Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Common things are common
- Deepak Kejariwal (2 May 2003)
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Is a PE the truth, the whole truth, and nothing but the truth?
- Anthony N Glaser (2 May 2003)
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It's easy to test....
- Andrew G Robinson (2 May 2003)
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?Pulmonary Embolism
- Sudipta Maitra (2 May 2003)
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A 42 year old man with acute chest pain-part 2
- Marin Marinovic, PO BOX3939 Dubai,UAE (2 May 2003)
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acute minor PE in IT Worker(?variation of economy class syndrome)
- krishna kumar jada (3 May 2003)
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remains 'aortic dissection until proven otherwise'
- M D Dominic Bell (3 May 2003)
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First do no harm!
- Malvinder S. Parmar (3 May 2003)
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proximal aortic dissection.
- nagmeldin hassan ibrahim (3 May 2003)
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can myocardial ischemia be excluded?
- Marco Biancardi (3 May 2003)
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IS IT VASCULITIS?
- KUMAR RS BHAMIDIMARRI (3 May 2003)
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Rapid Response from Peter Hartl- The patient´s point of view
- Peter Hartl (3 May 2003)
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New SoftwareTechnology for Diagnosing of Myocardia Ischemia and Assessment of Severity
- Hisham M.. Al-Qysi (3 May 2003)
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Don't forget the oesophagus
- David C Sprigings (4 May 2003)
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Unstable Angina
- Ganapathy Chidambaran (4 May 2003)
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confirmation of serious condition
- Dragan Trivanovic (4 May 2003)
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A 42 year old man with acute chest pain-part three
- Marin Marinovic (5 May 2003)
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Clinically this is dissection
- David J Bossano (5 May 2003)
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Reduce pain, rule out aortic dissection and then ...
- Axel Ellrodt, 91370 France (5 May 2003)
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Further investigations
- Birger B Møller (5 May 2003)
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Acute Aortic Dissection is giving us tips since the onset of symptoms
- Gustavo B.F. Oliveira (5 May 2003)
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aortic dissection
- amjad zaman (6 May 2003)
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aortic dissection remains the most likely diagnosis
- fergus joseph dignan (6 May 2003)
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Cardiomyopathy: diagnosis and treatment
- Moses N. Ndirangu (6 May 2003)
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Pleuritis
- sindis kareem (7 May 2003)
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Transthoracic Echocardiogram does not confirm Myocardial Ischaemia
- Masood Ali (7 May 2003)
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Acute chest pain in a 42yr.-old-male
- Jussi Mikkelsson (7 May 2003)
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Cardiology consultant's interim response
- Irene M Lang (7 May 2003)
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A GP perspective
- James A Heathcote (7 May 2003)
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atypical/boerhaave's
- J M Rumbold (7 May 2003)
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COULD IT BE ........................................
- SUBRAMANYA UPADHYAYA (7 May 2003)
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Question about cardiology consultants' report
- Malvinder S. Parmar (7 May 2003)
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aortic dissection but also consider oesophageal rupture leading to mediastinitis
- ravindhar vodela (9 May 2003)
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Aortic dissection is still a strong possibility
- Mohamad Abdelsalam Abdelkader (10 May 2003)
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Is it what it appears?
- Richard C Berglund, MD (11 May 2003)
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Is it special
- Dr. Prem Kapoor (12 May 2003)
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More questions than answers
- Stephen R Workman (13 May 2003)
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The suspense is killing me...
- Andrew G Robinson (13 May 2003)
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If it has udders and moos...
- Jonathan Treml (13 May 2003)
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two diseases
- manfredo turcios (14 May 2003)
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Re:PE
- saray mohammadi (17 May 2003)
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not circulatory pain
- david g connell (17 May 2003)
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Step wise Approach
- Dr Abdul Hafeez Qureshi (17 May 2003)
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Double diagnosis
- Juan Esteban Gómez Mesa, Gilberto Castillo (22 May 2003)
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Deepak Kejariwal, Senior SHO University hospital of Hartlepool, ts24 9ah
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Start antibiotics and low molecular wt heparin. Needs CT angio, to define the CXR findings better, as well as to look for pulmonary embolism. Sputum C/S and blood cultures will also help. Hypertension need to controlled better. Competing interests: None declared |
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Anthony N Glaser, Private practice of family medicine Summerville, SC, USA
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1 - What would you do next and why? The D-dimer and fibrinogen elevations, with the chest X-ray are suggestive of a pulmonary embolism (although the D-dimer elevation is not extreme, and is not conventionally high enough to rule in a PE). A pulmonary ventilation-perfusion (VQ) study would be appropriate ? but in the meantime, provided he has no contraindications, I would immediately give low-molecular weight heparin and start oral warfarin, and also obtain PT/INR and PTT, and administer oxygen by nasal cannula. If he continues to be haemodynamically stable, thrombolysis would not be indicated for the PE. I was puzzled by the assertion that a transthoracic echocardiogram could both rule in and rule out acute myocardial ischemia and thus determine whether thrombolysis was indicated. My training was that echo findings are of no use in determining indications for thrombolytics, and a brief Medline search (using the terms "thrombolysis and echocardiogram" shows no citation consistent with this (going back to 1997 at least). I would be very interested to know if the authors or other readers have evidence regarding this! His normal cardiac enzymes are reassuring, but as the duration of the pain is not clearly stated in the original report I would be happier seeing a series of 3 groups of cardiac enzymes at 6 or 8-hour intervals before being convinced that he does not have myocardial ischemia, so I would still treat him conservatively as previously discussed: I would admit him to the hospital to a monitored bed overnight, with aspirin, a statin, and keep him on his ACE inhibitor and beta-blocker. I would also obtain a fasting lipid panel and glucose level in the morning (he sounds like a reasonable candidate for metabolic syndrome ? what is his waist measurement?) ? and get a better history of possible factors putting him at risk of a PE (recent immobilization?) 2 - What issues does this raise for cardiovascular risk management in primary care? Apart from his as-yet-unknown family history (PEs, MIs, CVAs, repeated pregnancy loss, DVTs?), exercise habits, weight and lipid status, this patient has significant cardiac risk factors, and the elevated CRP only goes to add to this. He and his wife (does she smoke or exercise?) need persuasive advice regarding his smoking, and probably regarding his exercise and diet. He already has target organ damage (left ventricular hypertrophy) in at least one organ. When this additional data is obtained, a Framingham risk stratification would help determine target lipid levels and whether long-term aspirin is appropriate. Has his primary care physician failed? It would be interesting to see his family doctor?s/GP?s/internist?s chart ? have his lipids been checked? Has he been counselled about smoking, weight, diet, exercise? Has a risk stratification been performed? Competing interests: None declared |
