Chondromalacia Patella

                 

                                        DR KS Dhillon

Introduction

Chondromalacia is an affliction of the hyaline cartilage of the articular surfaces of the bone. There is softening and then subsequent tearing, fissuring, erosion, and degeneration of hyaline cartilage. Chondromalacia can occur in any synovial joint. It is, however, most commonly seen in the patellofemoral joint. In the patellofemoral joint, it is called chondromalacia patella, patellofemoral syndrome, or runner's knee. The articular surface of the patella is covered with hyaline cartilage and it articulates with the hyaline cartilage on the femoral groove (trochlear groove). 

Chondromalacia can result from direct trauma, patellar dislocation, chronic patellar instability/subluxation, patella alta, quadriceps imbalance, synovial plicae, and iatrogenic injections of medication. 

Etiology

A common cause of microtrauma leading to wear and tear resulting in chondromalacia patella is lateral subluxation or lateral positioning of the patella. It is more commonly seen in females who have a larger Q angle. 

The Q angle measures the pull of the quadriceps muscle relative to the pull of the patella tendon on the patella.  A normal angle is 17 degrees in women and 14 degrees in men. It is measured by drawing a line from the center of the anterior iliac spine to the center of the patella (quadriceps pull) and a second line from the mid-portion of the patella to the tibial tubercle (patella tendon pull). An abnormally high Q angle indicates lateral pull of the patella in the trochlear groove of the femur which leads to articular cartilage wear and tear [1].

The patella alignment in the vertical plane can also be abnormal. A high riding patella (patella alta) and a low riding patella (patella baja) have also been implicated as a cause of chondromalacia.

Chondromalacia can also result from injuries, immobilization, and surgical procedures that lead to quadriceps atrophy. Quadriceps atropy causes micro-trauma which is created by the decreased pull of the quadriceps muscle on the patella [1].

Lateral synovial plicas have also been implicated in the pathogenesis of chondromalacia patella. Patellofemoral stress caused by sporting activities, repeated stair climbing, and kneeling can contribute to the development of chondromalacia.

Iatrogenic injection of chondrotoxic medications into a joint can lead to chondromalacia patella. Intra-articular injections of bupivacaine and high doses or frequent intra-articular injections of corticosteroid are known to lead to softening and/or articular cartilage dysfunction [1]. 

Pes planus can cause an increased valgus orientation of the knee leading to increased lateral wear of the patellofemoral joint. High-heel shoes can increase stresses on the patellofemoral joint leading to chondromalacia [1].

Epidemiology

Chondromalacia patella is more common in women as compared to men. This is attributed to the presence of increased Q angles in women. There is no known hormonal cause of variation. Active young adults who participate in running sports and workers who have increased patellofemoral stress due to repeated stair climbing and/or kneeling have a higher incidence of chondromalacia.

About 20% of individuals with patellofemoral pain have chondromalacia patella. About 80% of patients with lower limb joint pain have patellofemoral pain [2]. 

History and Physical Examination

The chief complaint of patients with chondromalacia patella is anterior knee pain. The pain is aggravated by activities that increase the stress on the patellofemoral joint. These activities include stair climbing, squatting, kneeling, and running. 

There are several other causes of anterior knee pain. These include patellar tendonitis, infrapatellar fat pad syndrome (Hoffa disease), patellar instability, bi-partite patella, osteochondritis dessicans of the patellofemoral joint, patella alta, patella baja, and synovial plica.

The major symptom of chondromalacia is diffuse pain in the peripatellar or retropatellar area of the knee. The onset of pain is usually insidious and typically vague in nature. The pain is aggravated by daily activities such as going up and downstairs, prolonged sitting with knee bent, squatting, and kneeling.

Physical exam can show quadriceps muscle atrophy, signs of patella maltracking, lateral subluxation of patella or loss of medial patellar mobility, 

increased femoral anteversion or tibial external rotation, positive patellar apprehension test, palpable crepitus, pain with compression of the patella with knee range of motion, or resisted knee extension. 

The Clark’s test specifically evaluates the knee for chondromalacia. This test is performed by compressing the patella into the femoral trochlea and having the patient contract his/her quadriceps muscle. This pulls the patella through the groove and causes anterior knee pain in patients with chondromalacia.

Imaging

Radiographs

Three views of radiographs are recommended namely the AP, lateral, and Merchant’s view. The radiographs can show a shallow sulcus, patella alta/baja, and lateral patella tilt.

CT scan

CT scans are of not much use for the diagnosis of chondromalacia. CT scans can show patellofemoral alignment, fractures, trochlear geometry, and limb torsion.

MRI

MRI is the modality of choice for assessing patellar cartilage.

T1 sequence is a poor sequence for cartilage and surface irregularity and subtle signal change may not be apparent. Areas of hypointensity may be seen in cartilage. Subchondral reactive bone marrow edema pattern (low signal) may be seen.

T2/PD sequences are the best sequences for assessing cartilage. Most patients with chondromalacia patellae will have focally increased signal in the cartilage or focal contour defects in the cartilage surface. Abnormal cartilage is usually of high signal compared to normal cartilage. The findings can range from a subtle increase in signal to complete loss of cartilage. 

The modified Outerbridge grading of chondromalacia is divided into four grades based on T2/PD sequences. 

Grade I: focal areas of hyperintensity with normal contour. 

Grade II: blister-like swelling/fraying of articular cartilage extending to surface.

Grade III: partial-thickness cartilage loss with focal ulceration.

Grade IV: full-thickness cartilage loss with underlying reactive changes in the bone. 

Treatment

Nonoperative

In many individuals with chondromalacia patellae, the symptoms are self-limiting. The treatment is primarily nonsurgical. Conservative therapeutic interventions include the following:

• Isometric quadriceps strengthening and stretching exercises: Restoration of good quadriceps strength and function is important in achieving good recovery [3].

• Stretching exercises. Hamstring, quadriceps, calf, lateral hip, and thigh stretching exercises can be useful.

• Temporary modification of activity. Avoid activities that compress the

patella against the femur with force. This will include avoiding going up and downstairs and hills, deep knee bends, kneeling, step-aerobics, and high-impact aerobics. Do not wear high-heeled shoes. Do not do exercises sitting on the edge of a table and lifting leg weights

• Patellar taping. An elastic knee support that has a central opening cut out for the kneecap can help reduce pain.

• Foot orthoses. Orthotics which decrease pronation of the foot can be useful.

• Non-steroidal anti-inflammatory drugs are more effective than steroids.

Surgical treatment

Surgical management is indicated when there is a failure to respond to nonoperative management. Studies show that up to 20% of athletes fail to improve adequately with conservative treatment [4]. Surgical intervention often produces variable results. 

There are 2 approaches to surgical treatment of chondromalacia:

1.Treatment directed at malalignment and other abnormalities of the extensor mechanism and the patellofemoral joint. 

