Rate and factors associated with surgical site infection following aseptic revision fixation of orthopaedic trauma injuries.

PURPOSE: The primary aim of this study was to define the rate of infection following revision of fixation for aseptic failure. The secondary aims were to identify factors associated with an infection following revision and patient morbidity following deep infection. METHODS: A retrospective study was undertaken to identify patients who underwent aseptic revision surgery during a 3-year period (2017-2019). Regression analysis was used to identify independent factors associated with SSI. RESULTS: Eighty-six patients were identified that met the inclusion criteria, with a mean age of 53 (range 14-95) years and 48 (55.8%) were female. There were 15 (17%) patients with an SSI post revision surgery (n = 15/86). Ten percent (n = 9) of all revisions acquired a 'deep infection', which carried a high morbidity with a total of 23 operations, including initial revision, being undertaken for these patients as salvage procedures and three progressed to an amputation. Alcohol excess (odds ratio (OR) 1.61, 95% CI 1.01-6.36, p = 0.046) and chronic obstructive pulmonary disease (OR 11.1, 95% CI 1.00-133.3, p = 0.050) were independently associated with an increased risk of SSI. CONCLUSION: Aseptic revision surgery had a high rate of SSI (17%) and deep infection (10%). All deep infections occurred in the lower limb with the majority of these seen in ankle fractures. Alcohol excess and COPD were independent risk factors associated with an SSI and patients with a history of these should be counselled accordingly. LEVEL OF EVIDENCE: Retrospective Case Series, Level IV.

Percutaneous fixation of acute scaphoid waist fractures: Long-term patient-reported functional outcomes and satisfaction at a mean of 11 years following surgery.

The aim of this study was to report the long-term functional outcomes and complication rates following early percutaneous fixation of acute fractures of the scaphoid. A trauma database was searched to identify all skeletally-mature patients with an undisplaced or minimally-displaced scaphoid waist fracture managed with early percutaneous retrograde screw fixation over a thirteen-year period from 1997-2010. Medical records were retrospectively reviewed, and complications documented. Long-term follow-up was by a questionnaire-based review. The Patient-Rated Wrist Evaluation (PRWE) was the primary outcome measure. Secondary outcomes included the Quick version of the Disability of the Arm, Shoulder and Hand score (QuickDASH), the EuroQol 5-dimensions score (EQ-5D-5L), and complications. During the study period 114 patients underwent this procedure. The mean age was 28 years (range 17-62) and 97 patients (85%) were male. The median time from injury to surgery was nine days (range 1-27). Twelve patients (11%) reported a complication, all of whom required repeat surgical intervention (six revision ORIF for non-union, five elective removal of hardware, one early revision fixation due to screw impingement). Long-term outcome data was available for 77 patients (68%) at mean follow-up of 11.4 years (range 6.4-19.8). The median PRWE was 0 (IQR 0-7.5), median QuickDASH 0 (IQR 0-4.5) and median EQ-5D-5L 1.0 (IQR 0.837-1.0). There were 97% (n = 74) patients satisfied with their outcome. Early percutaneous fixation of acute non-displaced or minimally displaced scaphoid fractures results in good long-term patient reported outcomes and health-related quality of life. Although comparable with previous studies, the overall surgical reintervention rate is notable and can result in inferior outcomes. LEVEL OF EVIDENCE: Therapeutic level III (Retrospective Cohort Study).

The hidden blood loss after hip fracture.

INTRODUCTION: Despite advances in surgical and anaesthetic techniques the mortality after hip fracture has not significantly changed in the last 40 years. Pre-operative anaemia is a risk factor for peri-operative death. We speculate that a significant proportion of the blood loss related to hip fractures has occurred prior to surgery. Identifying patients at risk of pre-operative anaemia can facilitate appropriate medical optimisation. This study is unique in its attempt to quantify the blood loss associated with the initial hip injury. METHODS: In a retrospective study all patients with both a diagnosis of hip fracture and an operative delay of >48 h were assessed. The information collected included: fracture classification, serial haemoglobins and patient co-morbidities. The exclusion criteria included a pre-injury diagnosis of anaemia, anti-coagulation and gastrointestinal bleeds. RESULTS: Between 2007/2008 sixty-eight intracapsular and fifty extracapsular hip fracture patients had serial haemoglobins and operative delays of >48 h (mean 75 h, range 48-270 h). The mean lowest recorded haemoglobin prior to surgery for both extracapsular and intracapsular fractures were 95.0 g/L (+/-SEM 2.2) and 108.5 g/L (+/-SEM 2.2) respectively. This difference was statistically significant (Student's t-test p<0.05). The mean haemoglobin drop in the extracapsular and intracapsular fracture groups was 20.2 g/L (range 0-49 g/L) and 14.9 g/L (range 0-59 g/L) respectively. CONCLUSIONS: Hip fracture patients have a large drop in haemoglobin that is associated with the initial trauma rather than the operation. This highlights the need for anaesthetic and orthopaedic staff to be vigilant to the risk of pre-operative anaemia in this cohort of frail patients even when the initial haemoglobin is apparently normal.

Platelet serotonin concentration in schizophrenic patients.

Platelet serotonin (5-HT) concentration did not significantly differ between control subjects (N = 45) and schizophrenic (N = 62) or chronic schizophrenic (N = 39) patients. No clinical feature was associated with hyperserotonemia, but the subgroup receiving benzodiazepines had a significantly higher 5-HT level than other patients.

The effect of clonidine on plasma MHPG: evidence against tonic alpha 2-adrenoceptor control of noradrenergic function.

