an internist in kandahar prioritizing gim through leadership · 2020. 7. 6. · 4 volume 2, issue...

www.csimonline.comwww.csimonline.com

Volume 2, Issue 3

An Internist in KandaharKevin Patterson

Prioritizing GIM throughLeadershipDante Morra and Howard Abrams

Communication in the OfficeJonathan Silverman and Toni Laidlaw

An Internist in KandaharKevin Patterson

Prioritizing GIM throughLeadershipDante Morra and Howard Abrams

Communication in the OfficeJonathan Silverman and Toni Laidlaw

Publications Agreement Number 40025049 | 1911-1606

The CSIM is an organization committed torepresenting, promoting, and strengthening general internal medicine and the role of general internists in Canada.

Benefits of Joining CSIM and What It Can Do for YouCSIM offers you numerous awards to recognize, support, and acknowledge generalinternists and residents:• CSIM Osler Awards• Dr. David Sackett Senior Investigator Award• New Investigator Award (formerly the Young Investigator Award)• CSIM Awards for Excellence in Research• Ted Giles Clinical Vignettes

CSIM members benefit from reduced registration fees at CSIM meetings.The annual conferences will be:

October 10–13, 2007 St. John’s, Newfoundland

October 15–18, 2008 Montreal, Quebec

CSIM encourages and supports residents and medical students:• Resident and medical student membership is FREE.• Some support is provided for residents to attend the CSIM Annual Scientific Meeting.• Research and scholarly bursaries are available for resident initiatives.An upgraded CSIM website offers countless links to sites and tools of interest. Interactive teaching modulesand other educational information are also available. Visit www.csimonline.com.

CSIM advocates on your behalf to promote and strengthen general internal medicine in Canada.CSIM’s quarterly publication, the Canadian Journal of General Internal Medicine, is free with membership.Read about case reports and practice guidelines, brush up on clinical examination skills and drug

interactions, or submit your own research or journal commentary. Learn about job opportunities and linkup with what’s happening with GIM in Canada.

CSIM is an accredited provider under the Maintenance of Certification program. All CSIM meetingsare approved for CPD credits. If you have a program requiring CPD approval, please contact us.

CSIM is collaborative and liaises with other international internal medicine organizations to shareideas and discuss solutions to shared challenges.

Together we are strong! Your membership in CSIM can make a difference.

For an application form, visit www.csimonline.com or contact the CSIM office at [email protected]/1-800-668-3740, ext. 244.

Join the Canadian Society of Internal Medicine!

4 V o l u m e 2 , I s s u e 3 , 2 0 0 7 C a n a d i a n J o u r n a l o f G e n e r a l I n t e r n a l M e d i c i n e

ABOUT THE COVER

This photo was taken at sunset on OSA Lake in Killarney Provincial Park: “I was on a 4-day solo trip. I had been pad-dling against the wind all day to reach my campsite. That evening, I paddled out to a small island, got out of thecanoe, and pulled it up on the rocks, and just as I turned my back, a gust of wind blew the canoe back into the water.I jumped in and grabbed the boat at the last second; otherwise, I would have spent a long and cold night stuck onthe island!”

Peter Bowers is an amateur photographer who lives and works in Toronto. He gets a lot of photo opportunities whilecanoeing, kayaking, and skiing at his cottage in Haliburton. You can view other photos by Peter atwww.flickr.com/photos/mr_fabulous/.

8 Message from the PresidentThe Society of General InternalMedicine Annual MeetingDonald Echenberg, MD

11 Practice of GIMCommunication in the Internist’sOffice: Explanation and Planningwith PatientsJonathan Silverman, MD, Toni Suzuki Laidlaw,MD

14 Community GIMToo Few Subspecialists: A CriticalShortage of General Internists! Patrick Bergin, MD

15 Community GIMDoing More with Less: Managingthe Cardiovascular Cluster ofDisease in an Integrated HealthCare Clinic Tom Ashton, MD, Gerry Karr ,MD, BevArsenault, RN, Susi Wilkinson, RD, SusanCooper, MD, Nancy Serwo, RN

17 Women’s GIMGreater Impact of Diabetes onVascular Risk in Women: Memoriesof Pregnancy and Puberty?Noemie Chessex, MD, Kaberi Dasgupta, MD

20 EKG&U Two for One, or One for All?George Veenhuyzen, MD

21 Professional DevelopmentPrioritizing General InternalMedicine in a Large AcademicMedical CentreDante Morra, MD, Howard B. Abrams, MD

23 Special CommunicationAn Internist’s Eye on KandaharBy Kevin Patterson, MD

24 MedEdProviding Feedback: An EffectiveUse of Teaching Time?Michelle Elizov, MD

26 Images in GIMFistula Post Heart BiopsyAndy Ignaszewski, MD, Simona Bar, MD

27 Guidelines Review 2007Canadian Hypertension EducationProgram Recommendations:The Short Clinical Summary – An Annual UpdateCanadian Hypertension Education Program

33 GIM of AgingConsent to Clinical Treatment:Special Challenges in the FrailElderlyMichael Gordon, MD

35 Pharm-GIMSulfonylurea-Induced Hypoglycemia:Avoidance and TreatmentDavid Juurlink, MD

36 Dans la pratique de la médecine interne générale en françaisÊtes-vous à jour en français médical ?Donald Echenberg, MD

38 Examination SkillsArterial ExaminationMargot R. Roach, MD

40 Resident GIMThe R4 Match: Demystifying theProcessAngèle Brabant, MD, Karim Abou-Nassar, MD

C O N T E N T SVolume 2, Issue 3

E D I T O R - I N - C H I E F

Hector Baillie

E D I T O R I A L B O A R D

Hector Baillie, Pat Bergin

Benjamin Chen, Kaberi Dasgupta

Don Echenberg, Don Farquhar

Bill Ghali, Bert Govig

David Juurlink, Neil Maharaj

Suzanne Morin, Jock Murray

Kathryn Myers, Louise Pilote

Colin Powell, Margot Roach

Linda Snell, George Veenhuyzen

Gary Victor

C S I M S TA F F

Ms. Domenica UtanoMs. Alexi Campbell

P R O D U C T I O N E D I T O R

Susan Harrison

C O P Y E D I T O R S

Scott Bryant, Susan Harrison

A R T D I R E C T O R

Binda Fraser

P R O O F R E A D E R

Scott Bryant

A D V E R T I S I N G

John Birkby(905) 628-4309

[email protected]

C I R C U L AT I O N C O O R D I N AT O R

Brenda [email protected]

A C C O U N T I N G

Susan McClung

G R O U P P U B L I S H E R

John D. Birkby

Canadian Journal of General Internal Medicine is publishedfour times a year by Andrew John Publishing Inc., withoffices located at 115 King Street West, Suite 220, Dundas,ON L9H 1V1.

We welcome editorial submissions but cannot assumeresponsibility or commitment for unsolicited material.Any edi-torial material, including photographs that are accepted froman unsolicited contributor, will become the property ofAndrew John Publishing Inc.

The publisher and the Canadian Society of Internal Medicineshall not be liable for any of the views expressed by theauthors published in Canadian Journal of General InternalMedicine, nor shall these opinions necessarily reflect those ofthe publisher.

•••••Every effort has been made to ensure that the informationprovided herein is accurate and in accord with standardsaccepted at the time of printing. However, readers areadvised to check the most current product information pro-vided by the manufacturer of each drug to verify the recom-mended dose, the method and duration of administration,and contraindications. It is the responsibility of the licensedprescriber to determine the dosages and best treatment foreach patient. Neither the publisher nor the editor assumesany liability for any injury and/or damage to persons orproperty arising from this publication.

Adalat® XL® (nifedipine) is indicated in the management of mild to moderate essential hypertension. Adalat® XL® should normally be used in those patients in whom treatmentwith diuretics or beta-blockers has been ineffective, or has been associated with unacceptable adverse effects. Therapy should be initiated with Adalat® XL® 20 or 30 mg oncedaily. The usual maintenance dose with Adalat® XL® is 30 to 60 mg once daily.Adalat® XL® is indicated in the management of chronic stable angina (effort-associated angina) without evidence of vasospasm in patients who remain symptomatic despite ade-quate doses of beta-blockers and/or nitrates, or who cannot tolerate these agents. Therapy with Adalat® XL® should normally be initiated with 30 mg once daily.In hypertension: the most common adverse events reported with Adalat® XL® were edema, which was dose-related and ranged in frequency from approximately 10 to 30% inthe 30 to 120 mg dose range, headache (16.6%), fatigue (6.2%), dizziness (4.4%), constipation (3.5%) and nausea (3.5%).In angina: the most common adverse events reported were edema (10.1%), headache (3.1%), angina pectoris (3.1%).Please refer to the Product Monograph for complete prescribing information.

†Effort-associated angina without evidence of vasospasm in patients who remain symptomatic despite adequate doses of beta-blockers and/or nitrates, or who cannot tolerate these agents.®Adalat, Bayer and Bayer Cross are registered trade-marks of Bayer AG used under license by Bayer Inc. XL is a registered trade-mark of Bayer Inc. denoting its once daily nifedipine.

Reference: Product Monograph, Adalat® XL®, revised August 12, 2004.

Bayer Inc. 77 Belfield Road Toronto, Ontario M9W 1G6

Adalat® XL®

Demonstrated to get BP down. PrAdalat® XL® is also indicated in the management of chronic stable angina†

O U R M E S S A G E I S S I M P L E

XL1253AE

10 Message du présidentL’assemblée annuelle de la Sociétéde médecine interne généraleDonald Echenberg, MD

11 Pratique de la médecine interne généraleLa communication dans le bureaude l’interniste : Expliquer et planifi-er avec le patientJonathan Silverman, MD, Toni Suzuki Laidlaw,MD

14 La médecine interne générale communautaireTrop peu de surspécialistes :la pénurie criante d’internistesgénéralistes Patrick Bergin, MD

15 La médecine interne générale communautaireFaire plus avec moins : la prise encharge des maladies cardio-vasculaires dans une clinique desoins intégrés Tom Ashton, MD, Gerry Karr, MD, BevArsenault, inf. aut., Susi Wilkinson, diététiste,Susan Cooper, MD, Nancy Serwo, inf. aut.

17 Les femmes internistes généralistesL’effet dévastateur particulier dudiabète sur le risque vasculairechez la femme : des relents de lagrossesse et de la puberté?Noemie Chessex, MD, Kaberi Dasgupta, MD

20 Défi ECGDeux pour un ou un pour tous?George Veenhuyzen, MD

21 Développement professionnelPrioriser la médecine internegénérale dans un grand établisse-ment de soins universitaireDante Morra, MD, Howard B. Abrams, MD

23 Communication spécialeLe point de vue d’un interniste surKandaharKevin Patterson, MD

24 Éducation médicaleLa rétroaction : utilisation efficacede la période d’enseignement?Michelle Elizov, MD

26 Images en médecine interne généraleLa fistule à la suite de la biopsiecardiaqueAndy Ignaszewski, MD, Simona Bar, MD

30 Revue de lignes directricesRecommandations 2007 duProgramme éducatif canadien surl’hypertension : Bref résumé clinique – Mise à jour annuelleProgramme éducatif canadien sur l’hypertension

33 Médecine interne généraleet vieillissementLa personne âgée fragile devant leconsentement au traitementMichael Gordon, MD

35 Pharmacologie en médecine interne généraleL’hypoglycémie causée par les sulfonylurées : l’éviter et la traiterDavid Juurlink, MD

36 Dans la pratique de la médecine interne généraleen françaisÊtes-vous à jour en français médical ?Donald Echenberg, MD

38 SémiologieL’examen artérielMargot R. Roach, MD

40 Résident en médecine interne généraleLe jumelage en 4e année :démystifier le processusAngèle Brabant, MD, Karim Abou-Nassar, MD

Table des matières

AU SUJET DE LA PAGE COUVERTUREPhotographie prise au coucher du soleil sur le lac OSA dans le parc provincial Killarney : « Lors d’un voyage ensolitaire de quatre jours, après avoir ramé contre le vent tout le jour pour me rendre au site de campement, je mesuis rendu à une petite île en soirée. Comme je venais, à mon arrivée, d’asseoir le canot sur les rochers avant dem’éloigner un peu, voilà que le vent repousse le canot à l’eau. J’ai eu à peine le temps de le rattraper. J’ai échappéde justesse à une longue et froide nuit, tout fin seul sur une île ! »

Peter Bowers est un photographe amateur qui vit et travaille à Toronto. Il profite de toutes les occasions de prendrede magnifiques photos lorsqu’il fait du canoë-kayak ou du ski à son chalet situé à Haliburton. Vous pouvez voird’autres photos prises par Peter à l’adresse suivante. www.flickr.com/photos/mr_fabulous/.

C a n a d i a n J o u r n a l o f G e n e r a l I n t e r n a l M e d i c i n e V o l u m e 2 , I s s u e 3 , 2 0 0 7 7

CSIM Members of Council

Dr. Donald EchenbergPresident/Québec Region Representative

Sherbrooke, [email protected]

Dr. Mahesh K. RajuPast-President/Eastern Region Representative

Saint John, [email protected]

Dr. Bert GovigPresident-Elect/Québec Region Representative,

Secretary-Treasurer and Vice-President,Membership Affairs

Amos, [email protected]

Dr. Hector BaillieWestern Region Representative/

Executive MemberNanaimo, BC

[email protected]

Dr. Neil GibsonWestern Region Representative

St. Albert, [email protected]

Dr. Malcolm WilsonOntario Representative/Executive Member

Huntsville, ON [email protected]

Dr. Grant MacfarlaneOntario Representative

Collingwood, ON [email protected]

Dr. Jim NishikawaOntario Representative

Ottawa, ON [email protected]

Dr. Benjamin ChenOntario Representative

Kingston, ON [email protected]

Dr. Lucie OpatrnyQuébec Representative

Montreal, QC [email protected]

Dr. John RobbQuébec Representative

Sherbrooke, QC [email protected]

Dr. Patrick BerginEastern Region Representative/

Executive MemberCharlottetown, PEI

[email protected]

Dr. Finlay McAlisterChair, Research/Awards Committee

Montréal, QC [email protected]

Dr. Maria BacchusVice-President, Education

Saskatoon, SK [email protected]

Dr. Neil MaharajResident Representative

Ottawa, ON [email protected]

Dr. Barry O. KassenWestern Region Representative

Vancouver, BC [email protected]

Dr. Ann ColbourneChair, Annual Meeting Committee 2007

St. John's, [email protected]

M e s s a g e f r o m t h e P r e s i d e n t

8 V o l u m e 2 , I s s u e 3 , 2 0 0 7 C a n a d i a n J o u r n a l o f G e n e r a l I n t e r n a l M e d i c i n e

In April of this year I had the occasion to attend the 30th Annual

meeting of the SGIM held in Toronto. Spurred on by Bill Ghali, who

organized the First International Symposium in GIM, I packed my bike

and headed to the Big Smoke.

