Osteochondritis Dissecans

                             Dr. KS Dhillon

Introduction

Osteochondritis dissecans (OCD) was first described in 1888 by the German surgeon Franz König (1). Osteochondritis dissecans is also known as an osteochondral lesion. It is not a fully understood process, though it is believed to be multi-factorial in etiology. OCD is an idiopathic condition that can develop from childhood through adult life. The majority of patients present in their teenage years. The severity of these lesions can range from being asymptomatic to mild pain or in advanced cases having symptoms of joint instability and locking. The lesions can progress from stable to fragmentation of the overlying cartilage with the formation of a loose body in the joint space. Eventual early onset osteoarthritic changes of the joint can occur at any level of severity if not diagnosed and adequately treated. Therefore, early recognition and treatment are important to achieve good long-term outcomes.

Etiology

The etiology of osteochondritis dissecans has yet to be fully elucidated. It is believed to be multi-factorial. Postulated etiologies include spontaneous avascular necrosis, genetic predisposition, inflammation, and repetitive microtrauma. Originally it was believed to be related to osseous inflammation, hence the term osteochondritis. Multiple studies have failed to prove inflammation as the underlying cause. Spontaneous osteonecrosis is believed to occur during the maturation of the overlying cartilage during adolescence. At this time, the vascular supply to the subchondral bone moves from a juvenile perichondrial supply to mature supply from the medullary cavity. It is believed that during this transition period, the epiphyseal bone is predisposed to avascular necrosis. A higher prevalence of OCD in young athletes also suggests an etiology of repetitive microtrauma.  These theories have been studied with varying success in coming to a conclusion about the cause of this disease. The most commonly accepted etiology is that of repetitive microtrauma, with or without an inciting event. (2,3).

Epidemiology

The incidence of osteochondritis dissecans is approximately 15 to 29 per 100,000 patients (4). The majority of patients are 10 to 20 years of age although it can occur from childhood through adult life (5). Males are affected twice as often as females (5). There is a higher incidence in young athletes. The knee, particularly the lateral aspect of the medial femoral condyle, is the most affected joint. The elbow (capitellum) and ankle (talus) are also affected to a lesser degree (2,6).

Pathophysiology

Osteochondritis dissecans is an idiopathic focal joint disorder affecting the subchondral bone regardless of the etiology. Fragmentation of a small focus of subchondral bone creates a defect between the osteochondral lesion and the parent bone. This leads to decreased vascularization and osteonecrosis of the fragment. Fragments that are held in place by intact overlying articular cartilage are stable. Progression of the defect to involve the overlying cartilage is possible. This will lead to instability of the fragment. If lesions become unstable, they may displace from the parent site and become a loose body within the joint. In a large percentage of these affected patients, early-onset osteoarthritis occurs due to the altered articular surface caused by the osteochondral lesion.

History and Physical

Discovery and presentation of osteochondral lesions are variable. Patients can be asymptomatic. The lesion may be incidentally detected at imaging. This is true in patients who have been asymptomatic or those who never presented for evaluation but had remote chronic mild pain that resolved without treatment. Other patients present when they have chronic mild pain of the affected joint, with or without an acute injury. Typically these patients present several months to a year after the onset of symptoms. When there is a loose fragment, symptoms are generally more severe, with marked joint pain, swelling, locking, and joint instability (2,3).

Examination shows that these patients may have joint tenderness with painful or decreased range of motion of the involved joint, and swelling or effusion. Other injuries, such as ligamentous injuries and fracture has to be excluded (3).

Evaluation

Imaging plays a key role in the evaluation and treatment of these patients. Routine radiographs of the affected joint are obtained. Radiographs will show an ovoid lucency in the subchondral bone with adjacent sclerotic bone. Occasionally the bony fragment can be seen within the subchondral defect or, if displaced, elsewhere within the joint. Radiographs cannot determine the osseous fragment's stability and underestimate the lesion size. An MRI is usually used to confirm the diagnosis when an abnormality is detected on radiographs. It helps to differentiate a developmental ossification variation from OCD and aids in treatment planning, and helps to determine if the lesion is likely to be stable at the time of arthroscopy.  An MRI is highly sensitive and specific in the evaluation of fragment stability. Therefore, it is recommended for patients in whom stability is a clinical concern.

