60% off Selected Medicine Titles from Cambridge University Press

60% off Medicine Books from Cambridge University Press

 

For a limited time only, Cambridge University Press is proud to offer you* an exclusive 60% discount on selected titles from our renowned Medicine list.

 

*Offer ends 28th February 2013. Offer is valid for orders made via our website only. The discount cannot be used in conjunction with any other offer or discount. Offer available to customers within Europe, the Middle East and North Africa only.

TAVI and its role in treatment of aortic stenosis

submitted by Dr Gokulnath Rajendran & Dr Stephen T Webb both at Papworth Hospital NHS Foundation

Aortic stenosis (AS) is the most common type of valvular heart disease in developed countries. It is a progressive disease and the incidence of
severe stenosis increases with age, ~2% at 65 years and 4% at 85 years[1]. Patients may be asymptomatic or present with syncope, angina or exertional breathlessness. Surgical replacement of aortic valve is the standard treatment to improve quality of life in symptomatic severe AS. However patients who are considered too high risk for surgery could benefit from minimally invasive transcatheter aortic valve implantation (TAVI).

TAVI was first performed in 2002. Since then, technology has evolved rapidly and in the last decade, more than 50,000 procedures have been performed worldwide2. The procedure involves balloon valvuloplasty of the stenosed valve followed by deployment of a bioprosthetic valve by transfemoral or transapical route.
In UK, TAVI is currently performed in cardiac catheterisation suites with operating theatre facilities (‘hybrid’ catheter rooms) in specialist cardiothoracic centres by interventional cardiologists. Patients undergo comprehensive investigations including echocardiography, coronary angiography and computed tomographic (CT) angiography. Multi-disciplinary assessment of the patient is essential prior to the procedure.

Although TAVI can be performed under local anaesthesia, the majority of patients receive general anaesthesia. General anaesthesia provides
the patient immobility and facilitates the use of transoesophageal echocardiography. Anaesthetic management can be potentially challenging as these patients often have multiple comorbidities. The procedure involves rapid ventricular transvenous pacing to temporarily reduce cardiac motion. Pacing wires are inserted in case of bradyarrhythmias. Vasopressors are usually administered to treat intraoperative hypotension and maintain coronary perfusion pressure.

As the procedure may lead to potentially catastrophic haemodynamic instability, a cardiopulmonary bypass circuit and clinical perfusion team are kept on stand-by in the hybrid catheter room. Intraaortic balloon counterpulsation may be necessary to support patients with very poor ventricular function.

Complications of TAVI include delirium, seizure, stroke or TIA, myocardial infarction, cardiac arrhythmia, access site arterial injury and cardiac tamponade. Moderate to severe para-valvular regurgitation may occur after TAVI3.

Two-year survival rate is similar following TAVI compared to surgical procedure3 and is superior compared to medical treatment4. The UK National Institute for Health & Clinical Excellence (NICE) concluded that evidence for the efficacy of TAVI is sufficient to recommend the procedure for those unsuitable for surgery, but that there is0 insufficient evidence to support it for those considered suitable for surgery. Technological refinements could result in expansion of this less-invasive procedure to a broader spectrum of patients in the future.

1 Carabello BA, Paulus WJ. Aortic stenosis. Lancet 2009;373:956-66.
2 Vahanian A. Transcatheter aortic valve implantation: our vision of the future. Arch
Cardiovasc Dis. 2012 Mar;105(3):181-6.

AUB-P – How do polyps contribute to abnormal uterine bleeding? – Malcolm G. Munro, MD, FRCS(c), FACOG

Endometrial and endocervical polyps are localized epithelial proliferations that possess a variable vascular, glandular, fibromuscular and connective tissue component. Typically, such polyps are attached to the epithelial surface by a narrow stalk, but, in some instances, they may have a wide base when they are called “sessile”. In the vast majority of instances the lesions are benign, but 0.5 to 4.7% of symptomatic polyps have atypical or malignant features. (1, 2)

Polyps of the endometrium and columnar cervical epithelium have long been known to be associated with abnormal uterine bleeding (AUB) but it took the wide availability of diagnostic imaging and endoscopic techniques to provide greater insight into the relationship. Using such techniques to examine asymptomatic individuals allowed us to understand that these lesions have a prevalence of 12 – 25% in “normal” populations of premenopausal women. (3, 4) Consequently, those familiar with the varied causes of AUB in the reproductive years, detailed in FIGOs new classification system, will recognize that there are a large number of potential entities, both structural, and those unrelated to visible pathology, that could coexist with asymptomatic endometrial or endocervical polyps and be the actual cause of the abnormal bleeding.(5) So, you might ask, if that is the case, which polyps contribute to AUB and which do not?

