrointestinal paresis exists.

Total parental nutrition may then be required.The placing of a nasogastric tube may still berequired to relieve gastric distension as a resultof an ileus (Lanig & Peterson, 2000). A 40–45%loss in diaphragmatic muscle mass can occurwith malnutrition (Skeie et al., 1993), andadequate nutritional support can improverespiratory muscle function and pulmonaryventilatory gaseous exchange (Robb, 1997).

ConclusionHealthcare professionals aspire toevidence-based practice, but all to often theliterature has no bridges between the gaps(Kirrane, 2000). This is clearly the case whereliterature approaches the care of those withSCI and concomitant TBI, whereby theresource base for nurses aiming to providespecialist care is devoid of a firm grounding.This paper has sought to begin bridging thatgap through delineating the interventionsrequired to adequately maintain respiratoryfunction in those acutely ill, while preventingsecondary neuronal damage. Aggressiveefforts to maintain respiratory function andpulmonary hygiene result in dramaticdecreases in respiratory mortality in SCI from20 to 5% in the last 20 years (VanBuren et al.,1994), with the benefits well documented forthose with TBI.

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