All misconceptions that American general internists deal mainly in

primary care were quickly dispelled. In fact, the SGIM represents a

significant proportion of general internists who are practising in

academic centres, often in purely consultative roles, and who have the

same clinical, educational, and research profiles as their Canadian

counterparts.

The Society for Research and Education in Primary Care Internal

Medicine had 178 attendees at its 1978 inaugural meeting. It rolled over

into the SGIM in 1988 and has grown to over 2,800 members since

then. As does the CSIM, the SGIM is dedicated to improving patient

care, education, and research in general internal medicine. However, it

does mention primary care in its mission statement, which most

internists in Canada avoid.

The annual meeting is on a much larger scale than our own, with

1,300 registrants, including many from Canada and from countries

such as Argentina, Japan, New Zealand, and Switzerland. The theme of

the annual meeting titled the Puzzle of Quality was the subject of many

of the plenary sessions, each of which focused on a piece of the puzzle

from research to education to clinical practice.

I planned out my personal schedule and attended a variety of plenary

sessions, workshops, clinical vignettes, and up-to-date sessions. One of

the highlights of the meeting was the Meet the Professor session. I chose

to meet the president of the SGIM, Dr. Robert Centor, chief of the

Division of GIM at the University of Alabama in Birmingham. I walked

solemnly into a large conference room to find myself alone with Dr.

Centor. What an opportunity! We exchanged ideas. He talked about his

love for teaching, his passion for GIM, and his work at the VA Hospital

and the University of Alabama teaching hospital. I discovered that while

we work in different languages treating patients from different ethic

groups, we share many common interests and we are both devoted to

practising and teaching complex adult medicine.

I attended the International symposium in GIM and in fact was

invited to give the opening address. You will read more about the

symposium in a future issue.

While attending the other activities, I met some of the giants in GIM

such as Dr. Richard White, director of the anticoagulation service at UC,

Davis; Dr. Brian Gage from Washington University, who helped us

understand warfarin pharmacogenetics and rational dosing; and

Dr. David Simel, section editor of the JAMA’s Rational Clinical Exam

series.

I learned about selenium deficiency cardiomyopathy after bariatric

surgery and radiation induced coronary disease. I brought myself up to

date in the areas of venous thrombosis, physical diagnosis, perioperative

medicine, and medical education. I learned that beta-blockers could be

effective in preventing postoperative cardiac complications when the

dose is titrated to maintain a heart rate of 55–70 bpm.

I was struck by the marked concern that our fellow American

internists share with us in the management of many common chronic

diseases. They have a profound understanding of how inner-city

stressors influence their onset and severity.

My conclusion: the SGIM is relevant. The meeting widened my

horizons. Its annual meeting was definitely worth the trip. Perhaps I will

see some of you in Pittsburgh in April 2008. Pennsylvania is the home

of the editorial office of Bicycling Magazine, one of the best cycling

magazines in the word. There is surely some good riding in

Pennsylvania. And some good medicine to go along with it.

About the AuthorDon Echenberg is president of the Canadian Society of Internal Medicine and its Quebec regional representative. He has been

practising and teaching general internal medicine at the University Hospital in Sherbrooke for several years.

The Society of General Internal Medicine Annual MeetingDon Echenberg, MD

M e s s a g e d u p r é s i d e n t

En avril dernier, j’ai assisté à la 30e assemblée annuelle de la Société

de médecine interne générale (SMIG) à Toronto. Encouragé par Bill

Ghali, organisateur du premier symposium international en médecine

interne générale, je me suis dirigé vers la Ville reine, mon vélo sous le

bras.

L’idée préconçue voulant que les internistes généralistes américains

exercent principalement aux soins primaires a été vite dissipée. En

réalité, la SMIG représente un bon nombre d’internistes généralistes qui

pratiquent dans des établissements universitaires, pour beaucoup en

consultation exclusivement, avec le même bagage clinique, éducatif et

de recherche que leurs homologues canadiens.

La Society for Research and Education in Primary Care Internal

Medicine a attiré 178 personnes à son assemblée inaugurale en 1978.

Elle est devenue la SMIG en 1988, et elle compte désormais 2 800

membres. À l’instar de la Société canadienne de médecine interne

(SCMI), la SMIG est vouée à l’amélioration des soins, de l’éducation et

de la recherche en médecine interne générale. Sa mission mentionne

toutefois les soins primaires, ce dont la plupart des internistes canadiens

s’écartent.

Le congrès annuel est beaucoup plus imposant que le nôtre; il

rassemble 1 300 participants, beaucoup du Canada et d’autres pays

comme l’Argentine, le Japon, la Nouvelle-Zélande et la Suisse. Le thème

de cette année, le casse-tête de la qualité, a été repris dans la plupart des

sessions plénières, chacune centrée sur l’un des morceaux du casse-tête,

de la recherche à l’éducation en passant par la pratique clinique.

Je me suis concocté un programme personnel en choisissant des

sessions plénières, des ateliers, des vignettes cliniques et des séances de

mise à jour. La session « rencontre avec le professeur » est toujours très

courue. Pour ma part, j’ai rencontré le président de la SMIG, le

Dr Robert Centor, chef de la Division de médecine interne générale à

l’Université de l’Alabama à Birmingham. Je suis entré dans une salle de

conférence d’un pas solennel pour me retrouver tout fin seul avec le Dr

Centor. Quelle chance ! Nous avons échangé des idées, il a parlé de sa

passion à la fois pour l’enseignement et la médecine interne générale, et

de ses activités à l’Hôpital VA et à l’hôpital d’enseignement affilié à

l’Université de l’Alabama. Je me suis rendu compte que malgré que

nous ne travaillions pas dans la même langue et que nous traitions des

patients de groupes ethniques différents, nous partageons bien des

intérêts et nous nous consacrons tous les deux à l’exercice et à

l’enseignement de la médecine complexe de l’adulte.

J’étais présent, bien sûr, au symposium international de la médecine

interne générale, notamment parce qu’on m’avait invité à prononcer

l’allocution d’ouverture. Vous en saurez davantage à propos du

symposium dans un numéro futur.

J’ai eu également l’occasion de rencontrer des sommités en médecine

interne générale, dont le Dr Richard White, directeur du Service

d’anticoagulation à l’UC, le Dr Brian Gage de l’Université de

Washington, qui nous a enseigné les tenants et aboutissants de la

pharmacogénétique et de l’adaptation posologique de la warfarine, et le

Dr David Simel, éditeur de la rubrique sur l’examen clinique rationnel

de JAMA.

J’en sais plus maintenant sur la cardiomyopathie par carence de

sélénium à la suite de la chirurgie bariatrique et sur la coronopathie

radio-induite. J’ai actualisé mes connaissances dans les domaines de la

thrombose veineuse, du diagnostic physique, de la médecine

peropératoire et de l’éducation médicale. Enfin, je sais désormais que les

bêta-bloquants peuvent prévenir les complications cardiaques

postopératoires quand leur dose est modulée en fonction d’une

fréquence cardiaque allant de 55 à 70 battements à la minute.

J’ai été frappé de constater que nos collègues internistes américains se

consacrent tout autant que nous à la prise en charge des multiples

maladies chroniques courantes. Ils ont certes creusé la question de

l’influence des stresseurs de la grande ville sur leur apparition et leur

gravité.

Je conclu sur cette note : la SMIG est tout à fait pertinente.

L’assemblée m’a ouvert des horizons nouveaux. Cela valait assurément

la peine d’y être. Qui sait, peut-être verrai-je certains d’entre vous à

Pittsburgh en avril 2008? Pour ceux que cela intéresse, le bureau de la

rédaction de Bicycling Magazine, magazine sur le cyclisme de grande

renommée mondiale, se trouve en Pennsylvanie. J’imagine que les

parcours de vélo ne manquent pas dans cet État, comme la bonne

médecine d’ailleurs.

Au sujet de l’auteurDon Echenberg est président de la Société canadienne de médecine interne et son représentant régional au Québec. Il pratique

et enseigne la médecine interne au Centre hospitalier universitaire de Sherbrooke depuis plusieurs années.

L’assemblée annuelle de la Société de médecine interne généraleDon Echenberg, MD

1 0 V o l u m e 2 , I s s u e 3 , 2 0 0 7 C a n a d i a n J o u r n a l o f G e n e r a l I n t e r n a l M e d i c i n e

C a n a d i a n J o u r n a l o f G e n e r a l I n t e r n a l M e d i c i n e V o l u m e 2 , I s s u e 3 , 2 0 0 7 1 1

Why Bother Reading This?The problem in writing an article on communication is how to

persuade the busy internist to devote precious time to reading it. Why

should you consider the “soft” aspects of medicine when there are so

many technical and scientific aspects that you need to stay abreast of?

To make the investment of your time worthwhile, we need to provide

you with something that will be of direct practical use in your world,

rather than some abstract construct. What we want to offer you is

practical help to enable you to channel your hard-earned factual

learning and experience into more effective and satisfying medical

interviews that will truly make a difference to you, your patients, and

your practice of medicine. And in case you’re worrying, there is indeed

a large evidence base for the communication approaches we are going

to describe.

Explanation and Planning: The Cinderella Subject ofPhysician-Patient CommunicationWe have decided to concentrate on one area of communication –

explanation and planning. By this, we mean the second half of the

medical interview, where information gathered from talking to the

patient, physical examination, and investigations are brought to bear on

the tasks of giving information, providing explanations, and planning

future management.

But why have we chosen to focus here? Because explanation and

planning are consistently highlighted as key problem areas by

physicians, patients, and communication teachers alike.

PhysiciansDoctors increasingly state that explanation and planning are among the

major difficulties in their day-to-day work. Recently, one of the authors

(J.S.) conducted an informal survey of experienced internal medicine

physicians within his own teaching institution, asking what they found

difficult in their daily communication with patients. By far, the biggest

area identified was explanation and planning. The following problems

emerged:

• How to balance the conflict between giving full explanation and

overloading the patient

• How much detail to impart

• How to overcome what appears often to be an unbridgeable

comprehension gap

• How to deal with patients’ anxieties and concerns and, therefore,

their reduced ability to retain information

• What to do when patients’ expectations exceed what is possible or

conflict with the doctor’s opinion

• How to deal with an inadequate amount of time for discussion and

explanation

PatientsA raft of communication research shows that patients also struggle in

this component of the interview. They often

• would prefer more information than they receive (although 20%

would like less);

P r a c t i c e o f G I M

Communication in the Internist’s Office: Explanation and Planning with PatientsJonathan Silverman, MD, Toni Suzuki Laidlaw, MD

About the AuthorsJonathan Silverman is associate clinical dean at the University of Cambridge School of Clinical

Medicine and director of communication studies. He is one of the authors of the Calgary-

Cambridge Guide to the Medical Interview and has written two standard texts on teaching and

learning communication skills in medicine.

Toni Suzuki Laidlaw is a retired professor in the Faculty of Medicine, Dalhousie University, where

for 10 years she was director of the Communication Skills Program. She is co-author of a number of

published papers dealing with communication in health care.

Initiating the Session• preparation• establishing initial rapport• identifying the reason(s) for the consultation

Gathering Information• exploration of the patient’s problems to discover the: • biomedical perspective • patient’s perspective • background information context

Physical Examination

Explanation and Planning• providing the correct amount and type of information• aiding accurate recall and understanding• achieving a shared understaning: incorporating the patient’s illness framework• planning: shared decision making

Closing the Session• ensuring appropriate point of closure• forward planning

ProvidingStructure

Buildingthe

Relationship• making organization overt

• attending to flow

• using appropriate non-verbal behaviour

• developing rapport

• involving the patient

Figure 1. The enhanced Calgary-Cambridge Guide to the Medical Interview.Adapted from Kurtz SM et al.1

C o m m u n i c a t i o n i n t h e I n t e r n i s t ’ s O f f i c e @ L R H


• have difficulty remembering and understanding information given;

• feel disempowered to ask the questions they need to make sense of

the information given;

• leave the consultation with doubts and questions that they have not

voiced; and

• do not achieve their preferred level of involvement in decision

making.

A recent paper by the author (T.S.L.) and her colleagues confirms this

finding once again.2 Patients were satisfied with their physician’s care,

ability to put them at ease, listen to complaints, and create good rapport

but were unsatisfied with their physician’s information about the

presenting complaint and their own involvement in treatment plans.

Communication TeachersExplanation and planning have until recently been a relatively neglected

area of communication skills teaching. Most teaching programs have

concentrated on the first half of the interview and tended to underplay

this vital next stage. A recent series of training programs run by the

author (J.S.) teaching physicians to teach explanation and planning to

medical students has confirmed this problem. None of the physicians

had ever received any training in their own skills of explanation and

planning. Although all the skills highlighted in the course fitted their

experience of the subject as practising doctors, they had never before

broken down the task into separate components and were unable to

conceptualize how to teach this area to others.

So What Can We Do to Help Both Doctors andPatients in the Second Half of the Consultation?We would like to provide 12 simple strategies to alleviate both doctors’

and patients’ problems in explanation and planning. The prize on offer

is better patient and practitioner satisfaction, improved patient recall

and understanding, increased adherence to plans made, and eventually

better physiological outcomes. Research has demonstrated that all these

are achievable outcomes through better communication in this stage of

the interview.

1. Discover the patient’s starting point.

Always find out what the patient knows already, his or her starting

point. This can be a considerable timesaver; so often, doctors give

the same lecture to every patient, with information either

considerably above the patient’s head or that the patient knows

already. Discovering the patient’s starting point will help you tailor

the information to the individual and prevent much wasted time.

Doctor: “I don’t know how much you know about Parkinson’s disease

already.”

