Neglected hip dislocations are rare; reports in the literature are predominantly from developing countries5,7,8. The literature stresses that the risk of osteonecrosis is higher when the hip remains dislocated for longer periods of time. However, we present a missed traumatic hip dislocation that had been dislocated for over two weeks; there was no evidence of osteonecrosis at the two-year follow-up. Our patient originally presented to an outside emergency room with symptoms of knee pain. This demonstrated a referred pain pattern from the hip to the knee via the obturator or femoral nerves and underscored the importance of examining and imaging the joint above and below the area of the chief symptom.
Our patient had type-2 changes according to Barquet’s 1982 osteonecrosis classification scheme (Table I), yet no functional deficits or evidence of osteonecrosis were evident on MRI two years after the injury5. Because a more sensitive and specific assessment of osteonecrosis is available with MRI scans, Barquet’s classification scheme should be interpreted with caution. Osteonecrosis classification schemes have evolved10, and Barquet’s type-2 and 3 changes are not considered precursors to osteonecrosis; several sources attribute these changes to posttraumatic reactive hyperemia2,11,12.
Several publications agree that evidence of coxa magna (with the affected side having at least a 2-mm larger femoral head diameter) on follow-up of a traumatic hip dislocation has no correlation with a poor clinical outcome1,7. Vialle et al. reported a significant correlation (p < 0.05) between a younger age (<10 years) and the development of coxa magna following a traumatic hip dislocation4. This suggests an age-related difference in the physiological response to a traumatic hip dislocation. The vascular developmental anatomy may be one of these physiologic factors. Prior to four years of age, the blood supply to the femoral head is from the ligamentum teres and the medial and lateral femoral circumflex arteries. After age four, the principal blood supply to the femoral head is the medial femoral circumflex artery13; at skeletal maturity, the vessels form an anastomosis with less reliance on end arterial blood flow. Attention to the quadratus femoris and posterior capsule is warranted to avoid injury to the medial femoral circumflex artery.
It is accepted that joint hypermobility is inversely proportional to age, with the younger population experiencing joint dislocations with relatively less force. This relative increase in joint hypermobility in the younger population, especially in females14, can potentially have a protective effect on blood supply since a baseline increase in joint-tissue laxity can potentially withstand more tensile force without injury to the vascular supply, and allow for more capsular distension prior to tamponade of vessels by increased capsular pressure from a hematoma. By the time our patient was referred to us, she had no overt signs of pain, and ibuprofen was used as needed. According to pediatric hip fracture literature, this could in part be because of the rent in the joint capsule, allowing for capsular decompression, which in addition to alleviating pain could decrease the incidence of osteonecrosis13. Additionally, this case involved a low-velocity trauma, whereas with our patient, sledding caused the hip dislocation with increased baseline joint hypermobility (Beighton-Horan score of seven). We hypothesize that because of the baseline joint laxity, less force was required to dislocate the hip, thus decreasing the risk of future osteonecrosis. Similarly, in the pediatric hip fracture literature, there is increasing thought that the severity of the initial traumatic force is a more important factor than the timing of the reduction concerning the future development of osteonecrosis13.
To our knowledge, no studies have included an analysis of overall joint hypermobility as a predictive variable to the future development of osteonecrosis following traumatic joint dislocations. The majority of children have a Beighton-Horan score greater than four (Table II), which is the accepted standard measurement of joint laxity and could represent an unrecognized source of preexisting atraumatic hip instability14,15. Moreover, adults with benign joint hypermobility syndrome, a condition recognized in the rheumatology literature, may also be protected14. The guideline for urgent reduction within six hours may not be appropriate when age and baseline joint hypermobility are considered.
Our case represents an outlier of the six-hour reduction guideline, prompting the possibility of overlooked associations (including age, overall joint hypermobility, severity of trauma, time prior to reduction, use of MRI, and modern osteonecrosis classification) to the development of osteonecrosis following an index traumatic hip dislocation. Additionally, this case illustrates the importance of always considering hip pathology when knee pain is the presenting chief symptom as well as the fact that joint pathology with an associated capsular breach can present in a deceptively benign fashion.