Metastatic Disease of Extremity

                                    Dr. KS Dhillon

INTRODUCTION

Bone is the third most frequent site of metastatic disease. Primary tumors from the lung, breast, prostate, kidney, and thyroid are the most common cause of bone metastases (1). The primary presentation is pain and pathological fracture in 9%–29% of the cases. About 90% of pathological fractures require intervention (2,3). The orthopedic treatment of these bone metastasis significantly impacts both quality of life and probably survival rates (4).

Extremity bone metastases accounts for 66% of skeletal metastasis. Extremity metastases are one of the first presentations of disease in lung cancer, myeloma, renal cancer, and lymphoma (5). The median survival from diagnosis is 6 months in melanoma, 6–7 months in the lung, 6–9 months in the bladder, 12 months in the renal, 12–53 months in the prostate, 19–25 months in the breast, and 48 months in the thyroid carcinoma. The treatment involves a multidisciplinary team which includes an orthopedic surgeon, radiologist, orthopedic oncologist, radiation oncologist, medical oncologist, and other health-care personnel. The treatment varies on the specific site of involvement. 

MECHANISMS OF METASTASIS TO BONE

Bone metastasis commonly involves the axial skeleton and they present at multiple sites (3). This could be related to the hematopoietically active red bone marrow and the paravertebral network that may play a role in metastasis (5). Apart from the favorable microenvironment for tumor cell survival, the following are needed once the tumor cells are in circulation (3-7).

• Extravasation and adhesion to vascular tissues

• Microenvironmental support: As per the seed-and-soil hypothesis, for the growth and survival of cancer cells, the fertile ground is provided by the microenvironment

• Epithelial-mesenchymal transition: When the normal epithelial cells lose their epithelial features and transform into mesenchymal cells, they can migrate into new environments. This process of epithelial-mesenchymal transition occurs during embryogenesis. When the cancer cells undergo this transition, they transform into an invasive phenotype.

PRESENTATION AND EVALUATION

A complete workup must precede surgery when there is a pathological fracture (8). It can be the first sign of an unknown primary or it can be seen in cases with an established primary diagnosis. In cases where there is an established primary, the diagnosis of a second primary bone tumor as a differential diagnosis should be considered. Clinical features of multiplicity and typical axial presentation point toward bone metastases. A biopsy should be done to confirm the diagnosis before planning any intervention.

A painful solitary bone lesion without a history of metastatic disease or a primary malignancy needs a more extensive metastatic workup which includes laboratory investigations and imaging before the biopsy. Some of the commonly used laboratory investigations include β2- microglobulin, urine for Bence–Jones proteins and serum electrophoresis for multiple myeloma, CA-125 for ovarian cancer, prostate-specific antigen (PSA) for prostate cancer, CA-19.9 for pancreatic and biliary tumors, CA-15.3/CA-27.29 for breast cancer, carcinoembryonic antigen for colorectal and breast cancer, and calcitonin for medullary thyroid cancer. 

Imaging includes X-rays, bone scan, computerized tomography scan (CT), magnetic resonance imaging (MRI), and fluoride/fluorodeoxyglucose-positron emission tomography (PET) scan. Imaging may reveal an easier to access biopsy site or show the tract for a percutaneous biopsy (9). The possibility of bone sarcomas should be kept in mind in cases with a history of prior radiation exposure such as Paget's disease and fibrous dysplasia. The survival and final management depends on the primary tumor.

SURVIVAL PREDICTION

Irrespective of the primary tumor, the presence of skeletal metastases, visceral metastases, and multiplicity is associated with poor prognosis (10-12). The prognosis in patients with metastatic bone disease depends on several factors. For metastasis arising from breast cancer, the extraosseous disease, estrogen receptor status, age, disease-free interval, performance status, and histologic grade play a role in prognosis. In skeletal metastatic prostate cancer, the performance status, extraosseous disease, fall in alkaline phosphatase, and PSA levels are well-approved prognostic factors (13).

In multiple myelomas, β2- microglobulin and C-reactive protein are the main independent prognostic factors. The median survival is 6 months for those with high levels and 54 months for those with low levels (14).

Using predictive models like the Bayesian Belief Network (15), a patient's survival can be predicted which helps in deciding the final treatment plan. The clinical data can be used to calculate survival at 3 and 12 months. For patients with survival of less than 3 months, surgical treatment is not recommended. Those with 3–12 months of survival may require less invasive procedures without long rehabilitation. For those with more than 12 months of survival, a more durable reconstruction method is recommended (16).

Bauer reported that the overall survival of those who underwent fixation for pathological fracture was less than 6 months and was similar to those who received radiotherapy (RT) for bone pain (8,17). The incidence of solitary metastases is lower compared with those with multiple metastases. Solitary metastases have a better prognosis than those with multiple metastases (18,19).

The incidence and median survival of various primary malignancies with skeletal metastasis is as follows:

	Incidence advanced disease (%)	Median survival (months)	5 years survival (%)
Myeloma	95-100	20	10
Breast	65-75	24	20
Prostate	65-75	40	25
Lung	30-40	6	5
Kidney	20-25	6	10
Thyroid	60	48	40
Melanoma	14-45	6	5

Mechanical strength prediction

Prediction of mechanical strength and the risk of pathological fracture are considered to be important variables for decision-making when treating bone metastases. Mirel's scoring system is the most commonly used system to predict the risk of pathological fracture (20). The risk of a pathological fracture was 33% for a patient with a score of 9, 15% for a patient with a score of 8, and 4% for a patient with a score of seven. Excessive pain is one of the most significant indicators of an impending pathological fracture. Sometimes plain radiography alone is not diagnostic or a predictor of impending fracture. There is significant pathological fracture risk when more than 50% of trabecular bone is destroyed as seen on X-rays. Lesser trochanter avulsion indicates an impending hip fracture (21). CT rigidity analysis (CTRA) is a new method of predicting the pathological fracture probability. The density of the bone and the cross-sectional area at the maximal weakness point are recorded to estimate bending, torsion, and axial rigidity. Then the data are compared with a gender and size-matched normal femur CT. Reduction in axial, bending, or torsional rigidities of more than 35% are considered a significant risk for fracture (22).