Patient: “Well, I know a little about it – my mother’s best friend had

it.”

Doctor: “It would be helpful for me to understand a little of what you

already know so that I can try to fill in any gaps for you.”

2. Chunk and check.

Try not to give a lecture imparting all your knowledge in one go. A

common pattern is for doctors to give a long lecture at high speed

without breaks, assuming that the transmission of knowledge is all

that is required. In fact, transmission without checking is a recipe

for inefficiency for you and reduced recall and understanding for

your patient. Questions arise as you talk that need answering for the

patient to make sense of what you are saying. So, break up

information into small pieces and use the patient’s response as a

guide to how to proceed. If you give information in small chunks

and give patients ample opportunity to contribute, they will

respond with clear signals about both the amount and type of

information they still require.

Doctor: “So really, given the symptoms you have described and the very

typical way that you wheeze more after exercise and at night, I feel

reasonably confident that what you are describing is asthma and that

we should consider giving you some treatment for it. Does that make

sense so far?”

Patient: “Yes – I think so, but I’m not sure I really understand what

asthma is – is it something that runs in families?”

3. Ask patients what other information would be helpful.

It is all too easy to make assumptions about the information that the

patient requires. It is difficult to guess each patient’s individual

needs, and asking directly is an important way to provide the

patient with the information needed, rather than the information

we think he or she needs.

Doctor: “Are there any other questions you’d like me to answer or any

points I haven’t covered?”

Patient: “Do you think I could pass this on – I mean, is it infectious?

4. Use concise, easily understood statements; avoid or explain

jargon.

The use of jargon is a major problem in communication, and

patients rarely ask for clarification for fear of appearing ignorant.

Physicians even deliberately use technical language to control

communication and to limit questions – such behaviour occurs

twice as often when doctors are under pressure of time. Remember,

though, that many patients with chronic diseases are experts

themselves and are increasingly familiar with our medical jargon.

So be careful with your use of words by reducing the use of jargon

or explaining jargon when used.

5. Check the patient’s understanding of the information given.

Doctors often repeat statements to their patients in order to aid

recall. But few ask patients to restate in their own words what they

have heard, despite this being a much more effective way of

increasing patients’ recall of the information given. Patient

restatement has the added benefit of discovering what the patient

understands so that you can make appropriate corrections. The

difficulty of requesting patient restatement is that it is so easy to

sound patronizing by implying that the patient has limited capacity

to understand what you have said. But there are ways to do this that

work.

Doctor: “I know I’ve given you a lot of information today, and I’m

concerned that I might not have made it very clear. It would help me

if you repeated back to me what we have agreed on so far so that I can

make sure we are on the same track.”

S i l v e r m a n a n d S u z u k i L a i d l a w


6. Relate explanations to patients’ ideas, concerns, and expectations.

Consultations go wrong where there is incongruity between the

patient’s and the doctor’s explanatory frameworks. A 55-year-old

man with chest pain might well think that he has lung cancer as his

friend recently died from the disease. You might be perfectly happy

that it is musculo-skeletal condition. Unless you discover your

patient’s ideas and explain why you think that the pain is not due to

cancer, he may leave the interview with the nagging doubt that you

may not have considered the possibility. This doubt may block the

patient’s understanding and commitment to your explanations, and

undermine his acceptance of your diagnosis. Recall, understanding,

satisfaction, and adherence to plans are all likely to suffer when a

doctor’s explanation does not address the patient’s individual ideas,

expectations, and concerns.

Doctor: “You mentioned earlier that you were concerned that you

might have angina … I can see why you might have thought that, but,

in fact, I think it’s more likely to be a muscular pain. Let me explain

why …”

7. Provide opportunities and encourage your patient to contribute:to ask questions, seek clarification, or express doubts.

We know that when patients are left with doubts and concerns that

they are not able to voice within the consultation, they are much

more likely to misunderstand information and be unhappy with the

plans made. It becomes vital then to actively seek out such problems

if the patient and doctor are to come to a mutual agreement about

the way forward. You have to be very explicit here: many patients are

reluctant to express what is on the tip of the tongue and are

extremely hesitant to ask the doctor questions.

Doctor: “What questions does that leave you with? Is there anything I

haven’t covered or explained?”

8. Pick up and respond to your patient’s verbal and nonverbal cues.

Another means of discovering your patients’ thoughts and feelings

is to try to pick up their cues, both verbal and nonverbal. Remember

that most patients use indirect or oblique hints to express their

doubts or concerns rather than overt statements or questions. You

must therefore search for subtle cues that the patient wishes to

contribute information or ask questions.

Doctor: “You look unhappy – is it about the possibility of having

surgery?”

9. Offer suggestions and choices rather than give directives.

In order to involve the patient in the decision-making process,

outline the possible management options that are available rather

than proposing one particular course of action.

Doctor: “Given what you have said, I think there are two choices

available that we ought to consider together – firstly, starting treatment

for Parkinson’s disease now and, secondly, simply soldiering on for the

moment and seeing what happens to your symptoms over the next few

months.”

10. Explore management options with patient.

It is important to explore the options available to the patient in

more depth and to provide information about the risks and benefits

of each.

Doctor: “So to recap, we have agreed there are two approaches you

could take here. The first would be to consider taking treatment for

Parkinson’s disease now; the second would be to see how you go

without medication for the time being and revisit the issue at a later

date. Would it help if I ran through the risks and benefits of each course

of action now?”

11. Establish patient’s preferences.

Both your views and the patient’s can then be expressed, but be

careful to listen carefully to the patient’s ideas and responses.

Doctor: “What do you think overall? What would be your preference?”

12. Negotiate differences.

You can make it clear to the patient that you wish to share the

decision making, resolve differences, and negotiate a mutually

acceptable plan.

Doctor: “I do have some reservations about taking the approach you

suggest. Can I explain them to you, and then perhaps we can try to

find a solution that works for both of us?”

ConclusionsWe hope that the 12 steps we have outlined above will enable your and

your patients to have more effective and productive medical interviews.

All that we have said is backed by considerable research evidence; if you

wish to explore this further, please refer to Skills for Communicating with

Patients,3 from which many of the examples in this article are taken.

Interestingly, established physicians’ self-assessment always suggests

that explanation and planning are the key communication areas for

their personal development. However, they rarely, if ever, mention that

they might have any problems in information gathering or history

taking. Yet, there is considerable evidence that this too is a problem for

many physicians, leading to problems for patients and to ineffective

clinical reasoning. But that discussion will have to wait for another day.

References1. Kurtz SM, Silverman JD, Benson J, Draper J. Marrying content and

process in clinical method teaching: enhancing the Calgary-Cambridge guides. Acad Med 2003;78:802–9.

2. Laidlaw T, Kaufman DM, MacLeod H, et al. Patient satisfaction withtheir family physician’s communication skills: a Nova Scotia survey.Acad Med 2001;76:S77–9.

3. Silverman JD, Kurtz SM, Draper J. Skills for Communicating withPatients, 2nd edition. Oxford: Radcliffe Publishing; 2005.

C o m m u n i t y G I M


The future of general internal medicine (GIM) remains uncertain.

There has been a consistent trend during the past 35–40 years1 of

residents selecting subspecialties with better remuneration and a more

reasonable lifestyle, and there is now an imminent critical shortage of

general internists. The 2007 update of the CMA Masterfile2 reveals that

of the 2,400 general internists in Canada, 46% are over age 55 (with

23% of those being over the age of 65) and less than 10% are under the

age of 35. The medical subspecialties, including cardiology and

oncology, are estimated to have over 30% of their members over the age

of 55.

An aging population with increasingly complex medical problems,

heightened patient expectations, an inadequate number of resident

training positions, physician loss through attrition, and a visible shift

from physician willingness to personally absorb the increased work

demands will all contribute to a shortage of available specialty care.

With the “feminization of medicine” and the advent of the Generation

Xers, physicians are less willing to work endless hours at the expense of

their own well-being and at the risk of imbalance in family and

professional lives.3 Today’s doctors are no less dedicated than their

predecessors,3 but many have stepped off the pedestal of our forefathers.

A healthy physician will intuitively contribute to maintaining a healthy

community.

General internists have been quietly absorbing and upholding the

system’s deficiencies for years, partly because our predecessors naively

viewed our discipline as above speaking out for itself. Conscientious

generalists often endure a “forced altruism,” getting paid less or being

forced into “volume medicine.” To continue attracting residents and

students into GIM, we must insist on being treated equal to our

procedural-based colleagues – with the thinking hour being worth as

much as the procedural hour, teaching equally important as research,

and practising in communities such as Amos or Campbell River as

valuable as practising in Toronto or Vancouver.

In 2006, the Canadian Cardiovascular Society (CCS) published their

ad hoc committees’ report on the plight of cardiology in the future,

titled “Too Many Patients, Too Few Cardiologists to Care?”4 I commend

them for defending their futures but find their position disappointing.

In their quest for more residency positions, they suggest that general

internists may not be suitable for managing cardiac patients.4

Cardiologists may deal expertly with cardiac-related problems but are

less inclined to address other coexisting complex medical issues.

Generalists manage a significant portion of subspecialty patient care, as

well as many of the other complex problems these patients experience.

There are few general internists who would suggest that they have the

full expertise of a particular subspecialist; however, the majority of

disease states are effectively managed by general internists. For the

above-mentioned CCS ad hoc committees to suggest that you need a

cardiologist to manage conditions such as heart failure is simply

unfounded. Their arguments might speak more to the benefits of

multidisciplinary clinics in managing such chronic disease states.

Without question, we need more cardiology and other subspecialty

positions, but we also need many more GIM positions to sustain the

long-term delivery of health care in Canadian communities; otherwise,

our community hospitals may simply cease to function effectively as

referral centres.

Lengthening the training program for GIM has been proposed,

similar to changes made by Canadian cardiology training programs

over a decade ago. However, the recent CCS ad hoc report suggests that

they should now consider returning to the 2-year program for those

individuals desiring a community practice, and maintaining a 3-year

program for those desiring a university-based practice.4 An extended 5-

year GIM program might ultimately funnel residents toward a

university rather than a community-based practice. If adopted, it

should allow for the acquisition of further subspecialty skills that may

be useful in nonuniversity centres and be optional, rather than

mandatory.

General internists share the problems of an aging physician

population, the demographic shift with the baby boomers, and “elderly

Canadians living longer … with more complex medical problems.”4 We

too are severely understaffed. Do we need more subspecialty training

positions, or do we need to ensure that we train sufficient numbers of

general internists in the long term? Having more subspecialists at the

expense of general internists may serve larger communities and

university centres at the expense of smaller and medium-sized

communities. The point is not to diminish the obvious need for

subspecialists but, rather, to point out that generalists have a significant

role to play in a sustainable health care model.

Resource allocation and prioritization in medicine should consider

the current and future needs of university centres and, equally, the

sustainability of services in community hospitals. Major stakeholders

such as provincial health departments may need to exert greater fiscal

influence on training programs to meet their health care delivery needs.

It is also incumbent upon our profession, under the auspice of the Royal

About the AuthorPatrick Bergin is a community general internist working in Charlottetown, Prince Edward Island. He is an active member of

the CSIM executive and an examiner for the Royal College of Physicians and Surgeons.

Too Few Subspecialists: A Critical Shortage of General Internists!

A community internist’s perspectivePatrick Bergin, MD

Caring for chronic disease states consumes a growing proportion of

our health care resources. We know that there is a strong

association between diabetes, cardiovascular disease, and chronic

kidney disease. We proposed the creation of a dedicated clinic in our

community for the delivery of a patient-centred, multidisciplinary

program to help patients with these conditions. Critical elements in the

planning and implementation phases of the project are described. We

see this integrated model of care for the cardiovascular cluster of

diseases as perfectly suited to the skill set and values of the general

internist.

The NeedApproximately 80% of patients with diabetes die of a vascular event,

and as many as 30% of people with diabetes suffer from kidney disease.

The systemic response to this growth in chronic disease has been to

B e r g i n


College, and possibly with input from the Canadian Society of Internal

Medicine, the College of Family Practice, and the Canadian Medical

Association, to influence the allocation of our specialty resources in a

way that effectively serves our universal health care system. We need to

develop a balanced specialty resource plan and petition the government

for more residency positions based on patient and physician

demographic needs with supporting data. Simply presenting ad hoc

position statements or potentially biased opinions that state individual

group demands is not sufficient. There are expressed concerns that we

cannot afford health care delivery in Canada in its present format, and

promoting more, rather than less, subspecialization will likely increase

the cost of already unaffordable health care.

Issues for us to pursue in the future also include looking at the

benefits of alternate payment plans versus fee-for-service options,

improving on-call remuneration and working hours, attracting

residents to community rotations earlier in their training, and perhaps

most importantly, clarifying who we are and what we do across the

broad spectrum of our profession. There is a poor understanding by the

public, and therefore by our bureaucracy, of what an internist is and

does. Both medical and surgical general specialists are integral to

Canadian health care delivery and provide a strong foundation for our

health care system. With a calculated balance of generalists and

subspecialists, I believe we can sustain effective and efficient health care

for all Canadians.

References1. Petersdorf RG, Goitein L. The future of internal medicine. Ann

Intern Med 1993;119:1130–7.2. Canadian Medical Association. CMA Masterfile update April 2007;

www.cma.ca.3. The generation and gender shifts in medicine: an exploratory survey

of internal medicine physicians. BMC Health Serv Res 2006;6:55.4. Agarwala R. Too many patients, too few cardiologists to care? Can J

Cardiol 2006;22:901–2.

About the AuthorsTom Ashton is head of cardiology, Penticton Regional Hospital. Gerry Karr is medical director, Kidney Services, Interior

Health Authority, and championed the development of an integrated healthcare clinic. Bev Arsenault is past manager of

the Penticton Integrated Health Centre. Susi Wilkinson is current manager of the Penticton Integrated Health Centre.

Susan Cooper is a nephrologist at Penticton Regional Hospital. Nancy Serwo is director of Health Services for the South

Okanagan, Interior Health Authority. For information, contact [email protected].

develop disease-centred multidisciplinary programs (e.g., diabetes or

CKD clinics), each operating independently of one another. Most of

these programs are based on the Stanford Chronic Care Model. Usually,

patients with two or more of these conditions pay separate visits to two

or three clinics, resulting in duplicate investigations, conflicting or

redundant information, and considerable inconvenience. Yet, these

clinics have many similarities in operating systems and clinical goals

that offer great potential for improved efficiency and effectiveness

through an integrated patient-centred approach to care delivery.

