Australian and New Zealand journal of medicine
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Chronic heart failure (CHF) is associated with activation of the sympathetic nervous system. This activation provides short term haemodynamic support to the failing myocardium, but may be deleterious over longer periods as chronic catecholamine excess appears to contribute to disease progression and increased mortality in this condition. Therefore, blockade of sympathetic activation represents a logical, if somewhat counter-intuitive, approach to the management of the patient with systolic CHF. ⋯ Drugs such as carvedilol are also anti-oxidant, anti-proliferative and have anti-endothelin actions; the clinical significance of these properties is yet to be determined. Unanswered questions remain regarding the use of beta-blockers in heart failure. Ongoing studies are further examining mechanisms underlying the clinical benefits of these agents as well as their therapeutic potential in NYHA Class IV patients, heart failure post-myocardial infarction and patients with asymptomatic left ventricular dysfunction.
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Review Case Reports
Optic disc oedema and diabetes mellitus: a case report with review.
Optic disc oedema is a neurological complication of diabetes mellitus. Typically, the patient is a young diabetic with minimal symptomatology but severe bilateral optic disc oedema discovered on routine eye examination. It is a relatively benign condition which on occasion can result in a residual visual deficit, but requires no specific intervention and represents a subgroup of anterior ischaemic optic neuropathy (AION). We present a patient with insulin dependent diabetes and asymptomatic bilateral optic disc oedema, with a brief review of the syndrome and its pathogenesis.
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In diabetic ketoacidosis (DKA) and particularly in hyperosmolar coma, rapid normalisation of the measured extracellular fluid abnormalities cannot be equated with optimal management. In both disorders there are complex imbalances between extra- and intracellular compartments that are best corrected in a series of rational steps, based on an understanding of pathophysiology. Fluid administration in DKA can generally be divided into three successive phases: (i) a short period of rapid isotonic saline infusion, (ii) slower infusion of isotonic saline with potassium chloride, and (iii) glucose-potassium infusion until oral food intake is well established. ⋯ In the management of hyperosmolar coma, insulin and fluid therapy are more conservative, with the aim of achieving complete rehydration and normoglycaemia only after 36 to 72 hours. Pulmonary complications and the effects of tissue ischaemia, as well as thromboembolic events, remain important causes of death in both disorders. The frequent recurrences of DKA that occur in a group of psychiatrically-unstable young patients remain an unsolved problem.