MANAGEMENT

Skeletal metastases are rarely an emergency. The aim of treatment would be to get the patient back to their previous activity level. The following are the treatment strategies available:

• Medical management

• Radiotherapy (RT)

• Surgery.

Medical management

The most common debilitating symptom of malignancy is pain. It has a significant impact on daily activity and social life. Pain can be due to osteoclast activation, nerve compression, substances produced by tumor cells, and inflammatory reactions due to tumor growth and invasion into surrounding tissues. Pain management includes the use of opioids, bisphosphonates, nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, RT, and surgical management (23).

With metastasis, osteoclast activation has an essential role in the destruction of bone. Receptor-activated nuclear factor kappa-B ligand (RANKL) attracts tumor cells into the bone. It produces more RANKL (24). This increase in osteoclasts leads to accelerated bone destruction. Bisphosphonate therapy is commonly used to reduce morbidity among patients with skeletal metastases. They benefit the patient by only 30%–40%. They can produce complications such as osteonecrosis of the jaw. Intravenous administration may be required (25).

Denosumab is a monoclonal antibody against RANKL. It has shown improved efficacy in blocking osteoclast formation and osteoclast-mediated bone destruction (26). It is administered subcutaneously and is not excreted through the kidney. This is an advantage for patients with chronic kidney disease. It was reported that Denosumab was superior to zolendronic acid in relation to reduction of the skeletal-related events. The quality of life, pain, and overall survival are similar for both the drugs. Bisphosphonates have an additional antitumor action which may add to survival, especially in patients with breast cancer (26).

Radiotherapy (RT)

RT is often used for pain relief in bone metastases. There are reports of complete pain relief in one-third of the patients. More than 50% of the patients have pain relief beyond 6 months (27). Short-course regimen with 8 Gray (Gy) as a single fraction dose is as effective as the long-course RT regimens. Jeremic et al (28) compared short-course RT regimens (4 Gy vs. 6 Gy vs. 8 Gy) and found that 8 Gy is the “lowest” optimal single fraction.

Hartsell et al (29) compared the 8 Gy in a single fraction with 30 Gy in 10 fractions in 898 patients. They found that the results were comparable with regard to pain and narcotic relief. The risk of pathologic fracture was 4% in the 30-Gy group and 5% in the 8-Gy group. The 8-Gy group had a retreatment rate that was higher than the 30-Gy group (18% vs. 9%, P < 0.001).

The protective role of RT from pathological fractures has not been properly defined. A comparison between the outcomes of the surgical fixation of pathological fractures with or without RT has been done. It was concluded that postoperative RT is the only significant predictor for a successful outcome (30).

RT is started within 2 weeks following surgery and it covers the entire operative field and the whole length of the implant (31). The role of RT is limited in cases with endoprosthesis. One study reported poor bone remodeling distal to the prosthesis and less new bone formation around the prosthesis (32).

Surgical management

Surgical treatment can include intralesional curettage, marginal excision, or wide excision, depending on the aim of the intervention. Preoperative embolization can be carried out while dealing with vascular tumors such as skeletal metastases from renal cell carcinoma or to facilitate en bloc excision. Solitary lesions are treated with curative intent with added emphasis on pain control and functional recovery.

When reconstruction is done the general rule is to protect the whole length of the bone to avoid failure in cases of recurrence. Nailing, plating, or endoprosthesis can be used. There are maximal benefits in metastatic fixations when locked compression plates are fixed using minimally invasive techniques. Locked plates reduce the risk of pullout or loosening. There is reduced postoperative morbidity due to the minimally invasive approach (33).

Instead of allografts and biological cement types, bone cement is used for augmentation of the fixation since the lesion is not expected to heal. Bone cement allows early weight bearing (34). It also improves postoperative pain and function (35).

Intramedullary nailing can be done for lesions involving the diaphysis. Titanium nails have improved mechanical strength and smaller diameter. Repair or reconstruction of the capsule and reattachment of surrounding soft tissue to the implant should be done so that there is good functional strength, range of movement, and joint stability. Fifteen to twenty percent of the patients treated with surgery will have disease progression and loss of fixation, hence postoperative radiation is recommended (30).

Pelvis

The pelvis was classified into three distinct zones by Enneking (36). Zone 1 and 3 are nonweight bearing and the bone is expendable. Lesions involving Zone 2 alone or in combination with adjacent bones require curettage with cementing or reconstruction with custom-made prosthesis, or total hip replacements (37). In lesions requiring resection of Zone 2 and 3, an inverted ice cream cone prosthesis or pedestal cup is used (38).

Lower limb

The proximal femur is the most common site for bone metastases. It involves a significant risk of mechanical failure, hampering the quality of life. For lesions involving the neck and head of the femur, the choice of treatment is typically a bipolar hemiarthroplasty with a long stem. For lesions involving the acetabulum or trochanteric and peri trochanteric regions, endoprosthesis provides the best results. This allows early weight bearing and return to function with a lower failure rate (38,39).

For tibial and femoral diaphyseal lesions, curettage and cementing with nailing can be carried out. To avoid failure due to recurrence in the femoral neck, reconstruction nails that span the entire length of the bone can be used (9). In lesions involving the proximal tibia and distal femur, composite total knee replacement can be done. For lesions involving the proximal tibia, the management principles are essentially similar to the femur. It depends on the size of the lesion varying from curettage to resection and megaprosthesis (40).

