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.

           Unnecessary Surgeries   

                                   DR KS Dhillon

What is meant by unnecessary surgery? Unnecessary surgery is defined as any surgical intervention that is not needed or indicated and is not in the best interest of the patient [1,2].

In the USA, the threat of unnecessary surgery had been publicized as far back as 1953, when the Director of the American College of Surgeons,

Dr. Paul Hawley, stated that “the public would be shocked if it knew the amount of unnecessary surgery performed by dishonest doctors [3].

In 1976, the American Medical Association (AMA) called for a congressional hearing on unnecessary surgery. The association claimed that there were “2.4 million unnecessary operations performed on Americans at a cost of $3.9 billion and that 11,900 patients had died

from unneeded operations” [4].

In the USA it has been estimated that at least 20% of the money spent on health care is wasted which amounts to more than $700 billion dollars a year. Unnecessary medical care is a major contributor to this waste [5].

Types of unnecessary surgeries

There are many types of unnecessary procedures that are carried out. Some of them include [6]:

• Cardiac angioplasty and stents. According to a 2011 study in the Journal of the American Medical Association about 12 percent of all angioplasty interventions weren’t medically necessary. 
• Cardiac pacemakers. According to a 2011 study in the Journal of the American Medical Association, there was no medical evidence to support 22.5 percent of implantable cardioverter-defribrillator surgeries.
• Back surgery and spinal fusion. According to a 2011 study in the journal Surgical Neurology, over 17 percent of patients received unnecessary spinal surgery.
• Hysterectomy. About 70 percent of hysterectomies are unnecessary, according to a 2000 study for the American College of Obstetricians and Gynecologists.
• Knee and hip replacement. According to a 2012 study in Health Affairs, after patients received information on alternatives to joint replacement surgeries, researchers noted that approximately 26 percent of patients had fewer hip replacements and 38 percent had fewer knee replacements. 
• Cesarean section. According to a 2013 study in Health Affairs, C-section rates vary across hospitals. Even with lower-risk pregnancies, cesarean rates varied from 2.4 percent to 36.5 percent. 

There are many other areas of medical practice where unnecessary procedures are carried out.

In 2021, the existence of unnecessary surgery remains a daunting reality that continues to expose patients to unjustified surgical risk. There are multiple clinical trials that show that spinal fusions for back pain do not lead to improved long-term patient outcomes when compared to non-operative treatment [7,8]. Despite these insights from high-quality trials, spinal fusion rates continue to dramatically increase in the United States [9] and elsewhere in the world. 

Another example is arthroscopic partial meniscectomy. It is one of the most commonly performed surgical procedures in the world [10]. In the United States surgeons perform about 700,000 arthroscopic partial meniscectomies every year. A Finnish prospective randomized controlled trial that assessed patient outcomes after arthroscopic partial meniscectomy compared to sham surgery showed no benefit for patients from the surgical procedure at 12 months follow-up [11]. Although it is well known that any surgical procedure can be associated with a risk of severe intra- or postoperative complication [12] yet to date, a change in practice has not occurred, and arthroscopic meniscectomies continue to be performed on hundreds of thousands of patients in the USA every year [13,14].

In 2002 Moseley et al [15] published an article in the New England Journal of Medicine to show the futility of arthroscopic joint debridement for osteoarthritis of the knee but to date, such procedures are still carried out [15]. Moseley et al [15] did a randomized, placebo-controlled trial to assess the efficacy of arthroscopic knee surgery to relieve knee pain and improve function in patients with OA of the knee. They had three groups of patients who either had joint lavage, joint debridement, or sham incisions at the arthroscopic portals. Their study showed strong evidence that arthroscopic lavage with or without debridement is no better than placebo in relieving pain and improving self-reported knee function. The authors concluded that the billions of dollars spent annually on such procedures could be put to better use.

Kirkley et al [16] in 2008 published the outcome of a single-center, randomized, controlled trial of arthroscopic surgery in patients with moderate-to-severe osteoarthritis of the knee. They randomly assigned patients to arthroscopic joint debridement with surgical lavage and physical plus medical therapy or to treatment with physical and medical therapy alone. At 2 years follow-up, they found that arthroscopic surgery for osteoarthritis of the knee provided no additional benefit as compared to optimized physical and medical therapy.

The incidence of anterior cruciate ligament (ACL) reconstruction is increasing around the world and in Australia, it is among the highest in the world [17,18]. There is a general belief that all ACL injuries must be treated with reconstruction to minimize symptoms, improve quality of life and minimize the risk of future complications such as chondral and meniscal injury. Now, however, there is level 1 scientific evidence that the mid-term (5 years) patient-reported and radiographic outcomes between those patients treated with rehabilitation plus early ACL reconstruction and those treated with rehabilitation and optional delayed ACL reconstruction are the same in young active individuals [19]. Despite such good level I evidence the incidence of ACL reconstruction is increasing around the world.

There are many surgeons who recommend a repair of grade 3 injuries of the lateral ligament of the ankle but there is no evidence that such surgery gives better results than conservative treatment.

Pihlajamaki et al [20] did a prospective randomized controlled trial to compare surgical versus functional treatment for acute ruptures of the lateral ligament of the ankle in young men. They found that at a mean follow-up of 14 years, all patients in both groups had recovered the pre-injury activity level and they could walk and run normally. There was no significant difference in the ankle scores.

In the United States, more than 18.9 million adults report chronic shoulder pain each year and it accounts for over 4.5 million primary care visits every year [21]. Shoulder impingement can account for about 85% of all shoulder complaints. It is estimated that almost 300,000 surgical procedures for shoulder pathology including impingement are performed yearly in the USA, with the direct financial burden estimated to be over US$3 billion annually [22].

Impingement syndrome is treated by subacromial decompression often by arthroscopy. There has been a sevenfold increase in subacromial decompression surgery in the United Kingdom from 2000 to 2010 and a fourfold increase in the US from 1996 to 2006 [23,24,25].

These increases in the number of subacromial decompression rates exist despite the presence of high-quality evidence that shows that subacromial decompression does not provide clinically important benefits as compared to placebo as far as pain, function, and health-related quality of life is concerned [26,27].

In ENT there is one procedure that has been done unnecessarily on millions of patients and wasted tens of billions of dollars over the past several decades, with no evidence that it even works for most patients. This overused procedure is endoscopic sinus surgery (ESS) [5].