Treatment directed at malalignment and other abnormalities of the extensor mechanism and the patellofemoral joint include:

• Lateral retinacular release-- This is indicated when there is a tight lateral retinacular capsule, loose medial capsule and there is lateral patellar tilt. This can be carried out by open arthrotomy or arthroscopically. The majority of studies, however, show that over 80% of patients with chronic patellofemoral pain respond initially to lateral release of the patella but with increasing time there is a diminishing long-term benefit [4].
• Patellar realignment surgery- This is indicated when there is patellar malalignment. The following techniques can be used: Maquet anterior tubercle elevation, Fulkerson anterior-medialization for increased Q angle and patella instability, Elmslie-Trillat osteotomy, and medial patellofemoral reconstruction.

2.Treatment of the diseased cartilage.

 Arthroscopic debridement of the cartilage is usually carried out for Outerbridge grade 2-3 chondromalacia of the patellofemoral joint. Krüger et al [5] carried out a retrospective study of 161 patients who had undergone arthroscopic operation for chondromalacia of the knee joint. The average follow-up was 40 (range 10-72) months. They found that patients with severe articular cartilage lesions who had undergone articular lavage alone showed significantly poorer results. Generally, younger patients showed better results than older patients. According to the authors, the literature shows that aggressive subchondral abrasion in severely degenerated knees does not provide any benefits to the patient. They found that almost every second patient suffering from grade 4 chondromalacia complained of recurrent pain 1 year postoperatively. One of every 6 patients received a knee joint prosthesis within the 1st year after debridement surgery. 

Price et al [6] in a series involving cases of post-traumatic chondromalacia patellae found that arthroscopic shaving and lavage generally provided only partial relief of symptoms, and few patients showed improvement beyond 2 years from the date of injury.

Federico et al [7] found that patients with traumatic chondromalacia patellae had 57.9% good or excellent results with joint debridement, and the patients with atraumatic cases had 41.1% good or excellent results with surgery, indicating that many patients who were improved by the surgery still had functional limitations.

Some surgeons have resorted to patellofemoral arthroplasty and others to patellectomy for treatment of advanced chondromalacia of the patella. The clinical outcome after patellectomy is not good with one study showing only 29% of soldiers recovering to a fully fit category after patellectomy [8].

Patellectomy has its own set of problems, which include loss of extension power and increased risk of arthritis in the tibiofemoral compartment. It is hardly carried out nowadays.

Patellofemoral arthroplasty (PFA) is sometimes carried out in patients with severe isolated patellofemoral osteochondropathy not responding to nonoperative measures. The main contraindications for arthroplasty are uncorrected maltracking of the patella, uncorrected tibiofemoral malalignment, and other compartmental diseases. Success rates of PFA vary from 42% to 90% [9,10,11,12]. The published data is limited and the indications for surgery are varied in these studies and this could possibly explain the diversity of these success rates [13].

Other treatments

There are some newer techniques for the treatment of chondromalacia patellae, such as chondrocyte transplant and cartilage transplant. A definite conclusion cannot be drawn on the effectiveness of these techniques in the treatment of chondromalacia because the patients undergoing such treatment have not been followed up for a sufficient length of time [14]. 

Prognosis

Pain from chondromalacia usually disappears with time. Recovery can occur in a month. Sometimes it takes years before it disappears. Teenagers usually achieve long-term recovery because their bones are still growing, and their symptoms generally disappears once they reach adulthood.[15]

Reference

1. Habusta SF, Coffey R, Ponnarasu S, et al. Chondromalacia Patella at https://www.ncbi.nlm.nih.gov/books/NBK459195/#_NBK459195_pubdet_.
2. Glaviano et al. DEMOGRAPHIC AND EPIDEMIOLOGICAL TRENDS IN PATELLOFEMORAL PAIN. The International Journal of Sports Physical Therapy | Volume 10, Number 3 | June 2015. 
3. Natri A, Kannus P, Järvinen M. Which factors predict the long-term outcome in chronic patellofemoral pain syndrome? A 7-yr prospective follow-up study. Med Sci Sports Exerc. 1998 Nov;30(11):1572-7. doi: 10.1097/00005768-199811000-00003. PMID: 9813868.
4. Perry JD. Sports medicine: the clinical spectrum of injury. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, editors. Rheumatology 3rd ed. St Louis, MO: Mosby, Inc;2003. p 749.
5. Krüger T, Wohlrab D, Birke A, Hein W. Results of arthroscopic joint debridement in different stages of chondromalacia of the knee joint. Arch Orthop Trauma Surg. 2000;120(5-6):338-42. doi: 10.1007/s004020050478. PMID: 10853909.
6. Price AJ, Jones J, Allum R. Chronic traumatic anterior knee pain. Injury 2000;31:373-8.
7. Federico DJ, Reider B. Results of isolated patellar debridement for patellofemoral pain in patients with normal patellar alignment. Am J Sports Med 1997;25:663-669.
8. Pailthorpe CA, Milner S, Sims MM. Is patellectomy compatible with an army career? J R Army Med Corps 1991;137(2):76-9.
9. Cartier P, Sanouiller JL, Khefacha A (2005) Long-term results with the first patellofemoral prosthesis. Clin Orthop Relat Res 436:47–54.
10. Kooijman HJ, Driessen AP, van Horn JR (2003) Long-term results of patellofemoral arthroplasty. A report of 56 arthroplasties with 17 years of follow-up. J Bone Jt Surg 85(6):836–840.
11. Leadbetter WB, Ragland PS, Mont MA (2005) The appropriate use of patellofemoral arthroplasty: an analysis of reported indications, contraindications, and failures. Clin Orthop Relat Res 436:91–99
12. Leadbetter WB, Seyler TM, Ragland PS, Mont MA (2006) Indications, contraindications, and pitfalls of patellofemoral arthroplasty. J Bone Jt Surg Am 88(Suppl 4):122–137.
13. van Wagenberg JM, Speigner B, Gosens T, de Waal Malefijt J. Midterm clinical results of the Autocentric II patellofemoral prosthesis. Int Orthop. 2009 Dec;33(6):1603-8. doi: 10.1007/s00264-009-0719-z. Epub 2009 Feb 18. PMID: 19224212; PMCID: PMC2899175.
14. Adrian Roberts. Chondromalacia Patellae at https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/384485/chondromalacia_patellae.pdf.
15. Mouzopoulos G, Borbon C, Siebold R. Patellar chondral defects: a review of a challenging entity. Knee Surg Sports Traumatol Arthrosc. 2011 Dec;19(12):1990-2001.

Ivermectin for Prevention and Treatment of COVID-19 Infection

          Ivermectin for Prevention and Treatment of COVID-19 Infection

                                                 Dr. KS Dhillon

Ivermectin oral tablet is used to treat infections of parasites. These include parasitic infections of our intestinal tract, skin, and eyes. It is also available as a topical cream and topical lotion. Ivermectin oral tablet is available as the brand-name drug Stromectol. 