Upper limb

After the proximal femur, the humerus is the second most common site of long bone metastases. Mechanical stress on the humerus is far less than that on the lower limb. That is why humeral bone metastases can be managed nonoperatively by external beam irradiation (30). Proximal humerus hemiarthroplasty can be used in patients with lesions involving the neck or proximal humeral head provided the greater tuberosity, lesser tuberosity, and axillary nerve are intact. In large lesions involving the proximal half of the humerus proximal humerus endoprosthesis or nail cement spacer with meshplasty can be done. Soft-tissue repair to prevent subluxation of the humeral head (41). For lesions that extend 2–3 cm distal to the greater tuberosity and 5 cm proximal to the olecranon fossa, intramedullary nailing can be done. Distal humeral metastases can be managed with plating and cement augmentation. If the lesions are large and involve the elbow joint, total elbow replacement can be done. Segmental defects of long bones can be treated with a nail cement spacer. Irrespective of the treatment method more than 90% of patients with humeral metastases have pain relief and functional restoration for activities of daily living. They have restricted range of movements of the shoulder with normal functioning of the elbow and wrist joints (42). Scapular lesions can be treated by a total or partial scapulectomy, depending on the extent of involvement. The forearm is an uncommon site for metastasis which may require resection of the bone.

Minimal invasive modalities

Radiofrequency ablation, cryoablation, high-intensity focused ultrasound, and microwave therapy are percutaneous modalities that can be used to relieve pain and improve bone strength without additional risk of morbidity from open surgery (43,44). For lesions involving the pelvis cementoplasty plays a vital role. They help prevent fractures and provide significant pain relief and functional improvement in 80% of cases (45). Angioembolization can produce devascularization and tumor necrosis (46). Embolization along with antimitotic agents such as adriamycin and platinum, prolongs the analgesia and can produce partial-to-complete tumoral remission (47).

CONCLUSION

Adequate work-up and a biopsy are required to confirm the diagnosis of extremity metastasis. The management involves a multidisciplinary approach. It depends on the primary tumour as well as the expected survival. The aim of treatment ranges from pain relief by medical management or radiotherapy and curative intent in patients with solitary metastases. The final aim is to improve the patient's quality of life.

References

1. Macedo F, Ladeira K, Pinho F, Saraiva N, Bonito N, Pinto L, et al. Bone metastases: An overview. Oncol Rev. 2017;11:321.

2. Harrington KD. Orthopaedic management of extremity and pelvic lesions. Clin Orthop Relat Res. 1995;312:136–47. 

3. Cecchini M, Wetterwald A, Pluijm G, Thalmann G. Molecular and biological mechanisms of bone metastasis. EAU Update Ser. 2005;3:214–26.

4. Aaron AD. Current concepts review-treatment of metastatic adenocarcinoma of the pelvis and the extremities. J Bone Joint Surg. 1997;79:917–32.

5. Berrettoni BA, Carter JR. Mechanisms of cancer metastasis to bone. J Bone Joint Surg Am. 1986;68:308–12. 

6. Jones DH, Nakashima T, Sanchez OH, Kozieradzki I, Komarova SV, Sarosi I, et al. Regulation of cancer cell migration and bone metastasis by RANKL. Nature. 2006;440:692–6.

7. Langley RR, Fidler IJ. Tumor cell-organ microenvironment interactions in the pathogenesis of cancer metastasis. Endocr Rev. 2007;28:297–321. 

8. Bauer HC. Controversies in the surgical management of skeletal metastases. J Bone Joint Surg Br. 2005;87:608–17. 

9. Ogilvie CM, Fox EJ, Lackman RD. Current surgical management of bone metastases in the extremities and pelvis. Semin Oncol. 2008;35:118–28. 

10. Dijstra S, Wiggers T, van Geel BN, Boxma H. Impending and actual pathological fractures in patients with bone metastases of the long bones. A retrospective study of 233 surgically treated fractures. Eur J Surg. 1994;160:535–42. 

11. Sarahrudi K, Greitbauer M, Platzer P, Hausmann JT, Heinz T, Vécsei V. Surgical treatment of metastatic fractures of the femur: A retrospective analysis of 142 patients. J Trauma. 2009;66:1158–63. 

12. Hansen BH, Keller J, Laitinen M, Berg P, Skjeldal S, Trovik C, et al. The scandinavian sarcoma group skeletal metastasis register. Survival after surgery for bone metastases in the pelvis and extremities. Acta Orthop Scand Suppl. 2004;75:11–5.

13. Robson M, Dawson N. How is androgen-dependent metastatic prostate cancer best treated? Hematol Oncol Clin North Am. 1996;10:727–47. 

14. Bataille R, Boccadoro M, Klein B, Durie B, Pileri A. C-reactive protein and beta-2 microglobulin produce a simple and powerful myeloma staging system. Blood. 1992;80:733–7. 

15. Forsberg JA, Eberhardt J, Boland PJ, Wedin R, Healey JH. Estimating survival in patients with operable skeletal metastases: An application of a Bayesian belief network. PLoS One. 2011;6:e19956. 

16. Forsberg JA, Sjoberg D, Chen QR, Vickers A, Healey JH. Treating metastatic disease: Which survival model is best suited for the clinic? Clin Orthop Relat Res. 2013;471:843–50.

17. Bauer HC, Wedin R. Survival after surgery for spinal and extremity metastases. Prognostication in 241 patients. Acta Orthop Scand. 1995;66:143–6. 

18. Koizumi M, Yoshimoto M, Kasumi F, Ogata E. Comparison between solitary and multiple skeletal metastatic lesions of breast cancer patients. Ann Oncol. 2003;14:1234–40. 

