Evaluation of validity of the STOP-BANG questionnaire in major elective noncardiac surgery.

BACKGROUND: The STOP-BANG questionnaire screens for obstructive sleep apnoea (OSA) in surgical patients. In prior research, the association of STOP-BANG scores with comorbidities and outcomes was inconsistent. The objective of this study was to evaluate the validity of the STOP-BANG score. METHODS: We conducted a retrospective cohort study of patients undergoing major elective noncardiac surgery at the University Health Network (Toronto, ON, Canada) between 2011 and 2015. Cross-sectional construct validity was evaluated based on proportions with diagnosed OSA across STOP-BANG strata. Concurrent construct validity was assessed based on the correlation of STOP-BANG with ASA Physical Status (ASA-PS), the Revised Cardiac Risk Index, and the Charlson Comorbidity Index. Predictive validity was assessed based on the adjusted associations of STOP-BANG risk with 30-day mortality (logistic regression), cardiac complications (logistic regression), and length-of-stay (negative binomial regression). RESULTS: Of 26 068 patients in the cohort, 58% were in the low-risk STOP-BANG stratum, 23% in the intermediate-risk stratum, and 19% in the high-risk stratum. The proportion with previously diagnosed OSA was 4% (n=615) in the low-risk stratum, 12% (n=740) in the intermediate-risk stratum, and 44% (n=2142) in the high-risk stratum. The correlations of STOP-BANG with ASA-PS (Spearman ρ=0.28), Revised Cardiac Risk Index (ρ=0.24), and Charlson Comorbidity Index (ρ=0.10) were weak, albeit statistically significant (P<0.001). After risk-adjustment, STOP-BANG risk strata were not associated with 30-day mortality, cardiac complications, or length-of-stay. CONCLUSIONS: The STOP-BANG questionnaire has modest construct validity but did not predict postoperative mortality, hospital length-of-stay, or cardiac complications.

Association between preoperative ambulatory heart rate and postoperative myocardial injury: a retrospective cohort study.

BACKGROUND: Resting heart rate is well established as a predictor of morbidity and mortality in the general population. However, the relationship between preoperative heart rate and perioperative outcomes, specifically myocardial injury, is unclear. METHODS: This retrospective cohort study included patients undergoing elective major non-cardiac surgery from 2008 to 2014 at a multisite healthcare system. The exposure was ambulatory heart rate measured during the outpatient preoperative clinic visit, whereas the outcome of interest was myocardial injury (peak postoperative troponin I concentration >30 ng L-1). Covariates included patient characteristics, comorbidities, and preoperative medications. We constructed several multivariable regression models that each modelled heart rate in a different manner, including as a simple continuous variable, categories, and fractional polynomials. RESULTS: The cohort included 41 140 patients, of whom 4857 (11.8%) experienced myocardial injury. Based on pre-specified heart categories thresholds, a heart rate ≥90 beats min-1 was associated with an elevated odds of myocardial injury compared with a heart rate <60 beats min-1 (adjusted odds ratio, 1.22; 95% confidence interval, 1.06-1.39; P=0.005). This result was consistent regardless of the method used for categorisation. When fractional polynomials were used to model heart rate, a 'J-shaped' relationship between heart rate and odds of myocardial injury was observed. CONCLUSIONS: This cohort study found that both very high preoperative heart rates, and possibly also very low heart rates, are associated with increased risk of myocardial injury. Whether heart rate is a modifiable risk factor, or rather simply a marker of underlying cardiac pathology, needs to be determined in further research.

Reliability of the American Society of Anesthesiologists physical status scale in clinical practice.

