ABSTRACT

Elbow injuries is a common injury seen in the acute setting. Radial head fractures are fairly common and accounts for approximately one third of elbow fractures¹. Goals of management are directed at restoring early range of motion to prevent stiffness, pain and instability¹. Post traumatic complications do occur infrequently but if missed can contribute to significant stiffness or instability symptoms. Heterotrophic ossification (HO) is a complication seen in elbow injury post dislocation, fracture, ligament, or tendon injuries. Excess lamellar bone infiltrates non osseous soft tissue with subsequent elbow stiffness. Radiographic imaging often will show irregular calcification that lack organization of mature cancellous or cortical bone². Most papers cite the “Terrible triad” and Essex-Lopresti injury as a major contributor to HO. Terrible triad consists of radial head and coronoid process fractures with concurrent elbow dislocation^{3 4}. Essex-Lopresti involves further injury of the distal radio-ulnar joint⁴. Nevertheless, there are other types of lesser injuries that can also cause HO. This paper focuses a bit on radial head fracture management, HO pathophysiology, and current available treatment options.

CASE HISTORY

Demographics: 53 year-old right hand dominant Samoan female was referred to fracture clinic by her general practitioner (GP) for further assessment and follow up.

Presenting Complaint: Presents with one week old un-displaced right radial head fracture.

History of Presenting Complaint: Injured right elbow by falling on outstretched hand. She developed immediate pain post fall.

Past Medical History:  Obesity. Nil regular medications. No known drug allergies. Currently only taking paracetamol and ibuprofen as needed.

Examination:  Reduced flexion/extension range of motion of right elbow from 30 to 120 degrees. Supination and pronation short by 10 degrees from full range of motion. No mechanical block. Upper limb neurology normal.

Investigation: Xray showed un-displaced right radial head fracture with elbow joint effusion.  

Management: Rest in above elbow back-slab and sling for two weeks. Simple analgesia. At two weeks, she was referred to physiotherapy for early range of motion. She was monitored up to the three-month mark before discharging her from fracture clinic.

Clinical Question – Do I need to worry about HO in radial head/neck fractures?

DISCUSSION

The elbow joint articulation is made up of the humerus, proximal ulna and radial head. Together with the joint capsule, ligaments, tendons and muscles, the radial head is an important stabilizer of the elbow in valgus and supination⁴. Radial head fracture is a common injury accounting for a significant proportion of upper limb injuries. It is most commonly caused by axial load onto the radial head following a fall on an outstretched hand⁴. There are different types of radial head fractures. It was originally described by Mason in 1954 and was further modified by Hotchkiss in 1997⁴. The current classification commonly used is the “Broberg-Morrey Classification”⁴. Table 1 below illustrates the types of radial head fractures classification according to their authors¹.

Treatment options can be conservative, or surgical which can involve open reduction internal fixation, e.g., screws, plates or even arthroplasty. The figure below shows a simplified version of the treatment algorithm in radial head fractures⁴.

In this paper, special interest is placed on HO post trauma/injury. HO is the formation of abnormal lamellar bone within non osseous soft tissues such as joint capsule, muscle, tendons, or ligaments^{3 5}. Capsule contraction and adhesion remains the most common cause of post traumatic elbow stifness⁶. Anterior capsule contracture leads to flexion contracture and posterior capsule contracture causes extension contracture⁶. In the case of muscles, brachialis contracture limits extension and triceps contracture limits flexion movement⁶. HO can be genetically related or acquired. The main aetiologies for HO are: genetic predisposition, neurogenic from central nervous system injury; traumatic e.g., burns; or orthopaedic following a fracture, dislocation or surgical fixation^{3 7}. Some literature has suggested that in radial head fracture, HO occurrence can be as high as 56%⁷. Studies have suggested no propensity of HO between genders or ethnic groups⁵.

The exact mechanism of HO is still a grey area.  There is abundance of literature on HO over the years, albeit with significant heterogeneity in study methods³. HO leads to poor patient satisfaction and rehab progress. It leads to joint stiffness, oedema, reduced range of motion and ankylosis of joints³. The pathophysiology of HO is still not fully understood. Undifferentiated tissue respond to various signals which then stimulate the undifferentiated mesenchymal tissue to form fibroblast⁵. This fibroblast deposit collagen and extracellular matrix⁵. They form metaplastic tissue within the planes of HO which leads to subsequent formation of chondroblast and osteoblasts⁵. HO is also believed to be influenced by several factors such as prostaglandin E2, leukotrienes, bone morphogenic protein (BMP) and inflammatory process⁵. BMP production is stimulated by inflammation, venous stasis, and immobilization which then leads to increase in osteogenic cell differentiation⁵. HO typically occurs from one to three months post injury⁵. Xray can only pick up bone formation after 3-6 weeks of formation whereas bone scan is sensitive in recognizing bone metabolic activity as early as two weeks⁵.

