See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/261315591

Whiplash Injury

Article  in  Continuing Education in Anaesthesia, Critical Care and Pain · August 2014

DOI: 10.1093/bjaceaccp/mkt052

CITATIONS READS

5 4,388

3 authors:

Alifia Tameem Sandeep Kapur

The Dudley Group NHS Foundation Trust University Hospitals Birmingham NHS Foundation Trust
28 PUBLICATIONS   74 CITATIONS    101 PUBLICATIONS   239 CITATIONS   

SEE PROFILE SEE PROFILE

Hirachand Mutagi
Sakra World Hospital
55 PUBLICATIONS   192 CITATIONS   

SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Pain management View project

All content following this page was uploaded by Sandeep Kapur on 22 May 2014.

The user has requested enhancement of the downloaded file.

 Continuing Education in Anaesthesia, Critical Care & Pain Advance Access published October 1, 2013
Whiplash injury
Alifia Tameem MD FRCA
Sandeep Kapur FRCA FFPMRCA
Hirachand Mutagi FRCA FFPMRCA
Key points
Whiplash is the most common
injury associated with motor
vehicle accidents and a major
cause of disability and litigation.
Whiplash-associated disorders
(WAD) can be classified by the
severity of signs and symptoms
from Grade 0 to 4.
Patients usually complain of
neck pain and stiffness in the
acute phase, with the majority
recovering within 3 months.
Depression, anxiety, and mood
disorders are common in
patients with chronic whiplash.
Reassurance, early
mobilization, simple analgesic,
and physiotherapy are
recommended in acute
whiplash (WAD I–III).
In chronic WAD,
multidisciplinary pain clinic
referral followed by cognitive
behavioural therapy and
cervical radiofrequency
neurotomy plays an important
role.
Alifia Tameem MD FRCA
Specialist Registrar in Anaesthesia
Russells Hall Hospital
Dudley DY1 2HQ
UK
Sandeep Kapur FRCA FFPMRCA
Consultant in Anaesthesia and Pain
Management
Russells Hall Hospital
Dudley DY1 2HQ
UK
Tel: þ44 1384 244809
Fax: þ44 1384 244025
E-mail: sandeepkapur@doctors.net.uk
(for correspondence)
Hirachand Mutagi FRCA FFPMRCA
Consultant in Anaesthesia and Pain
Management
Russells Hall Hospital
Dudley DY1 2HQ
UK
Page 1 of 4
An acute whiplash injury follows sudden or ex-
cessive hyperextension, hyperflexion, or rotation
of the neck affecting the soft tissues. It typically
results from rear-end or side-impact motor
vehicle collisions. Patients commonly present
with pain and stiffness in the neck, headache,
and upper backache with or without paraesthesia
of the upper limbs. Chronic whiplash syndrome
is characterized by symptoms that persist for
more than 3 months.1 With over half a million
people making whiplash injury claims per
annum in the UK, it has a major impact on the
healthcare and legal systems and also the
economy.
Background
In 1995, whiplash-associated disorders (WAD)
was defined by the Quebec task force as ‘Whiplash
is an acceleration–deceleration mechanism of
energy transfer to the neck. It may result from
rear-end or side-impact motor vehicle collisions,
but can also occur during diving or other mis-
haps. The impact may result in bony or soft-
tissue injuries (whiplash-injury), which in turn
may lead to a variety of clinical manifestations
called Whiplash-Associated Disorders’.2
The incidence of WAD is very variable
among countries, averaging to about nine per
1000 people in the UK, the highest in Europe.
WAD is usually seen in rear-end, low-impact
collisions, in 90% cases at speeds of ,14 mph.3
The trunk is forced back on the seat with hyper-
extension of the neck and then forward recoil
(Fig. 1). The risk of whiplash injury is higher in
women (as they have thinner necks), people with
short necks, car seats with a low neck rest, and if
the rear-end collision is with a heavy vehicle.
Car seats with an elastic back minimize the risk
of neck injury after a car crash. Research indi-
cates that the source of the pain in a majority
(60%) of whiplash patients is the zygapophy-
sial (facet) joints (especially C2/3 and C5/6
levels), rather than the muscles.4
doi:10.1093/bjaceaccp/mkt052
Continuing Education in Anaesthesia, Critical Care & Pain | 2013
& The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.
All rights reserved. For Permissions, please email: journals.permissions@oup.com
Matrix reference 2E02, 3E00
Clinical features
WAD includes all indirect injuries to the cervical
spine. The affected individual most commonly
complains of neck pain and stiffness in the acute
phase. The other symptoms are headaches,
mainly occipital, upper back and shoulder pain,
Downloaded from http://ceaccp.oxfordjournals.org/ by guest on October 3, 2013
and upper limb pain. Patients may also complain
of paraesthesias, numbness, and/or weakness of
the upper limbs and may occasionally suffer
from dizziness, blurred vision, vertigo, dyspha-
gia, and tiredness. Based on the severity of the
symptoms, WAD is classified in five grades
(Table 1).
Chronic whiplash
Around 40% of patients suffer from symptoms
of WAD beyond 3 months (chronic whiplash)
and 2– 4.5% of patients are left permanently dis-
abled.3,5 Patients who are asymptomatic at 3
months continue to be so even after 2 yr. A
worse outcome is associated with severe and
rapid onset of neck pain and stiffness after the
initial injury, neurological deficit, arm pain,
headaches, and acute hospital admission. Older
age at the time of injury, pre-existing pain in the
neck, low back ache, female gender, part-time
employment, lower educational achievement,
and lawyer involvement have been established
as markers for delayed recovery in patients with
whiplash injury.3 Depression, anxiety, and mood
disorders are common in patients with chronic
whiplash. If one or more of the above adverse
indicators are noted, the patients usually need a
more intensive treatment and possibly an early
referral to a physiotherapist, pain physician, or a
specialist with interest in WAD.
Patients who develop chronic pain after
whiplash injury also suffer from central hyper-
sensitivity, possibly due to the sensitization of
dorsal horn neurones. Studies have shown that
these patients experience hyperalgesia to cutane-
ous and muscular stimulus not only in the neck
but also at sites away from the primary site of
injury. There is thought to be an alteration of the
Whiplash injury