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Andrew G Robinson, resident Vancouver
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1. What would I do next and why? Well, having initially thought that this patient may have had an aortic dissection, I am now going to revise my opinion. While the patient had a low pretest probability of pulmonary embolism (no predisposing factors, no typical features on presentation), the increased d-dimer and CXR findings have moved him up into a moderate probability. Hence, depending on the facility I was at, I would order a Helical CT for PE. This would also help me see any other pathology, and may show an aortic dissection. While the possibility of pneumonia (radiographic findings, chest pain) is there, the patient would need to be very sick (ie be almost septic) to also have elevated d-dimer levels - this patient is not septic and infection likely doesn't explain the d-dimer. Obviously, with the CRP elevated so much, the patient has some systemic inflammation. Is this consistent with pulmonary embolism (I think probably not, although I am unsure of the literature) The possibility, given the dilated aortic root, of a large vessel vasculitis (ie Takayasu's) is present, and a CT angio would better delineate the anatomy of the aorta. As there are no signs of cardiac decompensation, and my working diagnosis has switched to possible PE, I would consider heparinizing (without a bolus), this patient, but would not thrombolyze. In truth I'd be pushing for the CT scan first to ensure that I am not worsening his outcome. I would also look at the CXR on a bigger screen. QUESTION 2. What questions does this raise for primary care? There are several important things. The first is that inspite of the EKG which showed no evidence of LVH, the echocardiogram showed concentric LV hypertrophy. Basically there are false negatives on EKG when looking for end organ damage with hypertension. (Although I find it hard to believe that this EKG corresponds to a patient with LVH). The second is that an ACE-I and B-blocker are not an ideal combination in treating hypertension as they both essentially work on the same end pathway. An ACE-I and diuretic would have been a better choice. Also, the CRP level is elevated. This means nothing for this patients cardiac risk at this time, as it clearly represents active inflammation. However, CRP measurements may be coming into risk stratification tables for MI soon (ready or not). Competing interests: None declared |
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Sudipta Maitra, Registrar,Internal Medicine,Suraksha Hospital, Salt Lake City, Kolkata , India. 700091
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.V/Q scan , pulmonary and coronary angiogram . If +ve - heparin and thrombolyse, if RV dysfunction is present. If -ve- reduce pain,continue to treat as unstable angina , with further ECGs , serial Echos and enzymes. Competing interests: None declared |
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Marin Marinovic, Emergency Physician ER,American Hospital Dubai,, PO BOX3939 Dubai,UAE
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1.This young gentleman has obvious widening of the upper mediastinum with enlargement of the heart and aortic root on CXR.On transthoracic ECHO he has signs of mild Aortic Valve Insufficiency.In the Emergency Department setting this is a case of Dissecting Thoracic Aneurysm until proven otherwise.The next step is to do CT of the chest or transesophageal echocardiogram depending on the hospital and expertise in which this patient is.I beleive he already has two large iv cannulas/14-16 Gauge and plenty of blood crossmatched/.Luckily,he is already on Beta-blocker but he may need more of beta blocking agent.I would also already contact cardiac surgeon and discuss the case with him. 2.two issues 1.Not to recognice this as a real emergency 2.to treat it as AMI and thrombolyse it Competing interests: None declared |
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krishna kumar jada, future paediatric sho n9ogq
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The investigations done suggest a strong possibility of pulmonary embolism ,and also from the history that the patient is an IT employee which probably involves sitting in front of pc for long periods of time with no frequent active movement of legs(additional risk factor- smoking],the patient would have had venous thrombosis of legs which has embolised now. 1.an ventilation perfusion scan and ? spiral CT could be done to confirm.since VP scan is the most commonly used screening method and a normal scan makes any but the smallest embolus unlikely.And if it turns out to be positive then it is sensible to start him on heparin iv if there are no serious concens about anti-coagulation.it could help prevent thrombus extension and also venous thombosis of legs. 2.with inceasing number of people spending more time in front of PCs especially the IT professionals it could be a risk factor for developing leg vein thrombosis.so awareness should be created among such individuals in particular and population in general about such risk. Competing interests: None declared |
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M D Dominic Bell, Consultant in Intensive Care/Anaesthesia The General Infirmary at Leeds LS1 3EX
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Aortic dissection has not been ruled out by the investigations thus far. To consider anticoagulating this patient on the weakest evidence for pulmonary embolus before excluding significant surgical pathology could hardly be endorsed in view of the potential for fatal haemorrhage. Thoracic CT with contrast is indicated to rule out the dissection and justify use of anticoagulants only with definitive evidence of PE. Blood cultures and sputum specimens etc should also be pursued on the basis of the elevated CRP and WCC for diagnostic completeness. The relevant issues for primary care are overshadowed by the above considerations, but relate to serious attention to blood pressure control. Competing interests: None declared |
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Malvinder S. Parmar, Medical Director, Internal Medicine Timmins & District Hospital, Timmins, Ontario, Canada