19. Kobayashi T, Ichiba T, Sakuyama T, Arakawa Y, Nagasaki E, Aiba K, et al. Possible clinical cure of metastatic breast cancer: Lessons from our 30-year experience with oligometastatic breast cancer patients and literature review. Breast Cancer. 2012;19:218–37.

20. Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res. 1989;249:256–64.

21. Phillips CD, Pope TL, Jr, Jones JE, Keats TE, MacMillan RH., 3rd Nontraumatic avulsion of the lesser trochanter: A pathognomonic sign of metastatic disease? Skeletal Radiol. 1988;17:106–10. 

22. Damron TA, Nazarian A, Entezari V, Brown C, Grant W, Calderon N, et al. CT-based structural rigidity analysis is more accurate than mirels scoring for fracture prediction in metastatic femoral lesions. Clin Orthop Relat Res. 2016;474:643–51. 

23. Ahmad I, Ahmed MM, Ahsraf MF, Naeem A, Tasleem A, Ahmed M, et al. Pain management in metastatic bone disease: A literature review. Cureus. 2018;10:e3286. 

24. Silva I, Branco JC. Rank/Rankl/opg: Literature review. Acta Reumatol Port. 2011;36:209–18. 

25. Mauri D, Valachis A, Polyzos IP, Polyzos NP, Kamposioras K, Pesce LL. Osteonecrosis of the jaw and use of bisphosphonates in adjuvant breast cancer treatment: A meta-analysis. Breast Cancer Res Treat. 2009;116:433–9. 

26. 26. Kohno N. The treatment for cancer with bone metastases -whether to use zoledoronate or denosumab for bone metastases. Clin Calcium. 2014;24:1229–36.

27. Chow E, Harris K, Fan G, Tsao M, Sze WM. Palliative radiotherapy trials for bone metastases: A systematic review. J Clin Oncol. 2007;25:1423–36. 

28. 28. Jeremic B, Shibamoto Y, Acimovic L, Milicic B, Milisavljevic S, Nikolic N, et al. A randomized trial of three single-dose radiation therapy regimens in the treatment of metastatic bone pain. Int J Radiat Oncol Biol Phys. 1998;42:161–7.

29. Hartsell WF, Scott CB, Bruner DW, Scarantino CW, Ivker RA, Roach M, 3rd, et al. Randomized trial of short- versus long-course radiotherapy for palliation of painful bone metastases. J Natl Cancer Inst. 2005;97:798–804. 

30. Townsend PW, Rosenthal HG, Smalley SR, Cozad SC, Hassanein RE. Impact of postoperative radiation therapy and other perioperative factors on outcome after orthopedic stabilization of impending or pathologic fractures due to metastatic disease. J Clin Oncol. 1994;12:2345–50. 

31. Frassica DA. General principles of external beam radiation therapy for skeletal metastases. Clin Orthop Relat Res. 2003;415(Suppl):S158–64. 

32. Haentjens P, De Neve W, Opdecam P. Prosthesis for the treatment of metastatic bone disease of the hip: Effects of radiotherapy. Bull Cancer. 1995;82:961–70.

33. Gregory JJ, Ockendon M, Cribb GL, Cool PW, Williams DH. The outcome of locking plate fixation for the treatment of periarticular metastases. Acta Orthop Belg. 2011;77:362–70. 

34. Yazawa Y, Frassica FJ, Chao EY, Pritchard DJ, Sim FH, Shives TC. Metastatic bone disease. A study of the surgical treatment of 166 pathologic humeral and femoral fractures. Clin Orthop Relat Res. 1990;251:213–9. 

35. Weiss KR, Bhumbra R, Biau DJ, Griffin AM, Deheshi B, Wunder JS, et al. Fixation of pathological humeral fractures by the cemented plate technique. J Bone Joint Surg Br. 2011;93:1093–7.

36. Enneking WF, Dunham WK. Resection and reconstruction for primary neoplasms involving the innominate bone. J Bone Joint Surg Am. 1978;60:731–46. 

37. Harrington KD. The management of acetabular insufficiency secondary to metastatic malignant disease. J Bone Joint Surg Am. 1981;63:653–64. 

38. Müller DA, Capanna R. The surgical treatment of pelvic bone metastases. Adv Orthop. 2015;2015:525363. 

39. Ratasvuori M, Wedin R, Keller J, Nottrott M, Zaikova O, Bergh P, et al. Insight opinion to surgically treated metastatic bone disease: Scandinavian sarcoma group skeletal metastasis registry report of 1195 operated skeletal metastasis. Surg Oncol. 2013;22:132–8.

40. Agarwal MG, Nayak P. Management of skeletal metastases: An orthopaedic surgeon's guide. Indian J Orthop. 2015;49:83–100. 

41. Sim FH, Frassica FJ, Chao EY. Orthopaedic management using new devices and prostheses. Clin Orthop Relat Res. 1995;312:160–72.

42. Frassica FJ, Frassica DA. Evaluation and treatment of metastases to the humerus. Clin Orthop Relat Res. 2003;415(Suppl):S212–8.

43. Dupuy DE, Liu D, Hartfeil D, Hanna L, Blume JD, Ahrar K, et al. Percutaneous radiofrequency ablation of painful osseous metastases: A multicenter American College of Radiology imaging network trial. Cancer. 2010;116:989–97. 

44. Hoffmann RT, Jakobs TF, Trumm C, Weber C, Helmberger TK, Reiser MF. Radiofrequency ablation in combination with osteoplasty in the treatment of painful metastatic bone disease. J Vasc Interv Radiol. 2008;19:419–25. 

45. Moser TP, Onate M, Achour K, Freire V. Cementoplasty of pelvic bone metastases: Systematic assessment of lesion filling and other factors that could affect the clinical outcomes. Skeletal Radiol. 2003;415(Suppl):S212–8. 

