Shahbaz S. Malik

Bio: Shahbaz S. Malik is an academic researcher from University of Manitoba. The author has contributed to research in topics: Medicine & Surgery. The author has an hindex of 7, co-authored 21 publications receiving 125 citations. Previous affiliations of Shahbaz S. Malik include Royal Orthopaedic Hospital & University Hospitals Birmingham NHS Foundation Trust.

Acromioclavicular joint augmentation at the time of coracoclavicular ligament reconstruction fails to improve functional outcomes despite significantly improved horizontal stability

Abstract: Acromioclavicular joint reconstruction is a well-established and frequently performed procedure. Recent scientific and commercial interest has led to a drive to develop and perform surgical techniques that more reliably restore horizontal stability in order to improve patient outcomes. The aim of this systematic review was to evaluate the biomechanical evidence for procedures directed at restoring horizontal stability and determine whether they are associated with superior clinical results when compared to well-established procedures. A review of the online databases Medline and EMBASE was conducted in accordance with the PRISMA guidelines on the 23rd December 2017. Biomechanical and clinical studies reporting either static or dynamic horizontal displacement following acromioclavicular joint reconstruction (Coracoclavicular reconstruction or Weaver-Dunn) were included. In addition, biomechanical and clinical studies reporting outcomes after additional augmentation of the acromioclavicular joint were included. The studies were appraised using the Methodological index for non-randomised studies tool. The search strategy identified 18 studies eligible for inclusion: six biomechanical and 12 clinical studies. Comparative biomechanical studies demonstrated that acromioclavicular augmentation provided significantly increased horizontal stability compared to the coracoclavicular reconstruction and Weaver–Dunn procedure. Comparative clinical studies demonstrated no significant differences between coracoclavicular reconstruction with and without acromioclavicular augmentation in terms of functional outcomes (American Shoulder and Elbow Surgeon and Constant score), complication or revision rates. However, one comparative study did demonstrate an improvement in Taft (p = 0.018) and Acromioclavicular Joint Instability scores (p = 0.0001) after acromioclavicular augmentation. In conclusion, coracoclavicular reconstruction with augmentation of the acromioclavicular joint has been shown to provide improved horizontal stability in both biomechanical and clinical studies compared to isolated coracoclavicular reconstruction. However, comparative studies have shown no clinical advantage with respect to American Shoulder and Elbow Surgeon or Constant scores and, therefore, the results of this systematic review do not support acromioclavicular augmentation in routine clinical practice. IV.

Risk factors for onset of delirium after neck of femur fracture surgery: a prospective observational study

Abstract: Background : Delirium is a common complication after surgery in the elderly that leads to increased length of stay and other adverse outcomes. The aim of this study was to better understand the exact causes of post-operative delirium in patients undergoing surgery for neck of femur (NOF) fractures.Methods : We performed a prospective cohort study of 381 consecutive patients undergoing surgery for NOF fractures at a single institution. Baseline cognitive status and risk factors were recorded on admission. Post-operative cognitive status was assessed at regular intervals until discharge. Binary logistic regression was performed to identify independent predictors of delirium.Results : Patients who developed post-operative delirium (n = 70) were significantly older (average age 83 vs. 78, p = 0.019) and more likely to be female (79% vs. 67%, p = 0.062) than non-affected patients. The presence of delirium was associated with increased length of stay (13 vs. 10 days, p = 0.001) and 1-year mortality (25.7% vs. 15% p = 0.03). Independent predictors of delirium included age ≥65 years (Odds Ratio = 5.8), presence of anaemia (OR = 2.9), hypoxia (OR = 2.86), cardiac disease (OR = 2.8), Chronic Obstructive Pulmonary Disease (OR = 2.5), new onset electrolyte imbalance (OR = 2.2) and renal failure (OR = 1.9).Conclusion : Overall analysis demonstrated an increased incidence of delirium in older females with greater comorbid conditions. It was also found to be associated with increased morbidity and mortality. We recommend clinicians put greater effort into recognising risk factors of delirium and diagnosing it in a timely manner to mitigate its effects.

Cortisol shifts financial risk preferences

Abstract: * Freely available online through the PNAS open access option. Risk taking is central to human activity. Consequently, it lies at the focal point of behavioral sciences such as neuroscience, economics, and finance. Many influential models from these sciences assume that financial risk preferences form a stable trait. Is this assumption justified and, if not, what causes the appetite for risk to fluctuate? We have previously found that traders experience a sustained increase in the stress hormone cortisol when the amount of uncertainty, in the form of market volatility, increases. Here we ask whether these elevated cortisol levels shift risk preferences. Using a double-blind, placebo-controlled, cross-over protocol we raised cortisol levels in volunteers over eight days to the same extent previously observed in traders. We then tested for the utility and probability weighting functions underlying their risk taking, and found that participants became more risk averse. We also observed that the weighting of probabilities became more distorted among men relative to women. These results suggest that risk preferences are highly dynamic. Specifically, the stress response calibrates risk taking to our circumstances, reducing it in times of prolonged uncertainty, such as a financial crisis. Physiology-induced shifts in risk preferences may thus be an under-appreciated cause of market instability.

