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Pulmonary embolism in hospital practice: troponin, CT pulmonary angiography and echo are crucial in significant PTE.
- Adrian J.B. Brady (23 January 2006)
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View from Primary care, chest pain and breathlessness but not together
- john sharvill (25 January 2006)
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Probabilities are numbers not states
- GH Hall (27 January 2006)
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The obstetric perspective
- Murray JM Luckas, Eric Nijiforfut and David M Semple (30 January 2006)
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'Everyone' misquotes BTS guidance
- Peter D Strouhal (1 February 2006)
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Further orthopaedic risk factors
- David T Loveday (2 February 2006)
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Wells score
- fahim hassan (6 February 2006)
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DVT and varicose veins
- Duncan Drury, Willey Pillay (18 February 2006)
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Diagnosis and treatment of venous thromboembolism in arthroplasty patients
- Robert A. E. Clayton, Adam C. Watts, Paul Gaston, Colin R. Howie (20 February 2006)
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Sensitivity of CT in pulmonary embolism
- pradeep narayan, Suma Chakrabarthi (20 February 2006)
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Intravenous drug use is an important cause of Deep Vein Thrombosis (DVT)
- Arabella G Nott, Andrew J McBride Consultant Psychiatrist and Clinical Director. SCAS. Oxford. (6 March 2006)
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Overtreatment of pulmonary emboli
- Ian J Runcie (26 February 2009)
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Heparin-induced thrombocytopenia and thrombosis as a cause of pulmonary embolism should not be forgotten
- Thein H Oo (2 March 2009)
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Adrian J.B. Brady, Consultant Cardiologist Glasgow Royal Infirmary, Glasgow G31 2ER
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Dr Robinson's article on pulmonary thromboembolism (PTE) is timely and well written but has several crucial omissions and one important error. She rightly states that diagnosis can be difficult, but does not mention the available scoring systems which are useful in defining the likelihood of PTE (ref 1). Most importantly, Dr Robinson makes no mention of biomarkers in PTE, and does not emphasise the critial importance of echocardiography or CT scanning to identify right ventricular (RV) strain. Patients with an elevated troponin (I or T) and echo or CT evidence of RV overload have a 10-fold higher risk of death or major adverse event than individuals with a normal troponin and normal RV (refs 2,3). Importantly, the recommendation of low molecular weight heparin (LMWH) as initial therapy for all, is, in fact suitable only for stable patients. Patients with shock should receive intravenous heparin, since cutaneous perfusion is compromised, and LMWH may not be absorbed. Finally, Dr Robinson makes no mention of life saving surgical embolectomy, or percutaneous fragmentation procedures, which have a key role in a gravely ill individuals with massive pulmonary embolism (refs 1,4). Modern management of the patient with significant pulmonary embolism demands three investigations: an immediate troponin level; CT pulmonary angiography; and definition of RV involvement by CT or echo. Without these we will remain stuck in 1990s medicine. Dr Adrian J.B. Brady
UK representative, European Society of Cardiology Pulmonary Embolism Committee. Member, Steering Committee, International Trial of Thrombolysis in Pulmonary Embolism 1. Torbicki A, et al. Guidelines on diagnosis and management of acute pulmonary embolism. European Heart Journal (2000) 21, 1301–1336. 2. Kucher N, et al. Incremental prognostic value of troponin I and echocardiography in patients with acute pulmonary embolism. Eur Heart J 2003;24:1651-1656. 3. Konstantinides S, et al. Importance of cardiac troponins I and T in risk stratification of patients with acute pulmonary embolism. Circulation (2002);106:1263-8. 4. Brady AJB, Crake T, Oakley CM. Percutanous fragmentation and distal dispersion of proximal pulmonary embolus. Lancet 1991;338:1186-9. Competing interests: None declared |
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john sharvill, GP Deal Kent CT14 7AU