BACKGROUND: Previous studies, which relied on hypothetical cases and chart reviews, have questioned the inter-rater reliability of the ASA physical status (ASA-PS) scale. We therefore conducted a retrospective cohort study to evaluate its inter-rater reliability and validity in clinical practice. METHODS: The cohort included all adult patients (≥18 yr) who underwent elective non-cardiac surgery at a quaternary-care teaching institution in Toronto, Ontario, Canada, from March 2010 to December 2011. We assessed inter-rater reliability by comparing ASA-PS scores assigned at the preoperative assessment clinic vs the operating theatre. We also assessed the validity of the ASA-PS scale by measuring its association with patients' preoperative characteristics and postoperative outcomes. RESULTS: The cohort included 10 864 patients, of whom 5.5% were classified as ASA I, 42.0% as ASA II, 46.7% as ASA III, and 5.8% as ASA IV. The ASA-PS score had moderate inter-rater reliability (κ 0.61), with 67.0% of patients (n=7279) being assigned to the same ASA-PS class in the clinic and operating theatre, and 98.6% (n=10 712) of paired assessments being within one class of each other. The ASA-PS scale was correlated with patients' age (Spearman's ρ, 0.23), Charlson comorbidity index (ρ=0.24), revised cardiac risk index (ρ=0.40), and hospital length of stay (ρ=0.16). It had moderate ability to predict in-hospital mortality (receiver-operating characteristic curve area 0.69) and cardiac complications (receiver-operating characteristic curve area 0.70). CONCLUSIONS: Consistent with its inherent subjectivity, the ASA-PS scale has moderate inter-rater reliability in clinical practice. It also demonstrates validity as a marker of patients' preoperative health status.

Five year review of the Rotaglide total knee arthroplasty.

In this study we present the outcome for patients with the Rotaglide mobile meniscal knee prosthesis implanted for osteoarthritis. All patients reviewed had this prosthesis implanted as a primary total knee Arthroplasty in Crosshouse Hospital. The minimum follow-up period was 5 years (range 5-8.2). Patients were assessed clinically by the junior author (C.W.) and results were standardised using the Hospital for Specialist Surgery (HSS) knee score. Standard radiographs were taken in antero-posterior and lateral planes to assess for loosening using the Knee Society roentgenographic system. Case notes were then examined for evidence of peri and post-operative problems. Sixty-seven patients (71 knees) were reviewed. Ninety-four percent of patients had an excellent clinical outcome with HSS scores of 85 or more. Two knees were revised, one for meniscal fracture and one for meniscal dislocation. Both of these failures were early in our series and in a total of 312 knees to date there have been no other meniscal failures. No knees were revised for aseptic loosening and there have been no deep infections. We feel this prosthesis offers a safe and effective treatment for osteoarthritis with a good clinical outcome at 5 years with a low level of complications.

Utilisation of bone allograft by orthopaedic surgeons in Scotland.

The use of bone allograft in orthopaedic surgery has been predicted to increase, particularly in joint revision surgery. This has led to a potential problem with supply. Questionnaires were distributed to all 146 Consultant Orthopaedic surgeons working in Scotland in 2000. They were asked to indicate their current usage of bone and tissue allograft, any problems encountered with supply and if alternatives to allograft, such as processed bone, might be used. The questions asked were very similar to those asked in a previous study in 1995 to enable comparisons to be made. Replies were received from 125 Consultants (87%) of whom 93 reported using bone allograft. Forty-one consultants (46%) predicted an increase in their requirement for bone allograft, and 23 (26%) felt they could currently use more bone if this was available. Sixty percent of surgeons would consider using processed bone as an alternative. In comparison with figures from 1995, an increasing number of surgeons are prepared to use processed bone as an alternative to fresh frozen allograft.

Effect of ethinyl estradiol on the panic response to the panicogenic agent pentagastrin.

