Acute anterior compartment syndrome following low energy non-contact injury.
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Biomedical subjects
Publications and source records attributed to Mark Fitzgerald.
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The reaction between O-. and MeO-CH2-C identical to C-CDO in the ion source of a VG ZAB 2HF mass spectrometer gives a number of product anions including [H2CCCCO]-. and [HCCCCDO]-. (in the ratio 1:5). Neutralisation-reionisation (NR+) of [H2CCCCO]-. results in the sequential two-electron vertical oxidation [H2CCCCO]-.-->H2CCCCO-->[H2CCCCO](+.). Singlet H2CCCCO lies 158 kJ mol-1 below the triplet [at the CCSD(T)/aug-cc-pVDZ//B3LYP/6-31G(d) level of theory]. The majority of neutrals H2CCCCO are stable for the microsecond duration of the NR experiment, but some are energized and decompose to give H2CCC and CO. A similar NR+ experiment with [HCCCCDO]-. yields neutrals HCCCCDO, some of which are excited and rearrange. Calculations show that it is the singlet form of HCCCCHO which rearranges (the singlet lies 36 kJ mol-1 above the ground state triplet): the rearrangement occurs by the sequential H transfer process, HCCCCHO-->HCC(CH)CO<--H2CCCCO. Neutral HCCCCHO needs an excess energy of only 43 kJ mol-1 to effect this reaction, which is exothermic by 230 kJ mol-1. Both HCC(CH)CO and H2CCCCO formed in this way should have sufficient excess energy to cause some loss of CO. The anions [CC(CH)CHO]-. and [CC(CD)CHO]-. are formed in the ion source of the mass spectrometer by the reactions of HO- with Me3SiC identical to C-CH = CHOMe and Me3SiC identical to C-CD = CHOMe respectively. NR+ of these anions indicate that energized forms of CC(CH)CHO and CC(CD)CHO may rearrange to isomer(s) which decompose by loss of CO. Singlet CC(CH)CHO rearranges to HCC(CH)CO and H2CCCCO, both of which are energized and fragment by loss of CO.
The neutrals HCCCCCO and CCCCCHO have been studied by experiment and by molecular modelling at the CCSD(T)/aug-cc-pVDZ//B3LYP/6-31G(d) level of theory. Neutral HCCCCCO has been made by one-electron reduction of [HCCCCCO]+ in the dual collision cell of a VG ZAB 2HF mass spectrometer. The isomer CCCCCHO is also formed in the dual collision cell, but this time by one-electron oxidation of the anion [CCCCCHO]-. Comparison of the CID and +NR+ mass spectra of [HCCCCCO]+ indicates that neutral HCCCCCO, when energised, retains its structural integrity. If the excess energy of HCCCCCO is > or = 170 kJ mol-1, decomposition can occur to give HCCCC and CO (calculations at the CCSD(T)/aug-cc-pVDZ//B3LYP/6-31G(d) level of theory). The situation with the isomer CCCCCHO is different. Comparison of the -CR+ and -NR+ spectra of [CCCCCHO]- shows that both neutral and cationic forms of CCCCCHO partially rearrange to a species which decomposes by loss of CO. The peak corresponding to loss of CO is more pronounced in the -NR+ spectrum, indicating that the rearrangement is more prevalent for the neutral than the cation. Theoretical calculations suggest that the species losing CO could be CCCCHCO or HCCCCCO, but that HCCCCCO is the more likely. The lowest-energy rearrangement pathway occurs by successive H transfers, namely CCCCCHO-->CCCCHCO-->CCCHCCO-->HCCCCCO. The rearrangement of CCCCCHO to HCCCCCO requires CCCCCHO to have an excess energy of > or = 94 kJ mol-1. The species HCCCCCO formed by this exothermic sequence (214 kJ mol-1) has a maximum excess energy of 308 kJ mol-1: this is sufficient to effect decomposition to HCCCC and CO.