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Pleuritc chest pain in primary care is common. Usually with no other signs. What tests in those not 'ill', if any, need to be done to rule out small pulmonary emboli? Silent breathlessness is also common. What is the best investigation again from primary care to exclude a silent PE if a VQ scan is now obsolete and trying to get a CT related activity within a reasonable time scale not possible. I write as a GP who has seen 4 or 5 silent PE over the years (suggested by outpatient vq scans) and 2 deaths from missed emboli that recurred or extended.If it is a d-dimer what can we take as a value below which the risks are minimal? Competing interests: None declared |
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GH Hall, Retired EX1 2HW
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Diagnostic testing should cease when the treatment threshold probability has been exceeded. This is the point where the cost and benefit of treatment are equal. For pulmonary embolism this a probability of 0.15 (1.) Quite what high, intermediate or low probabilities are in numerical terms isn’t made clear, but it should be if informed decisions are to be made quickly. This is vital in this context. In my experience once you think of the possibility of pulmonary embolism you should start to treat unless there are clear and important contraindications. 1.Pauker SG, Kassirer JP,1994. New Eng Journ Med v. 293, 229-34. Competing interests: None declared |
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Murray JM Luckas, Consultant Obstetrician & Gynaecologist Mid Cheshire Hospitals NHS Trust, Eric Nijiforfut and David M Semple
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Editor - We read with interest Robinson’s review of pulmonary embolus(1). We would however like to correct two inaccuracies; firstly, Robinson states that amniotic fluid embolism carries an 80% mortality rate. Whilst this figure is historically correct, a contemporary UK register has reported a mortality rate of only 29.5%, this improvement being due to rapid diagnosis and supportative management(2). Secondly, Robinson highlights late pregnancy as a risk factor for pulmonary embolus. It is salient to remind your readership that early pregnancy is also a period of increased risk for pulmonary embolus as witnessed by the fact that in the latest triennial report of maternal deaths, three out of the five antenatal fatalities from pulmonary embolus occurred in the first trimester(3). It is vital that all healthcare professionals maintain a high index of suspicion for pulmonary embolism in women throughout their pregnancies and into the puerperium. 1. Robinson GV Pulmonary embolism in hospital practice 2006;332:156- 160 2. Tuffnell D J. United Kingdom Amniotic Fluid Embolism Register. BJOG 2005;112:1625-1629. 3. Why Mothers Die 2000-2002. Confidential Enquiry into Maternal and Child Health, RCOG press, London Competing interests: None declared |
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Peter D Strouhal, Consultant Radiologist Royal Wolverhampton Hospitals Trust, WV10 0QP
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GV Robinson writes a good summary of current practice of PE management in hospitals but, like many clinicians, fails to pick up on subtle nuances when dealing with a specialist topic - namely imaging. BTS guidelines on imaging in suspected acute PE still say, albeit in smaller print, that V/Q scans can be used first line if readily available and in the context of normal chest x-rays, or if no acute changes are present, and in the absence of severe cardiopulmonary disease; this is mentioned in the article but dismissively so. VQ scanning has not yet been "mostly superseded by CTPA" as stated and neither should it be. A normal VQ scan still has the highest negative predictive value of any test I know whatever the D-dimers result may be. A 6 month audit of my department by the Respiratory team revealed that, with careful vetting, the indeterminate rate for V/Q scans was only 5%. Not surprisingly much lower than in the PIOPED studies (where it approached 50%) at least in part because we use Krypton like much of the UK and not Xenon as do the Americans; and because PIOPED didn't involve pre-test chest x-ray evaluation as undertaken in many institutions as well as my own. The other contentious point relates to what advice is given when faced with a discordant VQ scan and calculated clinical probability, assuming the latter has actually been done. Does the author know of many causes of multiple mismatched perfusion defects in the setting of normal chest x-ray and normal ventilation images other than PE? Particularly if the clinical suspicion is such that PE imaging has been requested, rather than just imaging because the D-dimers are elevated? We still perform, according to our audit, as many VQ scans as CTPA studies and with an integrated perfusion-only service on days when no ventilation isotope is availablity, there is greater access than to our CT scanners in our busy cancer centre. VQ scans still have an important role to play, recognised by the British Thoracic Society but almost consigned to history by the recent article. A risky stance given the readership of the journal. Competing interests: None declared |