According to De Smet, the following four signs on MRI are associated with OCD lesion instability (7): 

• A discrete round focus of hyperintense signal deep to the OCD lesion measuring 5 mm or more

• Line of hyperintense signal equal to the fluid at the fragment bone interface measuring 5 mm or more in length

• Focal defect in the overlying cartilage measuring 5 mm or more

• Hyperintense signal equal to the fluid that traverses the articular cartilage and the subchondral bone which extends to the lesion.  

To evaluate for stability these same findings can be applied to any joint with an OCD lesion. These criteria have high specificity and sensitivity in the determination of OCD lesion stability.  MRI arthrography can be useful in difficult cases. Although CT arthrography is not as sensitive, it can be used in the patient when MRI is contraindicated.

MRI is also useful in monitoring treatment of the patients if conservative or surgical treatment is chosen.  The recommended time interval to perform an MRI to evaluate healing depends on the institutional protocol and surgeon. MRI findings that suggest healing following conservative management include: 

• Decrease or resolution in the surrounding bone marrow edema pattern

• A decrease in lesion size

• Decrease or the resolution of the hyperintense T2 signal rim or cyst-like foci

• Ingrowth of bone within the bed of the OCD lesion with osseous bridging.

After surgery, an MRI allows for noninvasive evaluation of the repair of the articular surface and the bone cartilage interface (7).

Treatment

The patient’s age, presentation time, severity of symptoms, and lesion stability will dictate treatment. Several systems to classify the lesions have been developed. The important feature is the degree of overlying cartilage involvement and mobility of the lesion fragment. In stable lesions, conservative management is the treatment of choice. Immobilization is carried out and protected weight-bearing is done for a length of time, depending on which joint is affected. When conservative treatment fails in patients with stable lesions they may be treated with drilling techniques (retroarticular or transarticular drilling). These drilling procedures have shown healing rates and symptom improvement in 92% to 100% of the patients. Transarticular drilling has slightly higher success rates. When lesions are displaced or unstable, surgical intervention is necessary. The drilling is typically performed arthroscopically. The knee lesions most often require surgery. Fifty-eight percent of procedures for OCD lesions are performed on the knee. There are various modalities and techniques that exist, such as debridement, fixation, microfracture, and cartilage grafting/transplantation. In situ fixation of lesions can be done using various types of bioabsorbable implants, metallic screws, or osteochondral plugs. Metallic screw fixation shows high successful healing rates of 84% to 100%. The disadvantage of using metallic screws is that there is a need for a second procedure to remove the screws. Bioabsorbable implants do not require a second procedure for removal. They show successful healing rates of around 90%. These implants however show higher rates of complications. Osteochondral autograft or allograft plugs can also be used. The clinical outcomes are “good to excellent” in 72% of patients receiving allograft plugs. The overall aim of surgery is to promote cartilage reformation and/or repair of the articular surface to prevent early-onset osteoarthritis (8).

Differential Diagnosis

Meniscus injury

Osteoarthritis

Prognosis

Stable osteochondral lesions have a better outcome as compared to unstable lesions. Spontaneous healing typically occurs when stable lesions are treated with conservative treatment alone. There is no single uniform grading scale for lesions treated surgically. Unstable lesions and those that fail conservative management undergo surgical treatment which has a success rate of 30% to 100% depending on the technique utilized (8). However, a large majority of patients treated surgically will still develop early-onset osteoarthritis. Patients presenting during adolescence tend to have a better outcome than adult patients.