The effect of the alpha 2-adrenoceptor agonist clonidine on plasma free MHPG levels was assessed in 12 normal volunteers. A significant fall in MHPG was produced by 1.5 microgram X kg-1 clonidine IV whereas saline had no effect. The peak fall in MHPG correlated strongly with the area under the curve (AUC). In addition, a strong correlation was seen between basal MHPG and the extent of the clonidine-induced fall. This suggests that plasma MHPG levels are not simply a reflection of central alpha 2-adrenoceptor function and argues against tonic alpha 2-adrenoceptor-mediated inhibitory control of noradrenergic output.

Intracerebroventricular administration of 5,7-dihydroxytryptamine to mice increases both head-twitch response and the number of cortical 5-HT2 receptors.

5-Hydroxytryptamine-containing (5-HT) neurones in brain of the mouse were selectively destroyed by intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT, 50 micrograms). Sham-lesioned controls received vehicle (2 microliters, i.c.v.). Two weeks later the head-twitch response induced by 5-methoxy-N,N-dimethyltryptamine (2.0 mg/kg) and mediated by 5-HT2 receptors was markedly enhanced in the lesioned mice. Furthermore, lesioning also increased 5-HT2 binding sites in the cortex, assessed by the binding of [3H]ketanserin in these animals, and decreased levels of 5-HT in the cortex (70%) and mid/hindbrain (64%) regions. A second group of mice, lesioned with less 5,7-DHT (5-20 micrograms, i.c.v.) showed unaltered head-twitch responses to 5-methoxy-N, N-dimethyltryptamine (2.0 mg/kg) and did not have increased 5-HT2 receptor binding in the cortex. Depletions of 5-HT were 32 and 40% in the cortex and mid/hindbrain, respectively. Comparison of the extent of depletion of 5-HT in the mid/hindbrain after lesioning, with the increase in head-twitch response, suggested that depletions of less than 40% did not affect this behaviour. However, depletions greater than 40% produced marked increases in this response and there was a good correlation between these two variables (r=0.701, P less than 0.01). In conclusion, these data suggest that enhanced head-twitch responses occurring after lesioning with 5,7-DHT may result from increased 5-HT2 receptors in brain. Moreover, the magnitude of the observed behavioural enhancement was dependent upon the extent of depletion of 5-HT produced by the lesioning.

The relationship between plasma catecholamines and severity of injury in man.

The relationship between plasma catecholamines and injury severity was investigated in order to determine: a) whether a correlation existed between the severity of injury as assessed by the Injury Severity Score (ISS), and circulating noradrenaline and adrenaline; and b) whether such measurements were of prognostic value. It was found that in the immediate postinjury period, both noradrenaline and adrenaline correlated positively with ISS over the range of injury studied (ISS = 0-54; r = 0.67, p less than 0.01). It appeared that part of the response might be attributed to psychological rather than physical factors; at lower levels of injury (ISS less than 9) these psychological factors were possibly responsible for the whole of the observed effect. In the subsequent recovery period (greater than 24 hr postinjury) no clear relationship between plasma catecholamines and injury severity was maintained. Studies on patients who died as a consequence of their injuries failed to confirm the previously suggested prognostic value of plasma catecholamine determinations in this later postinjury period. However, plasma noradrenaline levels in this group were significantly higher on admission than in the casualties who survived serious injury (p less than 0.05). It is concluded that plasma catecholamine concentrations, in combination with other indices of injury severity, may provide useful information on the response to injury in man, and aid in the assessment of its overall severity in physiologic terms.

The effects of acute and repeated administration of various antidepressant drugs on clonidine-induced hypoactivity in mice and rats.

Small doses of clonidine produce hypoactivity in mice and rats, probably by stimulating pre-synaptic alpha 2-adrenoceptors in the brain. When mice were injected with desmethylimipramine (DMI, 5 mg/kg) before clonidine it attenuated the hypoactivity, while pretreatment with amitriptyline (5 mg/kg) or mianserin (5 mg/kg) potentiated this behaviour. In rats, desmethylimipramine (20 mg/kg) inhibited and mianserin (5 mg/kg) potentiated the clonidine-induced hypoactivity. Amitriptyline (20 mg/kg), however, had no effect on this behaviour in rats. Mice were also given repeated injections of these 3 antidepressant drugs (5 mg/kg twice daily for 14 days) and were tested with clonidine 12 and 60 hr after the final treatment. At 12 hr desmethylimipramine and amitriptyline both attenuated the hypoactivity responses while the reduction by mianserin was marginal (potency DMI greater than amitriptyline greater than mianserin). At 60 hr, however, amitriptyline and mianserin both decreased the clonidine-induced responses while the attenuation by desmethylimipramine was slight (potency amitriptyline congruent to mianserin greater than DMI). In rats, repeated injections of desmethylimipramine (20 mg/kg), administered twice daily for 14 days, attenuated the clonidine-induced hypoactivity 12 hr after the final treatment and this effect persisted for at least 72 hr. Furthermore, the degree of inhibition of the behavioural responses did not correlate with plasma concentrations of desmethylimipramine and persisted after disappearance of the drug from plasma. In conclusion, these data suggest that after repeated injection, desmethylimipramine, amitriptyline and mianserin all produce an adaptive decrease in the function of central alpha 2-adrenoceptors but the time course of this change differs with the individual antidepressant drug administered.

Routine determination of plasma catecholamines using reversed-phase, ion-pair high-performance liquid chromatography with electrochemical detection.

A procedure is described for the determination of plasma catecholamines using reversed-phase, ion-pair high-performance liquid chromatography coupled with electrochemical detection. Optimisation of chromatographic conditions with respect to detector performance and adherence to procedures and precautions described, render the method applicable to both neurochemical research and routine clinical analysis. The limit of quantitative detection of the method was found to be approximately 30 pg per injection for individual catecholamines. A single chromatographic run, providing adequate resolution of each component, could be completed in approximately 12 min.