Ivermectin tablet works by binding to parts inside the parasite. It eventually paralyzes and kills off the parasite, and it also stops adult parasites from making larvae for some time. This results in the eradication of the parasitic infection. 

In recent years several groups have shown, in-vitro, that ivermectin has anti-viral activity against a broad range of viruses [1]. Due to its in vitro antiviral activity against a broad range of viruses, it has been used off-label for the treatment of some viral diseases. 

Several studies have reported antiviral effects of ivermectin on RNA viruses such as dengue, Zika, yellow fever, West Nile, Hendra, Newcastle, Venezuelan equine encephalitis, chikungunya, Semliki Forest, Sindbis, Avian influenza A, Porcine Reproductive and Respiratory Syndrome, Human immunodeficiency virus type 1, and severe acute respiratory syndrome coronavirus 2. There are also some studies that show antiviral effects of ivermectin against DNA viruses such as Equine herpes type 1, BK polyomavirus, pseudorabies, porcine circovirus 2, and bovine herpesvirus 1.

Ivermectin has been found to have antiviral action against the SARS-CoV-2 clinical isolate in vitro. A single dose of ivermectin is able to control viral replication within 24–48 hours by inhibiting IMPα/β1-mediated nuclear import of viral proteins [1].

Ivermectin has an established safety profile for human use [2,3,4] and is FDA-approved for several parasitic infections [2,4]. Recent reviews and meta-analyses indicate that high-dose ivermectin has comparable safety as the standard low-dose treatment [5]. There, however, is not enough evidence to make conclusions about the safety profile in pregnancy.

Many drugs with anti-inflammatory, antiviral, and immunomodulatory properties are currently used in the treatment of COVID-19. Unfortunately, none of them can provide a complete cure [6]. One of the drugs whose effectiveness has been and is being investigated in the treatment of  COVID-19 is ivermectin.

Up to February 2021, the Pan American Health Organization (PAHO) identified twenty-two ivermectin randomized clinical trials through a rapid review of current available literature [7]. In these studies, there is considerable heterogeneity in the population receiving ivermectin, with studies administering it to family contacts of confirmed COVID-19 cases as a prophylactic measure [8], other studies using ivermectin for treatment of mild and moderate disease [9], and even in patients who are hospitalized with severe disease [10]. 

Kim et al [11] recently published a systematic review and network meta-analysis that compared the efficacy and safety of pharmacological interventions for COVID-19 in hospitalized patients. The review included 110 studies (78 published and 38 unpublished) with 40 randomized clinical trials and 70 observational studies. Based on the observational data, they found that high-dose intravenous immunoglobulin, tocilizumab, and ivermectin were associated with a reduced mortality rate in critically ill patients. They also found that none of the analyzed drugs were significantly associated with increased non-cardiac serious adverse events compared to standard care.

Kow et al [12] carried out a meta-analysis to study the association between the use of ivermectin and mortality in patients with COVID-19. The study included 6 randomized controlled trials with a total of 658 patients who were randomized to receive ivermectin and 597 patients randomized in the control group who did not receive ivermectin. The meta-analysis showed significantly reduced odds of mortality with the use of ivermectin among patients with COVID-19 relative to non-use of ivermectin. The estimated effect of ivermectin indicated mortality benefits.

Rajter et al [13] carried out a study that showed that the use of Ivermectin is associated with lower mortality in hospitalized patients with coronavirus disease. Their study included 280 patients, 173 treated were treated with ivermectin and 107 without ivermectin. Most patients in both groups also received hydroxychloroquine, azithromycin, or both. Univariate analysis showed lower mortality in the ivermectin group. Mortality also was lower among ivermectin-treated patients with severe pulmonary involvement. No significant differences were found in extubation rates or length of stay. After multivariate adjustment for confounders and mortality risks, the mortality difference remained significant. Mortality was significantly lower in the ivermectin group. 

Okumus et al [14] carried out a study to evaluate the effectiveness and safety of adding ivermectin to treatment in patients with severe COVID-19.

It was a prospective, randomized, controlled, single-blind phase 3 multicenter clinical trial to assess the effectiveness and safety of ivermectin use in the treatment of patients without mutation. All patients in the study had severe COVID19 pneumonia. Ivermectin 200 mcg/kg/day for 5 days in the form of a solution prepared for enteral use was given to the study group in addition to the reference treatment protocol of hydroxychloroquine, favipiravir, and azithromycin. Patients in the control group were given only reference treatment with 3 other drugs without ivermectin. The study showed that ivermectin provided an increase in clinical recovery, improvement in prognostic laboratory parameters, and a decrease in mortality rates even when used in patients with severe COVID-19. The authors were of the opinion that ivermectin should be considered as an alternative drug that can be used in the treatment of COVID-19 disease or as an additional option to existing protocols.

Shoumann et al [15] carried out a randomized clinical trial to study the use of ivermectin for chemoprophylaxis for covid-19 infection. This was a  prospective interventional randomized open label-controlled study. Two arms were designed according to the use of ivermectin. In the ivermectin arm, contacts of a patient with covid infection received ivermectin on the day of the diagnosis of their index case. The nonintervention group received no ivermectin. Both groups were followed up for two weeks to look for symptoms suggestive of COVID-19.

In the Ivermectin group, there were 203 contacts (to 52 index cases). In the nonintervention group, there were 101 contacts (to 24 index cases). Fifteen contacts (7.4%) developed COVID-19 in the ivermectin arm as compared to 59 (58.4%) in the nonintervention arm. The authors concluded that Ivermectin is suggested to be a promising, effective, and safe chemoprophylactic drug in the management of COVID-19.

Bryant et al [16] carried out a systematic review and meta-analysis to assess the efficacy of ivermectin treatment and/or prophylaxis among people with, or at high risk of covid-19 infection. They searched bibliographic databases up to February 2021. Their study included 21 RCTs involving 2741 participants. Meta-analysis of 13 trials found that ivermectin reduced the risk of death compared with no ivermectin. The evidence was of low to moderate certainty. Low-certainty evidence found that ivermectin prophylaxis reduced covid-19 infection by an average of 86%.

The systematic review and meta-analysis were done using rigorous Cochrane methods. Evidence was assessed using the GRADE approach which judges the certainty of the evidence.

The authors concluded that the apparent safety and low cost of the drug suggest that ivermectin could have an impact on the SARS-CoV-2 pandemic globally. Ivermectin is not a new and experimental drug with safety concerns; it is a WHO ‘essential medicine’ usually used for the treatment of other diseases.

López-Medina et al [17] carried out a randomized clinical trial to determine whether ivermectin is efficacious in the treatment for mild COVID-19. In this double-blind, randomized trial a total of 476 adult patients with mild disease and symptoms for 7 days or fewer (at home or hospitalized) were enrolled

between July 15 and November 30, 2020, and followed up through December 21, 2020. The patients were randomized to receive ivermectin, 300 μg/kg of body weight per day for 5 days (n = 200) or placebo (n = 200).