BACKGROUND: Panic disorder (PD) symptomatology has been reported to be altered by hormonal events or treatments which affect estrogen levels. Coryell et al. [Arch. Gen. Psychiatry, 39 (1982) 701-703; Am. J. Psychiatry, 143 (1986) 508-510] have suggested that the increased cardiovascular risk associated with PD is significantly greater in males, alluding to a potential cardioprotective effect of female hormones in the context of panic attacks. In the present study, we were, therefore, interested in elucidating the role of estrogen in modulating the behavioural and cardiovascular responses induced by the panicogenic agent pentagastrin, a cholecystokinin-B (CCK(B)) receptor agonist. METHODS: A double-blind cross-over placebo-controlled design with randomization of the order of a 3-day pretreatment of ethinyl estradiol (EE) (50 microg/day) or placebo was used to assess the effect of a 30-microg i.v. bolus injection of pentagastrin on panic symptom intensity and on increases in heart rate (DeltaHR), systolic (DeltaSBP) and diastolic (DeltaDBP) blood pressure following each pretreatment. Subjects were 9 male healthy controls and 11 male PD patients. RESULTS: EE pretreatment did not significantly reduce the pentagastrin-induced panic symptom scale (PSS) scores and had no effect on DeltaDBP or DeltaSBP. EE did, however, attenuate the pentagastrin-induced increase in HR in both PD patients and healthy controls. LIMITATIONS: Only male subjects were included in the present study; however, we are currently investigating the influence of female gonadal hormones on the panic response to pentagastrin in female PD patients and healthy controls. CONCLUSION: Our results suggest that estrogens may display cardioprotective effects in the context of panic attacks.

Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative contribution of small, dense LDL to coronary heart disease risk.

The concentration of plasma LDL subfractions is described in four groups of normocholesterolaemic (total plasma cholesterol < 6.5 mmol/l) male subjects consisting of men with and without coronary artery disease (CAD+/-), as determined by angiography, post-myocardial infarct survivors (PMI) and normal, healthy controls. The CAD(+) and PMI groups were distinguished from the CAD(-) and controls by raised concentrations of plasma triglyceride, very low density lipoprotein (VLDL) cholesterol, small, dense LDL (LDL-III density (d) 1.044-1.060 g/ml) and lower concentrations of high density lipoprotein (HDL) cholesterol and large, buoyant LDL (LDL-I d 1.025-1.034 g/ml). In all groups, a subfraction of intermediate density, LDL-II (d 1.034-1.044 g/ml), was the predominant LDL species but was not related to coronary heart disease risk. Plasma triglyceride showed a positive association with LDL-II (r = 0.51, P < 0.001) below a triglyceride level of 1.5 mmol/l. Above this threshold of 1.5 mmol/l, LDL-II and LDL-I showed significant negative associations with triglyceride (LDL-II r = -0.5, P < 0.001; LDL-I r = -0.45, P < 0.001). Small, dense LDL-III showed a weak positive association with triglyceride that became highly significant above the 1.5 mmol/l threshold (r = 0.54, P < 0.001). While age was positively related to LDL-II within the control subjects (r = 0.3, P < 0.05), there was no difference in the percentage abundance or concentration of LDL-III within control and CAD(-) subjects above and below the age of 40 years. Smoking was associated with a relative deficiency of the LDL-I subfraction (LDL-I to LDL-III ratio in smokers = 0.77, in ex-smokers = 0.95, in non-smokers = 1.89; P < 0.01), as was beta-blocker medication (% LDL-I, users vs. non-users, P < 0.05). Both of these effects could be explained by their primary influence on plasma triglyceride. Analysis of the frequency distributions for the three LDL subfractions revealed the concentration of small, dense LDL-III to be bimodal around a concentration of 100 mg (lipoprotein mass)/100 ml plasma. The calculation of odds ratios based on this figure indicated relative risk estimates of 4.5 (chi 2: P < 0.01) for the presence of coronary artery disease and 6.9 (chi 2: P < 0.001) for myocardial infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Unnecessary arthroscopies.