46. Moser T, Buy X, Goyault G, Tok C, Irani F, Gangi A. Image-guided ablation of bone tumors: Review of current techniques. J Radiol. 2008;89:461–71. 

47. Layalle I, Flandroy P, Trotteur G, Dondelinger RF. Arterial embolization of bone metastases: Is it worthwhile? J Belge Radiol. 1998;81:223–5.

 

   Knee Dislocation

                                   DR. KS Dhillon

Introduction

A dislocation of the knee can be defined as complete congruency loss between the proximal tibial and distal femoral articular surfaces. Bicruciate ligament injuries are also equivalent to knee dislocations with regard to the mechanism of injury, severity of ligamentous injury, and frequency of major arterial injuries (1). A knee dislocation is a potentially devastating injury. It is often a surgical emergency. A knee dislocation requires prompt identification, evaluation, and consultation with a surgeon for definitive treatment. Vascular injury and compartment syndrome are complications that should not be missed in the workup of a knee dislocation (2,3). This is unlike patellar dislocations, which generally do not require immediate surgical or vascular intervention (4,5).

Etiology

High-energy trauma is usually required to produce a knee dislocation. With disruption of the joint, multiple concomitant ligamentous injuries and instability can also be expected. Motor vehicle accidents, high-velocity sports-related injuries, and falls can all cause knee dislocation. Most often posterior and anterior dislocations occur. Medial rotatory, and lateral rotatory dislocations are also possible.

Epidemiology

Knee dislocations are infrequently seen. They are potentially limb-threatening injuries. Associated undiagnosed vascular injuries can lead to limb ischemia which will require amputation (6-8). Knee dislocations represent about 0.001% to 0.013% of all orthopaedic injuries (9-11). The incidence of knee dislocation is however underreported, since almost 50% of knee dislocations reduce spontaneously at the scene, before arrival at the hospital, or are misdiagnosed. The incidence of knee dislocations is higher in men than women, with a ratio of 4:1. Obesity is an independent risk factor for sustaining this injury from an ultra-low energy injury.

Pathophysiology

Anatomy

The knee is a ginglymoid joint with 3 articulations. These include the tibiofemoral, patellofemoral, and tibiofibular. Four major ligaments stabilize the knee joint. These include the posterior cruciate ligament (PCL), anterior cruciate ligament (ACL), medial collateral ligament (MCL), and lateral collateral ligament (LCL). Multiligamentous disruption can occur with a knee dislocation. The normal range of motion (ROM) of the knee is 0 to 140 degrees. There is 8 to 12 degrees of rotation during flexion and extension.

Mechanism of Injury

Knee dislocation can occur following high-energy injuries such as traffic accidents, falls from heights, dashboard injuries, and crush injuries. Low-energy injuries can also result in a knee dislocation such as those seen in athletic injuries. Even ultra-low-energy injuries can result in a knee dislocation in patients who have morbid obesity.

Associated Neurovascular Injuries

The popliteal artery is at the highest risk of injury due to knee dislocation. The popliteal artery stretches across the popliteal space. It gives off several branches in a collateral system around the knee. Upto 40% of patients with a tibiofemoral disruption will sustain an associated vascular injury. These injuries are due to tethering at the popliteal fossa, proximally by the fibrous tunnel at the adductor hiatus, and distally by the fibrous tunnel at the soleus muscle. There is collateral circulation around the knee that is formed by the geniculate arteries that can provide vascular flow and palpable pulses that mask a limb-threatening vascular injury (2). The peroneal nerve is located at the fibular neck. It is injured in more than 20% of patients with knee dislocation (2). 

Associated Bony and Soft Tissue Injuries

Sixty percent of the patients with knee dislocations have associated fractures. Multiple soft tissue injuries can also be associated with knee dislocation. These include patellar tendon rupture, periarticular avulsion, and displaced menisci.

History and Physical Examination

Spontaneously Reduced Cases

About 50% of knee dislocations spontaneously reduce before contact with a clinician. Obtaining a thorough problem-oriented history is paramount when evaluating knee dislocations. Inquiries into the mechanism of injury and position of the lower leg immediately after the injury are necessary. When the emergency management services or the patient reports a change in the position of the tibia relative to the femur, the doctor should assume a knee dislocation occurred with subsequent return to normal anatomical position. Subtle signs of trauma, such as abrasions, bruising, ecchymosis, and effusion should be looked for. Hyperextension of the knee to more than 30 degrees when lifting the heel is indicative of gross joint instability and it strongly suggests a knee dislocation.

Cases Presenting With Notable Deformity

When a patient presents with an obvious deformity consistent with knee dislocation the diagnosis is more straightforward.  A significant joint effusion, ecchymosis, and swelling may be present. Buttonholing of the medial femoral condyle through the medial capsule, known as a "dimple" or "pucker sign," may occur. It indicates an irreducible posterolateral dislocation (5). A closed reduction is contraindicated in such situations due to the risk of skin necrosis.

Physical Examination

A comprehensive physical examination of the affected extremity is required if the patient gives a history suggestive of knee dislocation. Special attention should be paid to the neurovascular stability of the extremity and ligamentous stability of the joint.

Popliteal and distal pulses should be assessed and compared with the contralateral side. A vascular injury should be excluded before and after reduction of the dislocation. Serial examinations are usually necessary. A palpable distal pulse does not exclude the presence of a vascular injury. Limb-threatening vascular ischemia can result in the presence of palpable distal foot pulses. This is because collateral circulation can mask a complete popliteal artery injury (12). 