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The most important and life-threatening diagnosis to rule out in this gentleman is of acute aortic dissection. The likelihood of this is still high in view of clinical history (although limited), enlargement of the aortic-arch on chest x-ray (although non-significant) and mild aortic insufficiency noted on transthoracic echocardiogram. Now, a right posterobasal shadow raised the possibility of pulmonary embolism but I still wouldn’t anticoagulate this patient until aortic dissection is ruled out. In any case, I would control his blood pressure better. What would I do next? As the possibility of aortic dissection is still there and not ruled out completely and possibility of pulmonary embolism is raised by chest x-ray, so I would request a helical CT scan of chest – a single test that would provide me the information on both possibilities. It will rule in or out both aortic dissection and pulmonary embolism. I found it interesting that authors first performed a transthoracic echocardiogram and remarked “As there were no echocardiographic signs of cardiac ischemia, he was not given systemic thrombolytic drugs.” Current guidelines recommend giving thrombolytic therapy to a patient with classic symptoms of acute coronary syndrome, in association with either ST elevation (>1 mm) in two consecutive leads or in the presence of LBBB. I do not find any specific echocardiographic criteria, as an indication for thrombolytic therapy. Thrombolytic therapy in other acute coronary syndromes (non-ST elevation MI and unstable angina) was not found to be of any benefit in the randomized trials. Question for authors and others – Would you use thrombolytic therapy in a patient presenting with similar history, inconclusive ECG (without ST elevation) but echocardiography showing evidence of possible acute ischemia? Another point, I would like to make is of the definition of “severe” left ventricular hypertrophy. Authors state that this patient had severe left ventricular hypertrophy and give the interventricular septal thickness of 14 mm. Is this severe left ventricular hypertrophy? Normal interventricular thickness is 8-11 mm. I couldn’t find anywhere in the textbooks severe LVH being defined as interventricular thickness of 14 mm. I am not sure if it is typographical error. Standard definitions should have been used and if authors are mentioning LVH then they should have used left ventricular mass index (LVMI), a standard used in literature to define LVH. Before discussing the issues in regards to primary care, I think the most important issue for this case and for future physicians (physicians in training) is - What would have been the most important test in this patient when he presented – A transthoracic echocardiogram or a CT chest (helical, in view of question about pulmonary embolism)? The main issue it raises for CV risk management in primary care is that possibly blood pressure should have been better controlled (hindsight is always better) and assessment of his lipids if not done and treating the lipid values to target. In addition, smoking cessation should have considered (and this might have been considered by the primary care physician) but now should be strongly considered. If patient indeed has severe left ventricular hypertrophy, then this indicates that patient had poorly controlled hypertension for years (although diagnosed only two years ago, at age 40) and whether patient sought medical attention before that or not, is not known. Malvinder S. Parmar Competing interests: None declared |
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nagmeldin hassan ibrahim, Physician King Fahad National Guard Hosp. Riyadh .K.S.A. 1146
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This pt. most likly having proximal dissecion with extention to the aortic valves explaining the aortic murmur but not affectig the coranary ostia. Transoesphageal echo/ CT chest will be next appropriate tool. 2/ this pt. having cardiovascular risk should be taken seriously by the primary care physician&refering him immediately. moreover his hypertion should be controlled adequately. also there be mention about an old/new aortic murmur. Competing interests: None declared |
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Marco Biancardi, Internal Medicine Consultant Ospedale S. Carlo Borrmeo, 20153 Milano
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in the presence of ongoing chest pain in this 42-y-old hypertensive and smoking patient I would not exclude myocardial ischemia although initial tests are negative. I would carefulluy follow the clinical course in a chest pain unit monitoring ecg and cardiac enzymes. I would consider the radiographic hint of pulmonary embolism trying to calculate the clinical probability of such event (risk factors and clinical signs of PE). I would obtain blood gas analysis and helical thoracic CT scan. Competing interests: None declared |
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KUMAR RS BHAMIDIMARRI, SHO MEDICINE SOUTHPORT DISTRICT GENERAL HOSPITAL, PR86PN
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1]DIAGNOSIS ->IS IT AORTITIS +/-PULMONARY THROMBUS OVER VASCULITIC SEGMENT, AND IS THIS VASCULITIS DRUG INDUCED ->HOCM+PE DUE TO RIGHT ATRIAL THROMBUS,AS NO COMMENT ON ATRIAL DIMENSIONS IN ECHO AND SPECIFIC MENTION OF INTER-VENTRICULAR SEPTUM THICKNESS 2] TESTS ->VASCULITIS SCREEN ESR,C-ANCA,P-ANCA,ANTINUCLEAR ANITBODIES ->U&E,URINE ANALYSIS ->RENAL ULTRASOUND ->RENAL ANGIOGRAM ->SPIRAL CT CHEST TO CONFIRM/REFUTE THE DIAGNOSIS OF PE ->AORTIC ANGIOGRAM 3]AT PRIMARY CARE EVALUATION OF HYPERTENSION IN YOUNG TO EXCLUDE SECONDARY CAUSES VIZ RENAL,AORTIC,ENDOCRINOPATHIES AND TO FOLLOW UP PATIENTS TO RECOGNISE SIDE EFFECTS OF THE MEDICATIONS Competing interests: ACUTE MEDICINE |
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Peter Hartl, patient 1090 Vienna, Austria
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To begin with I want thank you for giving me the possibility to explain my case from my own point of view, its exciting. Now that the story is online I am reading the rapid responses regularly. I have even mailed the URL to friends and colleagues. When, three days before admission to hospital, I experienced a short episode of severe pain I thought I was having an acute myocardial infarction Fortunately, the pain lessened within minutes. Both, my wife, an experienced nurse, and I then thought the pain most likely originated from the stomach or the back. In the evening of the day of admission the pain recurred. I felt angry and did not want to be bothered by anyone. I cannot explain why I refused to seek help immediately. Suddenly I experienced extreme general discomfort, began sweating and got restless and fidgety, and had the urge to talk loudly with my wife. I shouted that I was going to die. At this point, my wife decided to go to the emergency department of the hospital where she is working. We did not call an ambulance as we wanted to go to this particular hospital. Ambulances bring you to the nearest hospital with available beds. Therefore we took a taxi. Since I know I can trust my wife in every situation I obeyed blindly, particularly as I started feeling worse every minute. Competing interests: None declared |
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Hisham M.. Al-Qysi, Head of Research Dept.-ICES ICES - P.O.Box 161 Amman 11941 Jordan
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First we are a cardiac research center engaged in noninvasive cardiac diagnostic expert systems namely (MID) for detecting myocardial ischemia based only on ECG manifestations other than the conventional ST-T wave abnormalities. Therefor we will leave the answer for question (1) to physicians and cardiologists. However, we will respond to the second question because our software technology plays a crucial role in the early noninvasive diagnosis of myocardial ischemia prior to myocardial infarction in patients presenting with chest pain suggestive of cardiac origin, independently of the pathogenetic mechanisms responsible for the development of myocardial ischemia. Based of his ECG, after analysing the ECG for this 42-year-old patient by (MID)software algorithm, it appeared he has myocardial ischemia with a severity assessment of 55.41%. According to (MID) sensitivity and specificity criteria, should the myocardial ischemia severity value of (MID) exceeds 43.55%, this suggests that the patient is classified as being at high risk for developing acute myocardial infarction (AMI). The above (43.55%) cutoff value of myocardial ischemia severity was determined by (MID) to be the myocardial ischemia severity threshold value beyond which the patient is classified as being at high risk for developing acute myocardial infarction (AMI).This patient should be triaged to hospital for relavant treatment protocol. Competing interests: Our company ICES is a research center engaged in noninvasive cardiac diagnostic expert systems namely (MID)for detecting myocardial ischemia based ONLY on ECG manifestations other than the conventional ST-T wave abnormalities. |
