Clavicle shortening after fracture

                                        Dr. KS Dhillon

Introduction

Clavicle fractures are quite common. They account for 2.6% to 4% of all fractures. About eighty percent of clavicle fractures are located in the middle third of the clavicle [1]. These fractures primarily occur in the younger population with male dominance of about 70% [2].

The most common mechanism of injury is a direct fall on the shoulder. Fractures can also be sustained during sporting activities and motor vehicle accidents. 

About 69–82% of fractures occur in the midshaft of the clavicle, 12–26% in the lateral part, and 2–6% in the medial part [3]. Fractures of the medial and lateral parts are less common because the medial and lateral parts are firmly secured by strong ligaments and muscles, while the middle part of the clavicle lacks any strong attachments and thus is more vulnerable to a fracture. 

Due to the muscle and other soft tissue attachment, the lateral fragment displaces caudally, anteriorly, and medially, leading to angulation and overall shortening of the clavicle.

Regardless of the type of fracture, clavicle fractures have traditionally been treated almost exclusively non-operatively. Studies in the 1960s showed good functional results for conservatively treated midshaft clavicle fractures and a low nonunion rate compared to fractures treated by primary open reduction [3]. Several more recent studies, on the other hand, have reported opposite results with newer methods of fracture fixation 

[3], “which may have contributed to the 705% increase in operative treatment of clavicle fractures in Sweden between 2001 and 2012” [4]. The optimal treatment of clavicle fractures however remains a debated subject.

A recent Cochrane review by Lenza et al [5] showed that there is low-quality evidence that surgical treatment has no additional benefits in terms of function, pain, and quality of life compared with conservative treatment of clavicle fractures.

Displaced fractures of the clavicle that are treated conservatively often lead to shortening of the clavicle. There are several studies that have reported that shortening is associated with greater disability of the shoulder [6-9], whereas other studies have reported no such association [10-14].

Measurement of clavicle shortening

Clavicle fracture shortening was often measured on dedicated anteroposterior (AP) view of the clavicle or shoulder girdle [15].

Posteroanterior (PA) chest x rays have been found to be equally useful for the measurement of clavicle length [16]. 

Jones et al. [17] carried out a study and concluded that using unilateral radiographs of the fractured clavicle was insufficient for determining the true degree of fracture shortening. 

Computed tomography (CT) imaging of the clavicle has been regarded as the gold standard for measurement of the actual clavicular length [16] and an important modeling tool to establish clavicular morphology [18,19]. CT allows for imaging of the clavicle in multiple planes without projection abnormalities. Therefore, many believe that CT is a more reliable modality for evaluating clavicular length.

Most often clavicle length is measured, using a PA view of a chest radiograph. The clavicle length is the distance between two points placed on the center of the proximal and distal ends of the clavicle. The center is determined by choosing a point that is halfway between the superior and inferior aspects of the proximal end of the clavicle. The same is repeated for the distal end of the clavicle. The difference in length between the two sides provides the value of relative shortening.

For measurement of the clavicle length on CT, a clavicle-specific plane is created by orienting an oblique reconstruction through the center of the sternoclavicular joint proximally and the center of the acromioclavicular joint distally. As with X-ray measurements, the length of each clavicle is measured from the midpoint of the medial end of the clavicle to the lateral end of the clavicle.

Omid et al [15] carried out a study to compare the accuracy of clavicle shortening measurements based on plain radiographs with those based on CT reconstructed images of the clavicle. They found that measurement of clavicle length using AP plain radiographs is inaccurate. The measurements made on chest radiographs correlated poorly with those made on the CT, and this variability was significant. The reason for this variability can be explained by the fact that no radiographic projection captures the length of the clavicle in its oblique plane as can be done with a CT reconstruction. There was length overestimation and subsequent miscalculation of the true length of the clavicle. 

Radiographic measurements overestimated the clavicular length by a mean of 6.42mm to 8.22 mm which resulted in underestimation of clavicle shortening as compared to CT-based measurements. 

In the AP chest x rays, due to the greater distance between the clavicle and X-ray film, there can be greater projection artifact, amplification effects, and measurement errors due to positioning and rotation [16].

Impact of clavicular shortening

Clavicle fractures have traditionally been treated conservatively in the past. In nonoperatively treated patients, closed reduction of the fracture is difficult to achieve and to maintain and therefore is not attempted. A certain degree of clavicular shortening usually remains after union due to overlap of the fracture fragments.

There are several studies that have reported that shortening is associated with greater disability of the shoulder [6-9], whereas other studies have reported no such association [10-14].

Woltz et al [20] carried out a systematic review of the literature to find out whether clavicular shortening after nonoperative treatment of midshaft fractures affects shoulder function. There were 6 articles included in this systematic review based on the selection criteria. The studies were published between 2006 and 2015 and evaluated a total of 379 patients.  Five studies were retrospective and one was prospective. In four of the studies, determining the relationship between shortening and shoulder function was the primary aim. Follow-up was at least 12 months in all studies, with a mean of 4.5 years.

