Introduction
Intersection syndrome was described as peritendinitis crepitans by Howard in 19371 and traumatic tenosynovitis in rowers by Williams in 1977.2 Grundberg recognised hypertrophy of the first compartment associated with the activities of rowing and canoeing, but related the symptoms to stenosing tenosynovitis of the second compartment extensor wrist tendons rather than to the overlying bulky muscles.3 Theories proposed by other authors4 5 include tenovaginitis and compartment syndrome.
Rowing has long been recognised as a sport with a considerable load on the forearms.6 Biomechanical errors, rough water and changes in equipment have been blamed for the development of intersection syndrome7 in rowers. Fast flowing, choppy water and high winds increased the incidence of presentation in elite paddlers.8 Training reduced the likelihood of developing pathology with those who had covered more than 100 km per week for 8 weeks prior to racing having a lower incidence of injury.
The diagnosis of intersection syndrome is clinical with tenderness on palpation of the intersection point, 3–8 cm proximal to Lister’s tubercle,9 focal swelling and crepitus to both palpation and auscultation.7
Ultrasound in intersection syndrome demonstrates tendon thickening compared with the contralateral asymptomatic side,10 peritendinous oedema and synovial fluid within the tendon sheaths between the first and second compartments, and hypervascularity on Doppler sonography.10 11 MRI findings have concentrated on changes in the muscle of the first compartment as well as increased T2 signal, representing peritendinous oedema.9 12 13
No publication has outlined an accurate pathogenesis in rowers. Wulle14 has described pathology similar to our findings in the German literature, where he suggested a thickened fascia from the first compartment as a cause for the symptoms.
Most authors5 15 advocate a protracted period of conservative treatment with rest, activity modification, splinting and injection with corticosteroids.
While many rowers respond to a conservative treatment regime of icing, stretching and massage in the acute situation, many eventually modify their wrist biomechanics to decrease symptoms,16 but symptoms cause interruption to training schedules at times of increased workload prior to important (career goal) events.17
Classically, the decision to perform operative release is based on a failure of conservative treatment (at the expense of lost time training) and appropriate surgical indications. Surgery is usually the last resort, but if the procedure has minimal downtime and a low-risk profile, we propose that it should be considered earlier in the treatment programme in rowers at the elite level.
In this report, we demonstrate the pathology of the condition to clearly be a fascial response to first compartment hypertrophy producing an attrition synovial disruption of the sheaths over extensor carpi radialis longus (ECRL) and/or ECR brevis (ECRB), resulting in the classical ‘audible crepitus’ that defines this condition. We also show the dramatic improvement and rapid return to world-class performance with surgery and the rationale for this condition to be treated with the early surgical release.