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The cost of severe spinal cord injuries and traumatic brain injuries in Victoria

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Page 1: The cost of severe spinal cord injuries and traumatic brain injuries in Victoria

Injury, Int. J. Care Injured 40S (2009) S1–S26

Contents lists available at ScienceDirect

Injury

journal homepage: www.e lsev ier .com/ locate / in jury

Abstracts Trauma Melbourne 2008Trauma research and clinical management conference,21st–22nd November 2008, Sofitel Melbourne on Collins Melbourne

0020–1383/$ – see front matter

Oral presentation abstracts (ORAL and INVITED)—ORAL–INVITED

PLENARY 1-1

The Victorian trauma system—Looking into the future

M. Lum 1,*, S. Doherty 2

1 Access and Metropolitan Performance Branch, Department of Human

Services, Melbourne, VIC 3000, Australia2 Acute Health Services Program, Department of Human Services,

Melbourne, VIC 3000, Australia*Corresponding author.

Introduction: The Review of Trauma and Emergency ServicesVictoria (ROTES) 1999 provided a blueprint for the development ofan integrated system of care for patients sustaining major injuriesin Victoria. The VSTS has been in place for seven years and themajority of the RoTES recommendations have been implemented.To build further on and refine these recommendations and newinterest areas, it was considered timely to develop a strategic plan.Trauma Towards 2014 (TT2014) 2008, identifies VSTS achieve-ments and provides directional areas for refinement.

Method: Qualitative research conducted was a two-tieredapproach via 35 stakeholder and departmental consultations. Aquestionnaire was developed for this purpose. Preliminary andsecondary consultation with trauma associated industry anddepartmental stakeholders has been completed. In additionquantitative analysis via data obtained from the Victorian StateTrauma Registry (VSTR) has been analysed.

Results: Trends via the above analysis have depicted a systemthat is working exceptionally well, but refinements are required toenhance the system’s performance.

The main trends identified are:

(i) S

ystem integration of sub-acute care: The involvement of thesub-acute system i.e. rehabilitation, was raised in recognitionof the long-term impact of major trauma on individuals.

(ii) E

ducation and training: Centralising trauma at the MajorTrauma Services has significantly increased patient outcomes,but in doing so has potentially resulted in a perceived ‘de-skilling’ of staff in non major trauma services, particularlyregistrars in emergency medicine.

(iii) T

he VSTR provides patient level data, depicting patientoutcomes <6 months, there is a view that the evaluationand monitoring of patient outcomes should be extended to 24months to consider the economic and psycho-social impact ofmajor trauma.

(iv) Q

uality and safety standards/guidelines: There was generalagreement that the trauma triage guidelines, which determinepatient destination, require review in the context of newdevelopments and approaches to trauma management.

(v) In

corporation of burns education, training, triage and identi-fication into the VSTS.

Conclusion: TT2014 2008 targets strategic areas of refinementwithin the VSTS. To initiate, build and further refine these areas thedepartment is working with industry stakeholders, particularly theMajor, Metropolitan and Regional Trauma Services, will achievethe highest possible whole of care approach for Victorian majortrauma patients.

doi: 10.1016/j.injury.2009.01.021

ORAL–INVITED

PLENARY 1-2

The cost of severe spinal cord injuries and traumatic brain injuriesin Victoria

J. Dore

Transport Accident Commission, Melbourne, VIC 3000, Australia

The Transport Accident Commission (TAC) is a VictorianGovernment owned organisation established to manage Victoria’stransport accident scheme. Our mission is to work with the Victoriancommunity to reduce road trauma and support those it affects.

Whilst the number of people injured or killed on Victorian roadshas reduced dramatically over time, each year between 110 and130 people sustain either severe spinal cord injury (SCI, includingparaplegia and quadriplegia) or severe traumatic brain injury (TBI)as a result of a transport accident. People in early to mid-adulthoodare most commonly affected, with over 60% of these injuriessustained by people aged under 39. Males are also over-represented in this cohort at almost 75% of claims lodged.

Page 2: The cost of severe spinal cord injuries and traumatic brain injuries in Victoria

Abstracts / Injury, Int. J. Care Injured 40S (2009) S1–S26S2

Whilst less than 1% of the total claims lodged with TAC eachyear (2007/08: 111 of 16,840) are associated with clients havingsustained severe TBI or SCI, this cohort of clients have a much moresignificant impact on the long-term liabilities of Victoria’stransport accident scheme. Just over 60% of TACs total claimsliabilities ($3.6B of $6B) as at June 2008 were associated with theseverely injured. The significant impact on liabilities is driven bythe higher exposure to younger clients, with ongoing supportneeds as a result of severe injuries commonly in the range of 20–40years post-injury.