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David T Loveday, Spr Orthopaedics Norfolk & Norwich Hospital, Colney Lane, Norwich, NR4 7UJ
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An important group of patients has been excluded from this article on hospital practice. Orthopaedic patients having cemented implants are at risk of pulmonary embolism1. The pressurization process of the cement creates a large amount of bone marrow cell and fat emboli, which pass into the venous circulation. This has been visualised with trans-oesophagus echocardiography2. These patients are already at risk with their immobility and if combined with a fracture and dehydration their risk is further increased. 1. Clark DI. Ahmed AB. Baxendale BR. Moran CG. Cardiac output during hemiarthroplasty of the hip. A prospective, controlled trial of cemented and uncemented prostheses. JBJS Br 2001; 83(3):414-8 2. Hagio K. Sugano N. Takashina M. Nishii T. Yoshikawa H. Ochi T. Embolic events during total hip arthroplasty: an echocardiographic study. J Arthroplasty 2003; 18(2):186-92 Competing interests: None declared |
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fahim hassan, SPR George Eliot Hospital, Nuneaton
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No one has mentioned about well's score in pretest probability which is less confusing and much accurate than BTS scoring system including
Signs of DVT = 3,
Everyone should have a pretest probability score before going for a VQ OR CTPA scans Competing interests: None declared |
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Duncan Drury, Vascular SpR Doncaster Royal Infirmary, Willey Pillay
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Dr Robinsons article on pulmonary embolism in hospital practice lists varicose veins being a major risk factor for DVT. On review of the references for Box 1, the study by Heitt et al (ref 1) actually investigated a previous varicose vein procedure as a risk factor for DVT, a fact supported by van Rij et al (ref 2) who reported an incidence of 5.3% for DVT following varicose vein surgery. In addition there is evidence that superficial vein thrombosis is a risk factor for DVT. (ref 1) However there is no clear evidence to support the hypothesis that primary varicose veins per se confer significant risk for deep vein thrombosis. 1. Heit, JA, Silverstein MD, Mohr D et al. Risk factors for deep vein thrombosis and pulmonary embolism. Arch Intern Med 2000;160:809-15. 2. Incidence of deep vein thrombosis after varicose vein surgery. Van Rij AM, Chai J, Hill GB, Christie RA. Br J Surg 2004 Dec;91:1582-5. 3. Cambell B. Thrombosis, phlebitis and varicose veins. BMJ 1996;312:198 Competing interests: None declared |
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Robert A. E. Clayton, Specialist Registrar in Orthopaedic Surgery Royal Infirmary if Edinburgh, LIttle France Crescent, Edinburgh EH16 4SU, Adam C. Watts, Paul Gaston, Colin R. Howie
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We read with interest the article “Pulmonary embolism in hospital practice” by Robinson. The author correctly states that lower limb orthopaedic surgery is a risk factor for venous thromboembolism (VTE). However it must be pointed out that the diagnostic and therapeutic algorithms proposed, while exemplary for spontaneous embolism, are not wholly appropriate in the patients who have undergone surgery, in particular arthroplasty. The routine use of the d-dimer test of fibrin degradation products is of no use in the post-operative setting as it will invariably be expected to be elevated as a consequence of surgery. To perform the test is therefore a waste of resources and the inevitable positive result may place the patient at risk of inappropriate anticoagulation or investigation. CT pulmonary arteriography remains the diagnostic modality of choice in the post arthroplasty setting. However its findings may need to be treated with caution if performed within the first 48 postoperative hours as false positive findings may result from