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David C Sprigings, consultant cardiologist Northampton General Hospital, Northampton NN1 5BD
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I agree with the majority of your respondents, that as an acute coronary syndrome has been effectively excluded, aortic dissection or pulmonary embolism are the most likely diagnoses. However, in any case of acute severe chest pain where the cause is not obvious - such as this one, in spades - oesophageal rupture (Boerhaave's syndrome)should be considered. The patient's picture is consistent with this diagnois, as is the lack of definitive evidence for alternative possibilities. I would do a CT scan to excude aortic dissection, and if none was found, start heparin to cover pulmonary embolism, and get a gastrograffin swallow. Competing interests: None declared |
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Ganapathy Chidambaran, Hon.Med.Officer VHS,Adayar,Chennai-60020,India
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Sir, Pt's C-Reactive Protein is high& also Blood Total WBC. TMT need not be done due to the risk of MI & an Angeograhy may be done or Radioneucleotide imaging may be done. A C-Reactive Protein estimation is required to avoid & anticipate an MI, so early Lytic Therapy will save the muscle & early failure. DrGC MI-Myocardial Infarction-WBC-WhiteCellCount- Competing interests: None declared |
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Dragan Trivanovic, dr General Hospital Pula, Negrijeva 6, 52100 Pula,Croatia
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1. Second, we have to confirm diagnosis with pulmonary scintigram and Thorax CT and start antibiotic therapy for protection. 2. This is common case in primary care where is hard to exclude serious condition with usual algorithm and technology limitations of primary care Competing interests: None declared |
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Marin Marinovic, Emergency Physician American Hospital Dubai,UAE,POBox5656
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There was a real pleasure to see a rapid response from Mr.Peter Hartl and his point of view.I am very happy to see that he is well and it looks to me he is recovering well/probably after major surgery/.I have sent all my answers from work on two very busy days in between seeing many different patients,although neither of them so sick as MrHartl on the night of his presentation.Hoewever,I still have not changed my mind.I beleive his condition was highly suspicios of Dissecting Thoracic Aneurysm and I approached it as such.For myself, in my clinical practice this will always be Dissecting Thoracic Aneurysm until proven otherwise.The elevetion of D-Dimer and Fibrinogen is indication to me that there is probable bleeding process or collection of the blood somewhere in the mediastinum rather than PE.Therefore I would NEVER heparinise this patient before doing CT of the chest or before discussing his condition with cardiologist or cardiac surgeon.Simply saying there are so many details from the history,clinical examination and investigation pointing towards Dissecting Thoracic Aneurysm that this condition has to be ruled out urgently.How? Simply,by talking to cardiac surgeon and than ordering CT of the chest or Transoesophageal ECHO.I sincerely beleive Mr.Hartl was at the right place and was treated appropriately. Diagnosis:Of course, Dissecting Thoracic Aneurysm until proven otherwise. Competing interests: None declared |
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David J Bossano, GP Robert Darbishire Practice, Manchester M22 4JE
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My immediate clinical impression was dissection thoracic aortic aneurysm & I don't think this possibility has been ruled out.
My interpretation of risk management in this context, is how does the GP manage patients presenting with acute chest pain?
Clearly this patient has severe pain and it is likely that admission would always be contemplated. Patients with less severe chest pain may still have significant underlying pathology. How does a GP rule this out safely, particularly without access to the range of investigations in this discussion?
Competing interests: I'm a GP |
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Axel Ellrodt, Emergency Dpt, American Hospital of Paris Verrières le Buisson, 91370 France
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Pain level should have be quicky assessed and documented and reduced. We should first have treated pain. But this should have be done with a TNT test and a new ECG after TNT administration. Then the patient should have been given IV analgesia, since sweating may indicate a severe pain it was likely to be morphine. Pain relief might allow a better record of the history and give clues to the diagnosis. This patient still has got to go through a rule out serious treatable urgent ailments process. First he did not meet the criteria for thrombolysis, were he having a coronary syndrome. So we have some time with regard to this diagnosis which now is very unlikely given the ulrasonographic data. What diagnoses should be considered first? Aortic dissection (AD): diagnose as soon as possible. No thrombolysis/ Anticoagulant can be given, hence this has to be settled quickly. Diagnosis is best ruled in with CT scan angiogram or Trans oesophageal Ultrasound. Pitfalls: ECG ischemic changes can be present - remember that classical signs are rare and often appear premortem, so we do not rely on their absence to delay / refuse diagnostic tests. The pain has not migrated downwards but is more and more severe, which is suggestive of AD.. Pulmonary embolism. Diagnose as soon as possible. What is the respiratory rate ? CT angiogram or isotope scan or limb ultrasound can be used to rule the diagnosis in. CT angiogram and isotope scan in certain circumstances can rule diagnosis out. D Dimer testing should be done with a sensitive test, but will not rule PE in. Chest X ray does not rule the diagnosis in. Laboratory data are consistent with PE, but do not establish the diagnosis. Elevated D-Dimer levels are not specific. Other less frequent diagnoses are likely to be done with CT scan.This includes oesophageal ailments with , in this case , mediastinal involvement. The history does not suggest nor rule out mediastinitis or oesophageal tear. What do we do ? It depends… For the sake of the quizz, the following assumes the 18 leads ECG and TNT test were not conclusive. Take advantage of pain relief to get a better history, pain description, symptoms suggestive of GE reflux, vomiting, oesophageal symptoms. I would choose immediate CT scan to rule out or in AD. I'd discuss the technique with the radiologist so that if no AD is diagnosed, PE diagnosis can be evaluated. Data available so far point to AD. Why CT rather than trans-oesophageal ultrasonography ? Because CT will establish the diagnosis of both AD and PE and probably, alternative diagnoses, whereas US cannot ascertain PE. This raises the concern of having the patient transported to a remote area. This patient should remain monitored for ECG and direct nurse or physician supervision. What is the most likely diagnosis ? I do not feel this is the right question. The answer is a mix of likely diagnosis and urgent diagnosis: what is/are the most urgent diagnosis /ses to be established or ruled out? I'd say aortic dissection, because of : pain radiating to the back and hypertension and ECG not showing clear- cut coronary syndrome,presence of subtle chest X ray abnormalities, and lab data that are aspecific but consistent with AD among others. DA still is the most likely diagnosis. This influences on which first test is to be performed. What did we tell his wife ? Well I first would have told THE PATIENT something : we are going to first and quickly relieve your pain and proceed to urgent diagnostic tests. We are concerned that you could have some serious problem in the heart or vessels of the thorax, or even the abdomen, that can be very efficiently treated. But these tests are going to keep him in the hospital for at least a few hours. Of course he may have nothing very serious, but we are going to err on the side of safety and investigate extensively. We will first look for the most emergent possibilities and keep him under close supervision. You should tell us if the pain recurs, or changes, or if you have new symptoms. Do you allow us to explain this to your wife ? If he does I'd say the same to his wife, with more details on what we are looking for if she requires more information. Competing interests: None declared |