The Opportunity In September 2003, clinical and administration leaders of British

Columbia’s Interior Health Authority met to discuss innovative

approaches to improve health service delivery. Among several

proposals, the integration of chronic disease management (CDM) was

Doing More with Less: Managing the Cardiovascular Cluster of Disease in an IntegratedHealth Care Clinic Tom Ashton, MD, Gerry Karr, MD, Bev Arsenault, RN, Susi Wilkinson, RD, Susan Cooper, MD, Nancy Serwo, RN

C o m m u n i t y G I M

D o i n g M o r e w i t h L e s s @ L R H


targeted as most likely to succeed, given strong existing programs and

clinical support for integration. The diabetes, heart, and kidney disease

cluster was regarded as best suited to the development of a pilot

program. From January through March 2004, a business case was

developed for the funding of an integrated CDM clinic in Penticton,

with the understanding that this would be initially limited to the three

diseases and carefully evaluated as a proof-of-concept initiative.

The PlanThe proposal called for the physical integration of clinics for the delivery

of multidisciplinary team–based care for these chronic disease patients.

Process integration would be implemented through centralized patient

reception, registration, and information management, and clinical

integration through cross-training of team members and harmonized

evidence-based clinical protocols. Patient intake was to be by physician

or self-referral for diabetes patients and by physician referral for kidney

and cardiac patients. General internists, cardiologists, and nephrologists

worked together in the clinic, seeing patients, carrying out chart

reviews, and participating in patient conferences. It was proposed that

this integrated approach would be more efficient and effective in health

care delivery, yet still supportive of patient self-care management

strategies.

Adoption: Process Was CriticalThis was an exercise in team building. Representatives from existing

programs came to accept ownership and the belief that this clinic model

offered their patients more. Key strategies included the appointment of

a physician leader and manager as co-chairs, the involvement of a

skilled facilitator, and the adoption of a set of guiding principles at the

outset. Around informal weekly lunch meetings over 3 months, a clinic

team was formed that took proud ownership of the concept of

integrated care. To other groups contemplating a similar cultural shift,

we would emphasize the importance of giving participants time to get

to know each other and the project at hand: patience has its reward.

Phase 1 Implementation: From Planning to OpeningIn space adjacent to the Penticton Regional Hospital, renovations began

in the fall of 2004 and were completed in the spring of 2005.

Concurrently, working groups of clerks, nurses, dietitians, social

workers, pharmacists, and physicians met to develop detailed plans

allowing for patient flow, education, and management. A cross-training

plan was also developed to allow skill transfer between the specialty

groups. The teams were committed to the use of evidence-based

protocols and to the development of an effective program supporting

patient education and self-management. Information technology and

business support services were used to develop an integrated

information management system and to incorporate the budgets of

three separate programs. The Penticton Integrated Health Centre (IHC)

opened its doors in June 2005. Its team members include a program

manager, clerical staff, nurses, dietitians, exercise specialists, a social

worker, a pharmacist, and physicians representing the clinical

disciplines, as well as a family physician liaison.

Phase 2 Implementation: From Opening to ImprovingIn the first year of operation, priorities were (1) to implement

improvements to various processes including referral, triage, and

development of detailed procedures for centre activities; (2) to develop

the information management system to include integrated

comprehensive scheduling and point-of-care clinical documentation

modules; and (3) to continue with ongoing cross-training of the

interdisciplinary team of professionals, with a focus on improving self-

management support competence.

In the period from April 1, 2006, to March 31, 2007, 2,104 individuals

accessed at least one service at the IHC (Table 1). As acceptance grew,

the percentage of local family physicians referring patients to the IHC

grew from 41 to 59% (2005–2006). Patients and families have

consistently rated their satisfaction with care at the IHC as high or very

high.

Table 1. Visits to the Penticton Integrated HealthCentre, April 1, 2006–March 31, 2007

Individual Phone Group TotalVisits Visits Visits

Diabetes 1,345 1,671 727 3,743Renal 1,740 1,121 188 3,049Heart 525 258 271 1,054NIC 120 53 19 192Total 3,730 3,103 1,205 8,038

Using information technology, we are able to compare process and

clinical outcomes with provincial and national data, thus assessing the

effectiveness of our care and participating in quality improvement.

Evaluation of the first 2 years of operation was scheduled for

completion in the summer of 2007.

The FutureFuture directions for the IHC include (1) exploring and testing new

ways to strengthen and support our primary health care system;

(2) increasing the number of family physician referring to IHC to 80%,

thus improving care and possibly offloading our local emergency

department; and (3) partnering with our municipality to offer

cardiopulmonary rehabilitation and health education services in their

recreation facilities. The IHC is currently participating in a Virtual

Learning Community with the Institute for Healthcare Improvement

and eight other U.S. sites. This 16-month project will demonstrate that

innovative, comprehensive, and effective self-management support can

be delivered in a community health setting.

This holistic and patient-focused approach to chronic care delivery

presents a wonderful opportunity for general internists to provide core

leadership in dissemination and implementation of a new paradigm in

health care delivery.

Bibliography Barrett-Connor E, Pyorala K. Long-term complications: diabetes,

coronary heart disease, stroke and lower extremity arterial disease.

In: Ekoe J-M, Zimmett P, Williams R, eds. The Epidemiology of

Diabetes Mellitus: An International Perspective. Chichester, UK:

John Wiley & Sons, Ltd.;2001:301–19.

Wagner EH. Chronic disease management: what will it take to improve

care for chronic illness? Effect Clin Pract 1998;1:2–4

W o m e n ’ s G I M


Type 2 diabetes is a well-established risk factor for cardiovascular

disease. Although the prevalence of type 2 diabetes does not differ

between men and women, type 2 diabetes confers a greater relative

increase in the risk for cardiovascular disease in women. In the Inter-

Heart study, for example, the presence of diabetes was associated with a

more than fourfold increase in the risk for myocardial infarction among

women and a 2.6-fold increase in risk among men. The reason for this

difference has not been clearly established. An examination of the

evolution of insulin resistance across the life span may provide some

insight.

Adolescence and PubertyType 2 diabetes is characterized by an increase in glucose levels resulting

from higher levels of insulin resistance. In an analysis of data from 1,802

adolescents without diabetes, girls were determined to have a higher

level of insulin resistance compared with boys, even with adjustment for

age and weight status.1 Consistent with this, a community-based study

from Britain detected a trend toward lower insulin sensitivity among

girls compared with boys,2 and a cross-sectional assessment for diabetes

among children and youth in Taiwan identified a higher prevalence of

diabetes among girls than boys (15.3/100,000 versus 9.0/100,000).3

In a cross-sectional study by Moran and colleagues,4 girls were

determined to be significantly more insulin resistant than boys even

after adjusting for body mass index (BMI), waist circumference, or hip

circumference (glucose uptake during insulin clamp 8.3 ± 0.2 in girls

versus 9.7 ± 0.2 in boys mg.kg-1.min-1, p < .0001). At the onset of puberty

(Tanner stages I and II), insulin sensitivity was lower than prior to

puberty in both boys and girls. At Tanner stage V, insulin sensitivity was

similar to the prepubertal period, suggesting that a decline in insulin

sensitivity during adolescence may be transient. Ball and colleagues5

followed 92 prepubertal children for at least 2 years, measuring their

insulin sensitivity throughout their development. Interestingly, as

observed by Moran and colleagues,4 in both boys and girls, insulin

sensitivity declined during Tanner stages I and early stage II, remained

stable during the latter part of II and stage III, and recovered to

prepubertal levels by Tanner stage V. However, Ball and colleagues did

not identify any boy-girl differences.5

It appears then that during pubertal development, insulin sensitivity

may decline temporarily. This reduction in insulin sensitivity may be

more marked among girls, but this issue requires further longitudinal

study. In both boys and girls, insulin sensitivity appears to recover

toward the end of the adolescent period.

Young and Middle Adulthood Most studies do not demonstrate a sex difference in the prevalence of

type 2 diabetes between men and women. However, women are

definitely more insulin resistant during pregnancy, which has been

described as a diabetogenic state characterized by the onset of significant

insulin resistance.1 While many women are able to maintain normal

glucose levels by increasing insulin production, others experience a rise

in glucose levels termed gestational diabetes mellitus (GDM), defined as

glucose intolerance that is first detected during pregnancy.6 Up to 50%

of women diagnosed with GDM will develop type 2 diabetes over the

following 20–30 years.1

GDM is associated not only with an increased risk of developing type

2 diabetes but also with increased risks for hypertension (20% versus

11% in non-GDM patients) and cardiovascular disease.7 In a cross-

sectional study by Carr and colleagues,8 women with a history of GDM

were at an increased risk of developing cardiovascular disease (OR 1.56,

95% CI 1.0–2.43) even after adjustment for ethnicity, age, menopausal

status, and the presence of type 2 diabetes.

Later Adulthood and Post-MenopauseInsulin resistance is a defining feature of metabolic syndrome, a cluster

of metabolic abnormalities associated with an increased risk for

cardiovascular disease. As a result of increased prevalence of

overweight, over the past 20 years the prevalence of the metabolic

syndrome in the United States has increased in both men and women,

but it appears to be rising more significantly among women. In the

1999–2000 National Health and Nutrition Examination Survey

(NHANES), the prevalence of metabolic syndrome was higher among

women than men (39.7% in men versus 46.1% in women), although

this difference was not statistically significant. The age-adjusted

prevalence in women also increased by 23.5% (p = .021) between the

1988–1994 and 1999–2000 NHANES data, while the corresponding

increase in prevalence in men was minor and not statistically significant

(2.2%, p < .831).9

About the AuthorsNoemie Chessex is with the Division of Internal Medicine at McGill University Health Centre. Kaberi Dasgupta is with the Divisions of Internal

Medicine and Clinical Epidemiology, Department of Medicine, McGill University Health Centre. Correspondence may be directed to

[email protected].

Greater Impact of Diabetes on Vascular Risk in Women:Memories of Pregnancy and Puberty?Noemie Chessex, MD, Kaberi Dasgupta, MD

G r e a t e r I m p a c t o f D i a b e t e s o n V a s c u l a r R i s k i n W o m e n


DiscussionSeveral studies suggest that insulin sensitivity declines during puberty

in both girls and boys but recovers prior to adulthood. There is some

evidence, however, that the decline in insulin resistance during puberty

is more marked among girls compared with boys. During young and

middle adulthood, although men and women have a similar prevalence

of insulin resistance and type 2 diabetes, women who become pregnant

experience a reduction in insulin resistance during pregnancy, a

physiological change that facilitates the nourishment of the fetus. In

some women, this diabetogenic state during pregnancy may lead to

GDM, which is associated with increased risk for hypertension, type 2

diabetes, and cardiovascular disease postpartum. The presence of

diabetes in older women confers a greater relative increase in the risk of

cardiovascular disease than among men. NHANES data suggest that the

prevalence of metabolic syndrome is rising faster among older women

than among older men, in the context of the rising prevalence of

overweight.

We speculate that the greater impact of diabetes on cardiovascular

risk among women compared with men may partly be attributable to

the impact of a reduction in insulin sensitivity – and its associated

changes – that women with type 2 diabetes likely experience during

pregnancy and/or puberty prior to the diagnosis of type 2 diabetes. Our

hypothesis stems from the established importance of disease duration

and control. Longer periods of exposure to vascular risk – whether to

type 2 diabetes, hypertension, or metabolic syndrome – are more likely

to lead to vascular injury. The presence of insulin resistance is associated

with a variety of metabolic abnormalities (e.g., endothelial dysfunction,

a procoagulant state, inflammation). Assuming that both intermittent

and sustained exposures to a “metabolically abnormal” environment

have deleterious impacts on vascular health, among women who

develop type 2 diabetes, previous episodes of insulin resistance during

puberty and pregnancy may exert an additive impact to that associated

with type 2 diabetes itself. In contrast, men with type 2 diabetes may be

less likely to have had similar “metabolic past experiences.”

A similar theory has been put forward to explain the results of the

follow-up study of the Diabetes Complications and Control Trial

(DCCT). Among patients with type 1 diabetes, DCCT demonstrated

that randomization to tight glycemic control is associated with a lower

incidence of microvascular disease. The Epidemiology of Diabetes

Interventions and Complications study (EDIC), the follow-up study to

the DCCT, demonstrated persistent vascular benefits among subjects

who were initially randomized to the intensive glycemic control group

compared with the subjects in the conventional treatment group,

although there was no significant difference in degree of glycemic

control following the DCCT intervention itself. This suggested that

early metabolic control could significantly influence the progression of

diabetes-related complications. The metabolic memory hypothesis

argues that the prolonged impact of the early metabolic environment

preceding the overt manifestation of diabetes is pivotal in the

development of macrovascular and diabetes-related complications.10

GDM is a risk factor for type 2 diabetes in women. At least one study

has suggested that even among women with type 2 diabetes, a previous

history of GDM confers an increased risk for the development of

cardiovascular disease.8 We speculate that women who eventually

develop type 2 diabetes are likely to have experienced episodes of

marked elevations in insulin resistance either during puberty or

pregnancy, although marked increases in glucose levels may not have

occurred. We suggest that these episodes of insulin resistance may have

an adverse impact on vascular health, further worsened by the

recurrence of insulin resistance later in life, and an eventual diagnosis of

type 2 diabetes. As a result, the relative impact of type 2 diabetes on the

likelihood of cardiovascular disease is greater among women than

among men. While these ideas require further study and confirmation,

the clinical implication is that for women to realize the “sex protection”

from cardiovascular disease that they enjoy as a group, it is important

for them to control their weight and remain physically active, perhaps

particularly during puberty and pregnancy.

References1. Lee AJ, Hiscock RJ, Wein P. Gestational diabetes mellitus: clinical

predictors and long-term risk of developing type 2 diabetes.Diabetes Care 2007;30:878–83.

2. Ehtisham S, Crabtree N, Clark P, et al. Ethnic differences in insulinresistance and body composition in United Kingdom adolescents. JClin Endocrinol Metab 2005;90:3963–9.