Bleeding, when it occurs, is thought to emanate from a fragile and friable vascular structure, a feature that would lead to the notion that polyp-related AUB would be a random event, manifesting in intermenstrual bleeding or spotting. Indeed the available evidence seems to support this hypothesis. (3) However, there is also some relatively high quality evidence that heavy menstrual bleeding in association with polyps also may respond to polypectomy with a measurable reduction in menstrual volume. (6)

How is the diagnosis of an endometrial or endocervical polyp to be made? We know that blind sampling with endometrial biopsy catheters or D&C is inadequate for the task and that accurate structural evaluation of the endometrial cavity requires imaging by ultrasonographic techniques and/or direct inspection with hysteroscopy. (7-9) Furthermore, while simple transvaginal ultrasound is a good screening test, it may miss some focal lesions, particularly flat polyps. Consequently evaluation for structural causes of AUB such as polyps is most reliably determined by hysteroscopy or contrast sonography).

So the “take home” message should be this: When endometrial polyps are found in women with AUB, they should be excised and sent for histopathological examination. And while polyps can be blindly removed with suitable “polyp” forceps, there is evidence that recurrence is relatively frequent when this technique is used. (10) Consequently it is preferable to remove the polyps under direct hysteroscopic visualization with one or a combination of hysteroscopic scissors, biopsy forceps, or an electrosurgical cutting loop.

More about AUB-P can be found in the book Abnormal Uterine Bleeding, from Cambridge Medical Press.(11)

1. Anastasiadis PG, Koutlaki NG, Skaphida PG, Galazios GC, Tsikouras PN, Liberis VA. Endometrial polyps: prevalence, detection, and malignant potential in women with abnormal uterine bleeding. Eur J Gynaecol Oncol. 2000;21:180-3.
2. Shushan A, Revel A, Rojansky N. How often are endometrial polyps malignant? Gynecol Obstet Invest. 2004;58:212-5.
3. Lieng M, Istre O, Sandvik L, Qvigstad E. Prevalence, 1-year regression rate, and clinical significance of asymptomatic endometrial polyps: cross-sectional study. J Minim Invasive Gynecol. 2009;16:465-71.
4. Savelli L, De Iaco P, Santini D. Histopathologic features and risk factors for benignity, hyperplasia, and cancer in endometrial polyps. American Journal of Obstetrics and Gynecology. 2003;188:927-31.
5. Munro MG, Critchley HO, Broder MS, Fraser IS. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. Int J Gynaecol Obstet. 2011;113:3-13.
6. van Dongen H, Janssen CA, Smeets MJ, Emanuel MH, Jansen FW. The clinical relevance of hysteroscopic polypectomy in premenopausal women with abnormal uterine bleeding. BJOG : an international journal of obstetrics and gynaecology. 2009;116:1387-90.
7. Valle RF. Hysteroscopic evaluation of patients with abnormal uterine bleeding. Surg Gynecol Obstet. 1981;153:521-6.
8. Gimpelson RJ, Rappold HO. A comparative study between panoramic hysteroscopy with directed biopsies and dilatation and curettage. A review of 276 cases. Am J Obstet Gynecol. 1988;158:489-92.
9. Loffer FD. Hysteroscopy with selective endometrial sampling compared with D&C for abnormal uterine bleeding: the value of a negative hysteroscopic view. Obstet Gynecol. 1989;73:16-20.
10. Liberis V, Dafopoulos K, Tsikouras P, Galazios G, Koutlaki N, Anastasiadis P, et al. Removal of endometrial polyps by use of grasping forceps and curettage after diagnostic hysteroscopy. Clin Exp Obstet Gynecol. 2003;30:29-31.
11. Munro MG. Abnormal Uterine Bleeding. Cambridge: Cambridge University Press; 2010.

AUB-L – When is the leiomyoma the culprit?

Blog Post by Malcolm G. Munro MD, FACOG, FRCS(c), Professor, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Director of Gynecologic Services, Kaiser Permanante, Los Angeles Medical Center, Los Angeles, CA, USA

I frequently am approached by surgically ambitious residents (registrars) with a pitch that goes something like this:

“I have a 47 year old patient with menometrorrhagia from a 13 week size symptomatic fibroid uterus who wants a hysterectomy. When can we do it?”