A review of the results of arthroscopies on patients taken from an 'open access' service waiting list has been carried out. One-third of all arthroscopies proved to be negative. Accuracy of clinical diagnosis was not related to the clinical grade of the examining doctor. The excess annual cost to the Northern Ireland Orthopaedic Service of unnecessary arthroscopies may have been of the order of 89,000 pounds.

Delayed diagnosis of injuries from the M1 aircraft accident. The Nottingham, Leicester, Derby, Belfast Study Group.

The incidence of a delay in the diagnosis of injuries from the 83 survivors of the M1 aircraft accident is described. A total of 32 injuries in 25 patients were not initially diagnosed, nine each in the upper and lower limbs and 14 in the spine. This was equivalent to 9.6 per cent of all the major injuries suffered by the survivors. Five patients required surgery for a late diagnosed injury. The incidence of a delayed diagnosis injury (DDI) was not related to the overall severity of injury. Delay in diagnosis of injuries after such a major accident was attributable to failure of clinical examination, failure to radiograph symptomatic areas and failure of radiographic interpretation.

17 Beta-hydroxysteroid dehydrogenases in human breast tissues: purification and characterization of soluble enzymes and the distribution of particulate and soluble forms in adipose, non-adipose and tumour tissues.

17 Beta-Hydroxysteroid dehydrogenase (17 beta-HSD) is present in multiple forms in human breast tissue. One soluble form, with a molecular weight of approximately 35 kDa, was purified to near homogeneity from whole normal breast tissue. This form catalysed the oxidation of oestradiol and the reduction of oestrone, with NADP+ and NADPH as the preferred coenzymes. Three other soluble forms with higher molecular weights (in the range 50-80 kDa) were isolated. They catalysed the oxidation of oestradiol but not the reduction of oestrone, and all of them had properties very different from those of the low molecular weight enzyme. Activities of 17 beta-HSD were measured in particulate and soluble fractions from normal breast adipose and non-adipose tissues, and from breast tumours obtained from post-menopausal women, in the oxidative direction with NAD+ and NADP+ as coenzymes and in the reductive direction with NADH and NADPH as coenzymes. Particulate fractions from tumours had much higher oxidative and reductive activities than those from normal tissues. Soluble fractions from tumours had higher oxidative activities than those from the normal tissues but similar reductive activities. The major soluble form of 17 beta-HSD in adipose tissue was the 35 kDa enzyme which had both oxidative and reductive activities. In contrast, the majority of the soluble activity in non-adipose tissue was due to enzymes, with molecular weights in the range 50-80 kDa, which had oxidative activity only. The soluble fractions of tumours, like those of non-adipose tissue, contained enzymes with molecular weights in the range 50-80 kDa. In addition, they contained a 35 kDa enzyme with properties different from those of the enzyme with the same molecular weight present in adipose tissue.

Multiple forms of 17 beta-hydroxysteroid oxidoreductase in human breast tissue.

17 beta-Hydroxysteroid oxidoreductase, the enzyme that catalyses the interconversion of oestradiol and oestrone, is known to be present in human breast tissue. However, it is not known whether one or more forms of the enzyme is present. Homogenates of breast adipose tissue and breast glandular tissue were fractionated and fractions assayed in the oxidative direction with NAD+ and NADP+ as coenzymes, and in the reductive direction with NADH and NADPH as coenzymes. Ultracentrifugation of homogenates showed that there was membrane-bound activity and soluble activity. The soluble activity was due to a number of forms of the enzyme with different molecular weights, three in breast adipose tissue and two in breast glandular tissue, as shown by fractionation with (NH4)2SO4 followed by chromatography on Sephadex G-200. The forms of the enzyme isolated differed in their affinities for substrates and coenzymes and in the relative rates at which they catalysed the oxidative and reductive reactions. Preliminary experiments with breast tumours showed that they also contained membrane-bound activity and more than one soluble form of the enzyme.

Paracrine influence of human breast stromal fibroblasts on breast epithelial cells: secretion of a polypeptide which stimulates reductive 17 beta-oestradiol dehydrogenase activity.