the detection of embolic material in the pulmonary vasculature that originates from the femoral medullary canal during pressurisation of cement in total hip or knee replacement. Whilst the prompt and appropriate diagnosis and management of postoperative VTE is essential, we would caution against rapid anticoagulation of patients post operatively. Low molecular weight heparin cannot readily be reversed and is associated with significant rates of operative wound complications The response to warfarin may be exaggerated in the post operative period due to concomitant use of opiate analgesics and the stress response to surgery. Wound haematoma may lead to increased rates of prosthetic infection which, while not categorised as a “massive bleed” may have a catastrophic effect for the surgical patient. Competing interests: None declared |
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pradeep narayan, Specialist Registrar Cardiothoracic surgery Bristol Royal Infirmary, BS2 8HW, Suma Chakrabarthi
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A very nicely written paper. However, the sensitivity of CTPA has been quoted as more than 95% in the paper but this has been questioned in the recent past. The sensitivity of CTPA varies from 53% to 100% with marked interobserver and intraobserver variablility.¹ At the segmental level the incidence of false positives is around 38% and pulmonary embolisms at the level of the subsegmental arteries, accounting for 20% of the pulmonary embolisms, can be missed. A recent study found the sensitivity to be 70%, comparable to a “low probability” VQ scan.² While the CTPA is a very commonly utilized and extremely useful investigation which is rapidly becoming the investigation of choice these limitations ought to be borne in mind. ¹Rahimtoola A, Bergin D J. Acute Pulmonary Embolism: An update on Diagnosis and Management. Curr Probl Cardiol 2005; 30: 61-114 ²Perrier A, Howarth N, Didier D, Loubeyre P, Unger PF, de Moerloose P et al. Performance of helical computed tomography in unselected outpatients with suspected pulmonary embolism.Ann Intern Med. 2001 Jul 17;135(2):88-97 Competing interests: None declared |
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Arabella G Nott, SpR Psychiatry Oxford SCAS.Rectory Road, Oxford OX41BU, Andrew J McBride Consultant Psychiatrist and Clinical Director. SCAS. Oxford.
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Editor- In her otherwise excellent review, Robinson does not list intravenous drug use as a risk factor for DVT (1). This is an increasingly prevalent and clinically relevant association, especially in younger age groups. Liu-HSY et al (2) published a retrospective study identifying characteristic features of venous thromboembolism in the Chinese population of Hong Kong. Among their 376 patients with thromboembolism the four most common conditions associated with DVT were medical illness, malignancy, orthopaedic surgery and intravenous drug use. Among patients younger than 45 yrs venous thromboembolism was associated with intravenous drug use, thrombophilia, pregnancy and use of oral contraceptives. Intravenous drug use is also identified as a contributor to DVT in a paper by Syed et al (3). This retrospective case note review looked at 232 episodes of DVT in a district general hospital. Intravenous drug use was the seventh most common risk factor for DVT in general but accounted for 48.4% of episodes in patients aged 40 yrs or less. The precise mechanism for DVT among injecting drug users has not been delineated. DVT is another good reason for helping drug users avoid and move away from intravenous drug use. 1 Robinson GV. Pulmonary Embolism in Hospital Practice. BMJ 2006, 332:156-60. (21 January) 2 Liu HSY, Kho BCS, Chan JCW, Cheung FMF, Lau KY, Choi FPT, et al.Venous thromboembolism in the Chinese population—experience in a regional hospital in Hong Kong. Hong Kong Medical Journal, Dec 2002,Vol.8, no.6, p.400-5. 3 Syed F F, Beeching NJ. Lower limb deep vein thrombosis in a general hospital: Risk Factors, outcomes and the contribution of intravenous drug use. QJM: monthly journal of the Association of Physicians, Feb 2005, Vol98,no.2, p.139-45. Competing interests: None declared |
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Ian J Runcie, Consultant Radiologist Princess Royal Hospital, Haywards Heath, RH164EX
