23 Whiplash is defined as an injury caused by a flexion-extension energy mechanism that is usually the direct result of a motor vehicle collision (MVC). Crowe first used the term “whiplash” in 1928, although injuries fitting the pattern of whiplash can be found in documents as early as the 17th century.1 The resultant injury can be manifested by multiple complaints, and common to all is often the lack of objective evidence supporting any pathology. In the United States, it is estimated that whiplash is diagnosed in 3 of every 1000 people every year. Studies have indicated that 15–40% of people involved in a MVC will complain of acute neck pain. The majority of whiplash cases resolve uneventfully, though 5–7% of patients will complain of permanent disability.2 Although whiplash is a common diagnosis, special care should be taken to evaluate for other causes of patients’ complaints. Whiplash is a popular medicolegal subject. The societal cost to the United States has been estimated at 4.5–29 billion dollars per year.3,4 Many studies have evaluated the effect of medicolegal variables on a patient’s recovery. Whiplash injury is the result of a low-velocity flexion-extension stress on the cervical spine. Fifty percent of cases can be related to rear-end MVCs at low speeds. The whiplash event has been shown to last fewer than 500 milliseconds.5 Energy is transferred from the bullet vehicle to the struck vehicle, through the frame and seat to the body of the patient. The body of the patient moves in concordance with the seat and the patient’s head lags behind, causing the head to go into extension and act as though on a whip. Once the head contacts the head restraint, a forward momentum is applied causing the flexion mechanism. The forward momentum can be affected by the height of the headrest. A low headrest acts as a fulcrum about which the neck can whip. Raising the headrest has been shown to decrease the number of claims of whiplash secondary to car manufacturing. Studies have shown that a collision from a velocity of 8.7 mph is necessary to damage a struck vehicle, while a collision with an increase of only 2.5 mph can produce complaints of neck pain in subjects. Furthermore, subjects not wearing seatbelts during airbag deployment were 1.7 times more likely to sustain major cervical injury than those wearing seatbelts.6 The resultant energy affects the structures of the spine in specifically described manners. The facet joints each show compression posteriorly, combined with distraction anteriorly. The annulus fibrosus of the disk, as well as ligamental constraints, may also be disrupted in the injury. Studies of the kinematics of the facet joint have shown that there is a multitude of possible injury patterns associated with a whiplash event. These may include capsular strain and/or tears, bony impingement, synovial fold pinching, and direct-impact injury. Any of these may result in contusion, intra-articular hemorrhage, and damage to subchondral bone, any of which may result in pain.7 Presentation after a whiplash injury can include complaints of neck pain, stiffness, headache, back pain, and parasthesias of the upper limbs. Pain described within 24 hours of an accident has been related to the more symptomatic one-third of patients who develop whiplash-associated disorder (WAD). Multiple studies have tried to evaluate the prognostic symptoms and signs associated with a rapid recovery from a whiplash injury. Ozegovic reviewed 2335 patients with traffic-related WAD and showed that postcollision neck pains, as well as depressive symptomatology, affected a patient’s ability for, and timing of, return to work.8 This indicates that there may be a psychologic component associated with recovering from WAD. Other psychologic complaints include impaired concentration, somatoform disorder, forgetfulness, post-traumatic stress disorder, and driving anxiety.9–11 The psychological response to a WAD may be as marked as a structural injury and should be appropriately addressed. The natural history of WAD has been well studied. It has been estimated throughout the literature that 50% of patients who initially complain of WAD will go on to full recovery by 2 years, while 4.5% remain permanently disabled. Gargan and Bannister have developed a classification system that can be used to predict the prognosis for WAD.9 Based on complaints in the first 3 months postinjury, 70% of patients’ outcomes can be predicted. Poor prognostic factors include: rapid onset and severity of neck pain, hospital admission, radiation, headache, neurologic deficit, stiffness, and tenderness. Depressive symptoms may be noticed at 6 weeks postinjury.12 Preinjury psychiatric disease, older age, lower educational status, part-time employment, and preinjury complaints of neck or back pain have also been shown to confer a worse prognosis. Female sex is a poor prognostic factor, and an estimated two-thirds of women experience sufficient pain from WAD to take time off from work.13,14 Gargan et al. reported on psychological test scores following whiplash injuries and showed that, while testing was initially normal in 82% of patients, by 2 years postinjury, 69% of patients had abnormal test results.9 The conclusion from this study was that psychological disturbance may be a sequela of enduring a WAD. A positive prognostic factor that reduces the return to work time is self-employment status, although timing to full asymptomatic recovery is unchanged. Gozzard et al. found that 7% of patients who suffered from WAD had not returned to work, with the strongest predictor of disability being the intensity of symptoms.15 It has been shown that injured workers do worse than others with similar injuries, and whiplash is no different. Litigation has also been sought as a prognostic factor. Swartzman et al. noted that patients with active litigation claims secondary to WAD complained of worse pain than those with completed claims, though there were no differences in function or employment status.16 Regional governments may influence the rates and recoveries from whiplash, as well. In 1987, Victoria, Australia, required that subjects reporting WADs pay the first 317 Australian dollars of medical care out of pocket. This decreased the rate of reported whiplash by 68%, though chronic disability from whiplash remained unchanged at ~ 10%.17 Multiple imaging modalities have been used to further identify the pathology of WAD (Fig. 23.1). No imaging modality has been shown to be effective for detecting WAD. A 10-year follow up of magnetic resonance imaging (MRI) in both WAD and asymptomatic patients showed no statistical correlation between MRI findings (disk signal change, foraminal stenosis, disk protrusion and narrowing) and neck pain in WAD patients.18 MRI should be used in specific cases when nerve root impingement is thought to be the result of disk herniation.19 The first step to evaluate a patient with acute neck pain suspected to be due to WAD is to ensure that a more serious injury does not exist. A thorough history and physical exam and possible imaging modalities may be needed as part of the workup. In case whiplash is the correct diagnosis, the initial treatment should consist of education and reassurance. It is imperative that patients resume normal daily activities despite discomfort. Patients who remain active have better outcomes than those who limit or avoid activities altogether.20,21 Medical treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and intravenous steroids has also been shown to decrease symptoms and shorten return to work time.22,23 It is currently thought that cervical orthoses add little if any benefit and may result in a poorer prognosis than if not used at all.23
Cervical Whiplash
Mechanism
Presentation
Workup
Natural History
Imaging
Treatment