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Orthopaedic Proceedings
Vol. 98-B, Issue SUPP_16 | Pages 38 - 38
1 Oct 2016
MacLeod R Whitehouse M Gill HS Pegg EC
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Femoral head collapse due to avascular necrosis (AVN) is a relatively rare occurrence following intertrochanteric fractures; however, with over thirty-thousand intertrochanteric fractures per year in England and Wales alone, and an incidence of up to 1.16%, it is still significant. Often patients are treated with a hip fixation device, such as a sliding hip screw or X-Bolt. This study aimed to investigate the influence of three factors on the likelihood of head collapse: (1) implant type; (2) the size of the femoral head; and (3) the size of the AVN lesion. Finite element (FE) models of an intact femur, and femurs implanted with two common hip fixation designs, the Compression Hip Screw (Smith & Nephew) and the X-Bolt (X-Bolt Orthopaedics), were developed. Experimental validation of the FE models on 4. th. generation Sawbones composite femurs (n=5) found the peak failure loads predicted by the implanted model was accurate to within 14%. Following validation on Sawbones, the material modulus (E) was updated to represent cancellous (E=500MPa) and cortical (E=1GPa) bone, and the influence of implant design, head size, and AVN was examined. Four head sizes were compared: mean male (48.4 mm) and female (42.2 mm) head sizes ± two standard deviations. A conical representation of an AVN lesion with a lower modulus (1MPa) was created, and four different radii were studied. The risk of head collapse was assessed from (1) the critical buckling pressure and (2) the peak failure stress. The likelihood of head collapse was reduced by implantation of either fixation device. Smaller head sizes and greater AVN lesion size increased the risk of femoral head collapse. These results indicate the treatment of intertrochanteric fractures with a hip fixation device does not increase the risk of head collapse; however, patient factors such as small head size and AVN severity significantly increase the risk


Orthopaedic Proceedings
Vol. 99-B, Issue SUPP_2 | Pages 75 - 75
1 Jan 2017
Li L Majid K Huber C
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Osteonecrosis of the femoral head is a complex pathologic process with many aetiological factors. Factors most often mentioned in the literature are mechanical disruption (hip trauma or surgery), steroid use, smoking, haemoglobinopathies and hyperlipidaemia. 1. Our case depicts a rare association of crack cocaine related to osteonecrosis of the femoral head which has never been reported in the available literature. Case Report: A 32 year old man was referred to our Orthopaedic clinic with right hip pain. He had a 9 pack-year history of cigarette smoking and had also smoked crack cocaine between ages 20 to 28; shortly after this the hip pain started. He denied antecedent injury. He had undergone a steroid injection into his right ankle abroad for swelling one year before referral, which was after onset of hip pain. MRI of his hip previously performed abroad had been normal. The patient had an indoor job and was otherwise fit and well. On examination he had reduced of movement in his right hip with 5–10 degrees of fixed flexion deformity. Plain radiography demonstrated cyst formation and sclerosis of both femoral heads. Repeat MRI confirmed bilateral osteonecrosis, worse on the right with risk of head collapse. The patient underwent bilateral core decompressions. Subsequent follow-up demonstrated a mobile patient with no need for arthroplasty and he was discharged after two years. Osteonecrosis is caused by the coagulation of the intra-osseous microcirculation leading to thrombosis formation and eventual reduction in osseous blood supply. Steroid use is associated with increased risk of osteonecrosis to the femoral head, however in these cases the patients often undergo either direct local or systemic infiltration of steroid. In this case steroid was administered after symptoms began to a far distant site and therefore cannot be the cause. Cigarette smoking is also known to cause osteonecrosis. Our patient had smoked cigarettes for fourteen years without problems, and it was after he ceased to smoke crack cocaine that his symptoms began. Cocaine blocks voltage-gated sodium-channels causing vasospasm. It is known to cause nasal and facial bone osteonecrosis due to its common intranasal method of delivery. We postulate that in this case crack cocaine was a synergistic factor towards development of femoral head osteonecrosis