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Birger B Møller, consultant DK-5500
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I would order a thoracic CT-scan as suspicion of aortic dissection seems to be high and an TTE doesnot exclude this possibility. An alternative could be an TEE, but I would prefer my first option. As D- Dimer is increased the investigation should perhaps beformed as a spiral CT to viasualize pulmonary lung emboli, which is my second considration (though oxygen-saturation seems OK). Competing interests: None declared |
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Gustavo B.F. Oliveira, Cardiologist/Research Associate Duke Clinical Research Institute, Duke University, Durham, NC, USA - 27710
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This patient was having epigastric pain two days before he presented with an acute anterior(substernal)chest pain in the local ER. In addition, he was having some intermittent periods of pain radiation to the back. His initial physical exam showed diaphoresis, but no complain or signs of dyspnoea (clear lung fields;no abnormal sounds). He had both elevated systolic blood pressure (high pulse pressure)and heart rate, which increase the shear-stress on the vessel walls. Although no abnormal cardiac sounds were heard, with this history of intense pain, with migration from the epigastric region to the chest and back, in a 42 yeard- old male patient with hypertension and smoking, we can not forget to think of two major clinical diagnosis: Acute coronary syndrom and acute aortic dissection. The latter is enhanced by the migration-pattern of pain, although it's possible to have this in an ACS setting. Going ahead on the ECG and chest X -ray, we can realize that first, the ECG reveals non- specific st-t findings, despite severe signs and symptoms; and the X-ray, for me it's clear that although the mediastinum was considered not enlarged, the ascending aorta is not normal, even with a possibly descending aorta also abnormal, which could explain the postero-basal finding. Again, it's impossible not to think of the Acute Aortic Dissection in this case, with agreat chance of proximal dissection evolving to aortic root and descending artery. The biochemical markers of myocardial injury were normal, which for a 48h of onset of symptoms were not expected. Of course, it could be an Unstable Angina if an intermittent pattern of pain was observed, but even in this situation, we were expecting for an elevation of Troponin and / or CKMB. The transthoracic Echocardiogram was not a significant tool for the clinical assessment, but the finding of a mild aortic valve insuficiency, which could have been missed on the physical exam or worsenly indicate possible aortic valva affected by an acute aortic dissection, enhanced the possibility of this diagnosis. What would I do now ( or in the same day of ER )? .Control his blood pressure and heart rate with a beta-blocker and nitroglycerine or nitroprusside, both via I.V. administration of course, titrating to the most well tollerated level without decresing blood flow to important organs ( brain, kidneys and coronary ). I would not give any type of antithrombin unless completely ruled out this hypothesis. Aspirin shold have been given on admission, as recommended by the current guidelines, untill a diagnosis of aortic dissection were confirmed. .As fast as possible, perform either a helycoidal thorax CT or a transesophagic echo, searching for a reliable assessment of aortic dissection ( the transthoracic echo does not have enough resolution to define the major images in this setting, mainly the aortic root and descending aorta ). .If none of these methods are available, and neither a MRI, the patient could undergo to the Cath Lab, where an aortography and coronary anatomy could be evaluated. Therefore, I think it would be possible to confirm ( or no ) the clinical diagnosis of an acute aortic dissection and propose the definitive treatment for this malignant condition. Thanks, and congratulations for the case! Gustavo Oliveira Competing interests: None declared |
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amjad zaman, PHYSCIAN s . arabia
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this pt who presented with severe chest pain ,ecg shows no acute ischemic changes with normal markers of acute cardiac ischemia . TTE show LVH and mild AR .he needs supportive care like analgesia BP cont and spiral CT thorax to rule in/out aortic diss ,PE then managment according to dx. Competing interests: None declared |
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fergus joseph dignan, cmp raf lyneham sn15 4pz
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1.A CT scan of the mediastinum will confirm the diagnosis.None of the blood tests cast doubt on the provisional diagnosis although a CRP of 171 mg/l does seem rather excessive.Perhaps there is an inflammatory aetiology for the dissection although the hypertension is the most likely cause(may be the hypertension itself is due to a vasculitis). 2.If I was his GP I would be concerned as to why the bp was so high when he attended the local emergency department as well as the fact that there was severe LVH on the Echo.Had he been having his bp regularly monitored,was he complying with his medication;indeed had I thoroughly evaluated the aetiology of the hypertension before commencing treatment? Should all newly diagnosed young (? age)hypertensives be initially referred to a consultant physician. Competing interests: None declared |
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Moses N. Ndirangu, just concluded epidmiology at pg level; awaiting SHO appointment Cambridge, CB4 3AL
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Given the progress so far, i think this patient might have one or other form of cardiomyopathy, more so either hypertrophic or restrictive cardiomyopathy. Accordingly, i would want to do pedigree and genetic analyses to gain any information that may support hypertrophic cardiomyopathy. In the light of elevated markers of inflammation and the chest findings, i would imagine that amyloidosis could complicate into restrictive cardiomypathy which would then warrant an endomyocardial biopsy of the hypetrophied left ventricle. Given that this patient has important cardiovascular risks that might warrant aggressive treatment at primary care level, it leads to the question whether that would be the right sort of treatment in a patient with cardiomyopathy. Aggressive treatment of hypertension in persons with hypertrophic cardiomypathy may aggaravate outflow obstruction and result in refractory hypotension. This poses the obvious question on whether the case definitions used at primary care level are specific enough to exclude from treatment patients with cardiovascular diseases that are not related to co-existent risk factors for coranary artery disease. Competing interests: None declared |