Complications

Chronic pain

Arthritis

Nonunion

Conclusion

The diagnosis and management of osteochondritis dissecans is carried out by an interprofessional team that consists of a radiologist, orthopaedic surgeon, physical therapist, and primary caregiver. The treatment is dictated by the patient’s age, time of presentation, the severity of symptoms, and stability of the lesion. There are several systems that have been developed to classify the lesions. The important feature is the degree of overlying cartilage involvement and mobility of the lesion. In stable lesions, conservative management is preferred with immobilization and protected weight-bearing for a length of time, that depends on which joint is involved. When conservative treatment fails the patient can be treated with drilling techniques (retroarticular or transarticular drilling). These procedures have shown healing rates and symptom improvement ranging from 92% to 100%. Transarticular drilling has slightly higher success rates. When lesions are unstable or displaced, surgical intervention is necessary. The outcomes of stable lesions are better than unstable lesions (9,10). 

References

1. Kessler JI, Jacobs JC, Cannamela PC, Shea KG, Weiss JM. Childhood Obesity is Associated With Osteochondritis Dissecans of the Knee, Ankle, and Elbow in Children and Adolescents. J Pediatr Orthop. 2018 May/Jun;38(5):e296-e299.

2. Edmonds EW, Polousky J. A review of knowledge in osteochondritis dissecans: 123 years of minimal evolution from König to the ROCK study group. Clin Orthop Relat Res. 2013 Apr;471(4):1118-26. 

3. Zanon G, DI Vico G, Marullo M. Osteochondritis dissecans of the talus. Joints. 2014 Jul-Sep;2(3):115-23.

4. Andriolo L, Candrian C, Papio T, Cavicchioli A, Perdisa F, Filardo G. Osteochondritis Dissecans of the Knee - Conservative Treatment Strategies: A Systematic Review. Cartilage. 2019 Jul;10(3):267-277. 

5. Michael JW, Wurth A, Eysel P, König DP. Long-term results after operative treatment of osteochondritis dissecans of the knee joint-30 year results. Int Orthop. 2008 Apr;32(2):217-21. 

6. Kubota M, Ishijima M, Ikeda H, Takazawa Y, Saita Y, Kaneko H, Kurosawa H, Kaneko K. Mid and long term outcomes after fixation of osteochondritis dissecans. J Orthop. 2018 Jun;15(2):536-539.

7. Zbojniewicz AM, Laor T. Imaging of osteochondritis dissecans. Clin Sports Med. 2014 Apr;33(2):221-50.

8. Bauer KL, Polousky JD. Management of Osteochondritis Dissecans Lesions of the Knee, Elbow and Ankle. Clin Sports Med. 2017 Jul;36(3):469-487.

9. Cheng C, Milewski MD, Nepple JJ, Reuman HS, Nissen CW. Predictive Role of Symptom Duration Before the Initial Clinical Presentation of Adolescents With Capitellar Osteochondritis Dissecans on Preoperative and Postoperative Measures: A Systematic Review. Orthop J Sports Med. 2019 Feb;7(2):2325967118825059. 

10. Yamagami N, Yamamoto S, Aoki A, Ito S, Uchio Y. Outcomes of surgical treatment for osteochondritis dissecans of the elbow: evaluation by lesion location. J Shoulder Elbow Surg. 2018 Dec;27(12):2262-2270.

 Increased risk of early and medium-term revision after post-fracture total knee arthroplasty

                          Dr. KS Dhillon

Introduction

Post-traumatic osteoarthritis (PTOA) of the knee is defined as osteoarthritis that develops following an acute traumatic episode commonly associated with intra/extra-articular fracture or significant ligamentous injury (1). PTOA represents 9.8% of the overall prevalence of symptomatic knee osteoarthritis. It costs an estimated $40 billion in direct and indirect costs (2). Femoral and tibial fractures represent the major causes of PTOA of the knee (3). PTOA is caused by intra-articular fractures, which result in direct ligament and osteochondral injury, and cause joint instability and incongruity. It can be secondary to malunion of extra-articular fractures around the knee, which alters the weight-bearing axis of the lower limb and increases the joint stress, and accelerates the joint degeneration. Patients sustaining distal femur or proximal tibia fractures are around twice as likely to require total knee arthroplasty (TKA) as compared to patients with soft-tissue injuries (4,5).