The reported mean shortening ranged from 9.2 mm to 25 mm. Three studies compared patients with a shortening of less than 20 mm with those having 20 mm or more shortening. In these studies, 19% of the study population had a shortening of ≥20 mm. 

The authors found that there is not enough evidence in the literature to show that shortening of a midshaft clavicle after a fracture is a risk factor for functional impairment.

The authors concluded that the existing evidence to date does not allow for a valid conclusion regarding the influence of shortening of the clavicle on shoulder function after union of nonoperatively treated midshaft clavicular fractures.

Conclusion

Fractures of the clavicle are common. Traditionally they have been treated conservatively without surgery. Conservatively treated fractures heal with some overlap leading to shortening of the clavicle. 

The gold standard for the measurement of clavicle shortening is a CT. Chest X rays can also be used to measure the clavicle length.

Shortening of the clavicle was believed to produce no functional disability. There are several publications that show that shortening of the clavicle produces no functional disability. However, in the recent past, there have been several authors who claimed that shortening of more than 2 cm is associated with shoulder dysfunction. Systematic review of the literature, however, shows that there is not enough evidence to show that clavicle shortening is a risk factor for functional impairment.

References

1. Lenza M, Buchbinder R, Johnston RV, Ferrari BA, Faloppa F. Surgical versus conservative interventions for treating fractures of the middle third of the clavicle. Cochrane Database Syst Rev. 2019 Jan 22;1(1): CD009363. doi: 10.1002/14651858.CD009363.pub3. PMID: 30666620; PMCID: PMC6373576.
2. Postacchini F, Gumina S, De Santis P, Albo F. Epidemiology of clavicle fractures. J Shoulder Elbow Surg. 2002 Sep-Oct;11(5):452-6. doi: 10.1067/mse.2002.126613. PMID: 12378163.
3. Kihlström et al. Clavicle fractures: epidemiology, classification and treatment of 2422 fractures in the Swedish Fracture Register; an observational study BMC Musculoskeletal Disorders (2017) 18:82. 
4. Huttunen TT, Launonen AP, Berg HE, Lepola V, Felländer-Tsai L, Mattila VM. Trends in the Incidence of Clavicle Fractures and Surgical Repair in Sweden: 2001-2012. J Bone Joint Surg Am. 2016 Nov 2;98(21):1837-1842. doi: 10.2106/JBJS.15.01284. PMID: 27807117.
5. Lenza M, Buchbinder R, Johnston RV, Ferrari BA, Faloppa F. Surgical versus conservative interventions for treating fractures of the middle third of the clavicle. Cochrane Database Syst Rev. 2019 Jan 22;1(1): CD009363. doi: 10.1002/14651858.CD009363.pub3. PMID: 30666620; PMCID: PMC6373576.
6. Eskola A, Vainionpaa S, Myllynen P, Patiala H, Rokkanen P (1986) Outcome of clavicular fracture in 89 patients. Arch Orthop Trauma Surg 105: 337-338. 
7. Hill JM, McGuire MH, Crosby LA (1997) Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J Bone Joint Surg Br 79: 537-539. 
8. Lazarides S, Zafiropoulos G (2006) Conservative treatment of fractures at the middle third of the clavicle: the relevance of shortening and clinical outcome. J Shoulder Elbow Surg 15: 191-194. 
9. Abbot AE, Hannafin JA (2001) Stress fracture of the clavicle in a female lightweight rower. A case report and review of the literature. Am J Sports Med 29: 370-372. 
10. Nordqvist A, Petersson CJ, Redlund-Johnell I (1998) Mid-clavicle fractures in adults: end result study after conservative treatment. J Orthop Trauma 12: 572-576.
11. Fuglesang HF, Flugsrud GB, Randsborg PH, Stavem K, Utvag SE (2016) Radiological and functional outcomes 2.7 years following conservatively treated completely displaced midshaft clavicle fractures. Arch Orthop Trauma Surg 136: 17-25.  
12. Rasmussen JV, Jensen SL, Petersen JB, Falstie-Jensen T, Lausten G, et al. (2011) A retrospective study of the association between shortening of the clavicle after fracture and the clinical outcome in 136 patients. Injury 42: 414-417.
13. Stegeman SA, de Witte PB, Boonstra S, et al. Posttraumatic midshaft clavicular shortening does not result in relevant functional outcome changes. Acta Orthop. 2015;86(5):545-552.
14. Goudie EB, Clement ND, Murray IR, Lawrence CR, Wilson M, Brooksbank AJ, Robinson CM. The Influence of Shortening on Clinical Outcome in Healed Displaced Midshaft Clavicular Fractures After Nonoperative Treatment. J Bone Joint Surg Am. 2017 Jul 19;99(14):1166-1172.  
15. Omid et al. Accuracy of Shortening Measurement after Clavicle Fracture: CT vs. Chest Radiography Clinics in Orthopedic Surgery  Vol. 8, No. 4, 2016.
16. Smekal V, Deml C, Irenberger A, Niederwanger C, Lutz M, Blauth M, Krappinger D. Length determination in midshaft clavicle fractures: validation of measurement. J Orthop Trauma. 2008 Aug;22(7):458-62. doi: 10.1097/BOT.0b013e318178d97d. PMID: 18670285.
17. Jones GL, Bishop JY, Lewis B, Pedroza AD; MOON Shoulder Group. Intraobserver and interobserver agreement in the classification and treatment of midshaft clavicle fractures. Am J Sports Med. 2014 May;42(5):1176-81. doi: 10.1177/0363546514523926. Epub 2014 Feb 26. PMID: 24573571.
18. Bachoura A, Deane AS, Wise JN, Kamineni S. Clavicle morphometry revisited: a 3-dimensional study with relevance to operative fixation. J Shoulder Elbow Surg. 2013;22(1):e15-21.
19. King PR, Scheepers S, Ikram A. Anatomy of the clavicle and its medullary canal: a computed tomography study. Eur J Orthop Surg Traumatol. 2014;24(1):37-42.
20. Woltz S, Sengab A, Krijnen P, Schipper IB. Does clavicular shortening after nonoperative treatment of midshaft fractures affect shoulder function? A systematic review. Arch Orthop Trauma Surg. 2017;137(8):1047-1053. 

