Emergency medicine journal : EMJ
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The Australian healthcare system at all levels is under increasing pressure. The Australian paramedic discipline has seen a remarkable change in a number of areas including education, training, healthcare identity and clinical practice, particularly over the past three decades. Preparing future healthcare graduates for these expected changes therefore requires careful alignment of graduate attributes to core curriculum. ⋯ It is critical that empirically-based paramedic graduate attributes are developed and agreed upon by both the industry and teaching institutions. Until this occurs, the national standardisation, accreditation and benchmarking of Australian paramedic education programmes will not be possible.
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A 62-year-old man presented 6 h after a mixed intentional overdose of dilatizem (Adizem-SR), atorvastatin, aspirin and isosorbide mononitrate. He was symptomatic, with vomiting, blurred vision and unsteady gait. Despite initial fluid resuscitation and calcium chloride, glucagon, and high-dose ionotropic therapy, his hypotension remained refractory to treatment. ⋯ Over the following 24 h, the patient was given 1140 units of accumulative insulin. This resulted in a significant improvement in arterial blood pressure values and metabolic indices, allowing contiguous weaning off inotropes. This case supports the use of rescue hyperinsulinaemic euglycaemia in patients with an overdose of calcium channel blockers who remain hypotensive despite standard pharmacological measures.
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To determine the incidence of deep vein thrombosis (DVT) in patients diagnosed with superficial thrombophlebitis (STP) after presenting to an outpatient DVT service. ⋯ Although STP is generally considered benign, there is a risk that it may coexist or develop into DVT. The underlying cause of STP should be considered and patients with significant risk factors should be advised to monitor their symptoms closely with regard to potential DVT formation.
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This paper describes a 21-year-old man who presented to the emergency department with a knife wound to his buttock. He had a witnessed cardiac arrest with pulseless electrical activity in hospital as a result of further haemorrhage. His post-resuscitation arterial blood gas revealed a severe lactic acidosis (pH 6.61, lactate 22.0 mmol/l). ⋯ Severe lactic acidosis occurs post cardiac arrest due to imbalance between cellular oxygen supply and demand. Severe lactic acidosis is associated with hypoxic brain injury but has a low specificity in its prediction. The case illustrates that, especially in younger adults, severe lactic acidosis may be a poor predictor of outcome if it reflects a period of relative hypoperfusion preceding cardiac arrest.