3. Wei JN, Sung FC, Lin CC, et al. National surveillance for type 2diabetes mellitus in Taiwanese children. JAMA 2003;290:1345–50.

4. Moran A, Jacobs D, Steinberger J. Insulin resistance during puberty.Diabetes 1999;48:2039–44.

5. Ball GDC, Huang TTK, Gower BA. Longitudinal changes in insulinsensitivity, insulin secretion, and b-cell function during puberty. JPediatr 2006;148:16–22.

6. Kjos SL, Buchanan TA. Gestational diabetes mellitus. N Engl J Med1999;341:1749–56.

7. Hollander MH, Paarlberg KM, Huisje AJM. Gestational diabetes:review of the current literature and guidelines. Obstet Gynecol Surv2007;62(2):125–35.

8. Carr DB, Utzschneider KM, Hull RL. Gestational diabetes mellitusincreases the risk of cardiovascular disease in women with a familyhistory of type 2 diabetes. Diabetes Care 2006;29:2078–83.

9. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of themetabolic syndrome among U.S. adults. Diabetes Care2004;27:2444–9.

10. LeRoith D, Fonseca V, Vinik A. Metabolic memory in diabetes: focuson insulin. Diabetes Metab Res Rev 2005;21(2):85–90.

E K G & U

Apreviously healthy 36-year-old man was admitted to hospital with

syncope. Telemetry monitoring (Figure 1) revealed a

tachyarrhythmia that correlated with palpitations, shortness of breath,

chest discomfort, and lightheadedness. What is the diagnosis?

Figure 1 is a two-lead rhythm strip where the top tracing corresponds

to lead 1 and the bottom tracing corresponds to lead V1. The tracing in

lead V1 has been clipped. This regular tachycardia has a wide QRS

complex with a left bundle branch block (LBBB) pattern for the first six

beats, and then a narrow QRS complex. The rate of the wide complex

tachycardia is approximately 170 beats per minute, while the rate of the

narrow complex tachycardia is approximately 200 beats per minute.

The first narrow complex beat occurs at precisely the time that a wide

complex beat would have been expected. The differential diagnosis

includes two different tachyarrhythmias (e.g., ventricular tachycardia

followed by a more rapid supraventricular tachycardia), or

supraventricular tachycardia (SVT) with functional LBBB aberrancy

that disappears.

It would be quite a coincidence for an SVT to initiate and begin

depolarizing the ventricles at the same instant that the preceding VT

would have been expected to do so. Furthermore, the most

parsimonious diagnosis is SVT with LBBB aberrancy that disappears;

but why would the left bundle start conducting just as the tachycardia

suddenly accelerates? The answer lies in the fact that the left bundle can

participate in the SVT mechanism.

Orthodromic atrioventricular reciprocating tachycardia (AVRT) is a

common type of SVT where the reentrant circuit involves

atrioventricular (AV) conduction over the usual AV conduction system,

conduction through ventricular myocardium to the base of the heart,

ventriculoatrial conduction over an accessory pathway (AP), and, to

finally complete the circuit, conduction through atrial myocardium

back to the AV conduction system. The rate of this SVT is determined

by the time it takes the tachycardia wavefront to make one revolution

around the complete circuit.

Consider a left-sided AP (the most common location of APs). When

the left bundle does not conduct (LBBB), the tachycardia wavefront

reaches the ventricle via the right bundle. The tachycardia wavefront

must then cross the septum and travel all the way to the base of the LV

to reach the AP (Figure 2, left). When the left bundle finally

accommodates, the tachycardia wavefront reaches the ventricle via the

About the AuthorGeorge Veenhuyzen is an adult cardiac electrophysiologist at the Libin Cardiovascular Institute of Alberta in Calgary. He is

interested in the diagnosis and management of all arrhythmias, particularly using catheter ablation.

Two for One, or One for All?George Veenhuyzen, MD


Figure 2. Left, An atrioventricular reciprocating tachycardia circuit involving aleft-sided accessory pathway during left bundle branch block. Right, Thesame tachycardia mechanism but without left bundle branch block. Thecircuit in the right image is shorter, so the rate of the tachycardia increasesinstantly after the left bundle begins conducting.

Figure 1. Telemetry monitoring of a 36-year-old man admitted to hospital with syncope. See text for details.

V e e n h u y z e n


The Canadian health care system is experiencing huge external

pressures as it changes its focus from the delivery of catastrophic

care to chronic disease management. General internal medicine (GIM)

is the key player in this transformation and will develop into the core

specialty of most hospitals. The subspecialty programs that many

institutions pride themselves on depend on a functional and well-

organized GIM presence to provide comprehensive care to patients with

multisystem illness. Internists must work with hospitals, the Ministry of

Health, and the public to create positive change for the system, even

though this process is difficult.

GIM at the University Health Network (UHN) in Toronto has rapidly

emerged as a key focus of senior management over the past year

through the Emergency Department – General Internal Medicine (ED-

GIM) Redesign project. This commentary explores the process of

reprioritization and reflects lessons learned in this rapidly changing

environment.

Initiating a New Perspective: GIM Is the Core Businessof Hospitals The UHN is one of the largest academic health science centres in

Canada, with an operating budget of over $850 million dollars.1 The

hospital has a bold vision statement of global impact and, for the past

decade, has focused on the high-profile programs of transplantation,

cancer, cardiac disease, neuroscience, and musculoskeletal health. Each

of these programs has large operating budgets and well-developed

research platforms, with extensive financial support from well-funded

foundations. Although GIM cares for the largest volume of in-patients,

contributes the most hours to medical education, and is one of the most

successful research divisions, it remained largely unnoticed within the

larger program grouping of community and population health (along

with family medicine, mental health, women’s health, and emergency

medicine).2

In the new Ontario health landscape, Local Health Integration

Networks (LHINs) were created to facilitate a regional model of health

care delivery, governance, and funding. The LHIN structure created

accountability agreements to set benchmarks for delivery of service

from the hospitals. Common case mix groupings (CMGs) were

established in the accountability agreements, of which a large number

fell into GIM diagnostic categories. The accountability agreements, in

conjunction with a focus on emergency room wait times, created a

strong external pressure on the hospital. As environments undergo

rapid change and shifting accountabilities, there is a tendency for

physicians and departments with a lower profile to hide and to protect

existing positions. We took a different approach and engaged the

hospital leadership in an attempt to communicate the strategic

importance of GIM. We chose to change our message from discussions

revolving around patient care and the needs of our population to the

importance of GIM in maintaining the organization’s profile, and

meeting its vision of global impact. After careful analysis provided in

part by the GIM Division, the hospital leadership embarked on a project

to transform the role of GIM in the ED.

Living the ED-GIM Tool Kit: Walking the TightropeThe UHN in partnership with North York General Hospital engaged the

About the AuthorsDante Morra is the clinical teaching unit director at the Toronto General Hospital for the University

Health Network in Toronto. Howard Abrams is the division head, General Internal Medicine, for the

University Health Network and Mount Sinai Hospital in Toronto.

P r o f e s s i o n a l D e v e l o p m e n t

Prioritizing General Internal Medicine in a Large Academic Medical Centre:The “ED-GIM Redesign” ExperienceDante Morra, MD, Howard B. Abrams, MD

left bundle and has a much shorter distance to travel to reach the

ipsilateral AP (Figure 2, right). Hence, the tachycardia accelerates

immediately after the LBBB disappears. Thus, the acceleration of a

tachycardia with the loss of functional bundle branch block (and vice

versa) implies a diagnosis of AVRT using an AP that is ipsilateral to the

blocked bundle. With the exception of a dual tachycardia, this

observation is diagnostic of AVRT.

SVT commonly produces symptoms of palpitations, light-

headedness, chest discomfort, and shortness of breath in individuals

who are otherwise completely healthy. Syncope is certainly possible but

less common, and should at least prompt the consideration of other

causes. The mechanism of syncope may include hypotension due to a

corresponding drop in cardiac output (note the hypotension recorded

at the top of the telemetry strip) or a neurally mediated vasodepressor

response. Catheter ablation is considered first-line therapy that is

offered on par with medical therapy for AVRT. This man has had no

recurrent symptoms more than 3 years after successful catheter ablation

of a concealed left lateral AP.

P r i o r i t i z i n g G I M i n a L a r g e A c a d e m i c M e d i c a l C e n t r e @ L R H


Brand Recognition: GIM as the Core Business of HospitalsGIM has an identity problem, especially at our “quaternary care”

organization. A disease, an organ, or a technology associated with a

subspecialty is relatively easy to create an identity around, but GIM

cannot be defined in simple terms. GIM operates and delivers care in a

complex environment. We are dealing with the new realities of future

health care delivery. Although we provide the largest volume of in-

patient care and support every other subspecialty program, we had a

great deal of difficulty explaining what we do and how important GIM

is for the organization. In fact, prioritizing GIM depends on senior

management understanding what we have to offer. Hence, we have to

understand what the institution needs and work together to solve

common problems.

Teamwork As physicians, we often approach problems from a truth knower

perspective, believing we are experts on everything that takes place in

our units. This can limit our ability to learn from highly sophisticated

project managers and corporate strategic thinkers. It is important to

keep an open mind and consider different approaches to common

problems.

Risk TolerancePhysicians need to take on risk in making changes to the health care

system, recognizing that these initiatives could fail. We have to

acknowledge that the best decisions may come from a team approach

rather than individual enterprise.

ConclusionIt is imperative that GIM take an active role in shaping the process of

health care delivery to meet future needs. Internists, armed with their

complex problem-solving skills and multisystem approach to care, are

uniquely suited to help enable systematic change. GIM leaders must

make an effort to understand what issues and challenges their

organization or regional units face in the short to medium term, and to

communicate the important role our specialty has. Internists must

convince their administrators that, as large stakeholders and skilled

problem solvers, we have the ability to bring about successful change. By

telling health care planners who we are, what we do, and what we are

capable of, we can develop a mutually beneficial partnership to improve

the delivery of care in hospitals everywhere.

AcknowledgementsWe would like to acknowledge Michael Baker, Catherine Zahn, and Bob

Bell for their tremendous leadership in helping to transform GIM at the

UHN, as well as Kumanan Wilson for the suggestion to write up our

experience and share the ED-GIM project with our colleagues.

References1. UHN Facts. Retrieved April 16, 2007, from

http://www.uhn.ca/About_UHN/corporate_info/index.asp.

2. UHN Program Structure. Retrieved April 16, 2007, from

http://www.uhn.ca/About_UHN/programs/index.asp.

Ontario Ministry of Health and Long-Term Care (MOHLTC) in

creating a project to deliver operational improvement through the ED-

GIM patient care axis. The goal was to create a “tool kit” of

interventions that could be used by other hospitals. As this project was

accepted, GIM was vaulted from isolation to a primary focus of the

hospital with a large project management office to support this change.

Senior management attended town hall meetings, the chief executive

officer toured the wards, and the hospital news section had features on

GIM. Consultants were brought in and, through a dizzying series of

meetings, the organization began to create interventions that could be

piloted and tested. After years of low visibility in the hospital’s strategic

planning process, it was refreshing to see the enhancement of GIM now

become a priority of senior management and the hospital board.

As physician leaders, we were aware that the project team’s short-term

focus on the tool kit would not create a solution. We felt it was

important to use this window of opportunity to establish a longer-term

transformation focus. As clinical leaders, we knew this would translate

into walking a tightrope of present and future trade-offs. It further

creates a tension of managing risk of failure through the speed of

change. There is a constant negotiation process that takes place while

navigating this narrow path; one must remain positive, engaged, and

helpful in creating interventions but provide constant cautions as to

why short-term interventions might not work in the current

environment. The attention is a real opportunity for change, but it is

risky because we know the problems are difficult to solve. How does one

provide the truth that is necessary for real change but by its very nature

might scare off the attention being provided? This became an awkward

courting process in which we attempted to create small operational

wins while introducing the hospital and the project teams to the real

deep-seated, systemic problems.

Where We Stand Today: Lessons LearnedThe tool kit was delivered to the MOHLTC in February 2007. There

were 30 documented interventions implemented in a whirlwind 8-

month period. The teams created to develop these interventions were

composed of project managers, an interprofessional group of clinicians,

performance measurement team members, and several high-level

administrators. The interventions ranged from new models of care

delivery to sophisticated electronic bed-tracking applications. The

interventions were measured through general hospital metrics (e.g.,

length of stay) and other more focused operational metrics (e.g., time

to clean bed from discharge). Some of the interventions required

minimal resources (e.g., preprinted admission order sets in the ED),

and others were complicated and were resource intensive (e.g., best

practice implementation of health care staffing – corrected for acuity

and workload). The GIM environment has certainly improved, but we

are far from the real transformation GIM requires. The emergency

room is still full of GIM patients, and GIM still has the organization’s

attention. Although the organization is committed to a multiyear

transformation, some project teams are beginning to move away. There

is a concern that GIM could drift back to its previous position as an

underrepresented service in a large specialized hospital.

Some key lessons learned from the ED-GIM process involve brand

recognition, teamwork, and risk tolerance.


S p e c i a l C o m m u n i c a t i o n

On Saturdays, at the military base in Kandahar, merchants come to

do business. They line up outside the gates before dawn, to be

registered and photographed by the military police. Even the 7-year-old

boys, who hock magnets for a dollar, need a photo ID. Hundreds of men

and boys who come out here to sell carpets, DVDs, clothing, and

antique rifles are searched by security and sniffed by their dogs. Dogs

are unclean to Muslims, and no one supposes that this is well received

by the merchants. Nevertheless, in the past 5 years, there have been no

bombings at the Saturday bazaar. This is in contrast, it seems, to every

market in Baghdad.

I went to Kandahar for 7 weeks this spring to work as a civilian

internist at the Role 3 hospital there. On Saturdays that didn’t feature

casualties coming in from the field, nearly the entire hospital staff went

to the market to buy carpets and chess sets and polished lapis lazuli. The

men and boys there – this is traditional Pashtun country and the

women are sequestered – exhibited a dignified solemnity with which

they called to passersby, displaying not a sign of the obsequious

desperation of street vendors in other less desperate places. Among the

carpet vendors, this was easy to understand. The muted crimsons of the

Mazaar-i-Sharif carpets and the almost New Mexican patterns of the

Bamiyahns – “You know Bamiyah, sir? Where the giant stone Buddhas

were blown up? Yes, very sad, sir” – were unlike anything anyone who

grew up conceiving of the word “shag” as the natural modifier of the

noun “carpet” could have been prepared for.