In all patients suspected of knee dislocation, the ankle-brachial index (ABI) should be measured (13). The patient should be monitored with serial examinations when the ABI exceeds 0.9. If the ABI is less than 0.9 further investigation with an arterial duplex ultrasonography or computed tomography angiography is necessary. If arterial injury is confirmed vascular surgical consultation is imperative.

Patients who have diminished or absent pulses should undergo immediate joint reduction. Joint reduction should be followed by reassessment and if the pulses remain undetectable or diminished, surgical exploration should be carried out. Amputation rates of up to 86% have been reported with ischemia of greater than 6 hours. If the pulses return following joint reduction, ABI measurements should be taken. This should be followed by observation and serial examination or angiography.

With vascular injuries concomitant neurological deficits can occur. Sensory and motor function should be assessed and documented. The ligamentous integrity of the 4 major knee stabilizers should also be assessed.

Evaluation

Ankle-Brachial Index

The ankle-brachial index (ABI) is defined as the ratio of lower extremity perfusion via the posterior tibial and dorsalis pedis arteries and upper extremity perfusion via the brachial artery. An ABI of 0.9 or greater is considered normal. An ABI of less than 0.9 indicates a vascular compromise (13). Pulse and perfusion examinations can be conducted. Such examination has limited utility unless there are hard signs of vascular compromise. When there is vascular compromise prompt evaluation by a surgeon is necessary. Normal pulses or ABIs do not necessarily rule out any injury. There are reports of popliteal artery contusion, intimal layer disruption, and delayed thrombus formation in patients with distal perfusion after knee dislocation.

Duplex Ultrasonography

Duplex ultrasonography can evaluate the vascularity at the bedside. Imaging with computed tomography angiography is carried out in patients with decreased ABI, asymmetric pulses, or abnormal duplex ultrasonography. Vascular surgeon consultation is necessary for patients with absent or weak pulses, pale or cool extremities, paresthesias, or paralysis (14).  

Imaging Studies

Anterior-posterior (AP) and lateral knee radiographs can confirm the status of the joint and any concomitant fractures. A 45-degree oblique radiograph may be useful in patients with associated fractures. The radiographs can be normal in patients with spontaneously reduced knee dislocations. The following radiographic findings can be seen in knee dislocation:

• Joint space asymmetry or irregularity

• Associated avulsion fractures such as Segond sign or lateral tibial condyle avulsion fracture

• Osteochondral fractures

• Defects.

Computed tomography (CT) is needed when fractures are identified in postreduction radiographs. CT better delineates the fracture patterns and the level of extension, into the tibial tubercle, tibial eminence, or tibial plateau. Magnetic resonance imaging (MRI) may be needed to assess soft tissue structures. It is best performed after reduction of the dislocation and before placement of hardware to obtain better-quality images (15).

Management

Nonoperative Management

Dislocation of the knee is an orthopedic emergency that requires acute closed reduction followed by evaluation of the vascular status (1,16). Hospital admission for vascular observation is an option only for patients with clearly strong distal pulses, normal ABI, and normal duplex ultrasonography. In other patients, vascular surgery consultation and CT angiography are required to rule out popliteal artery injury. For closed reduction of an anterior dislocation, axial traction is applied and anterior translation of the femur is done. For a posterior dislocation, axial traction is applied, and anterior translation of the tibia is done. In patients with medial, lateral, or rotatory dislocations, the technique comprises axial traction and manipulation opposite to the deformity present. After close reduction, the knee is splinted with 20 to 30 degrees of flexion.

Operative Management

Immobilization can be the definitive treatment following a successful acute closed reduction in the absence of vascular injury. Nonoperative treatment as a definitive treatment produces inferior outcomes. Prolonged immobilization can be complicated by an unstable knee with limitation of movements (17). 

Open reduction

An open reduction is indicated in knee dislocations that are recalcitrant to closed reduction and in those that present late (18). An open reduction is also indicated in posterolateral dislocations and open fracture dislocations. Obesity can pose a challenge to the closed reduction of dislocated knees. In such situations, an open reduction could be an alternative option. Open reduction is also indicated in patients with associated vascular injury.

Open reduction is carried out via a midline incision with a medial parapatellar approach. If the medial femoral condyle has buttonholed through the medial capsule, the condyle has to be reduced and the medial capsule repaired. Associated soft tissue injuries, such as meniscal tears, patella tendon rupture, or periarticular ligament avulsions, may require an acute repair. Concomitant bony injuries are treated by internal fixation or external fixation followed by planned delayed definitive management. External fixation is also indicated in patients with vascular repair and in cases complicated by obesity. Other indications for external fixation include open fracture–dislocation, polytrauma, and compartment syndrome (19). 

Early ligament repair or reconstruction

Arthroscopic management is not an option for early ligament repair or reconstruction, especially in patients with large capsular injury because there is a risk of fluid extravasation and compartment syndrome. Open reconstruction is usually indicated for the posteromedial and posterolateral corners, including the collaterals since they are subcutaneous and close to neurovascular structures. Meniscal, cartilaginous, and capsular injuries, can also be addressed acutely. Unstable knees are managed with ligament repair or reconstruction. There are improved outcomes if surgery is done within 3 weeks of the injury (20). A knee immobilizer should be kept until definitive management of the ligamentous injuries. Acute and staged reconstructive procedures have similar outcomes.

Differential Diagnosis

The differential diagnosis for knee dislocation includes the following:

• Medial collateral ligament injury

• Meniscus injuries

• Patellar injury and dislocation

• Anterior cruciate ligament injury

• Femoral shaft fractures

• Knee fractures

• Patellofemoral joint syndromes

• Tibia and fibula fractures.

Staging

There are 2 commonly used classification systems for knee dislocation i.e. the Kennedy Classification, which relies mainly on the direction of tibia displacement, and the Schenck Classification, which considers concomitant knee ligament injuries.