The median time to resolution of symptoms was 10 days in the ivermectin group compared with 12 days in the placebo group. By day 21, 82% in the ivermectin group and 79% in the placebo group had resolved symptoms. The authors concluded that among adults with mild COVID-19, a 5-day course of ivermectin, compared with placebo, did not significantly improve the time to resolution of symptoms. They said that their findings do not support the use of ivermectin for the treatment of mild COVID-19.

Despite the presence of several randomized clinical trials which show the effectiveness of Ivermectin in the treatment and prophylaxis of covid-19, WHO in its latest 2021 guidelines does not recommend the use of ivermectin for the treatment of covid-19 infections. According to WHO the current evidence on the use of ivermectin to treat COVID-19 patients is inconclusive. WHO recommends that the drug only be used within clinical trials. The WHO panel did not look at the use of ivermectin to prevent COVID-19. 

WHO strongly recommends the use of systemic corticosteroids for severe or critically ill COVID-19 patients. WHO does not recommend the use of remdesivir, hydroxychloroquine, and lopinavir/ritonavir for treatment of covid-19.  WHO provides conditional recommendation for the use of low-dose anticoagulants in hospitalized covid-19 patients. 

The WHO decision was based on the following factors. Their panel found that for most key outcomes, including mortality, mechanical ventilation, hospital admission, duration of hospitalization, and viral clearance, the evidence was of very low certainty. The evidence was rated as very low certainty mainly because of very serious imprecision for most outcomes: the aggregate data had wide confidence intervals and/or very few events. There were also concerns related to the risk of bias for some outcomes, specifically lack of blinding, lack of trial pre-registration, and lack of outcome reporting for one trial that did not report mechanical ventilation despite pre-specifying it in their protocol (publication bias) [18].

There has been some criticism of the WHO analysis [19]. According to the critics, the WHO analysis contains many flaws [19]: 

• Of the 58 studies (29 RCTs) available in the literature, WHO only included 16 in their analysis.
• They excluded all 14 prophylaxis studies (4 RCTs).
• There was no protocol for data exclusion.
• Trials included in the original UNITAID search protocol were excluded.
• They excluded all epidemiological evidence, although WHO has considered such evidence in the past.
• They combine early treatment and late treatment studies and do not provide heterogeneity information. Early treatment is more successful, so pooling late treatment studies will obscure the effectiveness of early treatment. They chose not to do subgroup analysis by disease severity across trials, although treatment delay is clearly a critical factor in COVID-19 treatment, the analysis is easily done, and it is well known that the studies for ivermectin and many other treatments clearly show greater effectiveness for early treatment.
• WHO downgraded the quality of trials compared to the UNITAID systematic review team and a separate international expert guideline group that has long worked with the WHO.
• They disregarded their own guidelines that stipulate quality assessments should be upgraded when there is evidence of a large magnitude effect (which there is), and when there is evidence of a dose-response relationship (which there is). They claim there is no dose-response relationship, while the UNITAID systematic review team found a clear relationship.
• Their risk of bias assessments does not match the actual risk of bias in studies. There is a clear treatment delay-response relationship and very late stage treatment is not expected to be as effective as early treatment. Much higher quality studies were classified as high risk of bias.
• Although WHO's analysis is called a "living guideline", it is rarely updated and very out of date. As of May 14, 2021, four of the missing RCTs are known to WHO and labeled "RCTs pending data extraction" [COVID-NMA]. 
• A single person served as Methods Chair, member of the Guidance Support Collaboration Committee, and member of the Living Systematic Review/NMA team.
• Public statements from people involved in the WHO analysis suggest substantial bias. For example, a co-chair reportedly said that "the data available was sparse and likely based on chance". The data is comprehensive, and we estimate the probability that an ineffective treatment generated results as positive as observed to be 1 in 9 trillion (p = 0.00000000000011). The clinical team lead refers to their analysis of ivermectin as "fighting this overuse of unproven therapies ... without evidence of efficacy", despite the extensive evidence of efficacy from the 58 studies by 519 scientists with 18,776 patients. People involved may be more favorable to the late-stage treatment of COVID-19, for example, the co-chair recommended treating severe COVID-19 with remdesivir.

It is not true that there is no evidence for the use of ivermectin in the prevention and treatment of covid-19 infections. There is evidence but the evidence is apparently weak.

In conclusion, research related to ivermectin use in COVID-19 has several limitations but the evidence continues to grow [20,21]. The use of ivermectin for prophylaxis or treatment for COVID-19 should be done based on trustable evidence, without conflicts of interest, with proven safety and efficacy in patient-consented, ethically approved, randomized clinical trials [22]. There remains a need for large randomized clinical trials to prove the efficacy of ivermectin in the prevention and treatment of covid-19 infections.

Reference

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5. Navarro M, Camprubí D, Requena-Méndez A, Buonfrate D, Giorli G, Kamgno J, Gardon J, Boussinesq M, Muñoz J, Krolewiecki A. Safety of high-dose ivermectin: a systematic review and meta-analysis. J Antimicrob Chemother. 2020 Apr 1;75(4):827-834. doi: 10.1093/jac/dkz524. PMID: 31960060.
6. Jean SS, Lee PI, Husueh PR. Treatment options for COVID-19: the reality and challenges. J Microbiol Immunol Infect. 2020;53(3): 436–43.
7. PAHO. Ongoing living update of COVID-19 therapeutic options: summary of evidence, 2021. Available: https://iris.paho.org/bitstream/handle/10665.2/52719/PAHOIMSEIHCOVID-19200030_eng.pdf?sequence=17&isAllowed=y.
8. Clinical Trial. Prophylactic ivermectin in COVID-19 contacts.. Available: https://clinicaltrials.gov/ct2/show/NCT04422561.
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10. Hashim HA, Maulood MF, Rasheed AM. Controlled randomized clinical trial on using ivermectin with doxycycline for treating COVID-19 patients in Baghdad, Iraq. medRxiv 2020:2020.10.26.20219345.
11. Kim MS, An MH, Kim WJ, et al. Comparative efficacy and safety of pharmacological interventions for the treatment of COVID-19: a systematic review and network meta-analysis. PLoS Med 2020;17:e1003501. doi:10.1371/journal.pmed.1003501 pmid:http://www.ncbi.nlm.nih.gov/pubmed/33378357.
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14. Nurullah Okumus, Nese Demirtürk, Rıza Aytac et al. Evaluation of the effectiveness and safety of adding ivermectin to treatment in severe COVID-19 patients. BMC Infectious Diseases (2021) 21:411.
15. Waheed M Shoumann, Abdelmonem Awad Hegazy, Ramadan M Nafae et al. Use of Ivermectin as a Potential Chemoprophylaxis for COVID-19 in Egypt: A Randomized Clinical Trial. Journal of Clinical and Diagnostic Research. 2021 Feb, Vol-15(2): OC27-OC32.
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17. Eduardo López-Medina et al. Effect of Ivermectin on Time to Resolution of Symptoms Among Adults With Mild COVID-19. A Randomized Clinical Trial. JAMA. 2021;325(14):1426-1435. doi:10.1001/jama.2021.3071.
18. WHO Therapeutics and COVID-19 living guideline at https://app.magicapp.org/#/guideline/5058/section/67421.
19. Ivermectin for COVID-19: real-time meta-analysis of 58 studies at https://ivmmeta.com/.
20. Chaccour C, Casellas A, Blanco-Di Matteo A, et al. The effect of early treatment with ivermectin on viral load, symptoms and humoral response in patients with non-severe COVID-19: a pilot, double-blind, placebo-controlled, randomized clinical trial. EClinicalMedicine 2021;32:100720.doi:10.1016/j.eclinm.2020.100720.
21. Hill A, Abdulamir A, Ahmed S. Meta-Analysis of randomized trials of ivermectin to treat SARS-CoV-2 infection. Research square 2021.doi:10.21203/rs.3.rs-148845/v1.
22. Garegnani LI, Madrid E, Meza NMisleading clinical evidence and systematic reviews on ivermectin for COVID-19BMJ Evidence-Based Medicine Published Online First: 22 April 2021. doi: 10.1136/bmjebm-2021-111678.