TKA for PTOA is technically demanding even for experienced surgeons

due to previous surgery, retained hardware, bone defects, and the extra-articular angular deformity created by a fracture. Patients with PTOA are also susceptible to higher rates of complications, including periprosthetic joint infection, aseptic mechanical failure, wound healing problems, and higher rates of reoperation compared with TKA performed for atraumatic osteoarthritis (6,7). Bala et al (6) evaluated the impact of PTOA versus primary osteoarthritis on postoperative outcomes after TKA in a large database of Medicare patients. They found that the PTOA patients had a higher incidence of periprosthetic infection (OR 1.72, P < 0.001), knee wound complications (OR 1.80, P < 0.001), cellulitis/ seroma (OR 1.19, P < 0.001), TKA revision (OR 1.23, P = 0.01), and arthrotomy/incision and drainage (OR 1.55, P < 0.001).

The literature in the past has found several risk factors for unsatisfactory outcomes after TKA for PTOA. Shearer et al (8) found that the location of post-traumatic deformity and compromise of the soft-tissue envelope influenced the pain and functional outcomes of TKA for PTOA. Patients with isolated articular deformities have the largest improvement in pain and function while patients with combined tibial and femoral deformities as well as patients with soft-tissue compromise experienced poor outcomes. Ge et al (9) found that patients with previous site-specific fractures suffered higher surgical site complications (22% vs 4.4%) and 90-day readmissions (14.8% vs 2.2%) after TKA than patients with previous soft-tissue knee trauma. El-Galaly et al (10) reported an increased risk of early and medium-term revision of TKAs due to previous fractures in the proximal tibia and/or distal femur. There is a scarcity of literature about the risk factors for surgical site complications and reoperations after TKA in patients with PTOA secondary to prior femoral and tibial fractures.

Background and rationale

The proportion of patients with a history of previous surgery before primary total knee arthroplasty (pTKA) is highly variable (6–34%). This variability may be due to overestimation, multiple counting, underestimation, patient recall bias, incomplete chart fill, insufficient anamnesis, different current practices from one country to another, and different time periods included. It is however not clear how a history of previous surgery influences the outcome after pTKA. Patients with previous surgery have primary arthroplasty at a younger age and have a 1.5 times higher risk of subsequent revision. The risk does not substantially change when restricting the inclusion to primary OA. The difference in implant failure at 5 and 10 years is notable: about twice the risk at both time points (6.6% vs. 3.3 and 8.4% vs. 4.5%, respectively). The timing of revision is substantially higher in the short term in patients with pre-dating surgeries.

Does history of previous surgeries influence the risk of revision of primary total knee arthroplasty?

The crude risk of all-cause revision after pTKA among patients with a history of previous knee surgery is about twice as high as among those without (8.3 vs. 4.3%). Baseline differences in age, American Society of Anesthesiologists (ASA) score, sex, BMI, smoking status, patellar resurfacing, type of tibial plateau, and surgery duration partly explained the higher risk. It was, however, still 1.5 times greater after adjusting for the baseline imbalances. Subgroup analysis considering only the first pTKA implanted reveals similar results. Patients who had previous surgery are substantially younger, more often men, have fewer comorbidities including obesity, and are more often smokers. Similarly, Lim et al (11) highlighted that pTKA after previous surgery was performed at a younger age (61 vs. 66 years).

 

What is the risk of revision according to the type of previous surgery?

The risk of revision varies according to the type of previous surgery and it is lowest, with a 4.1% (CI 1.7–9.5) 5-year cumulative failure rate in the case of previous osteotomy, and higher in the case of ligamentoplasty (7.1%), arthroscopy (7.9%), or previous osteosynthesis (8.3%). However, the confidence intervals around the estimates for different types are large and overlap considerably. This kind of surgery can alter knee mechanics. Typically, previous osteotomies around the knee, or posttraumatic conditions, make TKA technically more challenging in terms of ligament balancing and implant positioning. Their effect on the revision risk however is not evident. A study by Pearse et al (12) from the New Zealand Joint Registry showed a 3-fold increased risk of early revision in patients with a history of osteotomies around the knee, compared with pTKA without previous surgery. In a more recent study by El-Galaly et al (13) from the Danish Knee Arthroplasty Registry, the 10-year survival of pTKA after HTO was inferior (91% vs. 94%).  This however could be explained by lower age and male sex rather than the osteotomy (adjusted HR of 1.2 vs. acrude HR of 1.7). 