We have previously shown that a stroma-associated paracrine influence may occur in the human breast. In particular, human breast fibroblasts secrete a factor which stimulates reductive 17 beta-oestradiol dehydrogenase (HSD) activity, thereby regulating tissue concentrations of 17 beta-oestradiol. We report here the results of experiments designed to establish the nature of the enzyme activity stimulating factor. In vitro cell culture techniques were used, in which human breast fibroblast-conditioned medium was used to grow the human breast cancer cell line, MCF-7, for 6 days, after which the reductive HSD activity of the monolayers was assessed. The fibroblastic reductive HSD stimulating factor was found to be a trypsin-sensitive polypeptide. The polypeptide eluted from a Sephadex G-75 column as a peak corresponding to a molecular weight of about 50 kDa. The polypeptide exerts its effects by altering the Vmax of 2 of the cytosolic forms of HSD within MCF-7 cells. This is achieved by a protein-synthesis-dependent but calmodulin-independent mechanism. These results provide further evidence of a paracrine effect by stromal tissue within the human breast and have important implications with respect to the aetiology and treatment of breast cancer.

Transient shock and myocardial impairment caused by phaeochromocytoma crisis.

A patient admitted to hospital after injury to the abdomen was found to have transient hypertension which was followed by profound hypotension. ST elevation developed and extensive myocardial akinesia was seen at echocardiography, but coronary angiograms at this stage were normal. After treatment with intravenous fluids and dopamine he progressively recovered normal cardiac function. A partly necrotic catecholamine secreting tumour was later removed from the abdomen and it is likely that a kick to the abdomen had damaged the tumour and the consequent release of catecholamine had triggered a phaeochromocytoma crisis.

The role of cardioplegic solution buffering in myocardial protection. A biochemical and histopathological assessment.

The advantages of buffering cardioplegic solutions to improve adenosine triphosphate preservation and postarrest hemodynamic function have been previously promoted. We evaluated the benefit of histidine buffering (195 mmol/L) in a low sodium (27 mEq/L) cardioplegic solution (Roe's) in a canine model of multidose cardioplegic arrest. Four solutions, two unbuffered (K+ = 10 mEq/L and K+ = 30 mEq/L) and two buffered (K+ = 10 mEq/L and K+ = 30 mEq/L), were tested in four groups of dogs for a 4 1/2 hour arrest period followed by 1 hour of reperfusion. Use of the unbuffered solution resulted in a drop in myocardial adenosine triphosphate from 29 +/- 1 mmol/kg (mean +/- standard error of the mean) (K+ = 30 mEq/L) and 28 +/- 2 mmol/kg (K+ = 10 mEq/L) to 8 +/- 2 mmol/kg and 7 +/- 2 mmol/kg, respectively, during the arrest period. In both buffered groups, adenosine triphosphate remained at preischemic levels during the entire arrest period. Myocardial glycogen followed the same pattern as adenosine triphosphate in the buffered groups. Lactate production was markedly elevated in all groups during ischemia. Postarrest hemodynamic function, as assessed by intraventricular isovolumic developed pressure measurements, was better (p less than 0.05) in the buffered low-potassium group than in the other three groups. The extent of myocardial necrosis, measured by triphenyl tetrazolium staining and confirmed by electron microscopy, was minimal (2% +/- 1% of biventricular mass) in the buffered low-potassium group, significantly greater (7% +/- 2% and 10% +/- 2%) in the unbuffered high-potassium and low-potassium groups, respectively, and highest (35% +/- 9%) in the buffered high-potassium group. These findings indicate that significant buffering capacity (similar to that of blood) in a crystalloid cardioplegic solution can be effective in preserving myocardial adenosine triphosphate stores, improving postarrest contractile function, and minimizing myocardial necrosis, provided the combination of high extracellular potassium and high pH levels is avoided.