Lifetime support services including attendant care,accommodation and other substitutable services dominateliabilities for severe injury clients, followed by loss of earningsbenefits and a range of other hospital, medical and paramedicalservices. The changes in function caused by severe injuries(both mental and physical) are complex and produce a widerange of symptoms, making the determination of clientsupport needs and effective transition back into the communitycomplex.

Janet Dore (TAC CEO) will present on the cost of catastrophicinjuries in a TAC context, including current strategies andchallenges to improving client outcomes whilst maintaining thelong-term viability of Victoria’s transport accident scheme.

doi: 10.1016/j.injury.2009.01.022

ORAL–INVITED

PLENARY 1-3

Traumatic brain injury—Where are we today?

D.J. Cooper 1,2,3

1 Epidemiology and Preventive Medicine, Monash University, Mel-

bourne, VIC 3004, Australia2 National Trauma Research Institute, The Alfred Hospital, Melbourne,

VIC 3004, Australia3 Intensive Care Unit, The Alfred Hospital, Melbourne, VIC 3004,

Australia

In Australia, the human and financial costs of traumatic braininjury (TBI) are staggering. There are 1000 new patients withsevere TBI in Australia annually, and of these, 50% are never able tolive independently. They are dead or severely disabled. And everyyear, the 170 TBI survivors with severe disability begin theirlifetime costs of more than $3 million – each.

Against this background, a myriad of mainly industrysponsored clinical trials have failed to find a magic bullet – orindeed anything else to improve real patient outcomes in adevastating condition. But the times are changing. There havenow been 3 major clinical trials in which practice change hassignificantly improved TBI outcomes. One Victorian, one Aus-tralian, and both supported by competitive TAC and NHMRCresearch grants.

There are also three remarkable new NHMRC and TAC fundedresearch initiatives which have huge potential to improveoutcomes further in Australia, New Zealand and internationally.One is approaching completion, while two new bi-nationalprograms are commencing.

The international impact and clinical relevance of this Victorianand Australian lead research is very substantial – and there is moreto come.

doi: 10.1016/j.injury.2009.01.023

ORAL–INVITED

BREAKOUT 1-1

From cell death to neurogenesis: The broad-spectrum function ofbrain inflammation after trauma

M.C. Morganti-Kossmann 1,2

1 National Trauma Research Institute, Melbourne, VIC 3004, Australia2 Medicine, Monash University, Melbourne, VIC 3004, Australia

Since the early 1990’s the role of brain inflammation elicited inresponse to traumatic injury has received increasing interest fromthe neurotrauma community. However, although the literature haselucidated important aspects of immune mediator as well asimmune cell function, these studies generated a large number ofconflicting data supporting opposing roles of trauma-inducedinflammation. If inflammation can exacerbate the synthesis ofneurotoxic molecules thus contributing to delayed cell death andinhibiting neurogenesis, it also promotes the synthesis of neuro-trophic factors required for regenerative processes. The differencebetween the beneficial and detrimental function of brain inflam-mation seems to depend on the concentration at which immunemediators are released and the extent of time of their up regulation.Complete abolishment of inflammation seems to worsen theneurological deficit in injured animals whereas a mild attenuationseems to result in a better histological and neurological outcome.The purpose of our research is to elucidate the role of braininflammation in humans and rodent models of TBI with respect to itsexacerbation following post-traumatic hypoxia, delayed neuronalcell death, brain accumulation of blood derived leukocytes,neurogenesis and therapeutic intervention aimed at maintainingthe protective properties of inflammation to guarantee repair andattenuate toxicity. The presentation will show the interplaybetween the clinical and the basic research and demonstrate thesimilarity and the difference in human and rodent TBI to validate therole of molecular pathways relevant in humans and develop noveltherapies of potential patient application.

doi: 10.1016/j.injury.2009.01.024

ORAL–INVITED

BREAKOUT 1-2

Avoiding bias at the bench

D. Howells 1,2

1 National Stroke Research Institute, Heidelberg Heights, VIC 3081,

Australia2 Medicine, The University of Melbourne, Melbourne, VIC 3004,

Australia

In both neurotrauma and stroke research we are often left toponder the statement that ‘‘Everything works in rats but nothingworks in man.’’ Many explanations have been put forward to explainthis failure to translate apparent efficacy in animals to therapies forman. In the field of stroke neuroprotection, systematic failure toconsider two components of stroke biology and four facets ofexperimental design which contribute to this failure have beenidentified and have clear parallels for head and spinal cord trauma.Firstly, timing of therapy is critical. Whilst animal studies show amarked fall in neuroprotective efficacy 3–6 h after stroke, mostclinical trials of neuroprotection have been conducted with a meantime to treatment of 20 h. This has occurred despite clear evidencefor a nearly identical short time frame for successful thrombolysis