                  Cervical spondylosis

                                          Dr. KS Dhillon

Introduction

Cervical spondylosis is a natural age-related degenerative disease of the cervical spine. The term cervical spondylosis encompasses a wide range of progressive degenerative changes that affect all the components of the cervical spine including intervertebral discs, facet joints, joints of Luschka, ligamentum flavum, and laminae [1]. Degeneration of the cervical spine is a natural process of aging and presents in the majority of people after the fifth decade of life [1]. By the age of 65 years the prevalence of cervical spondylosis is 95%. 

Etiology

Age-related degeneration of the intervertebral disc and cervical spinal elements is the primary risk factor and contributor to the incidence of cervical spondylosis. Besides the disc, degenerative changes also occur in surrounding structures, including the uncovertebral joints, facets joints, posterior longitudinal ligament, and ligamentum flavum. These degenerative changes all combine to cause narrowing of the spinal canal and intervertebral foramina. The narrowing can cause compression of the spinal cord, spinal vasculature, and nerve roots. Patients with cervical spondylosis can present with axial neck pain, cervical myelopathy, and cervical radiculopathy.

Several factors can contribute to an accelerated disease process and early-onset cervical spondylosis. These include exposure to significant spinal trauma, a congenitally narrow vertebral canal, dystonic cerebral palsy affecting cervical musculature, and some athletic activities such as soccer, rugby, and horse riding [1].

Epidemiology

About 25% of individuals under the age of 40, 50% of individuals over the age of 40, and 85% of individuals over the age of 60 have some degree of cervical spondylosis. Most people with radiographic evidence of cervical spondylosis remain asymptomatic [1]. The most commonly affected segment is C6-C7, followed by C5-C6. 

Neck pain is the most common symptom of cervical spondylosis. The point prevalence of neck pain ranges from 0.4% to 41.5% in the general population, the 1-year incidence ranges from 4.8% to 79.5%, and lifetime prevalence may be as high as 86.8% [1]. Neck pain along with back pain remains the leading cause of years lived with disability. 

Pathophysiology

Cervical spondylosis pathogenesis involves a degenerative cascade that produces biomechanical changes in the cervical spine. There is an increase in the keratin-chondroitin ratio that prompts changes in the proteoglycan matrix resulting in loss of protein, water, and mucopolysaccharides within the disc. Disc desiccation results in loss of elasticity of the nucleus pulposus and it shrinks and becomes more fibrous. The nucleus pulposus loses its ability to maintain weight-bearing loads effectively. It begins to herniate through the fibers of the annulus fibrosus resulting in the loss of disc height. 

The annular and Sharpey fibers peel off from the vertebral body edges, resulting in reactive bone formation. This reactive bone formation leads to formation of spurs or osteophytes along the ventral or dorsal margins of the cervical spine. These osteophytes can project into the spinal canal and intervertebral foramina. The uncovertebral and facet joints also undergo degenerative changes which leads to hypertrophy or enlargement of the joints with bony spur formation into the surrounding neural foramen. These degenerative changes lead to reduction in the range of cervical movements and narrowing of the spinal canal [1].

Spondylotic changes in the cervical spine occur at a single disc space level in 15% to 40% of patients and at multiple levels in 60% to 85% of the patients. The discs between the third and seventh cervical vertebrae are most commonly affected.