                Talus dislocations

                                     DR KS Dhillon

Anatomy of the talus

The talus is the second largest tarsal bone, and it is situated posteriorly in the hindfoot between the tibia and the calcaneus. Two-thirds of the talar surface is covered with articular cartilage and it has a tenuous blood supply. It has 5 articular surfaces and there are no muscles or tendons attached to it. The talus has 3 parts, namely the head, neck, and body. There are two processes on the talus (the lateral and posterior process).

The talus has seven articular surfaces.

Superiorly the talus through the talar dome forms the mortise joint of the ankle with the tibia, medial and lateral malleoli.

Inferoposteriorly there is a large oblique facet that is concave which articulates with the calcaneus to form the talocalcaneal joint.

Anteroinferiorly there are two facets that articulate with the calcaneus to form part of the talocalcaneonavicular joint. The talar head articulates anteriorly with the navicular to form the talonavicular joint.

Blood supply is provided by the posterior tibial artery into the medial side of body and sinus, anterior tibial artery/dorsalis pedis artery into head and neck, and peroneal artery into the lateral side of the body and sinus. 

Robust peritalar ligaments provide stability to the talus. These include:

• Anterior talofibular ligament
• Posterior talofibular ligament
• Talocalcaneal ligaments
• Tarsal sinus ligaments
• Cervical ligament
• Talocalcaneal interosseous ligament
• Deltoid ligament
• Anterior tibiotalar ligament
• Posterior superficial tibiotalar ligament
• Posterior deep tibiotalar ligament
• Dorsal talonavicular ligament

Talus dislocation

There several types of talar dislocation given its multiple articulations. These include tibiotalar dislocation, subtalar dislocation, total talar dislocation, and talonavicular dislocation.

1.Total talar dislocation.

Total talar dislocation is also known as extrusion of the talus or pan-talar dislocation. It involves a tri-articular dislocation of the talus at the tibiotalar, talonavicular, and subtalar joints.  Most injuries are compound.

It usually occurs due to a high‐energy impact to an inverted, plantar‐flexed foot resulting from a fall from height or from a motor vehicle accident.

Total dislocation of the talus is a rare injury and it accounts for only 0.06% of all dislocations and only 2% of talar injuries [1]. 

Limited blood supply and numerous articulations of the talus along with the fact that the injuries are frequently open, make the treatment of total talar dislocation difficult. Such injuries are often associated with complications such as avascular necrosis (AVN), infection, and osteoarthritis [2]. 

In patients with close dislocation, a close reduction is carried out under GA and if the reduction is stable a cast is applied for 6 weeks. If the reduction is not stable percutaneous pinning can be carried out to maintain the talus in its position. If a close reduction is not successful, open reduction is carried out.

In patients with open dislocation, wound irrigation, debridement, and temporary internal or external stabilization of the ankle is carried out.

If the talus is lost and cannot be found, tibiocalcaneal fusion and fibular graft is a surgical option.

Primary talectomy is not recommended. All attempts must be made to preserve the talus even in patients with total extrusion of the talus with significant contamination.

Besides the total dislocation of the talus, neurovascular, capsular, and ligamentous injuries and pressure necrosis are early concomitant injuries.  Late complications include AVN, infection, and post-traumatic degenerative arthritis. Post-traumatic osteoarthritis can occur after several years. 

Incidence of AVN after total dislocation of the talus varies between 24% [3] and 88% [4]. The incidence of posttraumatic osteoarthritis (PT) varies between 10% [3] and 44% [4].

Open talar dislocations are often complicated by soft‑tissue infection. The incidence of infection ranges from 11.5% to 38% [5,6]. Infection rate as high as 88.9% has been reported in the older days [7]. Over the years, infection rates have been brought down through improvement of staged procedures for wound care and soft‑tissue management and adapted antibiotherapy.

2.Subtalar Dislocation

Subtalar dislocations are also known as peritalar dislocations. Subtalar dislocation is a rare injury that accounts for 1%–2% of all dislocations. In subtalar dislocations, there is a separation of the talonavicular and talocalcaneal articulations. These dislocations are commonly caused by falls from height, motor vehicle crashes, and twisting leg injuries. The dislocations are divided into anterior, posterior, medial, and lateral types based on the direction in which the distal part of the foot moves in relation to the talus. The most common type is medial dislocation which results from an inversion injury. A medial dislocation occurs in about 71.5 % of the patients, lateral in 26.0%, posterior in 1.6%, and anterior in about 0.8% of the patients [8]. Most of the dislocations are close. An open dislocation occurs in about 22.5% of the patients [8]. Sometimes subtalar dislocations are associated with fractures of the navicular, calcaneus, and talus. Additional bony injury is seen in about 61.4% of the patients [8].

During the physical examination, the neurovascular status must be carefully assessed. Subtalar dislocations are treated with closed reduction under sedation. In about 14% of the patients close reduction is unsuccessful. If close reduction fails, immediate open reduction should be carried out. After reduction of the dislocation, X-rays and if necessary computed tomography scan should be performed to evaluate the alignment of the bones and evaluate the presence of fractures.

The overall outcome of treatment of subtalar dislocations is good in 52.3%, fair in 25.2%, and poor in 22.5% of the patients.