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sindis kareem, psychiatrist Bkm mainkofen, 94469 deggendorf , germany
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Elevated D-dimer, fibrinogen, CRP, Leucocytosis must be due to an infection. So it could be the start of Pneumonia with pleuritis. Competing interests: None declared |
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Masood Ali, Cardiothoracic Intensive Care Fellow Freeman Hospital NE7 7DN
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Although Transthoracic Echocardiography is an important part of investigations in this scenario, it would not 'confirm' myocardial ischaemia. If chest pain is persistent or recurrent and/or there is electrocardiographic or biochemical evidence of myocardial damage, one should proceed to Coronary Angiography. Pulmonary Embolism remains an essential part of differential diagnoses of any acute severe chest pain especially in a setting of minimaml ECG and/or Chest X-Ray changes. Competing interests: None declared |
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Jussi Mikkelsson, cardiology resident Satakunta Central Hospital FINLAND
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The patient has several risk factors for coronary artery disease. However, no evident ECG of echocardiographic evidence of ischemia can be found. Also the aortic root seems enlarged in the chest X-ray. The patient is by age and sex in the group at a high risk of aortic dissection. He also has a history of hypertension. The logical next step would be transesophageal echocardiography or computed tomography of the chest. Competing interests: None declared |
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Irene M Lang, cardiologist at the University of Vienna, Austria AKH-Vienna, Währinger Gürtel 18-20,A-1090
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The clinical presentation with nocturnal resting chest pain, radiating into the epigastrium and into the back permits a variety of possible differential diagnoses. Many of the correspondents have immedately directed their guesses towards acute coronary syndrome and aortic dissection. In fact, the worst diagnoses need to be dealt with first. In the presence of precordial chest pain the patient qualifies as a patient with unstable angina until otherwise diagnosed. With unspecific ECG changes at rest (obviously in the absence of chest pain), a cardiac cause is not ruled out. Serial cardiac enzymes need to be measured, and serial ECGs need to be recorded. ECGs under chest pain should be recorded. If troponins are elevated, the patient should be given an oral load of clopidogrel and be scheduled for a cardiac catheterization. The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) study investigated the use of clopidogrel in the treatment of acute coronary syndromes. Clopidogrel treatment led to an impressive 20% relative risk reduction in the composite outcome measure of vascular death, myocardial infarction, and stroke. The addition of clopidogrel to aspirin represents a major advance in the treatment of acute coronary syndromes 1. This benefit persists over time and also applies to patients undergoing percutaneous coronary intervention 2. Dissection of a major vessel close to the heart is a rare, though a strongly competing differential diagnosis in the presence of negative TNT values and the patient’s immediate pain record as it can be read in his personal mail. Transthoracic echocardiography will visualize the the aortic root and allow to measure the diameter, as well as the right ventricle. In the presence of bicuspid aortic valve which occurs in about 2% of the population, aortic dilatation/dissection occurs more frequently 3. Abdominal aortic aneurysm is more likely to be associated with common risk factors for atherosclerosis. However, in the presence of negative TNT values, a CT scan of the chest and the upper abdomen will answer several torturing questions in this anxious patient. In addition, this exam may reveal a paraesophageal hernia, pancreatitis, an inflamed gallbladder, or kidney stones. 1. Mitka M. Results of CURE trial for acute coronary syndrome. Jama 2001; 285:1828-9. 2. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet 2001; 358:527-33. 3. Edwards WD, Leaf DS, Edwards JE. Dissecting aortic aneurysm associated with congenital bicuspid aortic valve. Circulation 1978; 57:1022–1025. Competing interests: None declared |
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James A Heathcote, GP South View Lodge, Bromley, BR1 3DR
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As Peter’s GP, my concern is not so much with what exactly is wrong with him, but with whether or not he is really ill or at serious risk. Inevitably, doing more tests will produce more results. Some results will be normal and give false reassurance; others may be abnormal, but of no consequence. Usually, the first and simplest tests give the most useful information and ordering more tests can sometimes be just displacement activity, when what is really needed is a careful review by an experienced and wise clinician. Even in chest pain, effective consultation skills are essential. If Peter’s tests remain inconclusive and he is sent home with a diagnosis of chest pain of unknown origin, he will probably come and see me and without the benefit of fancy tests, I will have ten minutes in which to make my decision – Is this stress-related or is he really ill? Should I reassure him or medicate him? Does he need a counsellor or should I send him back to the hospital? Chest pain is a high risk situation and one that GPs handle every day, often without even an ECG to guide them. Junior hospital staff may be reluctant to see atypical, ‘gut feeling’ presentations and with the wisdom of hindsight often disparage their GP colleagues, so referral to hospital is not an easy option. A wrong judgement can however be catastrophic for all concerned. Competing interests: None declared |
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J M Rumbold, private clinic B9 5PS
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an atypical pneumonia associated with pericarditis/pleuritis is still possible. certainly dissection hasn't been ruled out and the presense of aortic regurg warrants computed tomography (CT) of the thorax or Ttrans- oesophageal echocradiographyevaluation, CT having the additional benefit of assessing potential pulmonary pathology. there is no pneumomediastinum, pneumothorax or pleural effusion to suggest Boerhaave's but I have seen it present in a similar way to this case. Gastro-intestinal causes would fit with this case - as suggested oesophageal spasm is possible after exclusion of these other causes. i am surprised at the mention of genetic analyses - how would this be relevant acutely? also raised inflammatory markers do not automatically mean there is infection Competing interests: None declared |
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SUBRAMANYA UPADHYAYA, CLINICAL ATTACHMENT WREXHAM,LL137SA
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AS THE PATIENT IS A SMOKER,HYPERTENSIVE PRESENTED WITH ACUTE CHEST PAIN AND THE ECG SHOWED ISCHAEMIA MY FIRST DIAGNOSIS WOULD BE ACUTE CORONARY SYNDROME.BUT THE INCREASED CRP AND D-DIMERS GIVE A CLUE OF INFECTION/PULMONARY EMBOLISM.ECHO FINDINGS ARE COMPATIBLE WITH MYOCARDIAL STRAIN(LVH). SO GO FOR V/Q SCAN AND STRESS ECHO TO RULE OUT PE,M.STRAIN AND ACS.IN THE MEAN WHILE DO THE BLOOD CULTURE TO R/O INFECTION(PERICARDITIS,PLEURITIS) AS THE ECG FINDING COULD BE PERICARDITIS. Competing interests: None declared |
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Malvinder S. Parmar, Medical Director, Internal Medicine Timmins & District Hospital, Timmins, Ontario, Canada