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Pulmonary emboli (PE) are treated as an emergency with immediate anticoagulation. The reasons are well known: the disease carries a 30% mortality and is the most common cause of maternal death. This data is based mainly on post-mortem studies (PM) and diagnoses based on perfusion/ventilation (VQ) radioisotope scanning. The advice by Adrian Dixon1 recommending VQ scans in patients with normal chest X rays and CT in patients whose Chest X rays are abnormal has been replaced by the adoption of multislice helical CT. This examination is capable of diagnosing tiny emboli in peripheral vessels. These emboli (or embolus as sometimes only one is identified) are treated in the same way as the relatively massive emboli identified on VQ scans. Such tiny emboli would not be identified at PM, nor on VQ scans, yet the management of large PEs has been extrapolated to these defects. The morbidity and mortality, if any, caused by a single third or fourth branch thrombus is unknown and yet patients are treated with six months of warfarin. Even more worryingly, if two are found over a period of time the patient is condemned to the dangers of lifetime warfarin. A study in New York State over a ten-year period showed that, whereas the numbers of diagnosed PEs doubled, mortality rates stayed the same 2. The study stopped in 1994 and, with the near universal introduction of helical CT, it is likely that the numbers treated has continued to rise. This study implies that a great many people are being treated unnecessarily. When taxed with this physicians have replied ‘ But we can’t not treat a PE’ Maybe so, but this suggests defensive medicine utilising a drug with significant side-effects. Other theoretical reasons for treatment of a PE include avoidance of pulmonary hypertension and post-thrombotic leg syndrome for both of which there is no hard evidence. I submit that treatment of PE has failed to take into account the vast improvement in imaging techniques, to the extent, that it seems likely that large numbers of patients are being subjected to the dangers of long-term warfarin unnecessarily. 1. Dixon et al, The non-invasive diagnosis of pulmonary embolus, 2001, BMJ;323:412-413 2. Burge et al, Increased diagnosis of pulmonary embolism without a corresponding decline in mortality during the CT era. 2008, Clinical Radiology: 63; 381-386 Competing interests: None declared |
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Thein H Oo, Attending Physician/Consultant in Hematology & Medical Oncology, Assistant Professor of Medicine St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, USA
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Dear Sir I was reading this article with interest. Dr Robinson wrote a faily good review. However, she did not mention anything on a not uncommon acquired prothrombotic condition, "heparin-induced thrombocytopenia and thrombosis". With so many patients receiving heparin for deep vein thrombosis prophylaxis as well as for therapeutic purposes (e.g. acute coronary syndromes), we frequently see heparin-induced thrombocytopenia (HIT) which classically presents with thrombocytopenia or 50% drop in baseline platelet count on days 5-14 after exposure or perhaps earlier if the patient was exposed to heparin in the past 100-120 days. 50% of HIT leads to thrombosis including pulmonary embolism. Diagnosis is confirmed by heparin-platelet factor 4 antibody by ELIZA and/or serotonin release assay. The importance of this important clinical syndrome (HIT) is that management of pulmonary embolism in this setting is different. These patients must be treated with direct thrombin inhibitors such as argatroban or lepirudin instead of heparin. Warfarin should not be started straight away as it blocks vitamin K synthesis and can worsen prothrombotic state and can cause warfain-induced skin necrosis or worsening of the underlying thromboembolic process. If someone was recently on heparin for various reasons and presents with acute pulmonary embolism and thrombocytopenia or 50% drop in baseline platelet count, heparin-induced thrombocytopenia and thrombosis should be seriously considered as a differential diagnosis and should be treatment with direct thrombin inhibitors. Warfarin should be started a few days later. References: 1. Kelton JG, Warkentin TE: Heparin-induced thrombocytopenia: a historical perspective. Blood, 112(7):2607-16 2. Serasli E, Antoniadou M, Tsara V, et al. Successful management of acute thromboembolic disease complicated with heparin-induced thrombocytopenia type II (HIT II): a case series. Thromb J, 2;6:9. 2008 3. Prechel M, Walenga JM: The laboratory diagnosis and clinical management of patients with heparin-induced thrombocytopenia: an update. Semin Thromb Hemost. 34(1):86-96, 2008 Competing interests: None declared |
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