Crit Care Resusc
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To review the technology and the role of continuous intra-arterial blood gas monitoring in critical illness. ⋯ Over the last 10 years, a number of continuous intra-arterial blood gas monitoring systems have been developed. Only a few have reached commercial availability. While the performance characteristics of these systems are comparable, the levels of accuracy of these systems obtained in vitro are not consistently obtained in clinical trials. Arterial blood flow, wrist movement, wall effect and variability of blood gas analysers are some of the factors which determine the accuracy and reproducibility of these systems. Evidence to support the clinical usefulness of these monitors exists only in the form of case studies. Controlled studies demonstrating an improvement in outcome with the use of these monitors are lacking.
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To review the function and use of intravenous magnesium in magnesium depleted and non-magnesium depleted patients. ⋯ Magnesium is required in patients who are magnesium depleted and is also of benefit in non-magnesium depleted patients with pre-eclampsia. It may also be of benefit in non-magnesium depleted patients with acute coronary syndromes, arrhythmias, acute asthma, stroke, seizures and spinal cord injury.
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Clostridium perfiringens may cause myonecrosis (i.e. gas gangrene), acute food poisoning or necrotic enteritis (e.g. enteritis necroticans or Pig Bel). We describe a case of enteritis necroticans in a 33 year old man with acute myeloid leukaemia. ⋯ Treatment of enteritis necroticans requires urgent surgery to remove dead bowel and in adults intravenous penicillin (1g 2-hourly) and metronidazole (500 mg 8-hourly) or clindamycin (600 mg 6-hourly). While antibiotics may also reduce toxin formation, beta toxoid has not been found to be of benefit in established disease.
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To assess the effects of preoperative aspirin and/or intravenous heparin therapy on perioperative coagulation tests and postoperative blood loss for 24-hour after coronary artery bypass surgery. ⋯ There was no significant difference in either coagulation tests or postoperative blood loss (median of 860 mL with a range of 275 to 2800 mL, versus 833 ml with a range of 500-1380 mL) between the aspirin and no-aspirin patients. Preoperative heparin therapy affected most coagulation tests (e.g. international normalised ratio, activated partial thromboplastin time, thrombin clotting time, prothrombin time, activated clotting time and coagulation time of thrombelastography) before anaesthesia. The effects disappeared following protamine administration and after skin closure. Post operative blood loss was not significantly increased for the heparin group compared with the no-heparin group (median of 850 mL with a range of 700-1400 mL, versus 856 mL with a range of 275-2800 mL, respectively). Similar results were seen in patients receiving preoperative co-administration of aspirin and heparin compared with patients receiving aspirin alone. There was no suppression of platelet activity in patients receiving preoperative heparin or co-administration of aspirin and heparin. However, such suppression was found in patients receiving aspirin only. Conclusion: This study suggests that preoperative aspirin ingestion and intravenous heparin therapy should be administered as indicated and that concerns about the risk of postoperative bleeding should not lead to modification or cessation of such therapy.
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A case of hyponatraemia associated with subarachnoid haemorrhage is presented. The provisional diagnosis of an inappropriate antidiuresis was made and treatment with fluid restriction was instituted. However the patient continued to deteriorate as the diuresis continued and the hyponatraemia worsened, resulting in hypovolaema. ⋯ Cerebral salt wasting syndrome is an important and under-recognised cause of hyponatraemia in neurosurgical patients, particularly in patients with subarachnoid hemorrhage. It is essential to differentiate it from the syndrome of inappropriate antidiuretic hormone secretion to avoid complications of hypovolaemia and reduced cerebral perfusion as illustrated by this case. Brain natriuretic peptide may be responsible for this syndrome although this requires further investigation.