Clinical Sports Medicine (2nd edition) - A vital resource book for physicians, physical therapists masseurs and trainers.

Chapter 2

Sports Injuries

In this book sports injuries are divided into acute injuries and overuse injuries (Table 2.1). Some years ago most injuries were acute, traumatic injuries such as fractures, dislocations, ligament sprains and muscle tears. While these injuries are still common, overuse injuries such as stress fractures, compartment syndromes and tendinopathies appear to be increasingly prevalent. This is undoubtedly due to the increased load placed upon musculoskeletal structures by the increased training demands of modern day sport and the increased popularity of endurance events.

Acute injuries - THIS SECTION IS NOT AVAILABLE ON LINE

Overuse injuries

Overuse injuries have become an increasing problem in sports medicine and they present three distinct challenges to the clinician - diagnosis, treatment and understanding why the injury occurred. Diagnosis requires taking a comprehensive history of the onset, nature and site of the pain along with a thorough assessment of potential risk factors, for example, training and technique. Careful examination may reveal which anatomical structure is affected. It is often helpful to ask patients to perform the manoeuvre that produces their pain.

The treatment of overuse injuries involves relative rest, that is, avoidance of aggravating activities while maintaining fitness; the use of ice and various electrotherapeutic modalities; soft tissue techniques and drugs, such as the nonsteroidal antiinflammatory drugs (NSAIDs) (Chapter 7).

A cause must be sought for every overuse injury. The cause may be quite evident, such as a sudden doubling of training quantity, poor footwear or an obvious biomechanical abnormality, or may be more subtle, such as running on a cambered surface, muscle imbalance or leg length discrepancy. The causes of overuse injuries are usually divided into extrinsic factors, such as training, surfaces, shoes, equipment and environmental conditions, or intrinsic factors, such as malalignment, leg length discrepancy, muscle imbalance, muscle weakness, lack of flexibility and body composition. Possible factors in the development of overuse injuries are shown in Table 2.2.

Table 2.2 Overuse injuries: predisposing factors

Extrinsic factors

Intrinsic factors

Training errors
    Excessive volume
    Excessive intensity
    Rapid increase
    Sudden change in type
    Excessive fatigue
    Inadequate recovery
    Faulty technique
Surfaces
    Hard
    Soft
    Cambered
Shoes
    Inappropriate
    Worn out
Equipment
    Inappropriate
Environmental conditions
    Hot
    Cold
    Humid
Psychological factors
Inadequate nutrition

Malalignment
    Pes planus
    Pes cavus
    Rearfoot varus
    Tibia vara
    Genu valgum
    Genu varum
    Patella alta
    Femoral neck anteversion
    Tibial torsion
Leg length discrepancy
Muscle imbalance
Muscle weakness
Lack of flexibility
    Generalized muscle tightness
    Focal areas of muscle thickening
    Restricted joint range of motion
Sex, size, body composition
Other:
    Genetic factors, endocrine factors, metabolic conditions

Bone

Stress fractures

Stress fractures are a common injury among sports people, particularly among runners. They were first reported in military recruits in the nineteenth century and have become increasingly evident among athletes in the last two decades [6].

A stress fracture is a microfracture in bone that results from repetitive physical loading below the single cycle failure threshold. Overload stress can be applied to bone through two mechanisms:

the redistribution of impact forces resulting in increased stress at focal points in bone;
the action of muscle pull across bone

Histological changes resulting from bone stress occur along a continuum beginning with vascular congestion and thrombosis. This is followed by osteoclastic and osteoblastic activity leading to rarefaction, weakened trabeculae and microfracture and ending in complete fracture. This sequence of events can be interrupted at any point in the continuum if the process is recognized.

Similarly, the process of bony remodelling and stress fracture in athletes is recognized as occurring along a clinical continuum with pain or radiographic changes presenting identifiable markers along the continuum. Since radioisotopic imaging and MR can detect changes in bone at the phase of accelerated remodelling, these investigations can show stress-induced bony changes early in the continuum.

Stress fractures may occur in virtually any bone in the body. The most commonly affected bones are the tibia, metatarsals, fibula, tarsal navicular, femur and pelvis [7-9]. A full list of sites of stress fractures and the likely associated sports or activities is shown in Table 2.3.