The same group reported in another study an increased risk of early and mid-term revision of pTKA in the setting of OA after fractures around the knee (14).

How does previous surgery influence specific causes of revision and the time of revision?

The risk of revision after pTKA with previous surgery is about twice as high for any specific diagnosis, with aseptic loosening (2.1%) and infection (1.9%) being the most frequent cause of revision. The vast majority of patients are homogeneously treated making implant-related factors unlikely to explain the difference in revision rates due to aseptic loosening. Both younger age (15) and a BMI over 35 (16,17) are known patient-related risk factors for revision, due to high activity levels and a higher mechanical load across the bone–cement interface, respectively. The higher risk of infection encountered in patients with a history of previous surgery might be explained by an intrinsic risk due to previous interventions, as reported in a meta-analysis, with an RR of 3.0 (CI 1.5–5.9) (18), especially with open surgical procedures (19), as well as a history of resolved septic arthritis following surgery or prolonged surgery. Residual pain after pTKA is not unusual. High patient expectations, long chronic pain situations, and social/economic pressure to resume work might play a central role. There are substantially more short-term revisions in patients with previous surgery. There is no difference in the mid-term. In the long term, there is a higher number of revisions in those with previous surgery.

Conclusions

About 6–34% of patients undergoing pTKA have a history of previous surgery. The difference in implant failure at 5 and 10 years is notable, and baseline differences only partly explain the increased risk of revision. It is important to advise patients that their knee history adversely influences the outcome of pTKA, with a 1.5 times higher risk of revision. Future studies should analyze whether 1 vs. multiple surgeries prior to pTKA influences the survival differently and should focus on what causes of revision are related to a specific previous surgery. 

References

1. Houdek MT, Watts CD, Shannon SF, Wagner ER, Sems SA, Sierra RJ. Posttraumatic total knee arthroplasty continues to have worse outcome than total knee arthroplasty for osteoarthritis. J Arthroplasty, 2016, 31: 118–123.

2. Brown TD, Johnston RC, Saltzman CL, Marsh JL, Buckwalter JA. Posttraumatic osteoarthritis: a first estimate of incidence, prevalence, and burden of disease. J Orthop Trauma, 2006, 20: 739–744.

3. Muthuri SG, McWilliams DF, Doherty M, Zhang W. History of knee injuries and knee osteoarthritis: a meta-analysis of observational studies. Osteoarthr Cartil, 2011, 19: 1286–1293.

4. Wasserstein D, Henry P, Paterson JM, Kreder HJ, Jenkinson R. Risk of total knee arthroplasty after operatively treated tibial plateau fracture: a matched-population-based cohort study. J Bone Joint Surg Am, 2014, 96: 144–150.

5. Anderson DD, Chubinskaya S, Guilak F, et al. Post-traumatic osteoarthritis: improved understanding and opportunities for early intervention. J Orthop Res, 2011, 29: 802–809.

6. Bala A, Penrose CT, Seyler TM, Mather RC 3rd, Wellman SS, Bolognesi MP. Outcomes after total knee arthroplasty for post-traumatic arthritis. Knee, 2015, 22: 630–639.

7. Lonner JH, Pedlow FX, Siliski JM. Total knee arthroplasty for post-traumatic arthrosis. J Arthroplasty, 1999, 14: 969–975.

8. Shearer DW, Chow V, Bozic KJ, Liu J, Ries MD. The predictors of outcome in total knee arthroplasty for post-traumatic arthritis. Knee, 2013, 20: 432–436.