Repeated occupational trauma can contribute to the development of cervical spondylosis. An increased incidence of cervical spondylosis has been found in individuals who carried heavy loads on their heads or shoulders, in dancers, gymnasts, and in individuals with spasmodic torticollis [2]. Everyone does not agree that trauma is an important causal factor in the production of cervical spondylosis. In about 10% of patients, cervical spondylosis is due to congenital bony anomalies such as blocked vertebrae, malformed laminae-that place undue stress on adjacent intervertebral discs [2].

Histopathology

Disc herniation precedes the development of cervical spondylosis. The spondylotic discs and herniated discs undergo similar degenerative changes with macrophage infiltration, upregulation of growth factors, and cytokines. Herniated discs usually demonstrate more profound inflammatory reactions involving CD68-positive macrophage infiltration into the outer layer of the annulus fibrosus. Spondylotic discs have thicker bony endplates with a more diffuse expression of TNF-alpha and MMP-3 in the inner layer of the annulus fibrosus [3,4].

History and Physical Examination

Typically symptomatic cervical spondylosis presents as one or more of the following three clinical syndromes:

1.Axial Neck Pain

Usually, patients complain of stiffness of the neck. The pain in the neck is most severe in the upright position and it is relieved with bed rest.

Hyperextension and side-bending of the neck increases the pain.

In upper cervical disease, the pain radiates to the occiput and the back of the ear. In lower cervical spine disease the pain radiates into the superior trapezius or periscapular musculature.

Sometimes patients can present with atypical symptoms of jaw pain or chest pain.

2.Cervical Radiculopathy

Radicular symptoms from cervical spondylosis usually follow a myotomal distribution depending on the nerve root(s) involved. There can be unilateral or bilateral neck pain, scapular pain, arm pain, paresthesias, and weakness of the arm or hand.

Pain is usually exacerbated on tilting the head towards the affected side, on hyperextension of the neck, and side-bending toward the affected side.

Pain radiating down the upper limb with neck extension and ipsilateral head rotation to the affected side is considered as a positive Spurling test for cervical radiculopathy. A 2011 study by Shabat et al found that the Spurling test is 95% sensitive and 94% specific for diagnosing nerve root pathology [5].  

3.Cervical Myelopathy

Cervical myelopathy usually has an insidious onset with or without neck pain. It can initially present with hand weakness and clumsiness which results in an inability to carry out tasks that require fine motor coordination such as buttoning a shirt, tying shoelaces, and picking up small objects.

There can be frequent episodes of gait instability and unexplained falls.

Urinary incontinence can occur although it is rare and it typically appears at the late stage of the disease.

An electric shock-like sensation radiating down the spine and into the extremities with neck flexion is a positive Lhermitte's sign for cervical spondylotic myelopathy (CSM). A more specific sign for CSM is Hoffman’s sign. A Hoffman’s is positive if the thumb and/or index finger flexes when the distal phalanx of the middle finger is flicked by the examiner. 

Physical examination

A meticulous examination of all extremities should be carried to identify nerve root/roots compromise and/or myelopathy. Muscle strength is assessed, sensory examination is carried out and deep tendon reflexes are examined. 

The patient’s gait and balance are evaluated with a toe-to-heel walk test and Romberg’s test. In the toe-to-heel test, the patient is asked to walk 4 steps on the toes and then 4 steps on the heels. In the Romberg’s test, the patient is asked to stand with eyes closed, and arms held forward. A loss of balance is interpreted as a positive Romberg’s test. It is indicative of dysfunction involving the dorsal columns of the spinal cord.

The presence of spasticity, hyperreflexia, sustained clonus, extensor Babinski response would indicate the presence of myelopathy. The grip and release test is another screening test for CSM. Normally a person can make a fist and release it 20 times in 10 seconds, with some decrease in cut-off values with increasing age and lower cut-off values in females [6]. 

Investigations

X-rays

In patients with neck and upper extremity symptoms, plain radiographs of the cervical spine will be the appropriate initial imaging study. The degenerative changes seen on X-rays often poorly correlate with the presence of neck pain [7]. In patients with cervical scoliosis, the common radiographic findings include osteophytes, disc space narrowing, sclerosis of endplates, degenerative changes of uncovertebral and facet joints, as well as calcified/ossified soft tissues. Commonly, AP, lateral, and oblique views of the spine are obtained. These views are adequate to access foraminal stenosis, sagittal alignment, and the size of the spinal canal. 

The Torg-Pavlov ratio is obtained by dividing the sagittal length of the spinal canal by the sagittal diameter of the vertebral body. The normal value is 1.0, with a ratio of <0.8 indicating cervical stenosis. Flexion and extension views are carried out when ligamentous instability is suspected.

Magnetic Resonance Imaging (MRI)

MRI imaging is the modality of choice to evaluate neural structures and soft tissues. MRI allows for proper visualization of the cervical spine without exposing the patient to radiation. 