Table 2.3 Stress fractures: site and common associated activity

Site of stress fracture	Common associated sport or activity
Coracoid process of scapula	Trapshooting
Scapula	Running with hand-held weights
Humerus	Throwing, racquet sports
Olecranon	Throwing/pitching
Ulna	Racquet sports (especially tennis), gymnastics, vol- leyball, swimming, soft-ball, wheelchair sports
Ribs--first	Throwing, pitching
Ribs--second to tenth	Rowing, kayaking
Pars interarticularis	Gymnastics, ballet, cricket fast bowling, volleyball, springboard diving
Pubic ramus	Distance running, ballet
Femur--neck	Distance running, jumping, ballet
Femur--shaft	Distance running
Patella	Running, hurdling
Tibia--plateau	Running
Tibia--shaft	Running, ballet
Fibula	Running, aerobics, race-walking, ballet
Medial malleolus	Basketball, running
Calcaneus	Long distance military marching
Talus	Pole vaulting
Navicular	Sprinting, middle distance running, hurdling, long/triple jumping, football
Metatarsal--general	Running, ballet, marching
Metatarsal--base second	Ballet
Metatarsal--fifth	Tennis, ballet
Sesamoid bones of the foot	Running, ballet, basketball, skating

Patients with stress fractures usually complain of localized pain and tenderness over the fracture site. There will often be a history of a recent change in training or taking up a new activity. Stress fracture is primarily a clinical diagnosis. Clinical suspicion may be confirmed by performing an X-ray. X ray appearance of a stress fracture is often quite subtle with the most frequent finding a periosteal reaction (FIG 2.8) However, X-rays may fail to show a stress fracture until after it has been present for some time and some fractures are notoriously difficult to detect using plain X-ray. Beware that the old adage that plain X-rays will detect a fracture after '10 days' is a myth - there are no data to support this contention, and many stress fractures are not evident even after symptoms have been present for months. Thus, further investigation is often indicated in the patient in whom stress fracture is suspected but X-ray is normal.	Fig. 2.8 X-ray showing periosteal new bone formation indicative of a stress fracture
Fig. 2.9 Stress fracture; radioisotopic bone scan appearance (COURTESY OF Z.S. KISS)	A more sensitive examination is the radioisotopic bone scan (scintigraphy) which can demonstrate the location of an overuse bony lesion. A localized area of increased uptake or 'hot spot' indicates a stress fracture (Fig 2.9, was 2.7). Until the 1990s, a triple-phase bone scan was considered perfectly sensitive, so a negative bone scan essentially ruled out a stress fracture [10]. In recent years, a few authors have reported MR positive stress fractures with negative bone scans [11]. The clinical implication of these cases is that a negative bone scan only represents a 99% probability that there is no stress fracture, rather than a 100% probability. Thus, it bone scan remains a very valuable investigation.
The bone scan, however, is a non-specific investigation, and therefore, other bony pathologies such as tumours and osteomyelitis may cause similar pictures. It may also be difficult to precisely localize the site of the area of increased uptake, especially in an area such as the foot where numerous small bones are in close proximity. In most cases of stress fracture, a radioisotopic bone scan is sufficient to confirm the diagnosis and no further investigations are required. However, in a few sites that are known to present problems with treatment, such as the tarsal navicular, further information regarding the site and extent of the fracture is required. In these cases, a CT scan or MR imaging (Fig 2.10) may be performed to show the exact site and extent of the fracture. Magnetic Resonance Imaging (MRI) is being increasingly advocated as the investigation of choice for stress fractures. While MRI does not image fractures as clearly as CT scan it is of comparable sensitivity to isotope bone scan in assessing bony damage. The typical MRI appearance of a stress fracture shows periosteal and marrow edema plus or minus the actual fracture line (Fig 2.10).	Fig. 2.10 MRI of a stress fracture showing bony edema (white)
Fig. 2.11 The continuum of bone stress: from stress reaction through to stress fracture. At present, stress fracture is detected by changes on X-ray or CT scan. MRI and bone scan can both reveal the entire spectrum of bone strain.	Treatment of stress fractures generally requires avoidance of the precipitating activity. The majority of stress fractures heal within six weeks of beginning relative rest. Healing is assessed clinically by the absence of local tenderness and functionally by the ability to perform the precipitating activity without pain. In most cases it is not useful to attempt to monitor healing with X-ray or radioisotopic bone scan [6]. CT scan appearances of healing stress fractures can be deceptive as in some cases the fracture is still visible well after clinical healing has occurred [6].

Return to sport after clinical healing of a stress fracture should be a gradual process to enable the bone to adapt to increased load (Chapter 8n). An essential component of the management of an overuse injury is identification and modification of risk factors (Table 2.2). A prospective study of risk factors associated with stress fractures showed that, in female athletes, reduced bone density, menstrual irregularity, delayed menarche and reduced calf muscle strength were all positively associated with the development of stress fractures [12]. In the male athletes there were no statistically significant factors although those with reduced bone density exhibited a trend in that direction.

There are, however, a number of sites of stress fractures in which delayed union or non-union of the fracture commonly occurs. These fractures need to be treated more aggressively. The sites of these fractures and the recommended treatments are shown in Table 2.4.