Typically the patient hasn’t been adequately investigated as the assumption is that the leiomyomas (fibroids), detected with some combination of manual examination and ultrasound are indeed the cause of the abnormal bleeding – this, coupled with an irrational exuberance for surgery, results in a patient who “wants” a hysterectomy. So what is wrong with this story?

In the United States, at least, by the age of 50, leiomyomas are present in almost 70 per cent of Caucasians and more than 80 per cent of women of African ancestry. (1) Since most of these women don’t have any symptoms, an astute observer should conclude that most “fibroids” are asymptomatic. So when the symptom of abnormal uterine bleeding (AUB) occurs in a woman who can be demonstrated to have leiomyomas, the clinician should be challenged to distinguish AUB that is caused by the myomas from that which occurs for other reasons. Those familiar with the varied causes of AUB in the reproductive years, detailed in FIGOs new classification system, will recognize that there are a large number of potential entities, both structural, and those unrelated to visible pathology, that could coexist with asymptomatic leiomyomas and be the actual cause of the abnormal bleeding.(2) So, you might ask, if that is the case, which leiomyomas contribute to AUB and which do not?

To answer this, we should look to the FIGO system, which has a subclassification for leiomyomas. When a woman presents with AUB and is found to have one or more submucous leiomyomas (Types 0, 1, & 2), she is categorized as having AUB-Lsm; if the endometrial cavity is normal, meaning that none of the leiomyomas distort the cavity by deviating the endometrium (Types 3-8), she is categorized as having AUB-Lo (“o” standing for other leiomyomas or those outside the endometrial cavity). While we need more well-designed studies, the present hypothesis is that the leiomyoma likely must directly contact the endometrium for the lesion to contribute to the AUB; in other words, the leiomyoma must be submucous in location, a circumstance that can be noted in the FIGO system as “AUB-Lsm”.

What is the evidence for such a relationship? Until recently, most of the evidence was indirect, with studies showing that removal of submucous leiomyomas resulted in the predictable improvement in the symptom of heavy menstrual bleeding. However, more recently, we are beginning to assemble the molecular puzzle, as it is apparent that leiomyomas manufacture factors such as TGF-Beta3 that can impact the endometrium, if it is nearby, by interfering with the action of the unlikely substance bone morphogenetic protein (BMP), that adversely impacts some of the mechanisms involved in local control of menstrual bleeding.(3) It takes little imagination to see that if the leiomyoma is remote from the endometrium, such an impact would be reduced or eliminated altogether.

So when we interview the resident’s patient with a structured history, we frequently find that indeed the patient has the irregular bleeding typically associated with an ovulatory disorder (AUB-O) and, despite the presence of Type 4 and 5 leiomyomas, evaluation with office hysteroscopy, contrast sonography or MRI, demonstrates a normal endometrial cavity. In such instances, the endocrine etiology of the problem is amenable to a host of medical interventions including combination oral contraceptives and cyclical or continuous progestins – and, such patients may even have a discernable and treatable cause of the anovulation, ranging from hypothyroidism, obesity or personal stress. Alternatively, the hysteroscopy or contrast sonography might identify a polyp or smaller Type 0 or 1 lesion that can be removed easily, often in the office. So the patient’s options are frequently are far more numerous than hysterectomy, and often safer and relatively painless. So just because you find leiomyomas in a woman with AUB, doesn’t mean that the two are related – taking the time to critically evaluate all the potential contributors to the symptom of AUB may relieve your patient from the unlikely notion of “wanting” a hysterectomy.

More about AUB-L can be found in the book Abnormal Uterine Bleeding, from Cambridge Medical Press.(4)

1. Day Baird D, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188:100-7.
2. Munro MG, Critchley HO, Broder MS, Fraser IS. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. Int J Gynaecol Obstet. 2011;113:3-13.
3. Sinclair DC, Mastroyannis A, Taylor HS. Leiomyoma simultaneously impair endometrial BMP-2-mediated decidualization and anticoagulant expression through secretion of TGF-beta3. The Journal of clinical endocrinology and metabolism. 2011;96:412-21.
4. Munro MG. Abnormal Uterine Bleeding. Cambridge: Cambridge University Press; 2010.

FRCAQ.com, the new online testing resource for the Primary FRCA exam, includes Single Best Answer questions…

‘I love the two levels of reading you can do if you get a question wrong. And, importantly, it’s made by anaesthetists for anaesthetists…a brilliant resource.’ Alan Race, anaesthesia trainee

FRCAQ.com, the new online testing resource for the Primary FRCA exam, is the only website offering SBA (Single Best Answer) questions.