Another ENT operation that is frequently done when it is not necessary is tonsillectomies in children. About 88 percent of tonsillectomies carried out on children in the UK each year are unnecessary [28].

If surgery was a pharmaceutical drug, the procedure would be required

to undergo scrutiny of testing for its safety and feasibility in several trials. 

Subsequently, the efficacy would have to be proven in randomized controlled trials before the Food and Drug Administration (FDA) would approve it [19]. The FDA, however, does not regulate surgical procedures. Common sense would dictate that whenever new level 1 evidence disproves a benefit for a certain surgical procedure, the ineffective practice should be immediately abandoned. This, however, is obviously not the case as far as surgery is concerned.

Why do surgeons continue to perform unnecessary surgery?

The question which begs for an answer is why would a reasonable surgeon consider performing unneeded surgical procedures which carry the risk of morbidity and mortality. The only surgery without risk of complications is the surgery that is not performed. 

There are estimates that as many as 1.3 million Americans suffer disabling injuries in hospitals every year, and 198,000 of those may result in death,  seven out of ten of which were preventable (48% from faulty surgery), and a third from negligence [29].

Unnecessary surgical procedures can be associated with the following:

• Death
• Infection, paralysis, blood clots, and other surgical complications
• Unnecessary loss of organs or organ function
• The need for follow-up expensive procedures and surgeries
• Diminished health and quality of life
• Surgical scars and other cosmetic blemishes
• Days, weeks, or months of missed work
• Huge medical bills

Unnecessary surgeries also lead to a profound loss of trust in the surgeon.

Surgeons have stated 2 primary reasons why unneeded surgeries continue to be performed [30]:

1. “We perform surgery because we have been trained to do so and because “we have always done it this way” or we simply do not know any better. 

2. We are incentivized to perform surgical procedures, either for financial gain, renown, or both”.

The main incentive for performing unnecessary surgery is financial gain.

Financial conflicts of interest usually drive physicians to perform worthless surgeries, and the field of orthopedics "is one of the worst offenders,"[31].

In the USA there have been many headlines of lawsuit allegations, investigations, guilty pleas, and convictions concerning this problem [32].  

In the USA and probably in many other parts of the world there are a number of reasons that drive medical overtreatment. 

Fee-for-service model is part of the problem. A profit-driven surgeon agenda is a problem since over 70% of U.S. doctors themselves believe that doctors "are more likely to perform unnecessary procedures when they profit from them" [33]. Doctors acknowledge that conflict of interest occurs because surgeons "are paid approximately ten times more money to perform surgery than to manage your problem conservatively" [34]. Hence financial pressures can lead to unnecessary surgery. One doctor quotes his residency professor who said that "there is nothing more dangerous than a surgeon with an open operating room and a mortgage to pay" [35].

Some surgeons have speaking agreements with medical device manufacturers and pharmaceutical companies. These surgeons carry out large numbers of operations, many of which are unnecessary, using their devices and implants. Surgeons receive consultancy fees for talks at meetings and conferences where the surgeon encourages others to use these devices and implants. Payments are made by these companies for trips, travel, lodging, food, honoraria, gifts, etc [36].  A conflict of interest in this setting can lead the surgeon to use a particular type of surgical device, even when it is not the right one for the patient. Unfortunately, there are many surgeons who are “in bed with the device industry." [34].

This "symbiotic" relationship between medical device manufacturers and surgeons provides the surgeons with an important source of revenue [35].  

Many of the surgeons don't disclose these potential conflicts of interest in studies that they publish about these devices [36]. Surgeons often tend to perform a given surgery due to their relationship with the device manufacturer instead of what is in the best interests of the patient.  There are even cases where some device-makers have even paid millions of dollars to settle cases involving allegations of improper payments to surgeons [37]. 

There are teaching hospitals in the USA that have come under scrutiny for accepting revenue from medical device manufacturers as well [38]. There are also many surgeons who are owners or co-owners of ambulatory surgical centers. This ownership model can be associated with conflicts of interest that affect surgical decisions leading to a higher volume of surgeries [39].   

Hospitals are also sometimes involved in these conflicts of interest. They drive the surgeons to do unnecessary procedures. The hospital administrators put pressure on surgeons to generate more money by performing more procedures [34]. In some cases, hospitals have purchased very expensive surgical equipment or devices and they need to justify their use. Hospitals sometimes require surgeons to perform a minimum number of some procedures every year or two years. 

When is Unnecessary Surgery Medical Malpractice?

Unnecessary surgery can be medical malpractice. To file a malpractice lawsuit for unnecessary surgery, one has to prove negligence. There are several ways to prove negligence and these includes but are not limited to:

• Doctor failed to inform the patient of the risks or benefits of the surgery versus the risks of not having the surgery.
• Doctor recommends surgery without considering or offering reasonable alternative treatment.
• When there is a misdiagnosis and surgery is performed. 

A claim of medical negligence could be filed for a medical malpractice lawsuit if a medical mistake was made during the surgery. Compensation can be obtained for unnecessary surgery if medical negligence can be proved. 

In the USA a Virginia doctor was sentenced to 59 years in prison for performing irreversible hysterectomies, improper sterilizations, and other medically unnecessary surgeries on his patients. In November of 2019, Dr Javaid Perwaiz was charged with health care fraud and making false statements relating to health care matters. 

His conviction resulted from various patient complaints. One patient had her fallopian tubes removed without her consent, resulting in being unable to conceive naturally. In another patient, an unauthorized hysterectomy was carried out which resulted in a perforated bladder which resulted in a 6-day hospital stay. Besides performing irreversible hysterectomies he carried out improper sterilizations and other medically unnecessary surgeries on his patients. 

Perwaiz was an obstetrician-gynecologist in Chesapeake, Virginia, since the 1980s. From 2010 to 2019, he defrauded health insurance programs, resulting in about $20.8 million in losses to health care insurers. He would often trick his patients into having unnecessary surgeries by telling them they had cancer or needed the surgery to avoid cancer. 

In four years, from January 2014 to August 2018, he operated on 40% of his Medicaid beneficiaries, or a total of 510 patients. Out of those, 42% of the patients had at least two surgeries [40].

Unnecessary surgeries in Malaysia

Anecdotal evidence suggests that the number of unnecessary surgeries in Malaysia is also high. There are no studies published to show the high incidence of unnecessary surgeries in Malaysia. 