From a tower perch high above, a well-armed soldier eyes the scene

carefully. Every couple of weeks, rockets are shot into the compound,

serving as reminders of the war that percolates all around. Soldiers cycle

in and out of the base. The Canadian Combat Group comprises most of

those who venture into the hinterland of Kandahar, and the infantry

come in every 3 weeks or so for showers and rest. They and the Afghan

National Army soldiers comprise most of the uniformed casualties at

the hospital, though there are Dutch, British, Jordanian, Estonian, and

Danish soldiers on the base as well. Otherwise, it is the police and

civilians, a third of whom are children, who are burned or mined or

shot in crossfire. The market is a welcome relief from the business of

repairing these shattered boys and men and girls. Its colour and the

vibrancy are striking contrasts with the dusty gravel and air of military

tedium that otherwise dominate the base.

If the Saturday market proves insufficient for your needs, there is also

a Sunday market in the Special Forces compound. But the market and

the compound itself serve as adjuncts to the rest of the base. The Special

Forces personnel – almost entirely American – stick largely to

themselves, and it is not possible to enter their compound except on

business on any other day. You’ll see them in the DFACs, the huge

dining facilities run by Kellog Brown Root, but they sit only with one

another and any attempt to engage them in conversation will be

defeated by taciturn disdain. It isn’t clear why they open their

compound to operate their market, but the most tenable hypothesis, in

my view, is that they use it to reward Afghans who have helped them.

No one in uniform will say anything definitive about this.

I enjoy their Sunday market. It is smaller and the selection is worse,

but walking through their compound lends one the sense of being a

palace thief, an interloper in a forbidden place. Though the merchants

there are ready to engage in conversation, the Special Forces people are

no less mute than they are at supper. They nod, and flex, and observe

closely. They do not speak. This is in dramatic contrast to everyone else

About the AuthorKevin Patterson is an internist and author in Nanaimo, British Columbia. He has co-edited Outside the Wire: The War in

Afghanistan in Words of Its Participants, which will be published by Random House Canada in December 2007. The current

article is adapted from an article by Patterson that was first published in The New York Times.

An Internist’s Eye on KandaharKevin Patterson, MD

A n I n t e r n i s t ’ s E y e o n K a n d a h a r

in the facility, especially the Australians and the American regular army

soldiers, who will talk to you until your ears buzz. Fifteen months at a

stretch, the Americans are doing now. No wonder they’re keen to talk to

someone new.

One of the things the Special Forces do is mentor Afghan National

Army formations. These men grow luxuriant beards and carry AK-47s

and wear traditional clothing convincingly enough that when they

speak, in English, in flat mid-Western accents that could as easily be

overheard in line at the Piggly-Wiggly, anyone who doesn’t do a double

take should really be a poker professional. Walnut-coloured skin, rigid

postures, and utterly immiscible in the unbelieving ferenghie all around

them, they seem only as foreign as they really are.

I saw the pose break twice. The first time was when an SF sergeant

came in with an Afghan National Army casualty. The purpose of his

presence there was to ensure that his colleague would receive the best

possible care. When it became clear that this was the case, he told me

how his injured friend had run at the men who had ambushed them,

firing his rifle and yelling, so disconcerting their attackers that the

ambush turned into a rout of the attackers themselves. “You’ve never

seen heart like that,” he said. I nodded. Then it was as if he realized how

many words he had just said in a row and closed his mouth. He nodded

and lifted his AK and walked away.

The other time was when a Chinook CH 47 crashed in the mountains

with a Special Forces platoon on board. There were eight dead on the

site, and another 15 critically injured. The wounded were brought to us,

nearly frozen and exsanguinated after a 6-hour extraction time. That

day was mad, every surgeon and anesthetist on a constant sprint, and

the ICU full, blood everywhere. We emptied the blood bank and had to

activate the walking blood bank. Soldiers lined up outside the hospital

a hundred deep to donate; none of the wounded who arrived with a

pulse left without one.

I remember running to pick up another armful of blood bags. As I

came around a corner, I passed two very young soldiers who recognized

one another from the carnage and relayed to one another who had been

killed. Frozen looks and sobbing.

That Saturday’s market was particularly welcome.


M e d E d

Providing Feedback: An Effective Use of Teaching Time?Michelle Elizov, MD

About the AuthorMichelle Elizov is an assistant professor of medicine at McGill University and is the Jewish General Hospital site director of

the Internal Medicine Residency Training Program. She has completed a master’s degree in medical education and is a

member of the Centre for Medical Education at McGill, as well as a member of the Faculty Development committee. Her

interests are medical education and eating disorders.

General internists are often at the heart of much of the teaching that

goes on in our various practice settings. Through our frequent

interactions with learners, we have come to recognize the importance of

well-structured teaching as a means of effectively sharing our

knowledge and skills. We also recognize that the provision of feedback

is required as part of the teaching process. In fact, giving feedback is a

crucial part of the learning process. Providing well-structured feedback,

even informally, can enhance the learning experience, making it much

more effective without necessarily taking up more time.

How many times have you heard students or residents complain that

they didn’t get any feedback during an entire rotation? And how many

times have you scratched your head and said to yourself, “Well, of

course I gave him feedback!” Part of the problem with this all-too-

common scenario is that, unless the learners hear the words “I am now

going to give you some feedback,” they often do not recognize that they

are getting constant feedback. This usually highlights the difference

between summative and formative feedback.

Summative forms of feedback are, unfortunately, what tend to

preoccupy our learners. This type of feedback is often given at the end

of a rotation and indicates whether the learner has been successful. It is

an evaluation that determines if the learner has met the predetermined

expectations, such as the examination given at the end of the course that

determines the final grade for that course.

Formative feedback is evaluation that is ongoing with the intent of

providing the learners with information or guidance required for

appropriate modification of their performance. The emphasis is on the

provision of information rather than a judgment of performance. This

is the day-to-day verbal commentary on such things as the presentation

of a differential diagnosis or the successful insertion of a central line.

Viewed in this way, it then becomes clear how this feedback is really just

E l i z o v


another form of teaching. When done in partnership with the learners,

feedback promotes active learning.

Like the scenario described above, in many cases the learners are

correct: no feedback or only superficial positive feedback is given. Why

does this happen when feedback is clearly a powerful teaching tool?

There may be concerns that the feedback will have effects beyond its

intent, for both the teacher and the learners. The teacher may be afraid

of hurting the learners’ feelings or crushing their enthusiasm, or may

worry that providing “negative” feedback will damage the relationship

with the learners, leading to decreased effectiveness of the teacher in the

future. The learners may misconstrue the negative feedback as a

personal commentary, rather than a comment on their performance.

However, by avoiding giving proper feedback, we might create an

environment where mistakes are not corrected; learning occurs by trial

and error, and summative evaluations, such as written examinations,

take on inflated importance as learners may feel that these are the only

way to measure their abilities.

Given these concerns, how to give effective feedback becomes an

increasingly important question. Some basic principles of providing

feedback are outlined here. The “trick” is to apply these principles in the

context of our busy lives, making it an automatic part of our teaching

process, while remaining conscious of the subtleties of the language we

use to express our observations.

The following detail what feedback should be.

1. Expected by the learners. This is easier to understand in the

context of more formal feedback given halfway through a

rotation, for example. But if we learn to give feedback regularly,

it becomes expected and often even sought out by the learners,

which further enhances the active learning process. Unexpected

feedback, especially if it’s negative, will almost always be met

with an emotional response.

2. Timely. Ideally, feedback should take place at the time of the

observed event or soon thereafter while things are still fresh in

your mind. This may not apply if emotions (the learner’s or

yours) are running high; in this case, a “cooling off” period is

needed, but keep notes of your observations of the event for

future use.

3. Objective and specific. This is where language becomes so

important. The feedback should be given on what you have

observed, not second-hand information, and should address

modifiable behaviours rather than subjective interpretations of

intent or personality style. For example, to say, “I noticed you did

not keep eye contact with the patient,” might be more useful

than “You are too shy with patients.” Or, “You were late three

times this week for teaching rounds” might be more helpful than

“Your organizational skills need to be improved.”

4. Regulated. Giving too much information at one time will

overwhelm the learners, who will then disregard everything

rather than try to sift through and pull out the two or three

things felt to be most important. Equally undesirable would be

that the learners pull out the points they feel are most pertinent,

not the ones you believe are most important. The learners may

also pay attention only to points that confirm their own

impressions, which may not be accurate.

5. Balanced. Giving negatives without positives may seriously

undermine the learners’ confidence; but, positives without

negatives may lead to overconfidence and the pitfalls inherent to

that. Frequent superficial positive praise, such as “You’re

excellent!” may lead to the implication that the people, not their

work, are being assessed.

6. Given in a nonjudgmental manner. If you say, “That differential

diagnosis was completely inadequate,” your learner will shut

down and not really hear anything further, no matter how valid

the teaching point. It may be more helpful to say, “Your

differential diagnosis included only three items, one of which is

highly unlikely, and did not include these common problems …”

7. An opportunity for self-reflection and development ofalternatives. Using open-ended questions such as: “What do you

think went well?” “Where do you think you can improve?” or

“How do you think you can do that differently next time?”

encourages active learning, where the learners participate in

identifying strengths and deficiencies and in the development of

learning strategies in the context of their own previous

experiences and perspectives. The advantage of this is that the

learners will be able to better integrate the new information into

their own conceptual frameworks, which will make it easier to

use again in future situations.

8. Structured. Like any good teaching method, there is a beginning

(“Let’s go over how that line insertion went”), a middle, where

the observed behaviours are discussed (“I noticed that you …”),

and an end, where a plan of further action is developed with the

learners and preferably by the learners themselves (“Next time, I

think I’ll try …”). Ideally there would also be a follow-up, where

you have an opportunity to observe a similar clinical scenario

again and can link the previous feedback to the current situation.

ConclusionWhile trying to incorporate all the above points and concepts may seem

daunting in the 3 minutes you may have between cases, it is important

to realize that providing feedback effectively is, like much of what we do

in medicine, a learnable skill. It will initially take a very conscious effort

to recognize the opportunities in your interactions to provide feedback

and then to structure it and deliver it in a format that will be well

received and useful. However, as you repeatedly engage in this teaching

moment, you will find that the process becomes more fluent, more

automatic, and hence faster, all the while retaining its purpose, which is

to help us help our learners become better doctors.

Bibliography Ende J. Feedback in clinical medical education. JAMA 1983;250:777–81.Frye AW, Hollingsworth MA, Wymer A, Hinds MA. Dimensions of

feedback in clinical teaching: a descriptive study. Acad Med1996;71:79–81.

Hesketh EA, Laidlaw JM. Scottish Council for Postgraduate Medical andDental Education. Developing the teaching instinct: feedback.http://www.nes.scot.nhs.uk/courses/ti/Feedback.pdf.

Kaprielian VS, Gradison M. Effective use of feedback. Fam Med1998;30:406–7.

Spickard A III. Words hard to say and hard to hear: “May I give yousome feedback?” J Gen Int Med 1998;13:142–3.


I m a g e s i n G I M

A19-year-old man underwent a heart transplantation in 2003. In

2006, following a routine cardiac biopsy, a right-sided cervical

fistula was detected by auscultation. A carotid duplex ultrasound

revealed evidence of turbulent flow in the lower part of the internal

jugular vein and vertebral artery at its junction with the subclavian

artery (Figure 1). A subclavian angiogram (catheter positioned in the

right brachiocephalic artery) illustrated a fistula arising from the

proximal portion of the thyrocervical trunk and entering the origin of

the brachiocephalic vein (Figure 2). The thyrocervical trunk arises at the

same level as the vertebral and internal mammary arteries. Clinical and

angiographic assessment prior to the closing procedure demonstrated

no evidence of any arteriovenous fistula. The fistula thrombosed on its

own (Figures 3 and 4), and the patient did not need further

intervention.

Clinical assessment of heart transplant patients undergoing routine

heart biopsies is paramount for establishing the presence of

arteriovenous abnormalities related to the procedure.

About the AuthorsAndy Ignaszewski is the chief of Cardiology at St. Paul’s Hospital, Vancouver, and medical director of

the Heart Function Clinic and Healthy Heart Program. Simona Bar is a clinical surgical associate in

the Division of Cardiac Surgery at Vancouver General Hospital in British Columbia.

Fistula post Heart BiopsyAndy Ignaszewski, MD, Simona Bar, MD

Figures 1–4. Fistula post heart biopsy in a patient who had undergone a heart transplantation. C = common carotid artery; F = fistula; I = internal thoracicartery; S = subclavian artery.

Figure 1

Figure 2

Figure 3 Figure 4


G u i d e l i n e s R e v i e w

The year 2007 marks the eighth consecutive year that the Canadian

Hypertension Education Program has updated recommendations

for the management of hypertension. This year we have focused on the

need to assess blood pressure in all Canadian adults and to regularly

assess blood pressure in those with high normal values. In addition, the

2007 recommendations support the increasing evidence that

hypertension can be prevented through public health interventions to

reduce dietary sodium.

New Key Messages Identified in the 2007Recommendations Adults with high normal blood pressure require annual blood pressure

assessment. One in five adult Canadians have high normal blood

pressure (130–139/85–89 mm Hg). Of those who are overweight and

have high normal blood pressure, 40% will develop hypertension

within 2 years and 60% will develop hypertension within 4 years.

Therefore, annual or more frequent assessment of blood pressure and

appropriate lifestyle interventions to prevent hypertension are

recommended for those with high normal blood pressure.

Reducing sodium in the diet of Canadians. Excess dietary sodium is a

significant cause of hypertension. Patients and the general public need

to be educated to select foods that are low in sodium (to aim for a

sodium intake <100 mmol/d), and the food sector needs to reduce the

sodium content of food either voluntarily or by regulation.

Other Important Recommendations for theManagement of the Patient with HypertensionAll Canadian adults need to have blood pressure assessed at all appropriate

clinical visits. Blood pressure increases with age such that 50% of

Canadians over age 65 years have hypertension. For those with normal

blood pressure at age 65, over 90% will develop hypertension within

their lifespan. To identify those with hypertension all adults require

ongoing assessment of blood pressure throughout their life.