Kennedy Classification

Anterior dislocation

This occurs due to a hyperextension injury. It is the most common knee dislocation pattern and accounts for 30% to 50% of dislocation injuries. Anterior dislocations have the highest rate of peroneal nerve injury. Usually, the PCL is also injured. When there is concomitant vascular injury, it is usually an arterial intimal tear from traction.

Posterior dislocation

This is the second most common knee dislocation pattern. It comprises 30% to 40% of knee dislocations. It is caused by axial loading to a flexed knee, as occurs in a dashboard injury. Posterior dislocation has the highest rate of vascular injury. It is most commonly characterized by a complete popliteal artery tear.

Lateral dislocation

The mechanism of injury in lateral knee dislocations is either varus or valgus force. There usually is concomitant PCL and ACL injury. Lateral dislocations occur in about 13% of knee dislocation injuries.

Medial dislocation

The mechanism of injury is the same as for lateral dislocation. It is caused by a varus or valgus force. Both the PLC and PCL are usually injured. Medial dislocations are not common and account for only 3% of knee dislocations.

Rotational or rotary dislocation

Posterolateral dislocation is most common, with buttonholing of the femoral condyle through the capsule (21). This is usually an irreducible dislocation

Schenck Classification

It is based on a pattern of multiligamentous injury of knee dislocation (KD).

• KD I: Multiligamentous injury with involvement of either the ACL or PCL.

• KD II: Injury to 2 ligaments: the ACL and PCL only.

• KD III: Injury to 3 ligaments: the ACL and PCL, in addition to either the PMC or PLC.

• KD IIIM: Involves the ACL, PCL, and MCL

• KD IIIL: Involves the ACL, PCL, and LCL.

• KD IV: Injury to 4 ligaments, including the ACL, PCL, PMC, and PLC. KD IV injuries have the highest rate of concomitant vascular injury (5% to 15%).

• KD V: A multiligamentous injury with a periarticular fracture.[22]

Prognosis

Knee dislocation is a serious injury in which the knee rarely returns to its pre-injury state. The need for surgical intervention is common.

Complications

Complications are common in traumatic knee dislocations and they vary in incidence. The most common complication is arthrofibrosis. The most serious complication is vascular injury. Other commonly encountered complications include injuries to the peroneal nerve and nearby vascular structures.

Arthrofibrosis or stiffness of the knee is the most common complication of knee dislocation. It occurs in up to 38% of the patients. Prolonged immobilization of the affected joint is a risk factor for arthrofibrosis. Early mobilization of the joint is recommended as a preventative measure. Manipulation of the joint under anesthesia and arthroscopic lysis of adhesion are the treatment options.

Some degree of instability is present in upto 37% of patients with knee dislocation. Redislocation however is uncommon. Management will vary from bracing to revision reconstruction.

Peroneal nerve injuries occur in 10% to 40% of patients. Partial recovery occurs in up to 50% of the patients (23). Men, patients with obesity, and those with associated fibular fractures are at an increased risk for peroneal nerve injuries. Patients with peroneal nerve injury are treated with an ankle-foot-orthosis (AFO) to prevent equinus contracture. In acute injuries, neurolysis or exploration of the nerve at the time of the reconstruction can be carried out. In chronic cases, the treatment includes nerve repair, reconstruction, or tendon transfer. Usually, a transfer of the tibialis posterior tendon to the foot is done.

Vascular injuries are reported in 5% to 15% of knee dislocations. About 50% of all vascular injuries occur with anterior or posterior dislocations (24). The incidence of vascular injuries is highest with KD IV dislocations. Vascular injuries are managed with urgent vascular repair and prophylactic fasciotomies.

Postoperative and Rehabilitation Care

Rehabilitation after knee dislocation is highly demanding. There are no definitive protocols for rehabilitation. The rehabilitative principles, however, remain the same. A delay of 1 to 3 weeks between the injury and operative treatment allows the inflammatory reaction to subside. Straight leg raise exercises should be performed to avoid quadriceps muscle wasting (25). Early postoperative rehabilitation aims to protect the operative repair, especially if the PCL was reconstructed. Some protocols recommend the use of a limited extension brace (26-28). Delayed postoperative rehabilitation is injury, patient, and repair-specific.

Conclusion

Knee dislocation is a relatively uncommon injury seen in the emergency department. The dislocation can be associated with a neurovascular injury that can lead to the loss of a limb. Patients with a knee dislocation are best treated by an interprofessional team. The staff treating the patient must be fully aware that a dislocated knee can disrupt the vascular supply to the distal leg. Immediate admission and a vascular surgery consult are required if there is a loss of pulses in the leg. Orthopedic consultation is necessary in almost all cases. 

The outcomes are generally good for most patients with knee dislocations who obtain prompt management. A delay in treatment leads to a chronically unstable and painful knee (29,30). All patients will require physical rehabilitation following a knee dislocation injury.

References

1. Wascher DC, Dvirnak PC, DeCoster TA. Knee dislocation: initial assessment and implications for treatment. J Orthop Trauma. 1997 Oct;11(7):525-9. 

2. Medina O, Arom GA, Yeranosian MG, Petrigliano FA, McAllister DR. Vascular and nerve injury after knee dislocation: a systematic review. Clin Orthop Relat Res. 2014 Sep;472(9):2621-9. 

3. McKee L, Ibrahim MS, Lawrence T, Pengas IP, Khan WS. Current concepts in acute knee dislocation: the missed diagnosis? Open Orthop J. 2014;8:162-7. 

4. Fanelli GC. Knee Dislocation and Multiple Ligament Injuries of the Knee. Sports Med Arthrosc Rev. 2018 Dec;26(4):150-152. 