Apparently, every year about 2,000 to 4,000 deaths occur due to some form of medical negligence and a large number of these cases go unreported partly because of the out-of-court settlements and partly due to the fact that many patients accept the incidents as matters of fate. Many patients are not aware of their rights and others are too poor to afford litigation especially in Malaysia where there is no speedy and inexpensive system of administration of justice in medical negligence [41].

Some have estimated that medical errors could be the No 2 killer in Malaysia after heart diseases and cardiovascular disorders. Medical errors probably kill more Malaysians than either cancer, diabetes, or motor vehicle accidents. Apparently for every case of medical error reported, 10 cases go unreported. About 80 percent of medical procedures performed today have never been properly tested [42].

In Malaysia, there is a lack of proper machinery to deal with poorly performing doctors except through the court of law. Medical negligence cases and malpractice cases are excessively difficult to prove and they take a very long time to settle. 

The Malaysian Medical Council (MMC) is a “passive regulatory body”. It deals with complaints of ethics and professional behavior that are reported to it.  There is no inspectorate to detect offenses. The regulatory bodies as well as the regulatory processes in Malaysia do not show that they provide sufficient safeguards to protect the interests of the public [43]. 

There have been questions as to why aren't the interests and the safety of millions of patients in Malaysia protected against medical mishaps and errors? Patients are not only not assured of consistent quality medical care but they are also denied a speedy, effective, and fair avenue for justice when there is medical negligence and malpractice [44].

They are also victims of a lack of an effective system to protect their interests and safety. 

A careless, incompetent, or irresponsible medical professional has the power to kill, paralyze, disfigure or dismember his patients. The safety and well-being of all patients should be of paramount importance. Hence it is important that the medical profession is most stringently regulated. However, unfortunately, the medical profession and the way it deals with medical errors seems to be shrouded in mystery and secrecy. It lacks integrity, accountability, and transparency. 'Prevention is better than cure' should be practiced more by the medical profession in preventing medical negligence, malpractice and errors because there are no quick, cheap, or painless cures for botched-up medical procedures [44].