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I am writing in response to the cardiology consultant’s interim report on this interactive case. The consultant agrees that the worst diagnosis needs to be dealt first. I agree 100% with this statement. However, the consultant choice of ‘the worst diagnosis’ in this gentleman indicates poor critical evaluation of patient’s symptoms and results of initial investigations. This approach is thinking with in the box. Remember, the main principle, ‘first, do no harm.” If, as consultant feels, acute coronary syndrome is the worst diagnosis to consider with this presentation (pay attention to character, radiation and severity of pain with essentially normal ECG) giving patient loading dose of clopidogrel in addition to aspirin (that he likely received even before ECG might have been performed) and starting patient on anti-anticoagulants (unfractionated or low molecular weight heparin) – a standard therapy for acute coronary syndromes, would be inflicting harm to the patient at this stage without ruling out the most life-threatening diagnosis. The worst diagnosis and most urgent to rule out at presentation, before one gives a lecture on the effects of clopidogrel in acute coronary syndromes, is to rule out effectively an acute aortic dissection. Normal ECG tells us that there is no need for thrombolytic therapy, even if it later proves to be a coronary event. A mini-symposium (consultant used 7 of the 23 lines of response writing about clopidogrel) on efficacy of clopidogrel in acute coronary syndromes was out of context and raises suspicion about a conflict of interest. Yes, any type of chest pain could present with acute coronary event but this patient’s character of pain is not typical and especially with severe pain and normal ECG, the treating physicians must consider and rule out other diagnoses before treating it as a cardiac pain. I am not saying that we shouldn’t consider this diagnosis (as most of us did), but what I want to stress is that there are other organs in the chest and below the diaphragm that can present with symptoms mimicking coronary event. In patients presenting to the emergency departments with precordial chest pain and who are admitted as ‘unstable angina’ only about 30% of patients have true ischemic pain and in remaining 70% there are other causes. This could be further illustrated by one re-examining their hospital admissions for ‘unstable angina’ and for ‘acute myocardial infarction.’ For every single case of myocardial infarction admitted to hospital there are about 60-80 cases of unstable angina, in almost every hospital around the world. One could interpret it in two ways – either the physicians involved in the care of these patients are doing an excellent job and preventing great number of myocardial infarctions or the other view (sadly is more prevalent) is that ‘unstable angina’ is simply over-diagnosed. In some hospitals, a patient presenting with any pain above the belt is labeled as ‘unstable angina.’ No doubt, it is important to consider this diagnosis that has its own serious implications but before labeling the patient with this diagnosis it is important to apply the basic knowledge that are helpful in discriminating different causes of pain. If we are going to treat every precordial pain as angina without further classifying the origin and its most likely cause then what is the use of spending hours and hours teaching medical students about proper history-taking in relation to pain and the importance of various associated features that are important in evaluating pain. History is often the most important tool for diagnosis in most common and even rare disorders that gives often a major clue to the origin of patient’s symptoms. Some reader’s raised the possibility of right ventricular infarction as a cause of this patient’s pain with a normal ECG. Right- sided (V3R, V4R) leads would give essential information required to evaluate this possibility and in addition this patient is hypertensive (and not hypotensive as is the case often with RV infarct) and above all, the echocardiogram was normal and did not show RV hypokinesis or dilatation. Competing interests: None declared |
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ravindhar vodela, sho medicine the royal oldham hospital ,oldham ,OL1 2JH
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he needs transoesophageal echocardiography,high resolution spiral C.T.thorax,to look out for aortic dissection but his high crp ,raised white cell count and chest X ray worries me to consider oesophageal rupture leading to mediastinitis. hence i would also do gastro graffin study of oesophagus. in any case the above investigations are helpful. Competing interests: medicine |
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Mohamad Abdelsalam Abdelkader, 9 may 2003 King Fahd Hofuf Hospital&31982
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Despite the elevated plasma D dimer level and the radiographic evidence of a possible pulmonary embolism, it seems very unlikely that pulmonary embolism would present with such a severe chest pain without dyspnea and hypoxaemia ( spo2=97%). The elevated c-reactive protien and fibrinogen levels may be considered as non-specific markers of inflammation. Acute coronary syndrome is almost virtually excluded because of normal cardiac enzymes and absence of any segmental wall-motion abnormalities on echocardiography. The clinical picture of severe chest pain radiating to the back along with the radiological picture of widening of the superior mediastinum in a hypertensive patient strongly suggest aortic dissection. Competing interests: None declared |
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Richard C Berglund, MD, Boneventure Medical Group Hoffman Est, IL 60195
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1, The answers are not in yet! Although D-dimer is somewhat elevated, I am very concerned about the very high CRP. I would avoid anticoagulating pt until more definitive imaging is completed. "Just when is that STAT spiral CT going to be done?" 2, I think it was the former baseball manager, Yogi Berra, who so aptly put it: "It ain't over till its over."; well not enough information is present to make a sustainable and appropriate diagnosis. "Protocols" which are enjoying prominence in the modern medical community which are dictated by cost containment would probably have us barking up the wrong tree in this patients managment. I think in all to many instances this patient would have been relegated to a "protocol" for initial diagnosis and then his pre-dictated managment would have delayed his real diagnosis and appropriate management. Competing interests: None declared |
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Dr. Prem Kapoor, Consultant Internal Medicine Majeedia Hospital, Hamdard Nagar, New Delhi - 62
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Case History in BMJ means something special but I will go by the dictum of making a diagnosis which is most likely Very likely this is a case of pleuralitis in a patient who is a heavy smoker comes with severe chest pain has increasd CRP and TLC count 1)I would next ask for a CT - chest to confirm pleural thickening and parenchymal involvement if any. 2)In view of history of hypertension and presence of severe Left Ventricular Concentric Hypertrophy in a smoker the chances of future cardiac event are very high. I would like to treat his hypertension vigrously and exclude other major cardiac risk factors like dyslipidemia and diabetes mellitus. Competing interests: None declared |
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Stephen R Workman, Assistant Professor, Dalhousie University Halifax Nova Scotia B3h 3S9