Why are SBAs important?
SBAs are included in the Primary exam from the 13th September 2011 onwards. Are you taking the Primary FRCA exam after 13th September 2011, or do you know someone who is? If so, find out more about FRCAQ.com

What does the Primary FRCA MCQ paper consist of?
We can say with some certainty what the MCQ paper will consist of in September 2011 and for a few cycles thereafter. In the exams prior to and including the June 2011 exam, the paper consisted of 90 MTF questions to be answered in three hours. This gave 450 knowledge point tests.

From September 2011, the College will replace 30 of the MTF questions with SBAs. This will provide 300 knowledge point tests from MTF and 30 from SBAs. The two styles will run in a combined paper for some time while the College gathers data comparing performance across the two paper styles. This will allow a standard to be created for the SBA question bank.

How do I answer SBAs?
Hints and Tips to help you in the exam…
This will sound like an echo from your earliest days of education, but it doesn’t hurt for us to say ‘make sure you read the question carefully‘!

A good tactic is to read the stem and lead-in, cover up the options and ask yourself what the correct answer would be. If you are 100% confident of the answer and this answer appears in the options, it is most likely to be correct.

If you are not in the lucky position of definitely knowing the answer and are trying to work it out, it is very important to not just settle on the first option you see that looks correct. Read all the options against the lead-in and ask yourself: ‘Which one fits best?’

In trials of SBAs with trainees we have noticed that they often find that two of the options can be discounted immediately, leaving two or three options to whittle down to one. If this happens to you, go back and read the stem, looking to see if there is anything within the detail that will allow you to reduce the options further. It may end up with a wild guess between two final options, but at least your odds of guessing correctly have increased from 20% to 50%.

Even if you only have the vaguest notion about the subject area, apply any knowledge you have and make an educated guess. Do not leave a blank. It is also important to state that only one mark per question should be made on the answer sheet. More than one mark and the candidate will score zero for that question.

Make sure you have the edge in your exam…
Try a free demo of FRCAQ
Subscribe to FRCAQ

New dynamic self-testing website for trainee anaesthetists from Cambridge

Cambridge Medicine has launched a dynamic new self-testing website for trainee anaesthetists – www.FRCAQ.com

What is FRCAQ.com?
It is an online revision resource of over 1,450 questions, answers and explanations in anaesthesia for trainees preparing for the Primary FRCA MCQ exam. Four different test options give you the flexibility to tailor your exam preparation to your specific needs, and detailed reports allow you to monitor your performance over time and against your peers.

Tell me more…
The site contains questions in both SBA (Single Best Answer) and MTF (Multiple True False) format. The Editors have analysed very component of the Primary FCRA syllabus and written questions on every topic you will encounter in the exam. Each question contains a short and long explanation, giving extensive background information to enhance your anaesthetic knowledge.

Which countries is the site relevant for?
Due to similarities in exam content and structure, the questions and answers on FRCAQ.com are directly applicable to the Irish Primary FCARSCI exam, the European Diploma in Anesthesia, the Australian and NZ FANZCA Part 1 exam, the Hong Kong HKCA Intermediate exam and the South African FCA(SA) Part 1 exam. Trainees preparing for these exams will find the site an invaluable revision resource.

Who are the Editors?
The FRCAQ editors, James Nickells and Ben Walton, are not only highly experienced anaesthetists and intensivists, but also expert medical educators who run the highly regarded Frenchay Final FRCA Crammer course. Members of their writing team are recent successful Primary and Final FRCA candidates or recently appointed consultants, so FCRAQ.com is written by anaesthetists for anaesthetists!

What next?
Try a free demo of FRCAQ
Subscribe to FRCAQ

Which other resources will help with Primary FCRA preparation?
Check out the following bestselling books:
Fundamentals of Anaesthesia, 3rd Edition Edited by Tim Smith, Colin Pinnock, and Ted Lin
Physics, Pharmacology and Physiology for Anaesthetists: Key Concepts for the FRCA Matthew E. Cross, Emma V. E. Plunkett
Pharmacology for Anaesthesia and Intensive Care, 3rd Edition Tom E. Peck, Sue Hill
Dr Podcast Scripts for the Primary FRCA Edited by Rebecca A. Leslie, Emily K. Johnson, Alexander P. L. Goodwin
Concise Anatomy for Anaesthesia by Andreas G. Erdmann

How Common is AUB-C?