Reference

1. Stahel PF. Blood, sweat and tears — becoming a better surgeon. Shropshire, UK: TFM Publishing; 2016. p. 320.
2. Klaidman S. Coronary - a true story of medicine gone awry. New York: Scribner; 2007. p. 303.
3. Unneeded operating charged to surgeons. The New York Times, February 17, 1953.
4. A.M.A. scores ‘unneeded surgery’ report. The New York Times, May 12, 1976.
5. Arthur W. Curtis. Endoscopic sinus surgery: A tale of overuse at https://rightcarealliance.org/article/endoscopic-sinus-surgery-tale-overuse/
6. Did You Undergo Unnecessary Surgery? You May Be a Victim of Medical Malpractice at https://www.mallardlawfirm.com/library/be-aware-of-the-common-types-of-unnecessary-surgeries.cfm.
7. Raabe A, Beck J, Ulrich C. Necessary or unnecessary? a critical glance on spine surgery [German]. Ther Umsch. 2014;71:701–5.
8. Srinivas SV, Deyo RA, Berger ZD. Application of “less is more” to low back pain. Arch Intern Med. 2012;172:1016–20.
9. Why ‘useless surgery’ is still popular. The New York Times, August 3, 2016. 
10. Jarvinen TL, Guyatt GH. Arthroscopic surgery for knee pain. BMJ. 2016;354:i3934.
11. Sihvonen R, Paavola M, Malmivaara A, Itala A, Joukainen A, Nurmi H, Kalske J, Jarvinen TL. Arthroscopic partial meniscectomy versus sham surgery for a degenerative meniscal tear. N Engl J Med. 2013;369:2515–24.
12. Grelsamer RP. A patient guide to unnecessary knee surgery. AuthorHouse, 2015, pp.150.
13. Lyu SR. Why arthroscopic partial meniscectomy? Ann Transl Med. 2015;3:217.
14. Thorlund JB, Juhl CB, Roos EM, Lohmander LS. Arthroscopic surgery for degenerative knee: systematic review and meta-analysis of benefits and harms. Br J Sports Med. 2015;49:1229–35.
15. Moseley JB, O'Malley K, Petersen NJ, et al. A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med 2002;347:81-88
16. Kirkley A, Birmingham TB, Litchfield RB, Giffin JR, Willits KR, Wong CJ, Feagan BG, Donner A, Griffin SH, D'Ascanio LM, Pope JE, Fowler PJ. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008;359((11)):1097–107.
17. Janssen K, Orchard JW, Driscoll TR, et al. High incidence and costs for anterior cruciate ligament reconstructions performed in Australia from 2003–2004 to 2007–2008: time for an anterior cruciate ligament register by Scandinavian model? Scand J Med Sci Sports 2011; 22: 495-501.
18. Moses B, Orchard J, Orchard J. Annual incidence of ACL injury and surgery in various populations. Res Sports Med 2012; 20: 157-179.
19. Frobell R, Roos H, Roos E, Roemar F, Ranstam J, Lohmander L. Treatment for anterior cruciate ligament tear: five year outcome of randomized trial. BMJ 2013; 346: f232.
20. Pihlajamäki, Harri MD, PhD1; Hietaniemi, Kalevi MD, PhD2; Paavola, Mika MD, PhD3; Visuri, Tuomo MD, PhD1; Mattila, Ville M. MD, PhD4 Surgical Versus Functional Treatment for Acute Ruptures of the Lateral Ligament Complex of the Ankle in Young Men, The Journal of Bone & Joint Surgery: October 20, 2010 - Volume 92 - Issue 14 - p 2367-2374 doi: 10.2106/JBJS.I.01176
21. Khan et al. Surgery for shoulder impingement: a systematic review and meta-analysis of controlled clinical trials. CMAJ Open 2019, Jan -Mar; 7(1): E149-E158.
22. Colvin AC, Egorova N, Harrison AK, et al. National trends in rotator cuff repair. J Bone Joint Surg Am 2012;94:227-33.
23. Judge A, Murphy RJ, Maxwell R, et al. Temporal trends and geographical variation in the use of subacromial decompression and rotator cuff repair of the shoulder in England. Bone Joint J 2014;96-B:70-4.
24. Vitale MA, Arons RR, Hurwitz S, et al. The rising incidence of acromioplasty. J Bone Joint Surg Am 2010;92:1842-50.
25. Beard DJ, Rees JL, Cook JA, Rombach I, Cooper C, Merritt N, Shirkey BA, Donovan JL, Gwilym S, Savulescu J, Moser J, Gray A, Jepson M, Tracey I, Judge A, Wartolowska K, Carr AJ; CSAW Study Group. Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-controlled, three-group, randomised surgical trial. Lancet. 2018 Jan 27;391(10118):329-338.
26. Karjalainen TV, Jain NB, Page CM, Lähdeoja TA, Johnston RV, Salamh P, Kavaja L, Ardern CL, Agarwal A, Vandvik PO, Buchbinder R. Subacromial decompression surgery for rotator cuff disease. Cochrane Database Syst Rev. 2019 Jan 17;1:CD005619. doi: 10.1002/14651858.CD005619.
27. Why ‘useless surgery’ is still popular. The New York Times, August 3, 2016.
28. Dana Šumilo, Linda Nichols, Ronan Ryan and Tom Marshall. Incidence of indications for tonsillectomy and frequency of evidence-based surgery: a 12-year retrospective cohort study of primary care electronic records. : Br J Gen Pract 2018; DOI: https://doi.org/10.3399/bjgp18X699833.
29. Unnecessary surgeries at https://sweeneylawfirm.com/content/unnecessary-surgeries.
30. Stahel et al.Why do surgeons continue to perform unnecessary surgery?  Patient Safety in Surgery (2017) 11:1 DOI 10.1186/s13037-016-0117-6.
31. Cheryl Clark. Orthopedists' Financial Conflicts Can Hurt Patients, Surgeon Says at https://www.medpagetoday.com/surgery/orthopedics/50601.
32. Mark Clore. Unnecessary Surgery: When the Doctor Gambles, Who Puts Up the Stakes? at https://www.clorelaw.com/insights/unnecessary-surgery-when-the-doctor-gambles-who-puts-up-the-stakes.
33. Lyu Xu T, et al, Overtreatment in the United States, PLOS One (Sep. 6, 2017), pp. 4-5, at: https://doi.org/10.1371/journal.pone.0181970.
34. Crouch M, 45 Secrets Surgeons Won’t Tell You, The Healthy, Nov. 25, 2019, Updated Nov. 14, 2020.
35. Cox, CE, Physician Conflict of Interest Disclosures to Journals for Device Industry Ties Falls Short, tct/md the heart beat, Aug. 24, 2018, p. 2.
36. Wolters Kluwer Health, Financial conflicts of interest are often not disclosed in spinal surgery journals, at: https://medicalxpress.com/news/2020-07-financial-conflicts-disclosed-spinal-surgery.html
37. U.S. Attorney's Office, Dist. of NJ Release, Medical Device Maker to Pay $18 Million to Settle Allegations of Improper Payments to Physicians, Oct. 14, 2020, at: https://www.justice.gov/usao-nj/pr/medical-device-maker-pay-18-million-settle-allegations-improper-payments-physicians, and U.S. Dep't of Justice (DOJ), Public Affairs, Medtronic to Pay Over $9.2 Million to Settle Allegations of Improper Payments to South Dakota Neurosurgeon, Oct. 29, 2020, at: https://www.justice.gov/opa/pr/medtronic-pay-over-92-million-settle-allegations-improper-payments-south-dakota-neurosurgeon.
38. Adams K. Drug, device companies' payments to teaching hospitals may spark conflict of interest, study suggests. Becker's Hospital Review, Sep. 9, 2020.
39. Hollingsworth JM, Ye Z, et al, Physician-Ownership of Ambulatory Surgery Centers Linked to Higher Volume of Surgeries, Vol. 29, No. 4, Health IT.
40. Virginia doctor sentenced to 59 years in prison for performing unnecessary surgeries on patients at https://www.usatoday.com/story/news/2021/05/19/doctor-who-performed-unnecessary-sterilizations-faces-59-years-jail/5170521001/
41. Prof Dr Ali Mohamad Matta. Issues in Medical Law and Ethics , Medical Law and Ethics Unit, Law Centre, Ahmad Ibrahim Kulliyyah of Laws, IIUM Malaysia, Dec 2003, p21.
42. SM Mohd Idris, Can Doctors Be Trusted? How to protect Yourself against Medical Errors (2004), Consumers' Association of Penang.
43. Dr Nik Rosnah Wan Abdullah (September 2003) The Malaysian Medical Professionals: Serving the Public Interests? , FEA Working Paper 2003-9, University of Malaya.
44. Kumaraguru. Justice for victims of medical negligence at https://www.malaysiakini.com/letters/29600.

         Breakthrough Covid-19 Infections

                            Dr. KS Dhillon

A vaccine breakthrough infection is defined as the detection of SARS-CoV-2 RNA or antigen in a respiratory specimen collected from a person 14 or more days after they have completed all recommended doses of a COVID-19 vaccine.

We are all aware that COVID-19 vaccines are a critical tool for controlling the ongoing global pandemic. In large, randomized-controlled trials, some vaccines have been found to be safe and efficacious in preventing symptomatic, laboratory-confirmed COVID-19. Despite the relatively high level of vaccine efficacy, a small percentage of fully vaccinated persons do develop symptomatic or asymptomatic infections with SARS-CoV-2, the virus that causes COVID-19.

In the USA as of 30th April 2021, a total of 10,262 SARS-CoV-2 vaccine breakthrough infections had been reported from 46 U.S. states and territories. Sixty-three percent of the cases occurred in females, and the median patient age was 58 years (range = 40–74 years). Twenty-seven percent of vaccine breakthrough infections were asymptomatic, 10% of the patients were hospitalized, and 2% of patients died. Among the 995 patients who were hospitalized 29% were asymptomatic and they were hospitalized for a reason unrelated to COVID-19. The median age of patients who died was 82 years (range = 71–89 years). 

The percent of patients who develop breakthrough infections is small in vaccinated individuals. The breakthrough infections in vaccinated individuals range from 0.2% to 5.9% of the total Covid-19 infections according to statistics from various states in the USA. Ninety-four to 99.8% of the infections occur in non-vaccinated individuals.

The number of breakthrough infection cases are probably underreported because the national surveillance system in the USA relies on passive and voluntary reporting, and data might not be complete or representative. Many individuals with vaccine breakthrough infections, especially those who are asymptomatic or who experience mild illness, might not go for testing. 

