Audit-induced change reduces complications of the Ganz trochanteric flip approach

INTRODUCTION

The Ganz trochanteric flip approach aims to avoid the potential risk of avascular necrosis in hip conserving surgery and may reduce the risk of femoral neck fractures, neck thinning and femoral head implant migration in hip resurfacing. Our initial audit revealed the complications of non-union and trochanteric screw irritation to be associated with this approach. We, therefore, modified our selection criteria and re-audited our results.

SUBJECTS AND METHODS

The initial audit (IA) ran between January 2003 and November 2007 after which an age limit of 50 years was recommended. The re-audit (RA) ran between November 2007 and December 2008 where one of the senior authors stopped using the approach in the over 50 year age group whilst the other senior author continued on selected patients over 50 years.

RESULTS

There were 545 hips in the IA and 152 hips in the RA group. The incidence of non-union decreased in the RA after the change of selection criteria (6.2% [IA] vs 1.3% [RA]). In both audit groups, the incidence of non-union increased with age, and in the RA no non-unions were observed under the age of 50 years. The incidence of screw irritation and the necessity for removal remained relatively unchanged (20.7% [IA] vs 28.3% [RA]) with a combined incidence of 22.4%.

CONCLUSIONS

The trochanteric flip approach to the hip can be used safely with an acceptable complication rate in young adult impingement and resurfacing surgery. Caution must, however, be exercised in patients over 50 years of age as they have a higher incidence of trochanteric non-union. In addition, all patients should be consented for the possibility of screw removal as a second procedure.     

Fatigue during continuous 20 Hz stimulation of the rat phrenic nerve diaphragm preparation

The site and mechanism of action of fatigue was investigated in the isolated rat phrenic nerve diaphrigm preparation, with indirect and direct stimulation at 20 Hz and recording of tension and EMG. An equal decay of the subtetanic tension during indirect and direct stimulation, and a parallel decay of tension and EMG, suggested a mechanism of fatigue localized to structures that were ‘seen’ by the EMG electrodes. A comparison of the responses to sub- and supra-maximum direct stimulation did not show increased fatigue at sub-maximum stimulation. Therefore, the fatigue was probably not caused by an increased threshold of the excitability of the sarcolemma. However, prolongation of the stimulus pulse during direct stimulation from 0.5 ms to 5 ms in the Citigued preparation caused a two-phasic recovery of tension. The initial phase, but not the slow phase, was inhibited by tetrodotoxin (TTX). Thus a recovery of sarcolemma action potentials could explain the initial phase. The slow phase was probably caused by a mechanism localized at more distal potential-dependent sites, probably in the T tubules.     

Induction of DNA adducts and mutations in spleen, liver and lung of XPA- deficient/lacZ transgenic mice after oral treatment with benzo[a]pyrene: correlation with tumour development

We were interested to study the relationship between DNA lesions, DNA repair, mutation fixation, and tumour development. Therefore, mice harbouring lacZ reporter genes and being either wild-type or defective in the DNA excision repair gene XPA, were treated with the genotoxic carcinogen benzo[a]pyrene at an oral dose of 13 mg/kg b.w. (3 times/week). At different time points, i.e. 1, 5, 9 or 13 weeks after start of the oral administration, levels of BPDE-N2-dG adducts (the major formed DNA adduct by benzo[a]pyrene in mice), and lacZ mutation frequencies were measured both in target (spleen) and non-target (lung and liver) tissues. Both in wild-type and XPA-deficient mice, benzo[a]pyrene treatment resulted in increased BPDE-N2-dG adduct levels in all three tissues analysed. In XPA-deficient mice, BPDE-N2-dG adduct levels still increased up to 13 weeks of oral benzo[a]pyrene treatment, whereas in DNA repair proficient mice steady-state levels were reached after 5 weeks of treatment. After 13 weeks, the BPDE-N2-dG adduct levels observed in XPA-/- mice, were 2- to 3-fold higher than the steady state levels observed in XPA+/+ mice in the same tissues. Mutation frequencies in the lacZ reporter gene were the same in wild- type and XPA-deficient mice that were treated with the solvent only. Oral benzo[a]pyrene treatment resulted in an increase in mutation frequency in the lacZ marker gene in all three tissues, but this increase was most profound in the spleen. After 13 weeks of treatment, a 7-fold increase in lacZ mutation frequency was detected in the spleen of wild-type mice as compared to mutation frequencies in control mice. At the same time point, a 15-fold increase in lacZ mutation frequency was observed in the spleen of XPA-deficient mice. The data presented here show, that a defect in NER mainly results in enhanced mutation frequencies in lymphocytic cells after oral treatment with the genotoxic compound benzo[a]pyrene. Interestingly, as we established in a previously performed carcinogenicity assay, the same oral treatment with benzo[a]pyrene induced lymphomas residing in the spleen of XPA- deficient mice.      

The wandering spleen

Marfan's syndrome has diverse manifestations that overlap with those seen in other connective tissue disorders. Visceral diverticula have been described only once in four adults with marfanoid features of recessive inheritance. Two siblings of a consanguineous marriage with marfanoid features, visceral diverticula, and diaphragmatic eventration are reported.