Blog Post by Malcolm G. Munro MD, FACOG, FRCS(c), Professor, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Director of Gynecologic Services, Kaiser Permanante, Los Angeles Medical Center, Los Angeles, CA, USA

Among the varied causes of the symptom of heavy menstrual bleeding (HMB) in reproductive aged women are congenital disorders of hemostasis, commonly called coagulopathies. In the new FIGO PALM-COEIN classification system for causes of AUB in the reproductive years, such women are categorized as having AUB-C.(1) While there exist a number of such entities, by far, the most common is von Willebrand disease (vWD), a disorder that has a mean prevalence of about 13% in women of all ages with HMB.(2) There exist three recognized variants of vWD; the majority has the mild Type 1 form that can only be diagnosed with certainty using specific testing for von Willebrand factor (vWF). Type 2 vWD is a quantitative deficiency where vWF levels are typically 10-45% of normal while Type 3 is a serious deficiency that adversely impacts hemostasis even in the face mild injury or menses. Other less common factor-based coagulopathies are caused by deficiencies in Factors II, V, VII, VIII, IX, X, XI and XII. Of course, AUB-C can be also caused by iatrogenic means secondary to the use of anticoagulants. Because it is not clear to what degree the mild variants of inherited coagulopathies contribute to symptom of HMB in a given woman it is important to always perform a complete evaluation considering all of the elements in FIGO’s PALM-COEIN classification system.

AUB-C may present initially at menarche, when the adolescent, perhaps for the first time, has to attain satisfactory hemostasis over a large bleeding surface – the endometrium. The problem can be compounded because at menarche, many, if not most, such bleeds are anovulatory, where the endometrium is already deficient in endometrial vasoconstrictors such as PG F2-α and endothelin-1 that are largely dependent on the production of progesterone. When added to the delay in presentation fostered by the embarrassment and immaturity of the typical adolescent, menarcheal girls with von Willebrand disease and other disorders of systemic hemostasis are at great risk for a serious episode of HMB. Indeed, one study has reported that almost 20% of young girls who presented in the emergency department with acute HMB have AUB-C. (3)

So how does one diagnose AUB-C? The first step is to have a high index of suspicion. So when an adolescent presents around menarche with acute HMB, steps should be taken to evaluate for a systemic disorder of hemostasis. For other women, there is evidence that a structured history can identify about 90% of the women with laboratory evidence of von Willebrand disease. Any woman with lifelong heavy menstrual bleeding is at risk, as are those with a family history, or with a personal history of frequent bruising, bleeding with brushing teeth or unexplained bleeding associated with childbirth or surgical procedures.(4, 5) For women who fail the screen, the process should start with non-specific assays including prothrombin time (PT), partial thromboplastin time (PTT), ABO blood type and Ivy bleeding time as well as more specific assays measuring vWF, Ristocetin co-factor and Factor VIII . Other assays such as those for platelet aggregation or more rare factor deficiencies can be obtained as appropriate, depending on the clinical situation, and the advice of a consulting hematologist. Of course, the evaluation of any individual with AUB, including HMB, should be performed considering focal lesions of the lower genital tract as well as the other potential contributors to the bleeding categorized in FIGO’s PALM-COEIN system, two of which (AUB-E and AUB-O) have been discussed in previous editions of this blog.

Treatment of women with AUB-C will vary according to the severity of the disorder, the desires regarding current and future fertility, and the response to simple interventions such as tranexamic acid and local or systemic progestin-containing regimens. More about AUB-C can be found in the book Abnormal Uterine Bleeding, from Cambridge Medical Press.(6)

1. Munro MG, Critchley HO, Broder MS, Fraser IS. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. Int J Gynaecol Obstet. 2011;113:3-13.
2. Shankar M, Lee CA, Sabin CA, Economides DL, Kadir RA. von Willebrand disease in women with menorrhagia: a systematic review. BJOG. 2004;111:734-40.
3. Claessens EA, Cowell CA. Acute adolescent menorrhagia. American journal of obstetrics and gynecology. 1981;139:277-80.
4. Kadir RA, Economides DL, Sabin CA, Owens D, Lee CA. Frequency of inherited bleeding disorders in women with menorrhagia. Lancet. 1998;351:485-9.
5. Kouides PA, Conard J, Peyvandi F, Lukes A, Kadir R. Hemostasis and menstruation: appropriate investigation for underlying disorders of hemostasis in women with excessive menstrual bleeding. Fertil Steril. 2005;84:1345-51.
6. Munro MG. Abnormal Uterine Bleeding. Cambridge: Cambridge University Press; 2010.

Munro MG. Abnormal Uterine Bleeding. Cambridge: Cambridge University Press; 2010.

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