A review of Veterans Health Administration (VHA) medical records in the USA pertaining to COVID-19 breakthrough infections in Veterans with spinal cord injuries and disorders (SCI/D), showed that 17 out of 8,319 (0.20%) fully vaccinated Veterans with SCI/D had breakthrough infection as of April 20, 2021. Of those diagnosed with COVID-19 breakthrough infections, 6 (35.3%) were symptomatic and 11(64.7%) were asymptomatic. Of the six symptomatic cases, three were of mild severity, one was moderate, and two were severe. Three patients were hospitalized, and one patient died within 30 days of COVID-19 diagnosis.

A study was carried out at the largest medical center in Israel, to identify breakthrough infections among health care workers. Among 1,497 fully vaccinated health care workers, 39 SARS-CoV-2 (2.6%) breakthrough infections were detected. 

Most breakthrough cases were mild or asymptomatic, although 19% had persistent symptoms lasting more than 6 weeks. The alpha variant was found in 85% of the samples tested. 

A study was carried out in India to ascertain the number of breakthrough COVID19 infections after vaccinations in a chronic care, diabetes-centric healthcare facility. One hundred and seven (94.7%) out of 123 employees had completed their 2nd dose of vaccination. Symptomatic breakthrough infections after 14 days of the second dose occurred in 15 persons (13.3%). All 14 had mild COVID19 disease.  Symptoms lasted from 3 to 14 days. One patient required hospitalization for pneumonia. 

The Chicago Department of Public Health (CDPH) carried out a study to identify breakthrough infections among skilled nursing facility residents and staff members in Chicago, Illinois, between December 2020 and March 2021.

There were 627 persons with SARS-CoV-2 infection across 75 SNFs.  Breakthrough infections occurred in 12 residents and 10 staff members accounted for 16% (22 of 136) of the COVID-19 infections. Nearly two-thirds (14 of 22; 64%) of persons with breakthrough infections were asymptomatic; two residents were hospitalized because of COVID-19, and one died.

In the USA as of 2nd August 2021, more than 164 million people had been fully vaccinated against Covid-19. According to data from CDC, there have been 7,101 hospitalizations and 1,507 deaths due to breakthrough infections. Individuals who are fully vaccinated and develop breakthrough infections usually develop mild to moderate illness, if they develop symptoms at all.

Vaccines shorten the length of illness in individuals who develop breakthrough infections. Vaccination reduces disease severity and duration of illness in individuals who develop breakthrough infections. 

Previously, scientists believed that vaccinated individuals rarely transmitted the virus. However, the Delta variant has changed the game. Emerging evidence shows that vaccinated individuals can spread the Delta variant to some extent. Unvaccinated individuals transmit the virus at a higher rate than vaccinated individuals.

Individuals with weakened immune system are at higher risk of getting  breakthrough infection because the vaccines work less well for them. Immunocompromised individuals include organ transplant recipients, cancer patients, and those with advanced HIV or uncontrolled diabetes. Upto 46% of patients who had received solid organ transplants do not mount an antibody response after two doses of an mRNA vaccine. A booster shot may be required for immunocompromised individuals.

Older individuals are more at risk of developing severe complications from breakthrough infections. Around three-quarters of breakthrough infections that caused hospitalizations or deaths occur in those aged 65 and older.

Overall, the data in the USA, showed that approximately 1 in 900 vaccinated people had breakthrough infections. The vast majority of those infected have mild or no symptoms of Covid. About 1 in 17,000 need to be hospitalized. Approximately 1 in 83,000 vaccinated people die from Covid. 

In general, it's very, very rare to get Covid infection after being vaccinated.

Overall about 95% of breakthrough infections are mild and do not require hospitalization.

In Malaysia, the incidence of breakthrough infections is higher than in the USA. Between Aug 12 to Aug 29, 2021, there were 68,629 breakthrough infections comprising 17.8% of the total 385,542 Covid-19 cases. There has been a gradual increase in the percentage of breakthrough infections. On 12 August 2021 the percentage was 12.6% and on 29 August 2021, it was 23.9%. 

There were 8,159 patients in category 3 to 5 who were hospitalized. The percentage of fully vaccinated was 1.6% and 2.2% were not fully vaccinated. The number of ICU admissions of category 4 and 5 patients was 4,762. The percentage of fully vaccinated was 0.8% and not fully vaccinated was 1.3%.

In Malaysia, daily Covid-19 cases increased fourfold from 5,586 on June 27 to 22,070 on 27 August 2021, while daily deaths increased from 60 cases on June 27 to 339 on 27 August. 

As of 27 August 2021, 61.1 percent of the country's adult population had been fully vaccinated, while in the Klang Valley, 88.7 percent of the adult population had been fully immunized. New cases, however, continued to spike in Selangor (from 2,212 cases on June 27 to 5,920 on 27 August) and Kuala Lumpur (628 cases on June 27 to 1,809 on 27/8/21).

Death rates in Selangor also increased from 20 fatalities on June 27 to 103 on 27/8/21. In Kuala Lumpur, it spiked from 16 deaths on June 27 to 40 on 27/8/21.

An end to this pandemic does not appear to be in sight despite the large numbers of individuals having been vaccinated.

     Posterior cruciate ligament injuries

                                    Dr. KS Dhillon

Anatomy and Biomechanics

The posterior cruciate ligament (PCL) length averages between 32mm and 38mm from its origin to insertion, and its cross-sectional area narrows distally [1]. The PCL is mainly made up of two bundles, namely the anterolateral bundle (ALB) and posteromedial bundle (PMB). The femoral attachment of the ALB is nearly twice as big as the tibial insertion. The ALB is more lax in full extension and tight in full flexion. This bundle comprises about 65% of the total mass of the PCL. The PMB is taught in extension and lax in flexion. 

The PCL extends from the posterior tibial plateau to the roof of the femoral notch. It is intraarticular but extra synovial. The synovial membrane covers the entire ligament except for the posterior part. The PCL femoral insertion is half-moon shaped and the PCL tibial insertion is nonplanar and rectangular in shape.

The PCL is surrounded by the anterior meniscofemoral ligament known as the Humphrey ligament and the posterior meniscofemoral ligament which is known as the Wrisberg ligament, which emerges from the lateral aspect of the medial femoral condyle and inserts distally close to the posterior horn of the lateral meniscus. Both these ligaments are only present in 49% of the knees, providing up to 71% of the posterior stability in a PCL-deficient knee, particularly between 60° and 90° of flexion [2].