Fig 1 Mechanism of whiplash injury.

Table 1 Classification of WAD1,6

Grade Symptoms Radiography Pharmacotherapy

0 Asymptomatic, no complaints of neck pain or stiffness, absent physical signs Not required Not required
I Pain, stiffness, or tenderness of the neck as the only complaint, absent physical Not required Simple analgesics
signs
II Pain, stiffness, or tenderness of the neck along with musculoskeletal signs, e.g. Plain X-ray of cervical spine usually not † Non-opioid analgesics
decreased range of movement and point tenderness of the neck required unless † NSAIDs
† Suspected bony injury
† Impaired consciousness leading to
masked pain sensation
† High speed/impact collision

III Pain, stiffness, or tenderness of the neck and neurological involvement, e.g. Baseline X-ray of cervical spine, anterior– † Non-opioid analgesics
sensory deficits, motor weakness, and/or decreased or absent deep tendon posterior, lateral, and open-mouthed view † NSAIDs
reflexes May need specialized imaging † Opioids for a limited period
in acute severe cases

IV Pain, stiffness, or tenderness of the neck along with dislocation or fracture with or Specialized imaging, e.g. CT scan, MRI, † Non-opioid analgesics
without spinal cord injury myelography, discography † NSAIDs
† Opioids
† Immediate referral to
specialist surgeon

afferent nociceptive signal from a focus present deep in the tissues
of the neck and an imbalance occurring in the descending pain
modulation system.7
Diagnosis
Whiplash or WAD is essentially a diagnosis based on clinical find-
ings. Assessment of a person with an acute whiplash injury
(iii) Identifying possible psychosocial barriers to recovery, such as
includes:1
(i) Confirming a history of sudden or excessive neck extension,
flexion, or rotation. Symptoms may be delayed for hours or
days after the injury. The two most common symptoms are
headache and disabling neck pain, with or without referral to
the shoulder or arm.
(ii) Examining for signs of muscular spasm, point tenderness, and
neurological problems in the upper or lower limbs. Assess for
range of neck movements, if appropriate. Look for ‘red flag’
features suggestive of a serious spinal or other abnormality, in-
cluding compression of the spinal cord (myelopathy), cancer,
severe trauma or skeletal injury, and vascular insufficiency.
stress, anxiety, or depression (‘yellow flags’). WAD is especial-
ly likely to manifest in people with obsessive compulsive be-
haviour, anxiety, depression, hypochondriasis, and those with
high scores of somatization.