9. Ge DH, Anoushiravani AA, Kester BS, Vigdorchik JM, Schwarzkopf R. Preoperative diagnosis can predict conversion total knee arthroplasty outcomes. J Arthroplasty, 2018, 33: 124–29.e1.

10. El-Galaly A, Haldrup S, Pedersen AB, Kappel A, Jensen MU, Nielsen PT. Increased risk of early and medium-term revision after post-fracture total knee arthroplasty. Acta Orthop, 2017, 88: 263–268.

11. Lim J B, Loh B, Chong H C, Tan A H. History of previous knee surgery does not affect the clinical outcomes of primary total knee arthroplasty in an Asian population. Ann Transl Med 2016; 4(16): 303. doi: 10.21037/atm.2016.08.15.

12. Pearse A J, Hooper G J, Rothwell A G, Frampton C. Osteotomy and uni-compartmental knee arthroplasty converted to total knee arthroplasty: data from the New Zealand Joint Registry. J Arthroplasty 2012; 27(10): 1827-31. doi: 10.1016/j.arth.2012.05.031.

13. El-Galaly A, Nielsen P T, Jensen S L, Kappel A. Prior high tibial osteotomy does not affect the survival of total knee arthroplasties: results from the Danish Knee Arthroplasty Registry. J Arthroplasty 2018; 33(7): 2131-5 e1.doi: 10.1016/j.arth.2018.02.076.

14. El-Galaly A, Haldrup S, Pedersen A B, Kappel A, Jensen M U, Nielsen P T. Increased risk of early and medium-term revision after post-fracture total knee arthroplasty. Acta Orthop 2017; 88(3): 263-8. doi:10.1080/17453674.2017.1290479.

15. Khan M, Osman K, Green G, Haddad F S. The epidemiology of failure in total knee arthroplasty: avoiding your next revision. Bone Joint J 2016;98-B(1 Suppl A): 105-12. doi: 10.1302/0301-620x.98b1.36293.

16. Abdel M P, Bonadurer G F, 3rd, Jennings M T, Hanssen A D. Increased aseptic tibial failures in patients with a BMI ≥35 and well-aligned total knee arthroplasties. J Arthroplasty 2015; 30(12): 2181-4. doi: 10.1016/j.arth.2015.06.057.

17. Zingg M, Miozzari H H, Fritschy D, Hoffmeyer P, Lübbeke A. Influence of body mass index on revision rates after primary total knee arthroplasty.Int Orthop 2016; 40(4): 723-9. doi: 10.1007/s00264-015-3031-0.

18. Kunutsor S K, Whitehouse M R, Blom A W, Beswick A D. Patient-related risk factors for periprosthetic joint infection after total joint arthroplasty: a systematic review and meta-analysis. PLoS One 2016; 11(3): e0150866.doi: 10.1371/journal.pone.0150866.

19. Tan T L, Maltenfort M G, Chen A F, Shahi A, Higuera C A, SiqueiraM, Parvizi J. Development and evaluation of a preoperative risk calculator for periprosthetic joint infection following total joint arthroplasty. J Bone Joint Surg Am 2018; 100(9): 777-85. doi: 10.2106/JBJS.16.01435.

 

         Septic Arthritis of the Pediatric Hip

                                Dr. KS Dhillon

Introduction

Septic arthritis of the hip in children is an emergent surgical condition. If not treated rapidly, can lead to hip destruction, sepsis, and even death. Septic arthritis of the pediatric hip has to be differentiated from transient synovitis of the hip. Transient synovitis is a non-emergent and non-surgical condition. It can resolve with symptomatic pain management. Significant morbidity may result from the improper diagnosis of either of these conditions. To make a proper diagnosis the infecting organism has to be identified. The organism will vary depending on the comorbidities of the patient and the age of the patient (1-3).