The PCL is the primary restraint to posterior tibial translation on the femur and the secondary restraint to external rotation [3]. These functional roles are most when the knee is flexed to 90 degrees. When the knee is in full extension there is a minimal posterior translation with an isolated PCL lesion [3]. 

Studies show that kinematic differences increased significantly with combined PCL/posterolateral corner (PLC) lesions when compared with isolated lesions [4,5,6]. 

Mechanism of Injury

Three mechanisms have been proposed for rupture of the PCL:

1. Hyperflexion

Hyperflexion knee injury is common in sports. The individual falls on hyperflexed knee and the traumatic forces are directed proximally up the tibia which leads to posterior subluxation of the tibia and rupture of the PCL.  Nearly always an anterior isolated intrasynovial intrasubstance tear occurs and often the posteromedial bundle remains intact. The laxity is rarely greater than grade II. These lesions can heal to some extent and with time the laxity may often decrease to grade I [7].

2. Pretibial Trauma

The most common traumatic mechanism for injury to the PCL is the dashboard injury. The knee is in a flexed position and a posteriorly directed force is applied to the anterior aspect of the proximal tibia. Such an injury results in an intrasubstance tear at the level of the tibial plateau or a tibial avulsion. Severe trauma will result in damage to the meniscofemoral ligaments as well.

An anteromedial and a rotational force can cause a tear of the posterolateral corner. When the PCL and posterolateral corner is torn, the posterior instability will be greater. 

3. Hyperextension

Hyperextension injury can result in tearing of the PCL and the posterior capsule. Hyperextension can lead to dislocation of the knee and neurovascular compromise. The PCL injury is frequently a proximal disruption at the femoral attachment. 

Epidemiology

The incidence of PCL injuries in the literature varies widely and this disparity results from differences in the population of individuals examined. Miyasaka and Daniel[8] reported an incidence of 3% in the general population, whereas Fanelli and Edson [9] reported an incidence of 38% in patients with acute knee hemarthrosis in an emergency room.

There is an association between athletic injuries and `isolated' PCL injuries. The most frequent mechanism of injury in athletes is hyperflexion injury. In an emergency room setting, 56.5% of injuries are trauma-related and 32.9% are athletic-related [7]. Fanelli and Edson [9] reported that 96.5% of the PCL injuries occurred in combination with other ligamentous injuries. 

The majority of PCL tears occurred in motor vehicle and motorcycle accidents. They concluded that the incidence of PCL injuries is higher in patients with trauma as compared to patients with athletic injuries.

Most grade III PCL injuries occur with other ligament injuries (79% of cases) [10]. Isolated PCL injuries are rare and occur in 3.5% of the patients, whereas 96.5% of PCL injuries occurred in combination with other ligament injuries [9]. 

Classification

The appropriate treatment of PCL injuries remains uncertain. This is partly due to inaccurate classification of patients in follow-up studies. PCL injuries can be classified according to the structures damaged (isolated vs combined), the degree of instability, and the mechanism of injury [7]. 

• Type I- Where the PCL is stretched, laxity is less than 5mm and the tibial plateau is 5mm to 10mm anterior to the femoral condyle.
• Type II- Where the PCL is torn, MF ligaments intact, laxity is 5mm to 9mm and the tibial plateau is 0 to 5mm anterior to the femoral condyle.
• Type III-Where the PCL and MF ligaments are torn, laxity is > 10mm and tibial plateau is flush with the femoral condyle.
• Type IVA- Where there is PCL, LCL, and posterolateral injury, laxity is >12 mm and the tibial plateau is > 2mm posterior to the femoral condyle.
• Type IVB-  Where there is PCL, MCL, and posteromedial injury, laxity is >12 mm and the tibial plateau is > 2mm posterior to the femoral condyle.
• Type IVC- Where there is PCL and ACL injury, laxity is >15mm and the tibial plateau is > 5mm posterior to femoral condyle.

Grades I to III are isolated injuries and grade IV is a combined injury.

Clinical Evaluation

History

A thorough history including the mechanism of injury is useful. The chief complaint and level of activity need to be determined. Patients with acute isolated PCL tear will complain of mild swelling, pain and inability to bear weight. Patients with chronic PCL laxity complain of pain. The pain is most prevalent with long distance walking and descending stairs. The pain is predominantly felt in the retropatellar area and medial compartment of the knee. Other complaints include difficulty walking with the knee extended in mid stance. They also can have apprehension while descending stairs because they get a sense of unsteadiness or sliding of the joint when going downstairs. Athletes often complain of a decreased ability to rapidly change direction [7]. However, significant giving way of the knee or buckling that is commonly seen with an ACL deficient knee is usually not seen with an isolated PCL tears. Instability is common in patients with combined injury.

Physical examination

A physical examination for a posterior cruciate deficient knee following an acute injury must include inspection over the anterior tibia for abrasions, ecchymosis or lacerations, range of motion, gait assessment, and a neurovascular examination. 

Testing for an acute posterior cruciate ligament injury is usually difficult because of a tense hemarthrosis and pain. The most accurate test for determining a posterior cruciate rupture is the posterior drawer test at 90° of knee flexion. Following an acute injury, it is often difficult to achieve 90 degrees of knee flexion because of pain. Staubli and Jakob [11]described significant posterior translation of the tibia at 10 to 15° of flexion. The posterior tibial sag and Lachman test and reverse pivot shift tests can be useful.

Injuries to other ligamentous structures must be excluded. Examination of the ACL, collateral ligaments, and posterolateral corner must be carried out.

Slightly increased posterior translation at 30° but not 90° indicates a posterolateral injury. An isolated PLC injury increases external rotation at all angles of flexion, but this is maximal at 30°. Neurovascular examination must be carried out to exclude peroneal nerve and vascular injury.

Ancillary Tests

Radiographs are taken to rule out an avulsion fracture of the PCL at its tibial insertion. Fibular head fractures are indicative of a PLC injury. Magnetic resonance imaging (MRI) has been shown to be highly accurate in the diagnosis of a complete PCL tear. Associated collateral ligament, meniscal and chondral injuries can also be diagnosed with an MRI. A good history and physical examination is very accurate in diagnosing a PCL injury, and hence an MRI is not routinely required. 

