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Steve Meek, Consultant Emergency Physician Emergency Department, RUH Bath
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I was pleased to see Dr Collinson and Prof Kennedy raising the profile of chest pain rule out. I am, however , concerned that Dr Collinson's paper suggests than a clinical diagnosis of gastrooesophageal pain can be made on response to antacids, and Dr Kennedy has highlighted this. It is a shame the authors did not recall and measure troponins on all discharged patients. Our own experience in using troponins for MI rule out for 15 months confirms that typically gastro-oesophageal sounding pain is indeed occasionally cardiac in origin. Dr Kennedy suggests a 12 hour observation period with serial ecgs and biochemical tests as the way forward. Two or three centres in the UK are already doing this, ourselves included. Our ROMEO pathway(Rule Out Myocardial Events on Obs ward)has been running for 15 months and involves troponin I on presentation and 12 hours, a monitored observation bed on our observation unit and next working session ETT for suitable patients. Data will shortly be offered for publication but we have found it to be safe and effective at reducing length of stay, preventing unsafe discharge and risk stratifying those patients unexpectedly found to have a raised troponin. Telephone follow up has demonstrated a low incidence of continued problems. Many other Emergency Departments are looking to start similar rapid rule out strategies. I would suggest that there are three essential requirements for an effective rule out strategy, cardiac or otherwise - 1. an observation facility 2. 24 hour senior doctor presence in the ED (registrar minimum), 3. a single portal of entry for all emergency admissions. We call this the Holy Trinity of Emergency Medicine. Steve Meek MRCP FRCS FFAEM
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Victor A Inyang
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This paper raises an important issue in the current practice of emergency medicine in the UK. There are certain areas, which may need clarification for this paper to be truly applicable to the emergency department. The recruitment of patients does not indicate how long they had experienced chest pain prior to arrival in the emergency department. Without this information we are unable to give weight to the assertion in the paper that the diagnostic sensitivity for acute myocardial infarction of troponin T is equivalent to that of creatine kinase on first presentation with chest pain. This statement was not referenced A positive troponin T may be associated with renal failure, diabetes mellitus, pulmonary embolism, cardiac failure and myocarditis 2. These groups of patients will test negative to troponin I in the absence of an acute coronary event. Information on the medical history of the patients who tested positive to troponin T would have been helpful. Based on the data we are given in this study, the number of patients discharged from the emergency with prognostically important myocardial damage is not a true reflection of the spectrum of patients discharged from the emergency department. Testing of the 408 patients would have been needed to achieve this. A further compounding factor was the decision to exclude 30 % (122 ) patients on the basis of an electrocardiogram and history having noted in the introduction a 41-61% diagnostic sensitivity for the electrocardiograph. Could this group have had patients with a positive troponin T test? A strategy, using troponins, in the management of patients with chest pain plus an equivocal electrocardiogram is 1. Performance of a troponin I on patient arrival. If positive transfer to coronary care for further management. If negative 2. Perform a repeat troponin I 4 hours later (at least 6 hours from the onset of pain). If positive manage on coronary care unit. If negative look for another cause of the chest pain. Hamm et al have shown that this procedure is 100% sensitive. Using troponin T in the same strategy the sensitivity is 94%. Victor A Inyang FFAEM John Sutherland FRCSEd Consultant Specialist Registrar Emergency Medicine Accident & Emergency Medicine The Ipswich Hospital Ipswich IP4 5PD References 1. Collinson P O, Premanchandram S, Hashemi K. Prospective audit of incidence of prognostically important myocardial damage in patients discharged from the emergency department. BMJ 2000; 320:1702-5 2. Hamm C W, Goldmann B U, Heeschen C et al. Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I. N Engl J Med 1997; 337: 1648-1653. |
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Steve Goodacre, Research Fellow Northern General Hospital