Reverse Total Shoulder Arthroplasty: Biomechanics and Indications.

Abstract: Over the past decade, our understanding of the biomechanics of the reverse total shoulder arthroplasty (RTSA) has advanced, resulting in design adjustments, improved outcomes, and expanding indications. The purpose of this review is to summarize recent literature regarding the biomechanics of RTSA and the evolving indications for its use. While Grammont’s principles of RTSA biomechanics remain pillars of contemporary designs, a number of modifications have been proposed and trialed in later generations to address complications such as impingement and glenoid failure. Clinical and biomechanical literature suggest that less medialized, more inferior glenospheres result in less impingement and notching. On the humerus, a more vertical neck cut is associated with less impingement. Indications for RTSA continue to expand beyond the classic indication of cuff tear arthropathy (CTA). Patients without a functional cuff but no arthritis now have a reliable option in the RTSA. RTSA has also replaced hemiarthroplasty as the implant of choice for displaced three- and four-part proximal humerus fractures in the elderly. Finally, updated design options and modular components now allow for treatment of glenoid bone loss, failed arthroplasty, and proximal humerus tumors with RTSA implants. Reverse total shoulder arthroplasty design has been modernized on both the glenoid and humerus to address biomechanical challenges of early implants. As outcomes improve with these modifications, RTSA indications are growing to address complex bony pathologies such as tumor and bone loss. Longitudinal follow-up of patients with updated designs and novel indications is essential to judicious application of RTSA technology.

Acute Inflammation Alters Brain Energy Metabolism in Mice and Humans: Role in Suppressed Spontaneous Activity, Impaired Cognition, and Delirium

Abstract: Systemic infection triggers a spectrum of metabolic and behavioral changes, collectively termed sickness behavior, which while adaptive, can affect mood and cognition. In vulnerable individuals, acute illness can also produce profound, maladaptive, cognitive dysfunction including delirium, but our understanding of delirium pathophysiology remains limited. Here, we used bacterial lipopolysaccharide (LPS) in female C57BL/6J mice and acute hip fracture in humans to address whether disrupted energy metabolism contributes to inflammation-induced behavioral and cognitive changes. LPS (250 µg/kg) induced hypoglycemia, which was mimicked by interleukin (IL)-1β (25 µg/kg) but not prevented in IL-1RI-/- mice, nor by IL-1 receptor antagonist (IL-1RA; 10 mg/kg). LPS suppression of locomotor activity correlated with blood glucose concentrations, was mitigated by exogenous glucose (2 g/kg), and was exacerbated by 2-deoxyglucose (2-DG) glycolytic inhibition, despite preventing IL-1β synthesis. Using the ME7 model of chronic neurodegeneration in female mice, to examine vulnerability of the diseased brain to acute stressors, we showed that LPS (100 µg/kg) produced acute cognitive dysfunction, selectively in those animals. These acute cognitive impairments were mimicked by insulin (11.5 IU/kg) and mitigated by glucose, demonstrating that acutely reduced glucose metabolism impairs cognition selectively in the vulnerable brain. To test whether these acute changes might predict altered carbohydrate metabolism during delirium, we assessed glycolytic metabolite levels in CSF in humans during inflammatory trauma-induced delirium. Hip fracture patients showed elevated CSF lactate and pyruvate during delirium, consistent with acutely altered brain energy metabolism. Collectively, the data suggest that disruption of energy metabolism drives behavioral and cognitive consequences of acute systemic inflammation.SIGNIFICANCE STATEMENT Acute systemic inflammation alters behavior and produces disproportionate effects, such as delirium, in vulnerable individuals. Delirium has serious short and long-term sequelae but mechanisms remain unclear. Here, we show that both LPS and interleukin (IL)-1β trigger hypoglycemia, reduce CSF glucose, and suppress spontaneous activity. Exogenous glucose mitigates these outcomes. Equivalent hypoglycemia, induced by lipopolysaccharide (LPS) or insulin, was sufficient to trigger cognitive impairment selectively in animals with existing neurodegeneration and glucose also mitigated those impairments. Patient CSF from inflammatory trauma-induced delirium also shows altered brain carbohydrate metabolism. The data suggest that the degenerating brain is exquisitely sensitive to acute behavioral and cognitive consequences of disrupted energy metabolism. Thus "bioenergetic stress" drives systemic inflammation-induced dysfunction. Elucidating this may offer routes to mitigating delirium.