Treatment of isolated PCL injuries

There is no controversy about the treatment of PCL avulsion fractures, which are ideally treated by open reduction and internal fixation when the fragment is large enough to be fixed with a screw. Isolated injuries of the PCL usually produce a grade I to II posterior laxity of the knee while a grade III laxity is produced by a combined PCL and posterolateral corner injuries. What is the best method of treatment of isolated PCL injuries?

An acute midsubstance tear of the PCL may heal [12] unlike ACL mid-substance injuries which do not heal. Logically such injuries should be treated conservatively. The long-term natural history of isolated PCL injuries suggests that there is no indication for surgical treatment of such injuries because the outcome of conservative treatment is good. There are no studies to show that surgical treatment is better than conservative treatment for isolated tears of the PCL. Neither is there any evidence that surgical treatment reduces the incidence of osteoarthritis of the knee after PCL injuries [13]. 

Natural history of isolated PCL injuries

One of the earlier studies of the long-term outcome of non-operatively treated isolated PCL injuries was done by Parolie and Bergfeld in 1986 [14]. They studied 25 patients who were treated conservatively for isolated PCL injuries and followed up for a mean of 6.2 years (2.2 to 16 years). They found that 80% of the patients were satisfied with their knee and 84% had returned to their previous sport, with 68% at the same level of performance and 16% at a reduced level of performance. Patients who were satisfied with their knee and had returned to sports had quadriceps strength of more than 100% of the contralateral uninvolved knee and those who were dissatisfied with their knee and not returned to sports had less than 100% strength of the quadriceps as compared to the contralateral knee. 

Selbourne et al [15] prospectively studied the natural history of acute, isolated, nonoperatively treated PCL injuries in athletically active patients. The study included 133 patients all of whom completed a yearly questionnaire for an average of 5.4 years (2.3 to 11.4 years) and 51% of the patients (68 out of 133) returned for long-term clinical and radiological examination. The functional outcome was good with a mean modified Noyes knee score of 84.2 points, a mean Lysholm score of 83.4, and a mean Tegner activity score of 5.7. The grade of laxity had no correlation with subjective functional outcome. Fifty percent of the patients returned to the same sport at the same or higher level of performance, one-third (33.3%) returned to the same sport at a lower level and one-sixth (16.6%) did not return to the same sport.

The authors concluded that ‘athletically active patients with acute isolated posterior cruciate ligament tears treated nonoperatively achieved a level of objective and subjective knee function that was independent of the grade of laxity’.

The longest follow-up study of patients with acute, isolated PCL injuries treated non-operatively was reported by Shelbourne et al in 2013 [16]. The study included 68 patients who had a subjective follow-up at a mean of 17.6 years and 44 of the patients had a subjective and objective follow-up at a mean of 14.3 years (10-21 years). The mean quadriceps strength was 97% of the contralateral side and the range of knee motion was normal in all patients. 

Fifty percent of the patients had no osteoarthritis (OA) of the knee, 30% had mild OA, 9% (4 patients) had moderate and 2% (1 patient) had severe OA of the knee at a mean follow-up of 14.3 years. The mean IKDC (International Knee Documentation Committee) and modified CKRS (modified Cincinnati Knee Rating System) subjective scores were 73.4 ± 21.7 and 81.3 ± 17.4, respectively at 17 years follow-up and the subjective scores did not correlate with the degree of PCL laxity.

The authors concluded that long-term follow-up of patients, with isolated PCL injuries treated non-operatively, shows that patients remain active, have good muscle strength, full range of knee motion and they report good subjective scores, and that the incidence of post-traumatic OA is low.

In 2007 Patel et al [17] published a study involving 57 patients with acute isolated PCL injuries who were treated non-operatively with a mean follow-up of 6.9 years (2 to 19.3 years). Seventeen patients (29.8%) had a grade I and 41 patients (71.9%) had a grade II laxity of the PCL. The functional outcome at 7 years was good with a mean Lysholm-II knee score of 85.2 points (range 51 to 100 points) and a mean Tegner activity level of 6.6 (range 3 to 10). The Lysholm-II knee scoring system showed excellent results in 40%, good in 52%, fair in 3%, and poor in 5% of the knees. The incidence of mild medial compartment OA was 12% and moderate medial compartment OA 5% and none of the patients had severe OA.

These medium and long-term studies of the natural history of isolated PCL injuries reveal that the subjective functional outcome is good, without surgical intervention, with the majority of the patients returning to their pre-injury activity level. Are the results of PCL reconstruction better than conservative treatment?

Surgical treatment of isolated PCL injuries

Most of the published studies reporting the outcome of PCL reconstruction for isolated PCL injuries are small case series with a short follow-up, and the heterogeneity of the patients studied and the technique used makes it difficult to judge outcomes in these patients [18].

However, there are two studies that have reported the long-term outcome of PCL reconstruction in patients with isolated PCL injuries. 

Herman et al [19] studied 25 patients (22 male, 3 female) with an average age of 30.8 years who underwent single-bundle PCL reconstruction for pain and functional instability of the knee. The mean follow-up was 9.1 years (6.5 to 12.6 years). Twenty-two patients were evaluated clinically and 3 patients were provided telephone interviews.

The final mean IKDC score was 65, Lysholm score was 75 and the VAS (visual analog score) was 8. The functional scores were fair to good and were significantly better than the pre-operatively scores. The final Tegner score was 5.7. The functional results were significantly better in patients with no cartilage damage at the time of surgery and in those who underwent surgery within 1-year post-injury.

Jackson et al [20] evaluated the long-term outcome of PCL reconstruction in 26 patients after failed conservative treatment. At 10 years follow-up, the IKDC score was 87 and the Lysholm score improved from 60 to 90 postoperatively. Twenty-two patients had a radiological examination and 18% of the patients had grade II OA changes and another 18% had grade III OA changes.

A careful analysis of the subjective outcome reported by Shelbourne [12] and Patel [17] for non-operative treatment and that by Herman [19] and Jackson [20] for surgical treatment of PCL injuries appears to be very similar. 

Complications of PCL surgery

PCL injuries are rare and the indications for surgery of the PCL are limited since conservative treatment has a good outcome, therefore the number of PCL surgeries carried out by surgeons per year are small. This limited experience with such complex surgery can lead to a higher incidence of complications especially when there are vital neurovascular structures at the back of the knee. Furthermore catastrophic complications usually never get reported which can give surgeons a false sense of relative risks involved when undertaking such procedures. 