Axial and sagittal cuts can show the extent of nerve and cord compression, as well as show offending pathological changes such as herniated discs, bony spurs, ligamenta flava hypertrophy, and facet joint arthropathy. Hyperintense spinal cord signal on T2-weighted images can represent edema, inflammation, ischemia, myelomalacia, or gliosis [8]. MRI should not be a routine part of the diagnostic workup for cervical spondylosis unless indicated, because there is a high prevalence of degenerative findings on MRI in asymptomatic individuals [9].

Computed Tomography (CT)

 CT is more useful then X rays for evaluation of bony structures. CT is useful for assessing intervertebral foraminal stenosis. It is less useful than MRI for the evaluation of soft tissues and nerve root compression.

CT Myelogram

In patients in whom an MRI is contraindicated as in those with pacemaker and hardware, a CT with contrast (myelography) can be used to evaluate the location and amount of neural compression.

Electromyogram (EMG)

An EMG can be useful in supplementing neuroimaging findings in the diagnosis of cervical radiculopathy. It can differentiate nerve root compression from other concomitant neurologic conditions such as peripheral neuropathies, entrapment neuropathies, brachial plexus neuropathies, myopathies, and motor neuron diseases.

Management of cervical spondylosis

The treatment of cervical spondylosis will depend on the severity of the patient’s symptoms and signs. If there are no “red flag” symptoms and no significant myelopathy, the goals of treatment will be to relieve pain, improve function, and prevent permanent injury to neural structures. The treatment starts with non-operative management.

Neck pain will usually respond to conservative treatment but the optimal treatment for uncomplicated neck pain has yet to be established. Only a few treatments have been assessed in high quality randomised studies.

Non-surgical

Pharmacologic agents such as nonsteroidal anti-inflammatory drugs (NSAIDs), oral steroids, muscle relaxants, anticonvulsants, and antidepressants have been used for pain relief. No evidence however exists for the efficacy of non-steroidal anti-inflammatory agents or analgesics in the treatment of cervical spondylosis. The evidence that muscle relaxants relieve pain more than placebo is weak, while the incidence of side effects like drowsiness is high [10].

Opioid analgesics for refractory axial neck pain can be used but is not recommended as first-line or for long-term use due to their potential adverse effects.

A four- to six-week course of physical therapy, including isometric and resistance exercises to strengthen the neck and upper back muscles is the mainstay of non-surgical treatment. There are, however, two systematic reviews of small poor quality studies which showed that there is limited evidence of benefit for manipulation or mobilisation therapy [11,12].

There is very little evidence that home exercise regimens [13] pulsed electromagnetic field therapy [14], and multimodal therapy [15], is of benefit in treating neck pain.

Soft cervical collar can be used for short periods to alleviate acute neck pain and spasm. Nighttime use of a cervical pillow can also relieve neck pain by helping to maintain the normal cervical lordosis which would promote better quality sleep. 

In patients experiencing severe radicular pain, cervical traction may be useful to alleviate the nerve root compression that occurs with foraminal stenosis.

Surgical Treatment

Surgical intervention is usually considered in patients with severe or progressive cervical myelopathy, and in those patients with persistent axial neck pain or cervical radiculopathy following failure of non-operative treatment.

Indication for surgery

Before a decision to operate is made the diagnosis must be confirmed and that cervical spondylosis was the cause of the patients symptoms. Other  diseases such as motor neuron disease and multiple sclerosis must be  ruled out. The clinical diagnosis should be supplemented by appropriate imaging. Patients who are moderately or severely disabled on the first examination are usually candidates for surgery.

Surgical decompression of the cervical spine is indicated in patients with progressive impairment of function without sustained remission [16,17,18]. Patients with advanced neurological changes, diabetes, and alcoholism, are less suitable candidates because of the associated neuropathies. Those who are too old to engage actively in a postoperative rehabilitation programme are also less suitable candidates for surgery.

The surgical candidates must have a pathological condition on neuroimaging studies that corresponds to the clinical features. 

Types of surgery and surgical approach

The type of operation and surgical approach depends on the clinical syndrome and the site(s) of pathology.

An anterior approach is preferable in patients who have radicular pain due to central or bilateral disc herniation. In patients who have a lateral disc lesion, either an anterior or posterior approach is an option. Anterior cervical discectomy and fusion (ACDF) can be used to treat patients with myelopathy and pathological compression of up to three levels or when the cervical lordosis is lost.

The anterior approach involves a cervical discectomy or corpectomy followed by fusion with an allograft, autograft, or artificial intervertebral disc. Anterior plates, metallic cages, and synthetic spacers can be used in addition to the bone grafts. The fusion rates are comparable with these techniques. The long-term outcome of these procedures remains unclear.

The operations performed through the posterior approach include partial discectomy, laminoplasty, laminotomy-foraminotomy, and laminectomy. A foraminotomy alone is adequate in patients with foraminal stenosis due to osteophytes and/or lateral disc herniation. Laminectomy or laminoplasty is used to treat patients who require decompression at four or more levels or whose anterior column is already fused. Preservation of cervical lordosis is critical for a posterior approach as it allows the spinal cord to shift dorsally following the decompression. In patients with flexible cervical kyphosis  additional cervical posterior instrumentation is needed to help restore normal lordosis and maximize the posterior shift of the spinal cord [19].