Optimum management requires assessment of overall cardiovascular

risk. Over 90% of Canadians with hypertension have other

cardiovascular risks. Identifying and managing risk factors beyond

hypertension can reduce the overall risk of cardiovascular disease by

over 60% and can alter the blood pressure target (Table 1) and specific

classes of antihypertensive medications recommended (Table 2).

Lifestyle modifications are effective in reducing blood pressure and

cardiovascular risk. Hypertension can be prevented, blood pressure can

be reduced, and other cardiovascular risks are favourably impacted by a

healthy diet, regular physical activity, moderation in alcohol, reductions

in dietary sodium, and, in some, stress reduction (Table 3). Simple and

brief health care professional interventions markedly increase the

probability of a patient adhering to lifestyle changes.

Treat patients to the recommended targets to achieve optimum

cardiovascular risk reduction. Greater reduction in cardiovascular

disease is achieved by lowering the blood pressure to the stated targets

(see Table 1).

Combinations of therapies (both drug and lifestyle) are generally

necessary to achieve target blood pressures. Most patients require more

than one antihypertensive drug and lifestyle changes to achieve

recommended blood pressure targets. When using two drugs to lower

blood pressure, combinations of a beta-blocker, angiotensin-converting

enzyme (ACE) inhibitor or angiotensin receptor blocker produce less

than additive hypotensive effect.

Monitor patients whose blood pressure is above target at least every 2

months. To achieve blood pressure control, follow-up at short intervals

is required to both improve patient adherence and increase the intensity

of treatment.

Focus on adherence. Nonadherence to therapy is one of the most

important challenges to improving blood pressure control. Adherence

to therapy should be assessed at each visit; specific interventions can

improve adherence to therapy (Table 4).

2007 Canadian Hypertension Education Program Recommendations:The Short Clinical Summary – An Annual UpdateOn behalf of the Canadian Hypertension Education Program

Table 1. Target Values for Blood Pressure*

Condition Target (SBP/DBP mm Hg)

Diastolic ± systolic hypertension < 140/90Isolated systolic hypertension < 140Diabetes < 130/80Chronic kidney disease < 130/80

*It is recommended that normotensive adults with established cardiovascular diseasebe treated with an angiotensin-converting enzyme (ACE) inhibitor. Normotensive adultswho have had a stroke or transient ischemic attack should be treated with an ACEinhibitor and a diuretic.

Reproduced with permission of the Canadian Hypertension Education Program.

2 0 0 7 R e c o m m e n d a t i o n s @ L R H


Diastolic ± systolichypertension

Thiazide diuretics, beta-blockers,ACE inhibitors, ARBs, or long-acting calcium channel blockers(consider ASA and statins inselected patients)

Combinations of first-line drugs Beta-blockers are not recommended as initial therapy inthose over 60 years of age. Hypokalemia should be avoidedby using potassium-sparing agents in those who areprescribed diuretics as monotherapy. ACE inhibitors are notrecommended in Blacks. ACE inhibitors and ARBs areteratogenic and marked caution is required if prescribing towomen of child bearing potential.

HYPERTENSION WITHOUT OTHER COMPELLING INDICATIONS

Diabetes mellitus withnephropathy

ACE inhibitors or ARBs Addition of thiazide diuretics,cardioselective beta-blockers,long-acting calcium channelblockers or use an ARB/ACEIcombination

If the serum creatinine level is >150 mmol/L, a loop diureticshould be used as a replacement for low-dose thiazidediuretics if volume control is required.

Diabetes mellituswithout nephropathy

ACE inhibitors, ARBs,dihydropyridine CCBs, or thiazidediuretics

Combination of first-line drugs, orif first-line agents are nottolerated addition ofcardioselective beta-blockersand/or long-actingnondihydropyridine calciumchannel blockers

Albumin to creatinine ratio [ACR] < 2.0 mg/mmol in menand < 2.8 mg/mmol in women.

DIABETES MELLITUS

Angina Beta-blockers. ACE inhibitorsexcept in low-risk revascularizedpatients

Long-acting calcium channelblockers

Avoid short-acting nifedipine.

Prior myocardialinfarction

Beta-blockers and ACE inhibitors(ARBs if ACEI intolerant)

Long-acting calcium channelblockers

CARDIOVASCULAR AND CEREBROVASCULAR DISEASE

Heart failure ACE inhibitors (ARBs if ACEIintolerant), beta-blockers, andspironolactone

ARBs or hydralazine/isosorbidedinitrate (thiazide or loopdiuretics, as additive therapy)

Avoid nondihydropyridine calcium channel blockers(diltiazem, verapamil). Monitor potassium and renalfunction if combining and ACE inhibitor and ARB.

Isolated systolichypertension withoutother compellingindications

Thiazide diuretics, ARBs, or long-acting dihydropyridine calciumchannel blockers

Combinations of first-line drugs Same as for diastolic ± systolic hypertension.

Table 2. Considerations in the Individualization of Antihypertensive Therapy

Initial Therapy Second-Line Therapy Notes and/or Cautions

Left ventricularhypertrophy

ACE inhibitors, ARBs,dihydropyridine calcium channelblockers, diuretics (beta-blockersfor patients under 55 years)

Avoid hydralazine and minoxidil.

Past cerebrovascularaccident or TIA

ACE inhibitor/diureticcombinations

This does not apply to acute stroke. Blood pressurereduction reduces recurrent cerebrovascular events inpatients with stable past cerebrovascular disease.

Nondiabetic chronickidney disease withproteinuria

ACE inhibitors (ARBs if ACEIintolerant) diuretics as additivetherapy

Combinations of additional agents

Avoid ACE inhibitors or ARB if bilateral renal artery stenosisor unilateral disease with solitary kidney. Patients placed onan ACE inhibitor or an ARB should have their serumcreatinine and potassium carefully monitored.

Renovascular disease Similar to diastolic ± systolichypertension without compellingindications for other medications

Avoid ACE inhibitors or ARB if bilateral renal artery stenosisor unilateral disease with solitary kidney.

NONDIABETIC CHRONIC KIDNEY DISEASE

C a n a d i a n H y p e r t e n s i o n E d u c a t i o n P r o g r a m


Table 4. Strategies to Improve Adherence

Adherence can be improved by a multi-pronged approach:

1. Adherence to pharmacological and nonpharmacological therapy shouldbe assessed at every visit.

2. Simplify medication regimens using once-daily dosing of long-actingmedications, combination tablets, and medication compliance aids.

3. Tailor pill-taking to fit patients’ daily habits.

4. Encourage greater patient responsibility by encouraging monitoringhome blood pressure.

5. Coordinate with chronic disease management programs to improvemonitoring of adherence with pharmacological and lifestylemodification prescriptions.

6. Educate patients and patients’ families about hypertension and itstreatment.


AcknowledgementThis manuscript was written by Dr. N. Campbell with the assistance of

the CHEP Executive. The preliminary drafts were reviewed by

Drs. R. Feldman, A. Milot, R. Touyz, G. Tremblay, and R. Ward and

S. Matheson, RN.

Peripheral arterialdisease

Does not affect initial treatmentrecommendations


Avoid beta-blockers with severe disease.

Dyslipidemia Does not affect initial treatmentrecommendations


Global vascularprotection

Statin therapy for patients withthree or more cardiovascular riskfactors or with atheroscleroticdisease. Low-dose ASA in patientswith controlled blood pressure

Caution should be exercised if blood pressure is notcontrolled.

OTHER CONDITIONS

ACE = angiotensin converting enzyme; ASA = acetylsalicylic acid; TIA = transient ischemic attack.


Table 3. Lifestyle Therapy to Reduce the Possibility ofBecoming Hypertensive and to Reduce Blood Pressureand the Risk of Blood Pressure–Related CardiovascularComplications in Hypertensive Patients

1. Healthy diet: high in fresh fruits, vegetables, low-fat dairy products,dietary and soluble fibre, whole grains, and protein from plant sources;low in saturated fat, cholesterol, and salt in accordance with Canada’sGuide to Healthy Eating

2. Regular physical activity: accumulation of 30–60 minutes of moderateintensity dynamic exercise 4–7 days per week

3. Low-risk alcohol consumption (≤2 standard drinks per day and <14 perweek for men and <9 per week for women)

4. Attaining and maintaining ideal body weight (BMI 18.5–24.9 kg/m2)

5. A waist circumference of <102 cm for men and <88 cm for women.

6. Reduction in sodium intake to <100 mmol/d

7. A smoke-free environment


R e v u e d e l i g n e s d i r e c t r i c e s


2007 marque la huitième année consécutive de mise à jour des

recommandations pour la prise en charge de l’hypertension par le

Programme éducatif canadien sur l’hypertension. Cette année, nous

insistons particulièrement sur le besoin de mesurer la pression artérielle

de tous les adultes canadiens et de le faire de façon régulière chez les

personnes ayant une pression artérielle à la limite de la normale. En

outre, les recommandations de 2007 soutiennent les arguments plus en

plus probants qui montrent qu’on peut prévenir l’hypertension par des

interventions de santé publique visant à réduire la consommation de

sodium.

Voici les nouveaux messages clés desRecommandations 2007 :Les adultes ayant une pression artérielle à la limite de la normale doivent

subir une évaluation annuelle de leur pression artérielle. Au Canada, un

adulte sur cinq a une pression artérielle à la limite de la normale (de

130/85 à 139/89 mm Hg). Parmi les personnes qui présentent une

surcharge pondérale et une pression artérielle à la limite de la normale,

40 % développeront de l’hypertension d’ici deux ans et 60 % d’ici

quatre ans. C’est pourquoi on recommande aux personnes ayant une

pression artérielle à la limite de la normale de se prêter à une évaluation

annuelle ou plus fréquente de leur pression artérielle et d’apporter les

changements appropriés à leurs habitudes de vie afin de prévenir

l’hypertension.

Les Canadiens doivent réduire leur consommation de sodium. L’excès

de sodium dans l’alimentation est une cause majeure de l’hypertension.

Il faut enseigner aux patients et au grand public à choisir des aliments à

faible teneur en sodium et le secteur de l’alimentation doit réduire la

proportion de sodium dans ses produits, soit volontairement, soit par

contrainte réglementaire.

Voici d’autres recommandations importantes pour laprise en charge des patients atteints d’hypertension :Tous les adultes canadiens doivent faire mesurer leur pression artérielle à

toutes les visites appropriées. La pression artérielle augmente avec l’âge,

de sorte que 50 % des Canadiens de plus de 65 ans souffrent

d’hypertension. Parmi ceux et celles qui ont une pression artérielle

normale à 65 ans, plus de 90 % finiront par développer de

l’hypertension. Pour découvrir les cas d’hypertension, il faut

mesurer systématiquement la pression artérielle de tous les adultes,

tout au long de leur vie.

Pour une prise en charge optimale, il faut évaluer le risque

cardiovasculaire global. Plus de 90 % des Canadiennes et des Canadiens

atteints d’hypertension présentent d’autres facteurs de risque

cardiovasculaire. Si on décèle et prend en charge les facteurs de risque

autres que l’hypertension, on peut arriver à réduire de plus de 60 % le

risque global de maladie cardiovasculaire et à modifier la cible de

pression artérielle (tableau 1) et les classes de médicaments

antihypertenseurs spécifiques recommandés (tableau 2).

La modification des habitudes de vie est un moyen efficace de réduire la

pression artérielle et les risques cardiovasculaires. On peut prévenir

l’hypertension, réduire la pression artérielle et améliorer les autres

facteurs de risque cardiovasculaire en adoptant une alimentation saine,

en pratiquant une activité physique régulièrement, en modérant sa

consommation d’alcool, en réduisant l’apport de sodium dans son

alimentation et, pour certains, en réduisant son niveau de stress

(tableau 3). Par des interventions simples et brèves, les professionnels de

la santé peuvent accroître de beaucoup la probabilité que leur patient

observe ces changements d’habitudes de vie.

Pour réduire au minimum les risques cardiovasculaires, il faut traiter les

patients en vue d’atteindre les valeurs cibles recommandées. C’est en

abaissant la pression artérielle aux valeurs cibles établies (tableau 1)

qu’on arrive à une réduction maximale des maladies cardiovasculaires.

Des associations de traitements (médicaments et habitudes de vie) sont

en général indispensables pour atteindre les valeurs cibles de pression

artérielle. La plupart des patients ont besoin de prendre au moins deux

Recommandations 2007 du Programme éducatif canadien sur l’hypertension :Bref résumé clinique – Mise à jour annuelle Au nom du Programme éducatif canadien sur l’hypertension

Tableau 1 : Valeurs cibles de pression artérielle*

Affection Cible (PAS/PAD mm Hg)

Hypertension diastolique ± systolique < 140/90Hypertension systolique isolée < 140Diabète < 130/80Néphropathie chronique < 130/80

* On recommande d’administrer un inhibiteur de l’ECA aux adultes normotendus ayantune maladie cardiovasculaire établie. Aux adultes normotendus ayant subi un accidentvasculaire cérébral ou un AIT, il est recommandé de prescrire un inhibiteur de l’ECA etun diurétique.

AIT : accident ischémique cérébral.

Reproduit avec l’autorisation du Programme éducatif canadien sur l’hypertension.

P r o g r a m m e é d u c a t i f c a n a d i e n s u r l ’ h y p e r t e n s i o n


Hypertension diastolique± systolique

Diurétiques thiazidiques, bêta-bloquants, inhibiteurs de l’ECA,ARA ou bloquants des canauxcalciques à action prolongée(envisager l’AAS et les statineschez certains patients)

Association de médicaments detraitement initial

Les bêta-bloquants sont déconseillés en thérapie initialechez les patients de plus de 60 ans. Chez les patientsrecevant des diurétiques en monothérapie, il faut prévenirl’hypokaliémie en prescrivant des épargneurs de potassium.Les inhibiteurs de l’ECA ne sont pas recommandés chez lespatients de race noire.

HYPERTENSION SANS MALADIE COEXISTANTE

Diabète accompagné denéphropathie

Inhibiteurs de l’ECA ou ARA Ajout de diurétiques thiazidiques,de bêtabloquants cardiosélectifsou de bloquants des canauxcalciques à action prolongée ouassociation d’un ARA et d’un IECA

Si le niveau de créatinine sérique est >150µmole/L, il fautremplacer les diurétiques thiazidiques à faible dose par undiurétique de l’anse en cas de surcharge volumique.