The most frequent late complications following subtalar dislocations include pain, decreased motion, subtalar instability, and degenerative joint disease [9,10]. Other complications that have been reported include avascular necrosis of the talus, RSD (reflex sympathetic dystrophy), and recurrent dislocation [11]. Some authors have reported no AVN following subtalar dislocations [11,12] while others have reported a low incidence of 4% to 6% [9,10]. In patients with severe open fracture-dislocations of the subtalar joint a high incidence of 33% has been reported [13].

About 80% of patients with subtalar dislocation show significant restriction of motion and about 30% show roentgenographic evidence of arthritis [14].

3.Talonavicular Dislocation

Isolated dislocation of the talonavicular joint is a rare injury. These injuries are caused by severe adduction or abduction force applied to the forefoot. 

A medially or laterally directed force applied to the foot causes dislocation of the talonavicular joint without dislocation of the subtalar joint. The calcaneum along with the remaining foot swivels on the intact interosseous talocalcaneal ligament. The dislocation can be medial or lateral depending on the direction of the force applied to the foot. Medial dislocation is more common than a lateral dislocation.

The dislocation is treated by close reduction and cast immobilization. If close reduction fails, an open reduction is carried out, and if the reduction is not stable, internal fixation with K-wires can be done. The leg is immobilized with a cast. 

4.Tibiotalar dislocation

The tibiotalar joint is formed by the tibia, fibula, and talus. Stability is provided by the strong medial (deltoid) and lateral ligaments.

Tibiotalar dislocation is also known as talocrural or ankle dislocation. Tibiotalar dislocations without associated fractures are very uncommon. More than 50% of these dislocations are posteromedial and 25% are pure posterior dislocations [15]. The majority of dislocations are open injuries. On rare occasions, the dislocation can be anterior/anterolateral, medial, or lateral.

The usual mechanism of injury is a fall on a fully plantarflexed foot. The fall forces the talus into a position posterior to the tibia. Other causes of dislocation include motor vehicle accidents and sporting injuries. 

Most cases of closed tibiotalar dislocations can be treated by close reduction under sedation and cast immobilization for 6 to 9 weeks [15].  Open injuries are treated with thorough wound lavage and débridement followed by reduction of the dislocation, stabilization with K-wires if necessary, repair of ligaments and capsule, and immobilization in a slab followed by casting.

The overall prognosis for tibiotalar dislocations is favorable. The majority of patients are asymptomatic following appropriate treatment [16]. Those who are symptomatic (primarily female) complain of ankle stiffness. Ankle instability is rare. Closed dislocations are associated with fewer symptoms as compared to open dislocations. Some of the prognostic factors that are associated with worse outcomes include advanced age, presence of vascular injury, delay in reduction, and inferior tibiofibular ligament injury [16].  Late complications reported include stiffness, degenerative changes, joint instability, and capsular calcification [17]. 

The incidence of posttraumatic osteoarthritis is about 25% and it often occurs in patients with open dislocations [18]. 

Conclusion

There several types of talar dislocation given its multiple articulations. These include tibiotalar dislocation, subtalar dislocation, total talar dislocation, and talonavicular dislocation. Most of the time these dislocations result from falls from a height. Other causes include motor vehicle accidents and sports injuries. 

The injuries can be open or close. Open dislocations are treated with wound debridement. The dislocation can be treated with close reduction. If close reduction fails open reduction can be carried out. If the reduction is stable the limb is immobilized with a cast for 6 to 8 weeks. If the reduction is not stable then the fragments can be stabilized with k-wires or external fixation.

The complications include loss of motion, instability, AVN, and posttraumatic arthritis. Generally, the clinical outcome is good. Open dislocations can result in poorer outcomes.

Reference

1. Pavić R. Talocalcaneal transfixation in total dislocation of the talus and subtalar dislocations. Mil Med, 2009, 174: 324–327.
2. Wagner R, Blattert TR, Weckbach A. Talar dislocations. Injury. 2004 Sep;35 Suppl 2:SB36-45. doi: 10.1016/j.injury.2004.07.010. PMID: 15315877.
3. Weston JT, Liu X, Wandtke ME, Liu J, Ebraheim NE. A systematic review of total dislocation of the talus. Orthop Surg. 2015;7(2):97-101. doi:10.1111/os.12167.
4. Boden, Kaeleen A. BA1; Weinberg, Douglas S. MD1; Vallier, Heather A. MD1, a Complications and Functional Outcomes After Pantalar Dislocation, The Journal of Bone and Joint Surgery: April 19, 2017 - Volume 99 - Issue 8 - p 666-675 doi: 10.2106/JBJS.16.00986.
5. Palomo-Traver JM, Cruz-Renovell E, Granell-Beltran V, Monzonís-García J. Open total talus dislocation: Case report and review of the literature. J Orthop Trauma 1997;11:45-9.
6. Marsh JL, Saltzman CL, Iverson M, Shapiro DS. Major open injuries of the talus. J Orthop Trauma 1995;9:371-6.
7. Detenbeck LC, Kelly PJ. Total dislocation of the talus. J Bone Joint Surg Am. 1969 Mar;51(2):283-8. PMID: 4975068.
8. Hoexum F, Heetveld MJ. Subtalar dislocation: two cases requiring surgery and a literature review of the last 25 years. Arch Orthop Trauma Surg. 2014 Sep;134(9):1237-49. doi: 10.1007/s00402-014-2040-6. Epub 2014 Jul 4. PMID: 24993588.
9. Christensen SB, Lorentzen JE, Krogsøe O, Sneppen O. Subtalar dislocation. Acta Orthop Scand. 1977;48(6):707-11. doi: 10.3109/17453677708994821. PMID: 607761.
10. Zimmer TJ, Johnson KA. Subtalar dislocations. Clin Orthop Relat Res. 1989 Jan;(238):190-4. PMID: 2910600.
11. F. Rivera, C. Bertone, E. Crainz, P Maniscalco and M. Filisio. Peritalar dislocation: three case reports and literature review. J Orthopaed Traumatol (2003) 4:39–44.
12. Wang HY, Wang BB, Huang M, Wu XT. Treatment of closed subtalar joint dislocation: A case report and literature review. Chin J Traumatol. 2020;23(6):367-371. doi:10.1016/j.cjtee.2020.08.008
13. Goldner JL, Poletti SC, Gates HS 3rd, Richardson WJ. Severe open subtalar dislocations. Long-term results. J Bone Joint Surg Am. 1995 Jul;77(7):1075-9. doi: 10.2106/00004623-199507000-00015. PMID: 7608231.
14. Heppenstall RB, Farahvar H, Balderston R, Lotke P. Evaluation and management of subtalar dislocations. J Trauma. 1980 Jun;20(6):494-7. doi: 10.1097/00005373-198006000-00011. PMID: 7373681.
15. Grotz et al. Open Tibiotalar Dislocation Without Associated Fracture in a 7-Year-Old Girl. A Case Report & Literature Review. Am J Orthop. 2008;37(6): E116-E118.
16. Wight L, Owen D, Goldbloom D, Knupp M. Pure Ankle Dislocation: A systematic review of the literature and estimation of incidence. Injury. 2017 Oct;48(10):2027-2034. 
17. Wang YT, Wu XT, Chen H. Pure closed posteromedial dislocation of the tibiotalar joint without fracture. Orthop Surg. 2013 Aug;5(3):214-8.
18. Elisé S, Maynou C, Mestdagh H, Forgeois P, Labourdette P. Les luxations tibio-astragaliennes pures. A propos de 16 observations [Simple tibiotalar luxation. Apropos of 16 cases]. Acta Orthop Belg. 1998 Mar;64(1):25-34. French. PMID: 9586247.