Etiology

The most common mechanism for the development of pediatric septic arthritis is by hematogenous spread of bacteria into the hip joint. In about 80% of the cases the septic arthritis is preceded by an upper respiratory tract infection. The bacteria involved in about 70% of the cases is Kingella kingae a gram-negative coccobacillus. Staphylococcus organisms account for 10% of the cases. Haemophilus species have been the most common organisms causing septic arthritis of the hip in children younger than two years of age (4-6).

Blood pooling in the metaphyseal vessels of long bones permits bacterial seeding into this area. Bacteria then spread through the blood vessels of the bone into the bony epiphysis and result in an intracapsular infection of the hip joint hip.

Epidemiology

About 50% of children presenting with septic arthritis of the hip are younger than 2 years of age. It occurs twice as often in males as compared to females. Children who are immunocompromised, have sickle cell disease, or hemophilia are more likely to develop septic arthritis of the hip. In areas where Lyme disease is endemic, this condition should be considered as a possible diagnosis. This is especially true if other signs of Lyme disease such as transient polyarthralgia, typical erythema migrans (bull's eye rash), heart palpitations, and irregular heartbeat are present. Serological testing (Lyme titer /western blot) can be ordered to confirm the diagnosis of Lyme disease.

Pathophysiology

The release of cytokines in the pus within a septic joint leads to hydrolysis of collagen and proteoglycans in the hyaline cartilage covering the end of the bones within the joint. This leads to the destruction of the hyaline cartilage and articular bone which results in deformity, chronic loss of function, and pain. If the infection is left untreated, septicemia and death can occur.

History and Physical

Children with septic arthritis of the hip usually present with acute onset of pain in the hip joint. If they walk, they may be a limp. They will resist weight bearing on the affected leg. Children who do not walk will usually lie in bed holding their hip in the most comfortable position i.e. flexed and abducted. This is a position that allows the hip capsule to be lax, and it decreases pressure from intraarticular effusion that may be causing pain. They usually do not have fever. The children may have a history of a recent oropharyngeal infection.

When the children are in bed, log rolling of the child will produce severe hip pain. Passive movements of the hip joint are very painful.

Evaluation

It is difficult to differentiate acute hip pain caused by septic arthritis from that caused by transient synovitis of the hip. The best way to differentiate the two is by hip aspiration. The Kocher Criteria for diagnosing septic arthritis of the hip can be used to determine if an aggressive approach to the management of the patient is needed. The four criteria used in order of sensitivity in the Kocher criteria are:

• Fever higher than 38.5 C

• ESR more than 40

• Weight-bearing status (non-weight bearing)

• White blood cell count of more than 12,000

Children who meet 1 out of 4 of these criteria have a 3% incidence of septic arthritis, 2 out of 4 have a 40% incidence, 3 out of 4 have a 93% incidence, and 4 out of 4 have a 99% incidence (7-9).

X-rays of the hip should be done in older children to rule out the possibility of Perthes disease or a slipped femoral capital epiphysis (10).

Treatment

Children who have pain in the hip but only meet one out of the four Kocher criteria should be observed. They should be watched for further progression of the condition. Children with two or more of the criteria should have hip aspiration with a gram stain and cell count. If bacteria are identified or if the cell count reveals a WBC count of over 50,000 WBC/mm3 with greater than 75% PMN cells and a glucose level of more than 50 mg/dl less than that of the serum level, than the hip joint should be explored and irrigated with saline and an antibacterial agent (11,12).

The synovial fluid WBC count is considered more sensitive than the blood WBC count when diagnosing septic arthritis. A finding of 85% PMNs has an 88% sensitivity.

The duration of intravenous (IV) antibiotic use varies.  Usually, 2 days of IV antibiotics followed by a 3-week course of oral antibiotics is adequate. Some authors recommend one week of IV antibiotic therapy followed by 2  weeks of oral antibiotics. Kingella kingae is known to be resistant to clindamycin and vancomycin. These infections are treated with IV beta-lactamase antibiotics and then their oral forms. The sooner the treatment is started, the better the results. 

Surgical approaches to the hip for treatment of these patients are either anterior or anterior lateral.  Recent literature shows that the results are similar when comparing open drainage of the hip to arthroscopic drainage.