5. Gray SF, Dieudonne BE. Pucker sign in irreducible posterolateral knee dislocation. Pan Afr Med J. 2018;30:153.

6. Erivan R, Chaput T, Villatte G, Ollivier M, Descamps S, Boisgard S. Ten-year epidemiological study in an orthopaedic and trauma surgery centre: Are there risks involved in increasing scheduled arthroplasty volume without increasing resources? Orthop Traumatol Surg Res. 2018 Dec;104(8):1283-1289. 

7. Darcy G, Edwards E, Hau R. Epidemiology and outcomes of traumatic knee dislocations: Isolated vs multi-trauma injuries. Injury. 2018 Jun;49(6):1183-1187. 

8. Arnold C, Fayos Z, Bruner D, Arnold D, Gupta N, Nusbaum J. Managing dislocations of the hip, knee, and ankle in the emergency department [digest]. Emerg Med Pract. 2017 Dec 20;19(12 Suppl Points & Pearls):1-2. 

9. Brautigan B, Johnson DL. The epidemiology of knee dislocations. Clin Sports Med. 2000 Jul;19(3):387-97.

10. Azar FM, Brandt JC, Miller RH, Phillips BB. Ultra-low-velocity knee dislocations. Am J Sports Med. 2011 Oct;39(10):2170-4. 

11. Good L, Johnson RJ. The Dislocated Knee. J Am Acad Orthop Surg. 1995 Oct;3(5):284-292. 

12. Weinberg DS, Scarcella NR, Napora JK, Vallier HA. Can Vascular Injury be Appropriately Assessed With Physical Examination After Knee Dislocation? Clin Orthop Relat Res. 2016 Jun;474(6):1453-8. 

13. Mills WJ, Barei DP, McNair P. The value of the ankle-brachial index for diagnosing arterial injury after knee dislocation: a prospective study. J Trauma. 2004 Jun;56(6):1261-5. 

14. Lachman JR, Rehman S, Pipitone PS. Traumatic Knee Dislocations: Evaluation, Management, and Surgical Treatment. Orthop Clin North Am. 2015 Oct;46(4):479-93.

15. Bui KL, Ilaslan H, Parker RD, Sundaram M. Knee dislocations: a magnetic resonance imaging study correlated with clinical and operative findings. Skeletal Radiol. 2008 Jul;37(7):653-61.

16. Peskun CJ, Levy BA, Fanelli GC, Stannard JP, Stuart MJ, MacDonald PB, Marx RG, Boyd JL, Whelan DB. Diagnosis and management of knee dislocations. Phys Sportsmed. 2010 Dec;38(4):101-11. 

17. Richter M, Bosch U, Wippermann B, Hofmann A, Krettek C. Comparison of surgical repair or reconstruction of the cruciate ligaments versus nonsurgical treatment in patients with traumatic knee dislocations. Am J Sports Med. 2002 Sep-Oct;30(5):718-27.

18. Pardiwala DN, Subbiah K, Rao N, Yathiraj BR. Chronic Irreducible Knee Dislocations: Outcomes following Open Reduction and Reconstructive Surgery. J Knee Surg. 2023 Sep;36(11):1116-1124. 

19. Ramírez-Bermejo E, Gelber PE, Pujol N. Management of acute knee dislocation with vascular injury: the use of the external fixator. A systematic review. Arch Orthop Trauma Surg. 2022 Feb;142(2):255-261.

20. Levy BA, Dajani KA, Whelan DB, Stannard JP, Fanelli GC, Stuart MJ, Boyd JL, MacDonald PA, Marx RG. Decision making in the multiligament-injured knee: an evidence-based systematic review. Arthroscopy. 2009 Apr;25(4):430-8. 

21. KENNEDY JC. COMPLETE DISLOCATION OF THE KNEE JOINT. J Bone Joint Surg Am. 1963 Jul;45:889-904. 

22. Schenck RC. The dislocated knee. Instr Course Lect. 1994;43:127-36.

23. Bonnevialle P, Dubrana F, Galau B, Lustig S, Barbier O, Neyret P, Rosset P, Saragaglia D., la Société française de chirurgie orthopédique et traumatologique. Common peroneal nerve palsy complicating knee dislocation and bicruciate ligaments tears. Orthop Traumatol Surg Res. 2010 Feb;96(1):64-9. 

24. Stannard JP, Schreiner AJ. Vascular Injuries following Knee Dislocation. J Knee Surg. 2020 Apr;33(4):351-356.

25. Howells NR, Brunton LR, Robinson J, Porteus AJ, Eldridge JD, Murray JR. Acute knee dislocation: an evidence based approach to the management of the multiligament injured knee. Injury. 2011 Nov;42(11):1198-204. 

26. Chhabra A, Cha PS, Rihn JA, Cole B, Bennett CH, Waltrip RL, Harner CD. Surgical management of knee dislocations. Surgical technique. J Bone Joint Surg Am. 2005 Mar;87 Suppl 1(Pt 1):1-21. 

27. Larson RL. Combined instabilities of the knee. Clin Orthop Relat Res. 1980 Mar-Apr;(147):68-75.

28. Engebretsen L, Risberg MA, Robertson B, Ludvigsen TC, Johansen S. Outcome after knee dislocations: a 2-9 years follow-up of 85 consecutive patients. Knee Surg Sports Traumatol Arthrosc. 2009 Sep;17(9):1013-26.

29. Ménétrey J, Putman S, Gard S. Return to sport after patellar dislocation or following surgery for patellofemoral instability. Knee Surg Sports Traumatol Arthrosc. 2014 Oct;22(10):2320-6. 

30. Fairhurst PG, Wyss TR, Weiss S, Becker D, Schmidli J, Makaloski V. Popliteal vessel trauma: Surgical approaches and the vessel-first strategy. Knee. 2018 Oct;25(5):849-855.