Besides the standard complications, such as those associated with anesthesia and complication of surgery such as infections and thromboembolic complications which can occur with any orthopedic procedure, there are specific complications associated with PCL surgery, some of which includes neurovascular injury, osteonecrosis, fractures, stiffness, residual laxity and anterior knee pain. 

A survey of the frequency of complications associated with arthroscopic surgical procedures of the knee reported by Salzler et al [21], where the data was obtained from the ABOS (American Board of Orthopaedic Surgery) database, showed that the complication rate was the highest for PCL surgery as compared with other arthroscopic procedures. The complication rate for PCL surgery was 20.1%, ACL surgery 9.7%, meniscal repair 7.7%, meniscectomy 2.8%, and chondroplasty 3.5%. The overall pulmonary embolism rate was 0.11% and the infection rate 0.84%. These were self-reported complication rates and the authors believe that the actual rates may be higher.

Conclusion

Posterior cruciate injuries can be caused by a variety of different mechanisms. The usual cause is trauma and sports. It is important to differentiate isolated PCL injuries from combined ligament injuries. The diagnosis can be established by a good history and good clinical examination. If the diagnosis is uncertain an MRI will be useful. It is critical to rule out neurovascular injuries in patients who have combined injuries.

Most patients with isolated PCL injuries can be treated conservatively. The mainstay of treatment is quadriceps strengthening with avoidance of active hamstring exercises. 

Medium and long-term studies of the natural history of isolated PCL injuries reveal that the subjective functional outcome is good, without surgical intervention, with the majority of the patients returning to their pre-injury activity level.

The incidence of posttraumatic OA is low after PCL injuries. The incidence of mild medial compartment OA is 12% and moderate medial compartment OA 5% and none of the patients usually develop severe OA.

A careful analysis of the subjective outcome of non-operative treatment and  surgical treatment of PCL injuries appears to be very similar. 

The complication rate following  PCL surgery is the highest as compared with other arthroscopic procedures. The reported complication rate for PCL surgery is about 20% but in actual fact may be higher.

 

 References

1. Girgis FG, Marshall JL, Monajem A. The cruciate ligaments of the knee joint. Anatomical, functional and experimental analysis. Clin Orthop Relat Res. 1975 Jan-Feb;(106):216-31. doi: 10.1097/00003086-197501000-00033. PMID: 1126079.
2. Gupte CM, Bull AMJ, Thomas RD, Amis AA. The meniscofemoral ligaments: secondary restraints to the posterior drawer. Analysis of anteroposterior and rotary laxity in the intact and posterior-cruciate-deficient knee. J Bone Joint Surg [Br] 2003;85-B:765-773.
3. Castle Jr TH, Noyes FR, Grood ES. Posterior tibial subluxation of the posterior cruciate-deficient knee. Clin Orthop 1992; 284: 193-202.
4. Veltri DM, Deng XH. Torzilli PA, et al. The role of the cruciate and posterolateral ligaments in stability of the knee: a biomechanical study. Am J Sports Med 1995; 23: 436-43.
5. Noyes FR, Stowers SF, Grood ES, et al. Posterior subluxations of the medial and lateral tibiofemoral compartments: an in vitro ligament sectioning study in cadaveric knees. Am J Sports Med 1993; 21: 407-14.
6. Harner CD, Vogrin TM, Höher J, Injury to the posterolateral structures has profound effects on the function of the human posterior cruciate ligament [abstract]. Trans Orthop Res Soc 1998; 44: 47.
7. Janousek et al. Posterior Cruciate Ligament Injuries of the Knee Joint. Sports Medicine 2000, 28(6):429-41.
8. Miyasaka KC, Daniel DM. The incidence of knee ligament injuries in the general population [abstract], Am J Knee Surg 1991; 4: 3-8.
9. Fanelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: II. Arthroscopy 1995; 11 (5): 526-9.
10. Becker EH, Watson JD, Dreese JC. Investigation of multiligamentous knee injury patterns with associated injuries presenting at a level I trauma center. J Orthop Trauma 2013;27:226-231.
11. H-U. STAUBLI, R. P. JAKOB. Posterior instability of the knee near extension. A clinical and stress radiographic analysis of acute injuries of the posterior cruciate ligament. The Bone & Joint Journal. 1990, 72(2):225-30.
12. Shelbourne KD, Jennings RW, Vahey TN. Magnetic resonance imaging of posterior cruciate ligament injuries: assessment of healing. Am J Knee Surg 1999; 12:209-13.
13. Dowd GSE. Reconstruction of the posterior cruciate ligament: Indications and results. J Bone Joint Surg [Br] 2004; 86-B: 480-91.
14. Parolie JM, Bergfeld JA: Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 1986; 14:35-38.
15. Shelbourne KD, Davis TJ, Patel DV. The natural history of acute, isolated, nonoperatively treated posterior cruciate ligament injuries. A prospective study. Am J Sports Med. 1999 May-Jun; 27(3):276-83.
16. Shelbourne KD, Clark M, and Gray T. Minimum 10-Year Follow-up of Patients after an Acute, Isolated Posterior Cruciate Ligament Injury Treated Nonoperatively. Am J Sports Med July 2013 vol. 41 no. 7 1526-1533.
17. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The Nonoperative Treatment of Acute, Isolated (Partial or Complete) Posterior Cruciate Ligament-Deficient Knees: An Intermediate-term Follow-up Study. HSS J. 2007 Sep; 3(2): 137–146.
18. Montgomery SR, Johnson JS, McAllister DR, Petrigliano FA. Surgical management of PCL injuries: indications, techniques, and outcomes. Curr Rev Musculoskelet Med. 2013 Jun; 6(2): 115–123.
19. Hermans S, Corten K, Bellemans J. Long-term results of isolated anterolateral bundle reconstructions of the posterior cruciate ligament: a 6- to 12-year follow-up study. Am J Sports Med. Aug 2009; 37(8):1499-507.
20. Jackson WF, van der Tempel WM, Salmon LJ, Williams HA, Pinczewski LA. Endoscopically-assisted single-bundle posterior cruciate ligament reconstruction: results at minimum ten-year follow-up. J Bone Joint Surg Br. 2008 Oct; 90(10):1328-33. 
21. Salzler MJ, Miller CD, Lin A, Irrgang JJ, Harner CD. Complications Following Arthroscopic Knee Surgery. Orthopaedic Journal of Sports Medicine, September 2013 vol. 1 no. 4 suppl 2325967113S00044.