Table 2.4 Stress fractures that require specific treatment other than rest

Stress fracture	Treatment
Femoral neck	Undisplaced: initial bed rest for one week, then gradual weight-bearing Displaced: surgical fixation
Talus (lateral process)	6 weeks, non weight-bearing cast immobilization /surgical excision of fragment
Navicular	6 weeks, non weight-bearing cast immobilization
Metatarsal base second	4 weeks, nonweightbearing
Sesamoid bone of the foot	4 weeks, nonweightbearing
Stress fracture 5th metatarsal base (a)	Case immobilisation or percutaneous screw fixation.
Anterior tibial cortex	non weightbearing on crutches for 6-8 weeks, or intramedullary screw fixation.

Bone strain

In some cases in athletes there is uptake of radioisotope at non-painful sites. This is thought to represent bony remodelling at a very early subclinical level and has been termed 'bone strain'. Another situation encountered in clinical practice is the painful, tender focal area of bone that demonstrates a mildly increased uptake of radioisotope, insufficient to be classified as a stress fracture. This has been termed 'stress reaction'. It would appear that there is a continuum of bone response to stress that ranges from mild (bone strain) to severe (stress fracture). The clinical features of bone strain, stress reaction and stress fractures are summarized in Table 2.5.

The presence of bone strain, that is, an increased radioisotopic uptake in a non-painful site, is probably an early phase in remodelling. The presence of a stress reaction (i.e. a mildly increased uptake corresponding to a site of tenderness) is probably an indication that the patient is further along the continuum towards stress fracture. This is probably an indication for reduction or modification of activity.

Table 2.5 Continuum of bony changes with overuse

Clinical features	Bone strain	Stress reaction	Stress fracture
Local pain	Nil
Local tenderness	Nil
X-ray appearance	Normal	Normal	Abnormal (periosteal reaction or cortical defect in cortical bone, sclerosis in trabecular bone)
Radioisotopic bone scan appearance	Increased uptake	Increased uptake	Increased uptake
CT scan appearance	Normal	Normal	Freatures of stress fracture (as for X-ray)
MRI appearance	May show increased high signal	Increased high signal	Increased high signal ± cortical defect

Osteitis & periostitis, Apophysitis, Articular cartilage, join, ligament, muscle, focal tissue thickening/fibrosis, Chronic compartment syndrome, muscle soreness, tendon, tendinosis, tendinitis, paratenonitis, partial tears, bursa, nerve, skin, pain: where is it coming from? masquerades, The kinetic chain, - THESE SECTIONS ARE NOT AVAILABLE ON LINE

RECOMMENDATIONS FOR FURTHER READING

Brukner P, Bennell K, Matheson G. Stress fractures. Sydney: Blackwell etc, 1999. An up-to-date, easy-to-read, well illustrated monograph that provides essential background for the clinician who commonly treats stress fractures.

REFERENCES

1. Buckwalter JA. Articular cartilage: Injuries and potential for healing. The Journal of Orthopaedic and Sports Physical Therapy 1998;28:192-202.

2. Frank CB. Ligament healing: current knowledge and clinical applications. J Am Acad Orthop Surg 1996;4:74-83.

3. Frank C, Shrive H, Hiraoka H, et al. Optimisation of the biology of soft tissue repair. J Sci Med Sport 1999;2:190-210.

4. Schwellnus MP, Derman EW, Noakes TD. Aetiology of skeletal muscle cramps during exercise: a novel hypothesis. J Sports Sci 1997;15:277-285.

5. Bentley S. Exercise-induced muscle cramp. Proposed mechanisms and management. Sports Med 1996;21:409-420.

6. Brukner P, Bennell K, Matheson G. Stress fractures. Melbourne: Blackwell Scientific, Asia, 1999

7. Matheson GO, Clement DB, McKenzie DC, et al. Stress fractures in athletes. A study of 320 cases. Am J Sports Med 1987;15:46-58.

8. Brukner P, Bradshaw C, Khan KM, et al. Stress fractures: A review of 180 cases. Clin J Sport Med 1996;6:85-89.

9. Baquie P, Brukner P. Injuries presenting to an Australian sports medicine centre: a 12 month study. Clin J Sport Med 1997;7:28-31.

10. Matheson GO, Clement DB, McKenzie DC, et al. Scintigraphic uptake of 99mTc at non-painful sites in athletes with stress fractures. The concept of bone strain. Sports Med 1987;4:65-75.

11. Khan K.M., P.J. Fuller, P.D. Brukner, et al. (1992) Outcome of conservative and surgical management of navicular stress fracture in athletes. Eighty-six cases proven with computerized tomography. Am J Sports Med 20(6):657-666.

12. Keene JS, Lash EG. Negative bone scan in a femoral neck stress fracture. A case report. Am J Sports Med 1992;20:234-236.

13. Bennell KL, Malcolm SA, Thomas SA, et al. Risk factors for stress fractures in track and field athletes. A twelve-month prospective study. Am J Sports Med 1996;24:810-818.