Page 2 of 4 Continuing Education in Anaesthesia, Critical Care & Pain j 2013


(iv) Radiological investigations in the acute phase can lead to a
large number of false-positive cases. It is important to avoid
overinvestigating; these should be held in reserve for patients
with ‘Red flag’ features or for those with persistent problems of
pain down the arms.1 Pre-existing degenerative cervical spine
disease (especially spondylosis at the C5/6 level) is the most
common finding seen radiologically in patients complaining of
whiplash injury. Additionally, they may have a minimal loss of
the lordotic curve of the cervical vertebrae. Dynamic X-rays of
the neck during flexion and extension initially may show a
kyphotic angle possibly due to muscle spasm causing
decreased mobility at the cervical region with a resultant in-
crease in mobility at the adjacent vertebral level.5
Treatment
Whiplash injuries are quite difficult to treat because of interactions
of various factors such as patient psychology, socioeconomic
factors, legal issues, and physical health. The absence of radiologic-
al evidence of injury in the symptomatic group further complicates
the treatment process for this condition. It was traditionally believed
that bed rest and immobilization of the neck with a soft collar was
the initial treatment of choice, but this has been refuted. Reassurance,
resuming activity as normal, early mobilization, physiotherapy along
with isometric exercise with periods of rest intermittently have been
associated with better long-term outcomes.
Acute/subacute whiplash injury
Acute whiplash injury is defined as symptoms present up to 4 weeks
and subacute whiplash when symptoms persist beyond 4 weeks until
12 weeks. Active physiotherapy and manipulation in the acute phase
of the injury has a significant role in improving neck pain at 6
months and also increases range of movement of the neck similar to
an uninjured individual. Mobilization is more effective if started
within 96 h of the injury. A better range of neck movements at 2
weeks has been reported when non-steroidal anti-inflammatory drugs
(NSAIDS) have been used. Patients receiving high-dose methylpred-
nisolone within 8 h of injury have fewer disabling symptoms at 6
months and fewer sick leave days but is not recommended in WAD
I –III.6,8 Other physical treatments such as heat and cold packs,
pulsed electromagnetic field therapy, hydrotherapy, traction, ultra-
sound therapy, laser therapy, short-wave diathermy, transcutaneous
electrical nerve stimulation, acupuncture, and passive repetitive move-
ments have been tried with variable benefit. There is some evidence
that a multimodal treatment approach of postural training, eye fixation
exercises, manual treatment, and psychological support may be more
beneficial than physical therapy at both symptom improvement and
functional improvement.9 Recent work indicates standardized multi-
disciplinary rehabilitation programme aimed at fostering functional
recovery may reduce pain catastrophizing in patients with subacute
pain after whiplash injury.10 Various analgesics, antidepressants (es-
pecially amitriptyline), and neuromuscular blocking agents such as
Continuing Education in Anaesthesia, Critical Care & Pain j 2013
Whiplash injury
diazepam, azapropazone, epidural local anaesthetics, and epidural
corticosteroids have been used. Neuromuscular blocking agents are
not recommended in the acute phase.
Chronic whiplash injury
Many interventions have been tried for chronic whiplash injuries; of
which, cervical radiofrequency neurotomy (CRFN) facet joints have
shown reasonable relief from pain for up to 9 months. Some studies
have reported a benefit in nearly 70% of the patients from CRFN.11
Other interventions like cervical facet joint injections have been
used with short-term benefit. Intra-articular corticosteroids, tem-
poromandibular joint treatment, cervical traction, and botulinum
toxin injections have been described in the literature, with evidence
lacking to support their use currently. A multimodal approach to
treatment including cognitive behaviour therapy along with physical
and or mechanical therapy and patient education is more effective at
3 months with a higher percentage of patients being satisfied with
their pain management when compared with only physical treatment.9
For symptom management, along with simple analgesics, patients
may be commenced on antineuropathic medications according to
NICE clinical guideline 96.12
Patients with neurological deficits undergo more aggressive man-
agement including surgical treatment. One-third of the people suf-