Complications

Postoperative respiratory compromise due to trauma to the anterior soft-tissue and prolonged prone position has been reported to vary from 0%–14% [20,21,22,23]. This is probably caused by trauma to the anterior soft-tissue and prolonged prone position; both can cause upper airway oedema and impaired respiration [20,22].

Controlled hypotension used to reduce blood loss and facilitate surgical exposure during cervical surgery can cause spinal cord ischaemia and neurological damage. At least 65% of the usual spinal blood flow is required to maintain physiological integrity and a 12% decrease in blood flow can produce paralysis [24,25].

Long-term harvest site pain (3 months to 2 years) has been reported to occur in 2.5% of iliac crest bone grafting cases [26]. Anterior iliac crest bone graft harvest can be associated with injury to the lateral femoral cutaneous or ilioinguinal nerves due to direct injury, retraction, fracture or subfascial haematoma. Posterior iliac bone harvesting can cause injury to the superior cluneal nerves resulting in sensory deficit to the superior two-thirds of the buttocks.

The incidence of postoperative wound infections following anterior cervical discectomy and fusion is between 0.1%–1.6% [27]. Epidural abscesses can form and cause neurological complications. 

The risk of durotomy with CSF leak during cervical laminectomy is between 0.3%–13% and can be up to 18% following revision surgery [28,29]. Durotomies present with postural headache, vomiting, nausea, photophobia, dizziness, tinnitus and vertigo, but are usually asymptomatic. 

Persistent CSF leakage can lead to the formation of CSF fistulas or pseudomeningoceles.

The overall rates of complications following anterior cervical surgery in systematic review of literature by Timothy J. Yee, et al [30], were as follows: “dysphagia 5.3%, esophageal perforation 0.2%, recurrent laryngeal nerve palsy 1.3%, infection 1.2%, adjacent segment disease 8.1%, pseudarthrosis 2.0%, graft or hardware failure 2.1%, cerebrospinal fluid leak 0.5%, hematoma 1.0%, Horner syndrome 0.4%, C5 palsy 3.0%, vertebral artery injury 0.4%, and new or worsening neurological deficit 0.5%”. Carotid artery, cervical sympathetic chain, thoracic duct and tracheal injuries have also been reported [31].

Injury to the spinal cord and nerve roots can occur with both anterior and posterior surgery. Quadriplegia can occur with spinal cord injury. Graft dislodgement leading to failure of fusion and misplacement of screws leading to neurological or vascular injury has also been reported [31].

The incidence of kyphotic deformity after multilevel laminectomy is 20% [32].

Prognosis

Cervical spondylosis is a slowly progressive, degenerative disease of the cervical spine that deteriorates with age. The severity of symptoms, however, do not correlate with the degree of spondylosis seen on neuroimaging. Patients who present with axial neck pain usually improve with time but they can have a recurrence of pain. 

Gore et al [33] followed up 205 patients with neck pain for a minimum of 10 after onset of symptoms. They found that 79% of patients with neck pain improved or became asymptomatic on follow up. They also found that the presence or severity of pain was not related to the presence of degenerative changes, the spinal canal diameter, the degree of cervical lordosis, or to any changes in these measurements over the evaluation period.

Between 50 to 75% of persons with current neck pain will report neck pain again 1 to 5 years later. Psychosocial factors, including psychological health, coping patterns, and the need to socialize, are the strongest prognostic factors of neck pain [34].

Individuals who present primarily with axial neck pain do not develop more severe spondylotic changes leading to radiculopathy or myelopathy. Symptoms of cervical radiculopathy eventually resolve in 1 to 2 years without surgical intervention [35]. The long-term prognosis of cervical spondylotic myelopathy, on the other hand, is less clear.

The natural course of cervical spondylotic myelopathy is highly variable In patients with mild-to-moderate symptoms with the disease usually remaining static, and the symptoms occasionally improving [36]. Patients who have a progressive decline in neurologic function, and moderate to severe signs and symptoms, surgery is likely to be beneficial. 

A more recent Cochrane review by Nikolaidis et al [36] found that there is no good evidence in literature that surgery is beneficial for patients with cervical radiculopathy and myelopathy.

Conclusion

Cervical spondylosis is a natural age-related degenerative disease of the cervical spine. Degeneration of the cervical spine is a natural process of aging and by the age of 65 years the prevalence of cervical spondylosis is 95%. 

Most people with radiographic evidence of cervical spondylosis remain asymptomatic. The most commonly affected segment is C6-C7, followed by C5-C6. Neck pain is the most common symptom of cervical spondylosis. 

Patients can develop radiculopathy and/or myelopathy. 

