Jon Van Caspel and Leo P. Heere
Netherlands Sports Federation, Papendal, Arnhem, The Netherlands
Breithaupt (1855) first presented a clinical description of a stress frac-ture without fully understanding its exact etiology; Stechow (1897) was the flrst to establish its radiological aspects. In those years such fractures were mainly seen in army recruits, ea. 80o/o of the cases being localized in the metatarsal bones, usually the os metatarsale Ill (Doury et al., 1979). This type of fracture has also been referred to as a "march fracture" or a "fatigue fracture." Recently stress fractures have been described in various sites of the lower extremities in athletes, especially runners (Taunton et al., 1981).
The following case deals with a swimmer's stress fracture suffered in the course of an intensive training program in which extra large fins were used. Research of the literature has not revealed any previous presenta-tions of cases with a similar etiology. This type of fracture, moreover, is seldom seen in this particular locus (MT 1).
Case Report
A 14-year-old female swimmer with no previous history of foot trauma and good general condition was seen a few days after the onset of pain in her left foot and ankle. She felt this pain especially during swim-ming; it was relieved by rest. The patient had been a national selection of the Netherlands Underwater Sports Association for the 2 previous years and had been participating in four to five workouts a week of 1.5 hr each.
During competitive training, the swimmers wore extra large fins (Figure 1) to develop maximal speed. These fins were made of nylon, weighed 900 g each and were 85 cm long and 23 cm wide.
The patient denied having suffered any specific, acute injury. She stated, however, that , 1 week prior to her visit, she bad participated in a
Figure 1- Patient wearing swimming fins.
swimming contest wearing a pair of still heavier fins (made of rubber) be-cause the sharp edges of her own fins were not protected with tape.
Examination of the left foot revealed a slightly swollen metatarsus showing tenderness with pressure upon the os metatarsale I and over the area of the talocrural joint. There was no impairment of ankle joint and foot movement. Forced passive dorsal/plantar flexion of the foot and straining the m. extensor digitorum communis against resistance were painful and so were all movements of the hallux. The x-ray (Figure 2) demonstrated the presence of a ~mall fissure in the base of the os metatarsale I with no sign of dislocation.
The case was diagnosed as a stress fracture in the os metatarsale I of the left foot. The foot was immobilized using acrylastic bandage and tape, and the patient was prescribed crutches for 3 weeks with gradually increased loading of the foot. During that period, she was to abstain from any athletic activities.
Follow-up 5 weeks later showed the patient had no more complaint; upon examination, no clinical symptoms were found. Meanwhile, she had resumed training without suffering from foot trouble. In a follow-up x-ray of the left foot (Figure 3), the fracture line was no longer visible. Only a very small callus had formed.
Discussion
A great many theories have already been advanced to explain the cause of stress fracture. They have been compared, for instance, with fatigue
Figure 2-X-ray of the fracture. Figure 3-Healed fracture, 5 weeks later.
fractures within metals. This analogy, however, is only partly justified, for bone is a heterogeneous, anisotropic material; it requires stress for normal formation and remodeling (Stanitsky et al., 1977). On the histological level, the following processes are found to occur in bone tissue (Johnson et al., 1963): due to increased loading, microscopic changes develop which, combined with an increased blood flow resulting from enhanced muscle activity, give rise to piezo-electric potentials that stimulate the bone's remodeling process. However, a time lag occurs be-tween the onset of bone destruction and the beginning of new bone for-mation. At a given moment, therefore, there is a weakened area within the bone in which fractures are likely to occur under the impact of exter-nal forces. A major etiological factor in this process is the rhythmic, repetitive muscle contraction causing slight mechanical lesions which summate beyond the stress-bearing capacity of the bone {Stanitsky et al., 1977).