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Collinson and colleagues should be congratulated on a detailed and thoughtful audit. This is a large and very important health care problem[1]. The thoughtful commentary by Kennedy touches on a number of key issues as well as the obvious limitations of such a study. As Kennedy says, further follow-up data on the 7 patients with raised troponin would be useful. Kennedy also touched on the issue of definitions. The seven missed Mayday patients had myocardial damage but would not satisfy the classical WHO or MONICA definitions of acute myocardial infarction. However, Collinson is correct to point out that such patients have a less favourable prognosis. Should these classical definitions be reconsidered? The 6% of discharged patients with troponin T levels above 0.1ng/ml have a substantial short-term mortality and morbidity,[2] yet this can be improved by appropriate treatment.[3] Discharge of such patients should clearly be avoided, even if they fail to meet classical definitions of acute myocardial infarction. Chest pain observation units (CPOUs) may prevent these inappropriate discharges. One such unit has been operational in the Accident and Emergency Department of the Northern General Hospital in Sheffield since March 1999.[4] Similar follow-up has been used to monitor those discharged (ECG and troponin T at 72 hours post-attendance). So far 761 patients have been assessed on the unit, of whom 86% were successfully discharged. 580 of those discharged (88%) attended follow-up. Only one patient had a troponin T level > 0.1ng/ml (0.17%). Using Collinsons' recommended audit tool in this way suggests that the Sheffield CPOU performs well. However, longer-term follow-up data needs to be collected and ultimately only a randomised controlled trial can tell us whether the CPOU is superior to routine care. A recent systematic review has examined the efficacy of chest pain observation units and their apparent cost effectiveness.[5] However, most data come from the United States with its unique mix of commercial and emergency services. In conclusion, we suggest that there is an urgent need for a randomised-controlled trial in the very different circumstances of the British NHS. Steve Goodacre, Francis Morris Northern General Hospital, Sheffield Simon Capewell University of Liverpool 1. Capewell S & McMurray JJV. "Chest Pain-Please Admit", is there an alternative? BMJ 2000; 320: 951-2. 2. Ohman M E, Armstrong P W, Christenson R H et al. Cardiac troponin T levels for risk stratification in acute myocardial ischaemia. N Engl J Med 1996; 335: 1333-41. 3. Lindahl B, Venge P, Wallentin L for the FRISC study group. Troponin T identifies patients with unstable coronary artery disease who benefit from long-term antithrombotic protection. J AM Coll Cardiol 1997; 29: 43-8. 4. Goodacre S W. Should we establish chest pain observation units in the United Kingdom? A systematic review. J Accid Emerg Med 2000; 17: 1-6. 5. Goodacre S W, Morris F M, Campbell S et al. A descriptive study of a chest pain observation unit in a UK hospital (abstract). J Accid Emerg Med 2000; 17: 58. |
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Fiona Rae
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Dear sir - Collinson et al (1) identify a small group of patients who were sent home from their department with chest pain of unclear cause who subsequently were found to have abnormal Troponin-T concentrations. Since previous studies have shown Troponin-T to be a marker for myocardial damage and, more importantly, to be associated with adverse outcomes, they conclude that all of these patients had prognostically significant myocardial damage. This may or may not be true, but is certainly not shown by their study as they imply in their conclusion. The study has no control group, and excludes a number of patients who are notoriously mis-diagnosed - namely those assumed to have musculoskeletal or gastrointestinal causes for their pain. It would also have been interesting to know what the troponin concentrations were in those patients who were admitted for "exclusion of myocardial infarction". I am surprised at such a large group of patients with undiagnosed chest pain being discharged with no follow-up arranged. What were the differences between this group and those who were admitted for further investigation? There is no mention in the paper of who the clinician initally seeing the patient was - were they largely seen and discharged by SHOs or all reviewed by senior members of the department? Most importantly of all, whatever any other study has shown, we need to know the long term morbidity and mortality of these patients, though this would need to be a much larger study to be statistically significant. However, I would agree that there is room for improvement in chest pain management both in the emergency department and subsequently. I think as emergency physicians we should be vary wary of discharging a patient with undiagnosed chest pain home at all, let alone without follow-up. It is important to re-iterate that normal electrocardiographic and biochemical markers in such patients at the time of presentation do not exclude significant myocardial injury, and to accept that we investigate large numbers of patients without cardiac disease for each one whose morbidity or mortality we affect. The present system for most hospitals in the UK means admitting these patients to a medical ward, and until there is safe, proven alternative (such as a short stay cardiac assessment unit) I think this is where we should be aiming for these patients to be when their troponin-T is found to be elevated at 12 or 24 hours after inital presentation. Fiona Rae BM FRCS Senior Registrar in Emergency Medicine Royal Darwin Hospital Australia 1. Collinson PO, Premachandram S, Hashemi K. Prospective audit of incidence of prognostically important myocardial damage in patients discharged from emergency department. BMJ 2000;320:1702-5 |
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