X-rays and MRI imaging is used to confirm the diagnosis. The mainstay of treatment is conservative with the use of medications, exercises, collar and sometimes traction. Occasional surgery is necessary. Surgery can be associated with serious complications and should be used judiciously.

References

1. Kuo DT, Tadi P. Cervical Spondylosis. [Updated 2021 May 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan.
2. Clark E, Robinson PK: Cervical myelopathy; complication of cervical spondylosis. Brain 1956; 79:483-510.
3. Ferrara LA. The biomechanics of cervical spondylosis. Adv Orthop. 2012;2012:493605. doi: 10.1155/2012/493605. Epub 2012 Feb 1. PMID: 22400120; PMCID: PMC3287027.
4. Kokubo Y, Uchida K, Kobayashi S, Yayama T, Sato R, Nakajima H, Takamura T, Mwaka E, Orwotho N, Bangirana A, Baba H. Herniated and spondylotic intervertebral discs of the human cervical spine: histological and immunohistological findings in 500 en bloc surgical samples. Laboratory investigation. J Neurosurg Spine. 2008 Sep;9(3):285-95. doi: 10.3171/SPI/2008/9/9/285. PMID: 18928227.
5. Shabat S, Leitner Y, David R, Folman Y. The correlation between Spurling test and imaging studies in detecting cervical radiculopathy. J Neuroimaging. 2012 Oct;22(4):375-8. doi: 10.1111/j.1552-6569.2011.00644.x. Epub 2011 Sep 1. PMID: 21883627.
6. Machino M, Ando K, Kobayashi K, Morozumi M, Tanaka S, Ito K, Kato F, Ishiguro N, Imagama S. Cut off value in each gender and decade of 10-s grip and release and 10-s step test: A comparative study between 454 patients with cervical spondylotic myelopathy and 818 healthy subjects. Clin Neurol Neurosurg. 2019 Sep;184:105414. doi: 10.1016/j.clineuro.2019.105414. Epub 2019 Jul 5. PMID: 31306894.
7. Expert Panel on Neurological Imaging:, McDonald MA, Kirsch CFE, Amin BY, Aulino JM, Bell AM, Cassidy RC, Chakraborty S, Choudhri AF, Gemme S, Lee RK, Luttrull MD, Metter DF, Moritani T, Reitman C, Shah LM, Sharma A, Shih RY, Snyder LA, Symko SC, Thiele R, Bykowski J. ACR Appropriateness Criteria® Cervical Neck Pain or Cervical Radiculopathy. J Am Coll Radiol. 2019 May;16(5S):S57-S76. doi: 10.1016/j.jacr.2019.02.023. PMID: 31054759.
8. McCormick WE, Steinmetz MP, Benzel EC. Cervical spondylotic myelopathy: make the difficult diagnosis, then refer for surgery. Cleve Clin J Med. 2003 Oct;70(10):899-904. doi: 10.3949/ccjm.70.10.899. PMID: 14621236.
9. Brinjikji W, Luetmer PH, Comstock B, Bresnahan BW, Chen LE, Deyo RA, Halabi S, Turner JA, Avins AL, James K, Wald JT, Kallmes DF, Jarvik JG. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015 Apr;36(4):811-6. doi: 10.3174/ajnr.A4173. Epub 2014 Nov 27. PMID: 25430861; PMCID: PMC4464797.
10. Binder. Cervical spondylosis and neck pain. BMJ|10 march 2007| Volume 334.
11. Vernon HT, Humphreys BK, Hagino CA. A systematic review of conservative treatments for acute neck pain not due to whiplash. J Manipulative Physiol Ther 2005;28:443-8.
12. Canadian Chiropractic Association, Canadian Federation of Chiropractic Regulatory Boards, Clinical Practice Guidelines Development Initiative, Guidelines Development Committee (GDC). Chiropractic clinical practice guideline: evidence-based treatment of adult neck pain not due to  whiplash. J Can Chiropr Assoc 2005;49:158-209.
13. Dziedzic K, Hill J, Lewis M, Sim J, Daniels J, Hay EM. Effectiveness of manual therapy or pulsed shortwave diathermy in addition to advice and exercise for neck disorders: a pragmatic randomized controlled trial in physical therapy clinics. Arthritis Care Res 2005;53:214-22.
14. White AR, Ernst E. A systematic review of randomized controlled trials of acupuncture for neck pain. Rheumatology 1999;38:143-7.
15. Van der Heijden GJ, Beurskens AJ, Koes BW, Assendelft WJ, de Vet HC, Bouter LM. The efficacy of traction for back and neck pain: a systematic, blinded review of randomized clinical trial methods. Phys Ther 1995;75:93-104.
16. Cusick JF. Pathophysiology and treatment of cervical spondylotic myelopathy. Clin Neurosurg 199 1;37:661-8 1.
17. Uttley D, Monro P. Neurosurgery for cervical spondylosis. BrJr Hosp Med 1989;42:62-70.
