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Melbourne, Australia

Ho K.M.,University of Western Australia | Chavan S.,Center for Outcome and Resource Evaluation | Pilcher D.,Alfred Hospital
Chest | Year: 2011

Background: VTE is a preventable cause of death within hospitals. This study aimed to assess the association between omission of early thromboprophylaxis for > 24 h after ICU admission and mortality in critically ill patients. Methods: This study involved 175,665 critically ill adult patients admitted to 134 ICUs in Australia and New Zealand between 2006 and 2010. Results: The crude ICU and hospital mortality in patients who did not receive thromboprophylaxis within 24 h of ICU admission was higher than those who were treated with early thromboprophylaxis (7.6% vs 6.3%, P =.001; 11.2% vs 10.6%, P =.003, respectively), despite the former patients being associated with a slightly lower acuity of illness (mean APACHE [Acute Physiology and Chronic Health Evaluation] III model predicted mortality, 13% vs 14%; P =.001). The association between omission of early thromboprophylaxis and hospital mortality remained significant after adjusting for other covariates (OR, 1.22; 95% CI, 1.15-1.30; P =.001), particularly for patients with multiple trauma, sepsis, cardiac arrest, and preexisting metastatic cancer. The estimated attributable mortality effect of omitting early thromboprophylaxis for patients with multiple trauma, sepsis, cardiac arrest, and preexisting metastatic cancer was 3.9% (95% CI, 2.2-5.6), 8.0% (95% CI, 5.6-10.4), 15.4% (95% CI, 11.1-19.8), and 9.4% (95% CI, 6.4-12.4), respectively. Conclusions: Omission of thromboprophylaxis within the first 24 h of ICU admission without obvious reasons was associated with an increased risk of mortality in critically ill adult patients. © 2011 American College of Chest Physicians. Source

Dowrick A.S.,Alfred Hospital | Bhandari M.,McMaster University
Journal of Bone and Joint Surgery - Series A | Year: 2012

The placebo effect is based on the expectations of the patient regarding the effectiveness of the treatment. The high levels of stress and rituals involved with surgery can lead to a strong placebo effect. However, the ethical principles of performing sham surgery to measure any placebo effect have been questioned, and sham-controlled surgical trials are rarely conducted. While there are a number of ethical principles that must be considered to justify the implementation of a sham-controlled surgical clinical trial, four areas deserve particular attention: equipoise, risk minimization, informed consent, and deception. Particularly in orthopaedics, where equipoise is common, sham-controlled trials may be important to ensure that inferior or ineffective treatments do not become standard practice. Copyright © 2012 by The Journal of Bone and Joint Surgery, Incorporated. Source

Slattery D.,Alfred Hospital
ANZ Journal of Surgery | Year: 2010

Background: The presentation of a Chinese patient with unilateral Dupuytren's disease (DD) prompted a literature search and a review of the epidemiology of DD in the Asian population as it has never been cumulatively reported. The purpose of this paper is to review all the reported cases of DD in the literature and aetiological links to DD elsewhere. Methods: The literature was searched with a wide variety of terms, and subsequent references were analysed and further references investigated for other reported cases of DD in the Asian population. Results: This review found 595 cases and has shown that DD is present to a variable extent in China (96 cases), Thailand (19 cases), Vietnam (one case), India (15 cases) and Japan (474 cases). A total of 54% had bilateral disease. Risk factors (diabetes, trauma, epilepsy, alcoholism, manual labour) were reportedly present in 65% of the patients, and a positive family history was reported in 9%. The average patient age was 67 years. Conclusion: This review shows that there is a low but significant incidence of DD across Asia, which supports the hypothesis of a widespread genetic susceptibility to the disease. Therefore, the prevalence of DD in this community is not likely due to sporadic genetic mutation as previously presumed but rather individual genetic susceptibility and that risk factors play a major role in the expression of DD in this population. © 2010 Royal Australasian College of Surgeons. Source

Chan W.,Alfred Hospital
Journal of the American Heart Association | Year: 2013

Early diagnosis and knowledge of infarct size is critical for the management of acute myocardial infarction (MI). We evaluated whether early elevated plasma level of macrophage migration inhibitory factor (MIF) is useful for these purposes in patients with ST-elevation MI (STEMI). We first studied MIF level in plasma and the myocardium in mice and determined infarct size. MI for 15 or 60 minutes resulted in 2.5-fold increase over control values in plasma MIF levels while MIF content in the ischemic myocardium reduced by 50% and plasma MIF levels correlated with myocardium-at-risk and infarct size at both time-points (P < 0.01). In patients with STEMI, we obtained admission plasma samples and measured MIF, conventional troponins (TnI, TnT), high sensitive TnI (hsTnI), creatine kinase (CK), CK-MB, and myoglobin. Infarct size was assessed by cardiac magnetic resonance (CMR) imaging. Patients with chronic stable angina and healthy volunteers were studied as controls. Of 374 STEMI patients, 68% had elevated admission MIF levels above the highest value in healthy controls (> 41.6 ng/mL), a proportion similar to hsTnI (75%) and TnI (50%), but greater than other biomarkers studied (20% to 31%, all P < 0.05 versus MIF). Only admission MIF levels correlated with CMR-derived infarct size, ventricular volumes and ejection fraction (n = 42, r = 0.46 to 0.77, all P < 0.01) at 3 day and 3 months post-MI. Plasma MIF levels are elevated in a high proportion of STEMI patients at the first obtainable sample and these levels are predictive of final infarct size and the extent of cardiac remodeling. Source

Phase shift (PS) between oscillations in arterial blood pressure (ABP) and transcranial Doppler (TCD) cerebral blood flow velocity (CBFV) is thought to describe cerebral autoregulation. Ventilated patients show high amplitude and regular respiratory oscillations in ABP and CBFV, allowing reliable PS measurement. We analysed recordings of ABP, CBFV and intracranial pressure (ICP) from 187 TBI patients treated at Addenbrooke's Hospital, Cambridge, UK, from 1993 to 1998. Monitored data were recorded and PS, TCD autoregulation (Mx) and pressure reactivity (PRx) were calculated using ICM+. PS was computed by peak detection in the ABP/CBFV cross-spectrum. Recordings with low coherence (<0.5), unstable respiratory rate (RR), or PS wraparound were excluded. Median RR was 14 bpm (range 10-20 bpm). Group median PS was 13° (range -37-56°). Average PS (PSa) correlated with RR (Spearman's R = -0.302, p < 0.01, and cerebral perfusion pressure (R = -0.373, p < 0.01). Correlations of PS with Mx and PRx were weak but significant (p < 0.01). Kruskal-Wallis test for outcome vs. PS was non-significant (PSa: p = 0.14, minimum PS (PSm): p = 0.27). Mann-Whitney test for mortality vs. PS was significant (p < 0.05) for PSm only. Respiratory PS responds to changes in CPP and RR and correlates weakly with CA. Respiratory PS may have some prognostic value for patients with TBI. Source

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