Distal Humerus Fractures

                        Distal Humerus Fractures
  

                                        Dr. KS Dhillon

Introduction

Fractures of the distal humerus constitute about 2% of all fractures in the adult population [1]. The overall incidence of distal humeral fractures in adults is 5.7 cases per 100,000 in the population per year. The male to female ratio is about equal. There is a bimodal age distribution with the first peak in young individuals resulting from high-energy trauma and the second peak in the elderly osteoporotic population. Two-thirds of those affected are aged 50 years or older. The incidence of these fractures is rising. 

Simple falls are the most common overall cause of the fracture, and the majority of the fractures are extra-articular or complete articular fractures [2]. 

The aim of treatment is to restore a functional elbow in the functional range of motion between 30 to 130 degrees [3]. Loss of elbow movements can severely affect activities of daily living and lead to a loss of independence, especially in elderly individuals [4]. Treatment of these fractures can be challenging due to fracture comminution, poor bone quality as well as difficulty in restoring the complex anatomy of the distal humerus [5].

Most of the distal humerus fractures used to be treated non-operatively in the past and the treatment often resulted in significant functional impairment [2]. 

However, with evolution in implant design and surgical technique, the outcome of operative treatment has improved and this has made internal fixation of the fractures as the current standard of care. The aim of surgical treatment is to restore articular congruity and bony alignment while providing rigid, stable fixation that enables early active motion [6]. 

         

Anatomy of Distal Humerus

In the coronal plane, the distal humerus is triangular in shape. It is formed by the medial and lateral columns which are linked by the articular segment as shown in Fig.1. 

The distal end of the humerus includes two smooth articular surfaces (capitulum and trochlea), two depressions (fossae) that form part of the elbow joint, and two projections (medial and lateral epicondyles). The capitulum laterally articulates with the radius; the trochlea, a spool-shaped surface, articulates with the ulna. The articular surface is in 4-8 degrees of valgus relative to the shaft and flexed 40 degrees relative to the shaft.

               

                                                        Fig 1. Anatomy of distal Humerus

Classification of Distal Humerus Fracture

The AO classification divides distal humeral fractures into three groups namely, A, B, and C with complexity and severity increasing.

Müller’s classification of distal humeral fracture is part of the AO scheme. This region is marked 13, so each type has this prefix, e.g. 13-A1.

Type Description

Type A:   Extraarticular fractures:

13-A1:    Apophyseal avulsion

13-A2:    Metaphyseal simple

13-A3:    Metaphyseal multifragmentary (comminuted)

Type B:    Partial articular fractures:

13-B1:     Sagittal lateral condyle

13-B2:     Sagittal medial condyle

13-B3:     Frontal

Type C:   Complete articular fractures:

13-C1:     Articular simple, metaphyseal simple

13-C2:     Articular simple, metaphyseal multifragmentary (comminuted)

13-C3:     Articular, multifragmentary (comminuted)

Imaging for Distal Humerus Fractures

All attempts are made to obtain good-quality radiographs. This may be difficult due to patient discomfort. The AP is taken with the elbow flexed to 40 degrees. This facilitates olecranon disengagement from the fossa which allows for better visualization of the distal humerus. The lateral images are taken with the shoulder abducted to 90 degrees and the elbow flexed to 90 degrees with the plate underneath the medial aspect of the elbow. A CT scan is useful to assess articular involvement and aid surgical planning. 

Non-Operative Treatment

Over the decades, there are only a few conflicting reports available in the literature on the outcomes of conservatively treated fractures of the distal humerus. Non-operative treatment involves splintage for pain relief followed by gentle mobilization. 

Nauth et al [7] showed that in elderly patients, those treated non-operatively were almost three times more likely to have an unacceptable result as compared to those treated operatively. Non-operative treatment is usually reserved for undisplaced fractures, for patients with dementia, and those who are not fit for anesthesia. Recently Aitken et al. reported that non-operative treatment could give a modest functional result in low-demand patients while avoiding substantial surgical risks [8].

Operative treatment 

Distal humerus fractures are commonly treated by surgery if the fracture is displaced and the patient is fit for surgery.

There are three surgical approaches to the distal humerus, namely the triceps reflecting, triceps splitting, and the trans-olecranon approach. The trans-olecranon approach gives the best articular exposure but it carries the risk of non-union, future need for the removal of implants, and potentially limiting any future arthroplasty. 

The triceps splitting approach has the potential to result in triceps weakness. The triceps reflecting technique spares the triceps mechanism and has the advantage of avoiding damage to the extensor mechanism. This approach, however, provides limited exposure of the articular surface.

For complex intra-articular fractures (type C), an olecranon osteotomy is usually preferred.

The aim of treatment is to obtain anatomic reduction and rigid internal fixation which will allow early mobilization. Rigid plate fixation gives better functional outcomes as compared to fixation solely with Kirschner wires or screws [9]. Plate fixation is now the standard treatment for distal humerus fractures. Although perpendicular plating was originally advocated by the AO group, parallel plating has now grown in popularity. Studies have shown that parallel plating provides better stability compared with the perpendicular locking system [10,11]. Clinical studies show there are no differences between the groups (perpendicular and parallel plates) in terms of functional outcome or complication rate [12,13]. The use of locking compression plates has been advocated for osteoporotic fractures as they provide angular stability and the head-locking mechanism potentially results in a stiffer construct [24]. 

Different length plates are used for fracture fixation to avoid a stress riser at the end of the plates and avoid the risk of a peri-prosthetic fracture. Post-operatively a back slab used for one to two weeks to protect the wound. Passive mobilization is carried out from two weeks and active mobilization after six weeks.

Despite the improvements in surgical techniques and evolution of implant designs, operative fixation of distal humerus fractures have been associated with dissatisfaction in about 15% of patients and complication rates of up to 35% [14,15]. Some of the factors that are known to affect clinical outcome include fracture comminution, reduction accuracy, fixation stability, and quality of postoperative rehabilitation [16]. 

Complications of operative treatment of distal humerus fracture

Complications can include hardware failure, fracture, malunion, non-union, infection, heterotopic ossification, elbow stiffness, ulnar neuropathy, and complications from olecranon osteotomy [17].