18. Epstein JA. The surgical management of cervical spinal stenosis, spondylosis, and myeloradiculopathy by means of posterior approach. Spine 1988;13:864-9.
19. Rao RD, Currier BL, Albert TJ, Bono CM, Marawar SV, Poelstra KA, Eck JC. Degenerative cervical spondylosis: clinical syndromes, pathogenesis, and management. J Bone Joint Surg Am. 2007 Jun;89(6):1360-78. doi: 10.2106/00004623-200706000-00026. PMID: 17575617.
20. Emery SE, Smith MD, Bohlman HH. Upper-airway obstruction after multilevel cervical corpectomy for myelopathy. J Bone Joint Surg Am. 1991;73:544–551. 
21. McAfee PC, Bohlman HH, Ducker TB, Zeidman SM, Goldstein JA. One-stage anterior cervical decompression and posterior stabilization: a study of one hundred patients with a minimum of two years of follow-up. J Bone Joint Surg Am. 1995;77:1791–1800. 
22. Sagi HC, Beutler W, Carroll E, Connolly PJ. Airway complications associated with surgery on the anterior cervical spine. Spine (Phila Pa 1976) 2002;27:949–953. 
23. Zdeblick TA, Bohlman HH. Cervical kyphosis and myelopathy: treatment by anterior corpectomy and strut-grafting. J Bone Joint Surg Am. 1989;71:170–182.
24. Krengel WF, 3rd, Robinson LR, Schneider VA. Combined effects of compression and hypotension on nerve root function: a clinical case. Spine (Phila Pa 1976) 1993;18:306–309. 
25. Naito M, Owen JH, Bridwell KH, Sugioka Y. Effects of distraction on physiologic integrity of the spinal cord, spinal cord blood flow, and clinical status. Spine (Phila Pa 1976) 1992;17:1154–1158.
26. Younger EM, Chapman MW. Morbidity at bone graft donor sites. J Orthop Trauma. 1989;3:192–195.
27. Fountas KN, Kapsalaki EZ, Nikolakakos LG, et al. Anterior cervical discectomy and fusion associated complications. Spine (Phila Pa 1976) 2007;32:2310–2317.
28. Epstein NE, Hollingsworth R. Anterior cervical micro-dural repair of cerebrospinal fluid fistula after surgery for ossification of the posterior longitudinal ligament. Technical note. Surg Neurol. 1999;52:511–514.
29. Smith MD, Bolesta MJ, Leventhal M, Bohlman HH. Postoperative cerebrospinal-fluid fistula associated with erosion of the dura: findings after anterior resection of ossification of the posterior longitudinal ligament in the cervical spine. J Bone Joint Surg Am. 1992; 74:270–277.
30. Yee et al. Complications of anterior cervical spine surgery: a systematic review of the literature. Journal of spine surgery, March 2020;Vol 6, No 1.  
31. Cheung JP, Luk KD. Complications of Anterior and Posterior Cervical Spine Surgery. Asian Spine J. 2016;10(2):385-400. doi:10.4184/asj.2016.10.2.385.
32. Kaptain GJ, Simmons NE, Replogle RE, Pobereskin L. Incidence and outcome of kyphotic deformity following laminectomy for cervical spondylotic myelopathy. J Neurosurg. 2000;93:199–204.
33. Gore DR, Sepic SB, Gardner GM, Murray MP. Neck pain: a long-term follow-up of 205 patients. Spine (Phila Pa 1976). 1987 Jan-Feb;12(1):1-5. doi: 10.1097/00007632-198701000-00001. PMID: 3576350.
34. Carroll LJ, et al; Course and prognostic factors for neck pain in the general population: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine (Phila Pa 1976). 2008 Feb 15;33(4 Suppl):S75-82. doi: 10.1097/BRS.0b013e31816445be. PMID: 18204403.
35. Bono CM, Ghiselli G, Gilbert TJ, Kreiner DS, Reitman C, Summers JT, Baisden JL, Easa J, Fernand R, Lamer T, Matz PG, Mazanec DJ, Resnick DK, Shaffer WO, Sharma AK, Timmons RB, Toton JF; North American Spine Society. An evidence-based clinical guideline for the diagnosis and treatment of cervical radiculopathy from degenerative disorders. Spine J. 2011 Jan;11(1):64-72. doi: 10.1016/j.spinee. 2010.10.023. PMID: 21168100.
36. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine (Phila Pa 1976). 2002 Apr 1;27(7):736-47. doi: 10.1097/00007632-200204010-00011. PMID: 11923667.
37. Nikolaidis I, Fouyas IP, Sandercock PA, Statham PF. Surgery for cervical radiculopathy or myelopathy. Cochrane Database Syst Rev. 2010 Jan 20;2010(1):CD001466. doi: 10.1002/14651858.CD001466.pub3. PMID: 20091520; PMCID: PMC7084060.