Herman and colleagues performed systematic literature review on a few medical databases over a period of 26 years³. Strict inclusion and exclusion criteria were used to allow standardization of study selection. They also incorporated a grading system for HO i.e., Hastings and Graham classification system³. Anatomical sites looked at: distal humerus, proximal radius, proximal ulnar, terrible triad injury, elbow fracture dislocation and complex fracture³. The figure below illustrates the three grades of Hastings and Graham Classification³.

Figure 2. Hastings and Graham Classification System

There is limited literature on non-steroidal anti-inflammatory (NSAID) prophylaxis for HO after elbow injury. The paper by Migliorini F. and colleagues on NSAIDs for prophylaxis for HO after total hip arthroplasty comes close to the clinical question⁸. This meta-analysis of randomized controlled trials looks at different NSAIDs and the rates of HO⁸. Celecoxib proved to be most efficacious in preventing HO although the authors acknowledged there are some limitations in their study which might confound their study results⁸. The other advantage gained from Celecoxib is the lower gastrointestinal side effect profile. Naproxen and Diclofenac also had some positive findings in HO prevention but not as convincing as Celecoxib⁸. The rest of the NSAIDs were statistically not significant. There were some limitations in the study i.e., some of studies were old, variability in study techniques and protocol heterogeneity⁸.  On the other spectrum, NSAIDs have been notorious in delaying bone healing. NSAID’s initial role is inhibitory but long term effect is bone resorption by proliferation and formation of osteclasts².  The study by Chen and Dragoo reviewed the literature looking at non-selective and selective (COX-2) NSAIDs⁹. NSAID cause prostaglandin inhibition by acting on platelets, endothelial and mast cells⁹. They act mainly on the prostaglandin pathway involving cyclo-oxygenase, arachidonic acid, thromboxane and prostacyclin⁹. There are multiple pathways in tissue healing. Platelet derived growth factor (PDGF) is responsible for the mitogenic and chemotactic effects on other cells, e.g., smooth muscle cells, neutrophils, macrophages and fibroblasts⁹. The PDGF pathways remains unaffected by NSAIDs and the authors conclude that NSAIDs appears safe as other pathways are sufficient for bone healing⁹. Hence,  the use of anti-inflammatories post sports injuries or surgeries is reasonable unless there are risk factors for poor bone healing⁹. Only Indomethacin appears to have deleterious effect in bone healing with no compelling evidence for the other NSAIDs⁹.

Herman ZJ. et al. suggested in their paper the incidence of HO after surgery was as high at 28.7%³. They further concluded that rates of HO was higher in injuries such as proximal humerus fractures, “terrible triad” and elbow fractures compared to distal humerus fractures³. One useful treatment option for post traumatic elbow stiffness is arthroscopic arthrolysis. Dai J et al. did a retrospective review of 30 arthroscopic elbow releases⁶. There was an improvement in the elbow range of motion post operatively⁶. The paper had some weakness, i.e., it was a non-randomised retrospective study with a short term follow up of 30 patients. There was no treatment comparison group. Although, the results were good post op, it was not convincing enough. The author also further elucidates the importance of recognizing which soft tissue structures are affected to aid good outcome⁶.

To date, there is no goal standard effective treatment option for HO. There has been hypothesis on the use of radiotherapy based on the role of osteoprogenitor cells⁷. Radiation is used to suppress the pluripotent mesenchymal cells from proliferating and differentiating to osteoprogenitor and osteoblast⁷. Bone morphogenic protein (BMP) -7 is suppressed which plays a role in the formal of mature bone tissue from osteoblast⁷. Albeit there is no “gold standard” radiotherapy treatment regimen due to the paucity of literature. The amount of dose, timing and appropriate indication remains mainly anecdotal evidence⁷. The systematic review of literature by paper by Ploumis A. and colleagues looked at radiotherapy for HO  prevention⁷. Not surprising, out of the 27 studies, only one is a randomized trial and the rest being case reports and series⁷. Radiotherapy was not statistically significant with similar outcomes to NSAID use for prevention of HO. Moreover, radiotherapy had a list of adverse effects such as skin thinning, ulceration, poor wound healing, delayed/non-union, superimposed infection and risk of carcinogenesis⁷. Therefore, radiotherapy is not a first line or safe intervention for the prevention of elbow HO⁷.

CONCLUSION

There are multiple studies out there looking at HO prevention but the most effective treatment remains elusive⁸. Society’s paradigm of the ideal medical treatment for HO is vexatious. Failure to treatment can often lead to patient and clinician frustration.  The notion of every medical condition has an easy treatment is an erroneous assumption. HO pathophysiology is still not fully understood. Invariably, for treatment to be successful, the pathophysiology of the condition must be well understood. As new treatment strategies evolved, there is abundance of literature to provide an overview of HO and an effective treatment option¹. Coming back to my clinical question, we should follow up radial head or elbow injuries up to at least three months to identify HO. Early recognition of HO might lead to better outcomes. Patients can then be offered different treatment options.