• Mechanical failure-- Mechanical failure is known to occur in 7–27% of patients [18,19,20]. Risk factors for failure include bone quality, such as osteoporotic or osteopenic bone, the complexity of the fracture,  bone defects, mechanical properties of implants, and postoperative rehabilitation [21]. Poor surgical technique is another risk factor. 
• Ulnar neuropathy-- Ulna neuropathy as a complication of distal humerus fractures, preoperatively and/or postoperatively, occurs in 0% to 51% of the patients, with an average of 13% [17]. The palsy can occur either at the time of the injury or intraoperatively. It can also occur secondarily due to swelling, to scar tissue development and thickening in the fibro-osseous tunnel, or due to hardware irritation. The true incidence of ulnar nerve dysfunction after elbow injury remains unknown. It appears that anterior transposition of the ulna nerve does not decrease the development of ulnar neuropathy after internal fixation of the fracture [17]. 
• Heterotopic ossification--The incidence of heterotopic ossification (HO) after internal fixation of distal humerus fractures varies widely from 0% to 49%. However, pooled analysis of data from several studies shows an overall prevalence of 8.6% [17]. There are several risk factors for HO and these include, concomitant head and central nervous system injury, delayed internal fixation,33 use of bone graft or substitute, prolonged postoperative immobilization. A 48 hours delay in fixation can increase the rate of HO from 0% to 33%. Kundel et al reported an increase in the rate of HO from 29% to 80% when surgical treatment was delayed by more than 24 hours [22]. HO can be radiologically visible two weeks after surgery in 86% of patients who finally developed HO [23]. In some cases, HO can cause limitations in elbow motion and function, and in such patients excision of the HO may be necessary. The routine use of indomethacin for prophylaxis against HO following internal fixation of distal humerus fractures remains controversial.
• Elbow stiffness-- Elbow stiffness is the most common sequela after internal fixation of distal humeral fractures. Elbow stiffness can be often seen even after optimal stable fixation and proper rehabilitation. Some authors have reported that one-third of patients failed to get a functional range of motion in the elbow after fracture fixation [17]. Loss of elbow motion can result from intrinsic or extrinsic causes such as malunion, nonunion, incongruity of the articular surface, intra-articular and capsular fibrosis, and adhesions around the elbow callus formation, HO, prolonged postoperative immobilization, and prominent hardware [24]. Early mobilization remains the mainstay of the prevention of elbow stiffness. In some patients, surgical treatment of elbow stiffness is needed. In these patients arthrolysis and contracture release is necessary. Open release of elbow stiffness is usually more effective when HO is obstructing motion. Sometimes implants need to be removed. Sometimes refractures can occur after the removal of implants.
• Nonunion-- Nonunions after internal fixation of distal humerus fractures have been reported to be between 2% and 10% [25].  High-energy trauma, gross comminution, and poor bone stock are some of the reasons for nonunion. In elderly patients, fracture union rather than motion is the first priority, because motion can be restored later by contracture release after the fracture unites. Nonunions can severely compromise the patient’s quality of life [26]. Nonunions usually need revision of internal fixation, autogenous bone-grafting, and aggressive contracture release.
• Malunion-- Malunion is seen in about 30% of patients with distal humerus fractures. It is more common in patients with nonoperatively treated fractures as compared to operatively treated fractures. Malunions of the distal humerus are either extra-articular or intra-articular. Extra-articular malunions are treated with humeral osteotomy and fixation. Intra-articular malunions are more difficult to treat. Intra-articular corrective osteotomy is usually considered in young patients who present with moderate to severe functional disability and/or pain and secondary post-traumatic arthritis at an early stage [27]. The aim of treatment is to restore the articular anatomy in order to improve motion, relieve pain and enhance stability in active young patients. In the elderly low demand patients, a total elbow replacement is an option.
• Infection and wound complications--  The wound complications incidence after fixation of distal humerus fractures is substantial and can be associated with significant morbidity. The risk for serious wound complications after surgery is high because of soft tissue damage, relatively thin soft tissue envelope, postoperative swelling, and shear forces occurring when elbow motion is started [28].     Infection should be suspected in any patient with persistent wound discharge. Open fractures and the use of a plate to stabilize the olecranon osteotomy, are considered to be significant risk factors. Majority of wound complications can successfully be treated with debridement and primary or delayed wound closure. In some patients, myocutaneus flaps may be necessary.
• Failure of olecranon osteotomy-- Complications of olecranon osteotomy include nonunion, malunion, hardware failure, and skin irritation by prominent implants. The incidence of complications associated with olecranon osteotomy ranges from 0% to 31% [17]. The reported rate of nonunion is about 11.9% [29].

Elbow Arthroplasty

Total elbow arthroplasty (TEA) is being increasingly used for the treatment of comminuted intra-articular distal humerus fractures in the elderly patients [30]. Because of its limited longevity due to aseptic loosening, TEA is only recommended in patients with sedentary lifestyles who can comply with the post-operative rehabilitation program [5].  A study by Prasad et al showed that survivorship of the implants, with revision and definite loosening as end-points, was 89.5% at ten years in those patients who were followed for a minimum of ten years [31]. 

A study by Mansat et al [32] which analyzed the outcome of treatment of 87 patients over the age of 65 with a distal humeral fracture treated who were treated with TEA found that 63% of patients had a pain free elbow at 37.5 months follow up, 48% had a mean flexion-extension arc of at least 100º, and 79% of the patients had normal function. 

There were complications in 23% of the patients and revision surgery was necessary for 9% of the patients. 

Conclusion

Fractures of the distal humerus constitute about 2% of all fractures in the adult population. The overall incidence of distal humeral fractures in adults is 5.7 cases per 100,000 in the population per year. Distal humerus fractures are difficult to treat especially in the elderly with poor bone stock. Improvements in implant design and surgical technique have resulted in better clinical outcomes following open reduction and internal fixation of distal humerus fractures. Open reduction and internal fixation is now standard treatment for displaced fractures of the distal humerus. 

However, the open reduction and internal fixation of these fractures can be challenging and can be associated with a high rate of complications. Total elbow arthroplasty has been advocated as a treatment option for elderly patients especially in those with unreconstructable distal humerus fractures.

References

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10. Stoffel K., Cunneen S., Morgan R., Nicholls R., Stachowiak G. Comparative stability of perpendicular versus parallel double-locking plating systems in osteoporotic comminuted distal humerus fractures. J. Orthop. Res. 2008;26(6):778–784. doi: 10.1002/jor.20528. 
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13. Lee S.K., Kim K.J., Park K.H., Choy W.S. A comparison between orthogonal and parallel plating methods for distal humerus fractures: A prospective randomized trial. Eur. J. Orthop. Surg. Traumatol. 2014;24(7):1123–1131. doi: 10.1007/s00590-013-1286-y. 
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