Multidose blood versus crystalloid cardioplegia. Comparison by quantitative assessment of irreversible myocardial injury.

The relative efficacy and safety of blood-based potassium cardioplegic solutions compared to crystalloid arresting solutions has been a major controversy in the field of intraoperative myocardial protection for cardiac operations. In this study multidose potassium (K+ = 30 mEq/L) blood cardioplegia was compared to multidose potassium crystalloid cardioplegia in a dog model in which hearts were arrested for periods of 4 1/2 and 6 hours. The cardioplegic solution was given as an initial bolus of 500 ml and then as 250 ml doses every 30 minutes of arrest. In the 4 1/2 hour arrest group, six animals received blood cardioplegia, six received a low-sodium crystalloid cardioplegia (modified Roe's solution), and 10 received a high sodium crystalloid cardioplegic solution of our own design. In the 6 hour arrest group, four animals received blood cardioplegia, four received the low-sodium solution, and four received the high-sodium solution. Myocardial temperature was precisely controlled at 27 degrees +/- 1 degree C in all groups. The hearts were reperfused for periods of 2 to 4 hours after the arrest periods and then examined morphologically for injury. The extent of myocardial damage was quantified in 5 mm thick transverse sections through the ventricles by using a tetrazolium enzyme-mapping technique. In the crystalloid groups the hearts arrested for 4 1/2 hours were significantly injured. The percentage (+/- SEM) of necrosis was 12.3 % +/- 5.6% in the low-sodium cardioplegic (modified Roe's) group and 9.3% +/- 3.4% in the high-sodium group. In the 6 hour arrest group the hearts were severely injured, with contracture occurring in all cases. The percentage of necrosis was 56.5% +/- 13% in the low-sodium cardioplegic group and 71.3% +/- 12% in the high-sodium group. In striking contrast all hearts protected with blood cardioplegia failed to show any evidence of tissue damage either on tetrazolium staining or on electron microscopic examination. We conclude that blood cardioplegia offers superior protection to the arrested heart at moderate hypothermia compared to crystalloid cardioplegia.

Intraoperative detection of spinal cord ischemia using somatosensory cortical evoked potentials during thoracic aortic occlusion.

Paraplegia remains a devastating and unpredictable complication of surgical procedures requiring temporary occlusion of the thoracic aorta, interruption of important spinal radicular vessels, or both. Intraoperative monitoring of the physiological integrity of the spinal cord should permit the early detection of spinal cord ischemia, the judicious and timely institution of corrective measures, including bypass or shunting, and the preservation of important intercostal arteries in appropriate circumstances. A model of spinal cord ischemia was created by temporary proximal and distal occlusion of the canine thoracic aorta. Serial measurement of somatosensory cortical evoked potentials (SCEP) generated by peripheral nerve stimulation, reflecting the status of long-tract neural conduction, was used to monitor alterations in spinal cord function during ischemia. Twelve animals subjected to aortic occlusion demonstrated a characteristic time-related deterioration of the SCEP with virtual extinction of the signal at a mean interval (+/- standard error of the mean) of 12.4 +/- 1.5 minutes. Six animals in which reperfusion was established immediately following the loss of the SCEP (Group 1) demonstrated complete recovery without neurological sequelae, as assessed by clinical and histological criteria. In 6 animals (Group 2), the period of aortic occlusion was extended for an additional 15 minutes following loss of the SCEP (27.3 +/- 2.3 minutes); postoperatively, 4 of 6 animals sustained major neurological lesions characterized by spastic paraplegia and histological evidence of spinal cord infarction (Group 1 versus Group 2, p less than 0.05). We conclude that distinctive alterations in the SCEP are indicative of reversible ischemic spinal cord dysfunction. On-line monitoring of spinal cord function using the technique of SCEP provides a rational basis for determining of SCEP provides a rational basis for determining operative strategy during surgical procedures on the thoracic aorta.