fering from brachialgia after chronic whiplash injury may benefit
from cervical fusion procedures and nearly half of the patients with
nerve impingement have reported pain relief from subacromial
decompression.
Medicolegal implications
Whiplash injuries cost the economy of the UK approximately £3.64
billion per annum and have increased in number by 25% since
2002, probably the highest in Europe. They constitute 76% of
motor-insurance claims. There is a prevalent view that a claimant’s
symptoms will improve once litigation has finished, but this is un-
supported by the literature. However, claimants who seek therapy
from a physician initially or do not seek care at all are more likely
to have their claims closed faster than those who look for help from
physical therapists or chiropractors, as active manipulation may
worsen symptoms.11 Residual pain was slightly higher in the
no-fault compensation era suggesting that, although claims were
less frequent, the symptoms were more severe and the pattern of
disease of whiplash injury was unaltered. Since patients with more
severe symptoms attract greater compensation, litigation in their
cases is likely to be more keenly contested and therefore more pro-
tracted. Unfortunately, there seems to be a perverse incentive for
everyone involved, including claimants, insurance companies, soli-
citors, and medical experts, all of which is funded by increased
premiums for car insurance.5 In Lithuania and Greece, where there
is no compensation culture, the development of chronic pain after
whiplash injury is rare and claimants recover faster.1,13
Page 3 of 4
Whiplash injury
Conclusion
Current evidence supports early mobilization, simple analgesics, re-
assurance, and active interventions as the best treatment options for
WAD I– III. Immediate specialist referral should be made for severe
symptomatic WAD III and for all patients with WAD IV. Recovery
from whiplash injury can be predictable in most cases. Most patients
who are symptomatic at 3 months remain so indefinitely, especially
if psychosocial and economic factors are involved.5
Declaration of interest
None declared.
References
1. NICE. Neck pain - whiplash injury. Available from http://cks.nice.org.uk/
neck-pain-whiplash-injury (last accessed 26 September 2013)
2. Spitzer WO, Skovron ML, Salmi LR et al. Scientific monograph of the
Quebec Task Force on Whiplash Associated Disorders: redefining ‘whip-
lash’ and it’s management. Spine 1995; 20(8 Suppl.): 8S– 58S
3. Bannister G, Amirfeyz R, Kelley S, Gargan M. Review article: whiplash
injury. J Bone Joint Surg 2009; 91-B: 845 –50
4. Bamsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of chronic
cervical zygapophysial joint pain after whiplash. Spine 1995; 20:
20 – 5
Page 4 of 4 Continuing Education in Anaesthesia, Critical Care & Pain j 2013
View publication stats
5. Rodriquez AA, Barr KP, Burns SP. Whiplash: pathophysiology, diagnosis,
treatment, and prognosis. Muscle Nerve 2004; 29: 768–81
6. The Working Party Recommendations. Guidelines for the Management of
Whiplash-associated Disorders. Australia: Motor Accident Authority, January
2001. Available from http://www.whiplashprevention.org/SiteCollection
Documents/Research%20Articles/Medical%20-%20Whiplash/Guidelines
DiagnosingWhiplash.pdf (last accessed 26 September 2013)
7. Curatolo M, Peterson-Felix S, Arendt-Nielson L, Giani C, Zbinden AM,
Radanov BP. Central hypersensitivity in chronic pain after whiplash injury.
Clin J Pain 2001; 17: 306– 15
8. Petterson K, Toolanen G. High-dose methylprednisolone prevents exten-
sive sick leave after whiplash injury. A prospective, randomised, double-
blind study. Spine 1998; 23: 984–9
9. Binder A. Neck pain. Clinical Evidence 2008; 8: 1103
10. Scott W, Wideman TH, Sullivan MJ. Clinically meaningful scores on pain
catastrophizing before and after multidisciplinary rehabilitation: a pro-
spective study of individuals with subacute pain after whiplash injury. Clin
J Pain Advance Access published on 1 April 2013, doi: 10.1097/
AJP.0b013e31828eee6c
11. Prushansky T, Pevzner E, Gordon C, Dvir Z. Cervical radiofrequency
neurotomy in patients with chronic whiplash: a study of multiple
outcome measures. J Neurosurg 2006; 4: 365–73
12. NICE clinical guideline 96. Neuropathic pain. Available from http://www.
nice.org.uk/nicemedia/live/12948/47949/47949.pdf (last accessed 26
September 2013)
13. Cassidy JD, Carroll LJ, Cote P, Lemstra M, Berglund A, Nygren A. Effect
of eliminating compensation for pain and suffering on the outcome of in-
surance claims for whiplash injury. N Engl J Med 2000; 342: 1179–86