As to the diagnostics of stress fractures, we emphasize the importance of an early diagnosis. The average time from the onset of symptoms to the request for medical help is 7.4 weeks (Taunton et al., 1981). The ex-istence of a stress fracture should be suspected in any athlete complaining of pain in some part of the body which has been loaded during a period of intensive training. The pain develops during exercise and is relieved with rest but the athlete may not have suffered any acute injury. In most cases, physical f"mdings will be limited to localized point tenderness over the bone and soft-tissue swelling. A stress fracture shows a characteristic picture in an x-ray-a "radiolucent hairline.'' In an early stage, however,
this hairline crack is seldom visible in an ordinary x-ray. In some cases it may be detected in a tomogram which, with the help of a specialized radiographic technique, presents a kind of cross-section of an organ. X-ray examination, therefore, should be repeated after 2-3 weeks. If a stress fracture actually is present, a periosteal callus formation may be detected at the fracture site.
Another method now used frequently for early diagnosis is bone scan-ning with 99 m Tc polyphosphate-scintigraphy, in which a radiophar-macon formed by joining polyphosphates, tin and the radioactive ele-ment 99 m technetium is used. At the site of the fracture, an area of heightened radioactivity will become visible (so-called "hot spots'') as the polyphosphates become involved in the increased bone turnover develop-ing at the specific site as a result of the mechanism described above.
Stress fracture treatment should aim at minimizing the period during which the athlete will be unable to train. Usually, a combined treatment is applied including modified rest, ice massage, antiphlogistic medica-tion, physiotherapy (especially for muscle training), maintaining car-diovascular fitness, and correcting, if necessary, static abnormalities (differences in leg length, forefoot varus). Not until the athlete has become asymptomatic can training resume and then only with a gradual build-up to the previous level. The physician should make sure that the training program will be well-balanced.
Comment
Returning to the patient, one can imagine the enormous forces acting upon the feet during swimming with these fins because of the huge masses of water they have to move. Both the m. tibialis anterior (dorsal flexion of the foot) and the m. peroneus longus (pronation, abduction and plantar flexion of the foot) insert partly on the os metatarsale I. The m. extensor hallucis longus and brevis pass across the os metatarsale I and insert on the bases of the two phalanges of the hallux. In swimming the front crawl, all of these muscles are used, meaning the os metatarsale I will be subjected to continuous forces.
Swimming without fins may cause an equal number of complaints, which has been described previously (Kennedy et al., 1978). Intensive training in front and back crawl strokes may give rise to surmenage le-sions of the extensor tendons along the dorsum of the foot. At the site of the retinaculum musculi extensorium inferius (cruciate-cruralligament) these tendons pass through a narrow sheath. With the movements the foot makes during these strokes ("flutter kick"), it is carried in extreme plantar flexion, causing these tendons to be stretched continuously. At the same time friction occurs within the sheath, giving rise to irritation of the tendons, resulting in edema, inflammation and adhesions.
training intensity were factors that may have contributed to the ap-pearance of the stress fracture in this young girl. In this still little known branch of sport, more surmenage lesions are likely to occur if the train-ing intensity is not adapted to the swimmer's physical capabilities (e.g., muscle development, age group).
References
BREITHAUPT, M.D. 1855. Zur Pathologie des menschlichen Fusses. (The pathology of human feet.) Med. Zeit. 24:169-171, 175-177.
DOURY, P., Delahaye, R.P., Pattin, S., Metges, P.J., and Mine, J. 1979. Frac-tures de fatigue. (Fatigue fracFrac-tures.) In: L. Simon (ed.), Le Pied du Sportif. Masson, Paris.
JOHNSON, L.C., Stradford, H.T., and Geis, R.W. 1963. Histogenesis of stress fractures. Armed Forces Institute of Pathology Annual Lectures. J. Bone Joint Surg. 45A:1542.
KENNEDY, J.C., Hawkins, R., and Kissof, W.B. 1978. Orthopedic manifesta-tions of swimming. Am. J. Sports Med. 6:309-322.
STANITSKY, C.L., McMaster, J.H., and Scranton, P.E. 1978. On the nature of stress fractures. Am. J. Sports Med. 6:391-396.
STECHOW, A.W. 1897. Fussoedem und Roentgenstrahlen. (Foot edema and x-rays.) Deuts. Milit. Aerzl. Zeit. 26:465-471.
TAUNTON, J.E., Clement, D.B., and Webber, D. 1981. Lower extremity stress fractures in athletes. Physician Sports Med. 9:77-86.