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The differential diagnosis includes pulmonary embolism (PE), dissection, cardiac ischemia, or non cardiac type pain. We are not told if there is right ventricular dysfunction on the echo, a poor prognostic sign in PE, suggesting that this is not a massive or submassive PE. At this point the goal is to minimize morbidity and mortality, and from this perspective it is necessary to realize, account for and accept responsibility for the risks of both treatment and delaying treatment. A CT scan would likely differentiate PE from dissection. If this is not immediately available, what next? The immediate treatment options include heparin, ASA, beta blockade, and intravenous or topical nitrates. There is no indication for thrombolytics. One must attempt to balance the risks of 'on spec' treatment. How dangerous is heparin if this is a dissection? (I don't know-call and speak to a thoracic surgeon perhaps?) What is the risk increase with delayed heparinization if this is a PE? (High I suspect.) How dangerous are beta blockers and IV nitrates in hemodynamically stable PE. (Safe likely if given cautiously and volume status maintained.) Such qualitative assessments can only truly be made at the bedside. However, in the absence of both diagnostic tests and a live patient to help further refine the diagnosis, careful beta blockade, gradual blood pressure reduction with intravenous nitrates, anticoagulation with heparin and ASA, and continous heart rate monitoring in a cardiac unit should all be initiated. Competing interests: None declared |
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Andrew G Robinson, Resident Vancouver
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I can't wait to hear the results of the CT Scan and further investigations. According to the case and responses so far, here are what I feel are the current odds: 1. Aortic Dissection-an early favourite, thoracic aortic dissection is felt to be favoured be some due to the history of severe chest pain radiating to the back, a history of HTN, no obvious other causes, and a borderline enlarged mediastinum. Working against the diagnosis of aortic dissection are the lack of a BP difference in the arms, or significant brachial-femoral delay. If one believes that the CXR does not show a widened mediastinum, then the chances that this is dissection range from 10-20%, if one believes that it is widened, then the chances are closer to 50%. With the lack of a widened mediastinum, and the lack of a pulse difference, the dissection would most likely be of the descending aorta. Current Vegas Odds of dissection: 2:1
2. Acute Coronary Syndrome:
Working for the diagnosis of acute coronary syndrome are the high
prevalence of this syndrome, the patients risk factors, and the non-
specific EKG changes. Working against ACS in this patient are the normal
troponins (despite 48hrs+ of pain)and sweating, the fact that an ACS
doesn't explain the X-ray findings.
Current Vegas Odds: 8:1 3. Pulmonary Embolism : Although a dark horse initially, this diagnosis is always considered in anyone with chest pain. The factors favouring this diagnosis are apparently the CXR (I haven't figured out how to enlarge this picture, but will assume the radiologist knows of what they speak. In reality, I would interpret the X-Ray and the report based on what I knew of who was reading it - ie a resident, staff person, etc.), and the elevated d-dimer and crp. The factors against this are the lack of a sinus tachycardia (although the patient is on B-blockade), the lack of a typical history, the normal O2 sat (assumed to be on room air). Current Vegas Odds 5:1 4. Pericarditis : Although no friction rub is noted, the echo was normal, there was no history of connective tissue disease, viral infection, uremia etc., and no typical EKG changes, pericarditis is always in the differential, especially with such an elevated CRP (lots of reasons for this). Current Vegas Odds: 12:1 5. Esophageal disease:
6. Vasculitis: -Anti-GBM disease, Wegener's etc., presenting with lobar hemorrhage looking like consolidation without kidney involvement yet (assuming no urine protein) in a smoker, or takayasu's arteritis presenting with aortic pain. Going against this are the rarities of these diseases, the lack of a pulse deficit etc. Current Odds: 100:1 7. Tertiary Syphillis, other weirder and wonderful things: 1000:1 Competing interests: None declared |
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Jonathan Treml, Specialist Registrar in Geriatric Medicine East Surrey Hospital, Redhill, RH1 7NH
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1. If an animal has udders and moos it is a cow until proven otherwise. In this case, a hypertensive man with chest pain, equivocal ECG, basal shadowing on CXR (?small pleural effusion) and aortic incompetence on ECHO should be considered to have aortic disection until proven otherwise. Certainly this must be excluded before any potential harm is done with anti-thrombotic therapy or, worse, thrombolysis. He needs an urgent CT thorax. 2. This case teaches us several things: Common things are still common Medicine is still about pattern recognition and not just about evidence from the latest trials. D dimers may have high sensitivity but they have low specificity. Always exclude the serious and treatable conditions first. The rule of halves applies - only half of all hypertensives are diagnosed, only half of those are treated and only half of those are treated adequately. Of course, it could be a wildebeest... Competing interests: None declared |
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manfredo turcios, internal medicine hospital escuela zc 504
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1.-confirm pulmonary embolism and acute aortic dissection. 2.-we need pulmonar scan ventilation/perfution and chest ct Competing interests: emergency room hospital, escuela tegucigalpa, honduras c.a. |
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saray mohammadi, MS Iran medical center
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PTE is our first differntial diagnosis.V/Q scan can help us to rull out this. also this pain may be related to hypertrophic CMP. Start LMWH & oral Warfarin,NG drip is first therapiutic effort. Competing interests: None declared |
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david g connell, gp oldmeldrum
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consider acute cholecystitis/biliary colic from the nature of the pain and associated features with the basal CXR finding suggesting a subphrenic focus Competing interests: None declared |
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Dr Abdul Hafeez Qureshi, Senior Medical Officer The Aga K han University Hospital Karachi Pakistan
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History and investigations done already guide to proceed as follows (1)To do CT scan or MRI TO rule out Dissecting aortic aneurysm and less likely diagnosis of mediastinal mass (2)If CT is negative for above mentioned diagnoses then to proceed fod for V/Q scan to look for PE Competing interests: General Practice |
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Juan Esteban Gómez Mesa, Cra 98 Nro 18-49 Clinica Valle del Lili, Gilberto Castillo
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In order of importance, we consider the following diagnosis:
Currently, paraclinics report high fibrinogen and D-dimer, and the ECG and cardiac markers are between normal limits. In fact, there is no current risk factors for embolism other than hypertension and active smoking, but we don´t know the rest of the personal record of this patient. Initially, we consider a V/Q G or 3D Scan for diagnosing pulmonary embolism, besides, control of blood pressure and, depending of the findings, cardiac markers control, ECG control and a conventional echocardiogram. Waiting for the final diagnosis, maybe unsuspected, but still waiting. Juan Esteban Gómez
Competing interests: None declared |
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