Stomaching the pain of spinal fusion: gastrointestinal discomfort is as severe as back pain in 50% of adolescent idiopathic scoliosis patients following posterior spinal fusion.

PURPOSE: There have been no prospective studies investigating gastrointestinal (GI) symptoms of patients with adolescent idiopathic scoliosis (AIS) following posterior spinal fusion (PSF). The purpose of this study was to evaluate the incidence and severity of self-reported GI symptoms following PSF. METHODS: In all, 40 AIS patients undergoing PSF were prospectively enrolled between March 2015 and October 2016. Patients completed a survey on each postoperative, inpatient day regarding nausea, emesis, constipation, abdominal pain and back pain, rating their pain on a scale of 1 to 10. RESULTS: Abdominal pain (50%), emesis (63%), nausea (65%) and constipation (68%) were experienced by the majority of patients. Of those reporting back pain, the mean pain level during the postoperative period was 5.1 (0.2 to 9.6). Of those reporting abdominal pain, the mean pain level during the postoperative period was 5.5 (1.4 to 8.6), which was not different than the severity of their back-pain levels (mean = 6.0, p = 0.31). CONCLUSIONS: Gastrointestinal issues in AIS patients following PSF are common. Abdominal pain was as severe as the back pain for half of the patients. LEVEL OF EVIDENCE: II.

The effect of canal fill on paediatric femur fractures treated with titanium elastic nails.

PURPOSE: Traditional teaching for fixation of paediatric femur fractures recommends 80% nail diameter/medullary canal diameter ratio (ND/MCD) for successful maintenance of reduction. Prior studies have investigated this with stainless steel Enders nails. Our aim was to assess the impact of ND/MCD on maintenance of reduction and malunion rates in paediatric femur fractures treated with flexible intramedullary nails (FINs). METHODS: Retrospective data was collected on all paediatric patients treated with FINs for diaphyseal femur fractures at a single tertiary care institution over a ten-year period. Patients with co-morbidities affecting bone quality were excluded. Patients were subdivided into groups based on ND/MCD. RESULTS: A total of 66 patients met inclusion criteria. Mean ND/MCD was 76.3% (32.9% to 98.8%, SD 14.3). In all, 50% (n = 33/66) of patients had > 80% ND/MCD, and only 13.6% (n = 9/66) of patients had less than 60% ND/MCD. When controlling for fracture stability, ND/MCD had no correlation with mean shortening (p = 0.07) There was no correlation between ND/MCD and angulation in the sagittal (p = 0.96) or coronal plane (p = 0.20). Three patients fit malunion criteria. ND/MCD for these patients were 40%, 67% and 79%. CONCLUSION: There was no correlation between ND/MCD and shortening or malangulation. The majority of patients in this series with less than 80% fill with FIN healed within acceptable parameters. LEVEL OF EVIDENCE: III.

The effects of body mass index on treatment of paediatric femur fractures managed with flexible intramedullary nails.

PURPOSE: Traditionally, flexible intramedullary nails (FINs) are not to be used to fix femur fractures in patients > 50 kg (110 lbs). However, studies have not examined the efficacy of this technique in overweight and obese patients who may be under this 'weight cutoff'. The purpose of this study was to assess how patient body mass index (BMI) impacts the treatment of paediatric femur fractures managed with FINs. METHODS: Retrospective data was collected on all paediatric patients treated with FINs for diaphyseal femur fractures at a single tertiary care institution over a ten-year period. BMI was calculated and categorised according to the Centre for Disease Control BMI Calculator for Children and Teens. Patients with comorbidities affecting bone quality were excluded. RESULTS: A total of 54 patients met inclusion criteria. In all, 14 patients were underweight, 20 were within a normal weight range, and 20 were overweight/obese. There was no correlation between BMI and mean shortening (underweight: 7.1 mm, normal weight: 5.2 mm, overweight/obese: 7.2 mm; p = 0.55). There was no correlation between BMI and mean anterior/posterior angulation (underweight: 3.1°, normal weight: 3.8°, overweight/obese: 3.3°; p = 0.93). There was no correlation between BMI and varus/valgus angulation (underweight: -0.86°, normal weight: -0.5°, overweight/obese: -1.25°; p = 0.89). Three cases fit malunion criteria. One of these patients fell into the 'underweight' category and two patients fell into the 'normal weight' category. CONCLUSION: We found no association between BMI and malunion in FIN fixation of femoral diaphyseal fractures in children. All cases of malunion were seen in underweight or normal weight patients.

Regulation of de novo sphingolipid biosynthesis and the toxic consequences of its disruption.

Complex sphingolipids are 'built' on highly bioactive backbones (sphingoid bases and ceramides) that can cause cell death when the amounts are elevated by turnover of complex sphingolipids, disruption of normal sphingolipid metabolism, or over-induction of sphingolipid biosynthesis de novo. Under normal conditions, it appears that the bioactive intermediates of this pathway (3-ketosphinganine, sphinganine and ceramides) are kept at relatively low levels. Both the intrinsic activity of serine palmitoyltransferase (SPT) and the availability of its substrates (especially palmitoyl-CoA) can have toxic consequences for cells by increasing the production of cytotoxic intermediates. Recent work has also revealed that diverse agonists and stresses (cytokines, UV light, glucocorticoids, heat shock and toxic compounds) modulate SPT activity by induction of SPTLC2 gene transcription and/or post-translational modification. Mutation of the SPTLC1 component of SPT has also been shown to cause hereditary sensory neuropathy type I, possibly via aberrant oversynthesis of sphingolipids. Another key step of the pathway is the acylation of sphinganine (and sphingosine in the recycling pathway) by ceramide synthase, and up-regulation of this enzyme (or its inhibition to cause accumulation of sphinganine) can also be toxic for cells. Since it appears that most, if not all, tissues synthesize sphingolipids de novo, it may not be surprising that disruption of this pathway has been implicated in a wide spectrum of disease.