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Mixtures of Ln(SC(6)F(5))(3) and Ln(EPh)(3) (E = S, Se) react with elemental E to give chalcogen-rich clusters with fluorinated thiolate ancillary ligands. The structures of both (THF)(6)Yb(4)S(SS)(4)(SC(6)F(5))(2) and (THF)(6)Yb(4)Se(SeSe)(4)(SC(6)F(5))(2) have been established by low-temperature single-crystal X-ray diffraction. Both compounds contain a square array of Yb(III) ions connected by a central mu(4)-E(2-) ligand. The edges of the square Yb(4) array are bridged by four mu(2)(EE) ligands, and two terminal SC(6)F(5) are on the same side of the Ln(4) plane that is capped by the mu(4)-E(2-) ion. Redox inactive (THF)(6)Tm(4)Se(SeSe)(4)(SC(6)F(5))(2) was also prepared to establish the extension of this chemistry to the redox inactive Ln. These clusters are soluble in toluene.
BACKGROUND: The Parkland formula is established as the "gold standard" for initial fluid resuscitation for major burns. The purpose of this study was to review our fluid resuscitation practice for major burns to determine whether anecdotal observations of significant variations from the Parkland formula were wide spread and whether any difference could be used as a basis for a revision of fluid resuscitation in major burns. METHODS: A retrospective review of 127 presentations to The Alfred Burns Unit with total body surface area (TBSA) affected > or =15% was conducted. A retrospective review of the resuscitation data from these patients was compared with the Parkland formula as well as other studies. RESULTS: A total of 49 patients with complete data on fluid administration and uncomplicated burns were included in the analysis. Significantly larger volumes of fluid (5.58 mL/kg per %TBSA) were given to these patients in the first 24 h than predicted by the Parkland formula. Mean arterial pressure, pulse rate and urine output were at satisfactory levels. Clinically evident complications from fluid administration were minimal. Mortality was similar to that in other centres. CONCLUSION: Fluid resuscitation volumes significantly higher than those predicted by the Parkland formula were given, without adverse consequences. This retrospective review supports a prospective, multicentre, randomized, controlled study comparing this study with the Parkland formula, resulting in a better guide to initial fluid resuscitation in major burns.
OBJECTIVE: Application of the Trauma and Injury Severity Score (TRISS) to a trauma population identifies patients with 'unexpected survival'. This study used TRISS analysis to identify 'unexpected survivors' suffering major thoracic trauma, who survived to hospital discharge. Further analysis determined prehospital interventions that appeared to contribute to 'unexpected survival'. METHODS: The present study was a single-centre, retrospective case review with comparative statistical analysis. Patients were identified from the Alfred Trauma Registry between 1 July 2002 and 30 June 2003. RESULTS: There were 336 adult trauma patients treated at The Alfred Trauma Centre with an Injury Severity Score >15 (major trauma) and at least one thoracic Anatomical Injury Score of 3 (severe) or greater. Of the eligible patients, 322/336 (95.8%, 95%[confidence interval] CI 95.1-96.5%) had complete data available for analysis. The study population mortality was 42/322 (13.0%, 95% CI 12.3-13.7%). There were 20 'unexpected survivors' (5.9%) and 5 (1.5%) 'unexpected deaths' on TRISS analysis. Chest decompression and/or endotracheal intubation prehospital was performed on 16/20 'unexpected survivors'. GCS for 'unexpected survivors' and 'expected deaths' (3.8 vs 3.5, P = 0.27) was not a predictor of survival. Respiratory rate per minute (16.2 vs 8.8, P = 0.01) and systolic blood pressure - mmHg (98 vs 80, P = 0.03) were significantly greater in the 'unexpected survivors' group compared with the 'expected death' group. CONCLUSION: For patients sustaining severe thoracic blunt trauma, prehospital intubation and chest decompression appear to be associated with unexpected survival. A low GCS at scene is not predictive of 'unexpected survival' or 'expected death'.