Long-term follow-up is necessary to detect complications of septic arthritis of the hip.  These complications can include growth disturbances of the hip, avascular necrosis of the femoral head, and the development of post-infection arthritis of the hip.

Differential Diagnosis

• Crystalline Arthritides

• Drug-Induced Arthritis

• Arthritis of Intrinsic Bowel Disease

• Postinfectious Diarrhea

• Postmeningococcal

• Postmeningococcal Arthritis

• Vasculitis

Conclusion

Swift diagnosis and treatment significantly impacts outcome in children with septic arthritis of the hip. Staphylococcus aureus, especially methicillin sensitive strains prevail. Resistant strains are however increasing. Early treatment is crucial. Delays, high CRP/ESR levels, and younger age correlate with worse outcome. Accurate diagnosis can be made by clinical examination and ultrasound. Treatment can include surgery and less invasive methods, often combined with tailored antibiotics. Antibiotic resistance can pose a challenge, requiring ongoing vigilance. Further research is needed to address the evolving landscape of antibiotic resistance and explore potential interventions to improve outcomes in septic arthritis of hip patients.

References

1. Chewakidakarn C, Nawatthakul A, Suksintharanon M, Yuenyongviwat V. Septic arthritis following femoral neck fracture: A case report. Int J Surg Case Rep. 2019;57:167-169.

2. Akgün D, Müller M, Perka C, Winkler T. High cure rate of periprosthetic hip joint infection with multidisciplinary team approach using standardized two-stage exchange. J Orthop Surg Res. 2019 Mar 13;14(1):78.

3. Hoswell RL, Johns BP, Loewenthal MR, Dewar DC. Outcomes of paediatric septic arthritis of the hip and knee at 1-20 years in an Australian urban centre. ANZ J Surg. 2019 May;89(5):562-566.

4. Momodu II, Savaliya V. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 3, 2023. Septic Arthritis. 

5. Deore S, Bansal M. Pelvic Osteomyelitis in a Child - A Diagnostic Dilemma. J Orthop Case Rep. 2018 Jul-Aug;8(4):86-88.

6. Tretiakov M, Cautela FS, Walker SE, Dekis JC, Beyer GA, Newman JM, Shah NV, Borrelli J, Shah ST, Gonzales AS, Cushman JM, Reilly JP, Schwartz JM, Scott CB, Hesham K. Septic arthritis of the hip and knee treated surgically in pediatric patients: Analysis of the Kids' Inpatient Database. J Orthop. 2019 Jan-Feb;16(1):97-100.

7. Mooney JF, Murphy RF. Septic arthritis of the pediatric hip: update on diagnosis and treatment. Curr Opin Pediatr. 2019 Feb;31(1):79-85. 

8. Amanatullah D, Dennis D, Oltra EG, Marcelino Gomes LS, Goodman SB, Hamlin B, Hansen E, Hashemi-Nejad A, Holst DC, Komnos G, Koutalos A, Malizos K, Martinez Pastor JC, McPherson E, Meermans G, Mooney JA, Mortazavi J, Parsa A, Pécora JR, Pereira GA, Martos MS, Shohat N, Shope AJ, Zullo SS. Hip and Knee Section, Diagnosis, Definitions: Proceedings of International Consensus on Orthopedic Infections. J Arthroplasty. 2019 Feb;34(2S): S329-S337. 

9. Mue DD, Salihu MN, Yongu WT, Ochoga M, Kortor JN, Elachi IC. Paediatric Septic Arthritis in a Nigerian Tertiary Hospital: A 5-Year Clinical Review. West Afr J Med. 2018 May-Aug;35(2):70-74.

10. Cruz AI, Anari JB, Ramirez JM, Sankar WN, Baldwin KD. Distinguishing Pediatric Lyme Arthritis of the Hip from Transient Synovitis and Acute Bacterial Septic Arthritis: A Systematic Review and Meta-analysis. Cureus. 2018 Jan 25;10(1):e2112.

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