Blunt cardiac injuries are a leading cause of fatalities following motor-vehicle accidents. Injury to the heart is involved in 20% of road traffic deaths. Structural cardiac injuries (i.e. chamber rupture or perforation) carry a high mortality rate and patients rarely survive long enough to reach hospital. Chamber rupture is present at autopsy in 36-65% of death from blunt cardiac trauma, whereas in clinical series it is present in 0.3-0.9% of cases and is an uncommon clinical finding. Patients with large ruptures or perforations usually die at the scene or in transit--the rupture of a cardiac cavity, coronary artery or intrapericardial portion of a major vein or artery is usually instantly fatal because of acute tamponade. The small, rare, remaining group of patients who survive to hospital presentation usually have tears in a cavity under low pressure and prompt diagnosis and surgery can now lead to a survival rate of 70-80% in experienced trauma centres. As regional trauma systems evolve, patients with severe, but potentially survivable cardiac injury are surviving to ED. Two distinct syndromes are apparent--haemorrhagic shock and cardiac tamponade. Any patient with severe chest trauma, hypotension disproportionate to estimated loss of blood or with an inadequate response to fluid administration should be suspected of having a cardiac cause of shock. For patients with severe hypotension or in extremis, the treatment of choice is resuscitative thoracotomy with pericardotomy. Closed chest cardiopulmonary resuscitation is ineffective in these circumstances. Blunt traumatic cardiac injury presenting with shock is associated with a poor prognosis. The majority of survivors of blunt or penetrating cardiac injury present to the ED/trauma centre with vital signs. The main pathophysiologic determinant for most survivors is acute pericardial tamponade. The presence of normal clinical signs or normal ECG studies does not exclude tamponade. In recent years the widespread availability and use of ultrasound for the initial assessment of severely injured patients has facilitated the early diagnosis of cardiac tamponade and associated cardiac injuries. Two cases of survival from blunt traumatic cardiac trauma are described in the present paper to demonstrate survivability in the context of rapid assessment and intervention.
BACKGROUND: There are no published studies that have assessed whether adding long-acting beta 2-agonist bronchodilators and/or inhaled steroids to chronic therapy with tiotropium would provide additional clinical benefit to patients with moderate to severe chronic obstructive pulmonary disease (COPD). METHODS: The Canadian Optimal Therapy of COPD Trial is a randomized, prospective, double-blind, placebo-controlled, multicentre trial funded by the Canadian Institutes of Health Research that has been designed to determine which combination of inhaled medications will most effectively prevent exacerbations and optimize disease-specific quality of life in patients with COPD. The trial is the first to evolve from the Canadian Thoracic Society Clinical Trials Group. The study will randomize 432 patients with moderate to severe COPD to one of three parallel treatment arms for 52 weeks: tiotropium and fluticasone/salmeterol; tiotropium and salmeterol; or tiotropium and placebo inhaler. The participants will be allowed to use salbutamol as required throughout the trial period. OUTCOMES: The primary outcome measure is the proportion of patients in the three treatment groups who experienced a respiratory exacerbation within 52 weeks of randomization. Other outcomes that will be assessed over the 52-week trial period will include: changes in disease-specific quality of life and changes in dyspnea, health care use and changes in lung function. A pharmacoeconomic analysis will also be performed to evaluate the cost of these therapies. RESULTS: The study commenced recruitment in October 2003. It is currently operating at 22 centres across Canada and has randomized 137 patients during the first four months of recruitment. Recruitment is scheduled to continue until April 2005 or until 432 patients have been randomized. CONCLUSION: The present randomized, placebo-controlled trial offers a unique opportunity to answer the question, what is the best combination of inhaled medications to use for COPD patients? It is hoped that optimal use of inhaled medications will improve patient health and quality of life, reduce patient respiratory exacerbations, and ultimately, reduce health care resource use.
Australian hospitals need to be prepared to deal with mass casualties from terrorist strikes, including bomb blasts and chemical, biological and radiation injury. Injuries from bomb explosions are more severe than those commonly seen in Australian hospitals. In disasters involving mass casualties in urban areas, many of the injured make their own way to hospital, often arriving before the more seriously injured casualties. Major hospitals in Australia should plan for large numbers of undifferentiated and potentially contaminated casualties arriving with minimal warning. It is critical that experienced and trained senior medical officers perform the triage of casualties in emergency departments, with frequent reassessment to detect missed injuries (especially pulmonary blast injury). Hospitals require well developed standard operating procedures for mass casualty events, reinforced by regular drills. Preparing for a major event includes training staff in major incident management, setting up an operational/control unit, nominating key personnel, ensuring there is an efficient intra-hospital communication system, and enhancing links with other emergency services and hospitals.