Diabète sansnéphropathie

Inhibiteurs de l’ECA, ARA, BCC detype dihydropyridine oudiurétiques thiazidiques

Association de médicaments detraitement initial ou, en casd’intolérance aux médicaments detraitement initial, ajout debêtabloquants cardiosélectifs et(ou) de bloquants des canauxcalciques non dihydropyridiniquesà action prolongée

Rapport albumine/créatinine (RAC) < 2,0 mg/mmole chezles hommes et < 2,8 mg/mmole chez les femmes.

DIABÈTE

Angine Bêta-bloquants et inhibiteurs del’ECA, sauf chez les patientsrevascularisés à faible risque

Bloquants des canaux calciques àaction prolongée

La nifédipine à action brève est déconseillée.

Antécédents d’infarctusdu myocarde

Bêta-bloquants et inhibiteurs del’ECA (ARA en cas d’intoléranceaux IECA)

Bloquants des canaux calciques àaction prolongée

MALADIES CARDIOVASCULAIRES ET CÉRÉBROVASCULAIRES

Insuffisance cardiaque Inhibiteurs de l’ECA (ARA en casd’intolérance aux IECA), bêta-bloquants et spironolactone

ARA ou hydralazine/dinitrated’isosorbide (diurétiquethiazidique ou diurétique del’anse comme traitementd’appoint)

Les bloquants des canaux calciques nondihydropyridiniques (diltiazem, verapamil) sontdéconseillés. Si on administre un inhibiteur de l’ECA enassociation avec un ARA, il faut surveiller le niveau depotassium et l’activité fonctionnelle rénale.

Hypertrophieventriculaire gauche

Inhibiteurs de l’ECA, ARA,bloquants des canaux calciquesde type dihydropyridine,diurétiques (bêtabloquants chezles patients de moins de 55 ans)

L’hydralazine et le minoxidil sont déconseillés.

Antécédents d’accidentvasculaire cérébral oud’AIT

Association d’un inhibiteur del’ECA et d’un diurétique

Cette recommandation ne s’applique pas aux accidentsvasculaires cérébraux aigus. La réduction de la pressionartérielle diminue le risque de récurrence des évènementsvasculaires cérébraux chez les patients ayant desantécédents de maladie cérébrovasculaire stabilisés.

Hypertension systoliqueisolée sans maladiecoexistante

Diurétiques thiazidiques, ARA oubloquants des canaux calciquesde type dihydropyridine à actionprolongée

Association de médicaments detraitement initial

Même que pour l’hypertension diastolique +/- systolique.

Tableau 2 : Facteurs à considérer avant d’envisager de personnaliser le traitement antihypertenseurTraitement initial Traitement en Remarques et avertissements

deuxième intention

R e c o m m a n d a t i o n s 2 0 0 7 @ L R H


Tableau 4 : Recommandations pour améliorer

l’observation des ordonnances antihypertensives

On peut aider les patients à suivre leur traitement par une approche à volets

multiples :

1. Évaluer la fidélité aux traitements pharmacologiques et non

pharmacologiques à chaque consultation.

2. Simplifier la prise de médicaments en prescrivant des médicaments à

action prolongée à prendre une seule fois par jour ou des comprimés

associant plusieurs médicaments, et en employant des outils d’aide à

la prise de médicaments.

3. Prescrire sur mesure en tenant compte des habitudes quotidiennes des

patients.

4. Encourager les patients à prendre plus de responsabilités en les

incitant à mesurer leur pression artérielle à domicile.

5. Travailler de concert avec les programmes de gestion des maladies

chroniques afin d’améliorer le suivi des ordonnances

pharmacologiques et des modifications apportées aux habitudes de

vie.

6. Informer les patients et leur famille au sujet de l’hypertension et du

traitement.


Néphropathie chroniquenon diabétique avecprotéinurie

Inhibiteurs de l’ECA (ARA en casd’intolérance aux IECA),diurétiques comme traitementd’appoint

Association d’autres médicaments Les inhibiteurs de l’ECA et les ARA sont à déconseiller encas de sténose bilatérale des artères rénales ou de sténosesur un rein unique. Si on administre un inhibiteur de l’ECAou un ARA, il faut surveiller de près le niveau de créatinineet de potassium sérique.

Maladie rénovasculaire Même que pour l’hypertensiondiastolique +/- systolique sansmaladie coexistante requérantd’autres médicaments

Les inhibiteurs de l’ECA et les ARA sont à déconseiller encas de sténose bilatérale des artères rénales ou de sténosesur un rein unique.

NÉPHROPATHIE CHRONIQUE NON DIABÉTIQUE

Maladie artériellepériphérique

Aucune influence sur lesrecommandations de traitementinitial


Les bêta-bloquants sont déconseillés en cas de maladiegrave.

Dyslipidémie Aucune influence sur lesrecommandations de traitementinitial


Protection vasculaireglobale

Statines pour les patientsprésentant 3 facteurs de risquecardiovasculaire ou plus ouatteints d’une maladieathérosclérotique AAS à faibledose chez les patients dont lapression artérielle est maîtrisée

Il faut se montrer prudent si la pression artérielle n’est pasmaîtrisée.

AUTRES AFFECTIONS

ECA : enzyme de conversion de l’angiotensine; AIT : accident ischémique transitoire; ARA : antagoniste des récepteurs de l’angiotensine II.


Tableau 3 : Modifications des habitudes de viesusceptibles de réduire les risques d’hypertension,d’abaisser la pression artérielle et de diminuer lesrisques de complications cardiovasculaires associées àla pression artérielle chez les patients hypertendus

1. Un régime alimentaire sain : riche en fruits et légumes frais, enproduits laitiers à faible teneur en gras, en fibres alimentaires solubles,en céréales à grains entiers et en protéines d’origine végétale, etpauvre en gras saturés, en cholestérol et en sel, conformément auxRecommandations alimentaires pour la santé des Canadiens.

2. La pratique d’une activité physique régulière : un total de 30 à 60minutes d’activités physiques dynamiques d’intensité moyenne, de 4 à7 fois par semaine.

3. Une consommation modérée d’alcool : un maximum de deux verresnormaux par jour; moins de 14 consommations par semaine pour leshommes, moins de 9 consommations par semaine pour les femmes.

4. La perte de poids et le maintien d’un poids santé (IMC de 18,5 à 24,9 kg/m2).

5. Un tour de taille de moins de 102 cm pour les hommes et de moins de88 cm pour les femmes.

6. Une réduction de la consommation de sodium à moins de 100 mmole/jour.

7. Un environnement sans fumée.


P r o g r a m m e é d u c a t i f c a n a d i e n s u r l ’ h y p e r t e n s i o n


médicaments antihypertenseurs et de modifier leurs habitudes de vie

pour atteindre les cibles de pression artérielle recommandées. Si on

associe deux médicaments pour abaisser la pression artérielle, les

combinaisons d’un bêta-bloquant, d’un inhibiteur de l’ECA ou d’un

inhibiteur des récepteurs de l’angiotensine produisent un effet

antihypertenseur moins qu’additif.

Assurer un suivi mensuel ou plus fréquent des patients dont la pression

artérielle est supérieure aux valeurs cibles. Pour arriver à maîtriser la

pression artérielle, il faut assurer un suivi à intervalles rapprochés, à la

fois pour aider le patient à observer son traitement et pour accroître

l’intensité du traitement.

Insister sur l’observation du traitement. L’inobservation du traitement

par les patients est l’un des plus grands obstacles à la maîtrise de la

pression artérielle. L’observation du traitement doit faire l’objet d’une

évaluation à chaque visite médicale. Par ailleurs, certaines interventions

spécifiques peuvent améliorer le taux d’observation (tableau 4).

RemerciementsLe présent manuscrit a été rédigé par le Dr N. Campbell. Les versions

préliminaires ont été révisées par les docteurs R. Feldman, A. Milot,

R. Touyz, G. Tremblay et R. Ward, et par S. Matheson, IA. Le présent

manuscrit a reçu l’approbation de la direction du PECH.

Consent to Clinical Treatment: Special Challenges in the Frail ElderlyMichael Gordon, MD

One of the cardinal principles in medical practice is the concept of

consent to treatment. In North America especially, this has

become a complex undertaking because of the ethical and legal

implications and the assumptions on which the consent process is

based. Physicians can play a key role in ensuring that the underlying

principles and actuality of the consent process are respected when

dealing with the frail elderly. This is especially important as there is an

understandable tendency to overlook or ignore the frail elder’s

involvement at one level or another in the decision-making process.

In the past in North America, the consent process was less formal.

The assumption of consent assumed that if a physician recommended

a necessary treatment, it was almost the duty of the patient to accept it.

The question would have been asked, “If you came for an opinion and

advice, why on earth would you [the patient] not take it?” It is the

development of the contemporary framework of medical ethics and its

translation into law that have led to the more rigorous concept of

consent to treatment whether for clinical care or research endeavours.1

The Ethical Underpinnings of ConsentWhen beneficence by the doctor was the overriding ethical principle

that governed the relationship between doctors and patients, the

consent process was fairly straightforward and virtually a given; that is,

recommended treatment would be accepted and, for the most part,

verbal acceptance was the norm. The contemporary framework of

medical ethics further developed with an often dominant focus on the

ethical principle of autonomy. When this was combined with an

increasingly risk-averse approach to medical interactions so as to avoid

litigation, the result was further formalization of the consent process.

Autonomy is a key ethical principle among the four foundational

ones described by Beauchamps and Childress.2 It requires an

operational framework to demonstrate that it has been respected – that

is, the legal process of consent to treatment. In most Western

jurisdictions, consent to treatment legislation requires two essential

components: an understanding of the treatment being proposed and an

appreciation of the implications of accepting or rejecting the proposed

treatment. For most people, the cognitive component of the consent

About the AuthorMichael Gordon graduated from the University of St. Andrews in Scotland and took further studies in Aberdeen, Haifa, Boston,

Montreal, and Jerusalem. He is currently staff geriatrician at the Mount Sinai Hospital and Baycrest Centre for Geriatric Care

in Toronto, and professor of Medicine at the University of Toronto.

G I M o f A g i n g

C o n s e n t t o C l i n i c a l T r e a t m e n t @ L R H


process is the easier part, even though some medical interventions are

more complex than others. Physicians and other health care providers

are usually adept at explaining medical interventions and what might be

achieved through them. It is the appreciation component of the consent

process that poses the greatest challenge at all ages, but more so when

dealing with the elderly, especially those who are frail and at risk of and

vulnerable to adverse reactions from many clinical interventions.

Even within the framework of the formalized and heavily constrained

consent process, in emergency situations, most jurisdictions allow for

clinical interventions to be undertaken even without formal consent in

order to salvage life or limb.

The Role of SurrogatesConfounding factors in the consent process when dealing with frail

elders are the issues of capacity to consent and the role of surrogates.

Previously, it was often assumed that a diagnosis of Alzheimer’s disease

or other form of dementia implied de facto incapacity to make any

health care decisions. We now recognize that decisional capacity is

variable and may be domain specific. This means that we should work

on the assumption that a frail elder, even with some degree of cognitive

impairment, should be allowed to participate in the decision making to

the extent that appears consistent with his or her ability to understand

and appreciate the issues at some acceptable, if basic, level.3

Since surrogates often make health care decisions, it is important that

those involved understand the basis by which such decisions should be

made. It is critical that clinicians understand the ethical and legal

frameworks as well as the array of family dynamics and emotional

investments that impact on how surrogate decision makers, whether

family members or others, make their decisions. Clinicians, who have

personally experienced the role of surrogate decision maker often more

readily empathize with and support family members who are struggling

with difficult choices.

Types and the Nature of DecisionsMany, but not all, decisions affecting frail elders fall within the category

of end-of-life decisions.4–6 There are those that are less dramatic but

important in terms of quality of life and one’s future well-being. It is

within these often daily activities that we must remember that even

impaired frail elders can make many decisions important to their

quality of life. As noted by B. M. Dickens, “Demented patients are

entitled to favourite foods, including those contraindicated on health

grounds but not actually dangerous, to wear unorthodox clothing of

their choice, and to lead unhygienic lifestyles. ‘Incompetent’ does not

mean that a person ceases to have choices, or that his or her wishes

should never be respected. ‘Incompetent’ does not mean that others are

free to do with you as they please.” He goes on to say, “Procedures

cannot be pursued on incompetent patients who, by word or action,

resist them at the time of their proposed performance,” which reflects

the high degree with which we must regard the decision-making

process in this population.3

Included in the decisions that often lead to enormous conflict and

guilt on the part of family caregivers is the contemplation of a move

from one’s historic home to a supportive housing venue or long-term

care facility; this can be emotionally charged. It often leads to conflict

between the person for whom the move is being considered and those

promoting the decision. The physician may be in the middle of the

decision-making process and can be of enormous support to the patient

and family members. The physician can recount examples of successful

and beneficial moves when holding discussions. The person may deny

the imperative for a move, especially if he or she suffers from a degree

of cognitive impairment.

The most challenging and heart-wrenching decisions that require

consent are those related to tube feeding and modification or

withdrawal of life-maintaining treatments.7 In such situations, the

individual may no longer be able to effectively articulate his or her

wishes on treatment decisions. Sometimes indirect evidence can be

gleaned by facial expressions and movements that can be interpreted as

rejection of treatments, such as infusions or feeding tubes, which might

help clinicians and families come to care decisions.3

The key to the surrogates’ decision-making framework is to

remember that the decision, while legally theirs to make, should be

based on what they honestly believe would have been the decision taken

by their loved one. That understanding should be reflected in advance

directives when available, previous personal discussions, or evidence of

expressed preferences from known cultural and religious values. When

such values are not possible to discern, the standard of “best interests”

of the person in terms of comfort and quality of life becomes

paramount.

ConclusionThe clinical care consent process for the frail elderly is one of the

challenges frequently encountered by health care providers and

surrogate decision makers. As clinicians, we must strive to ensure that

beyond the ethical and legal frameworks that govern decision making

we feel certain that, as much as possible, the dignity and humanity of

the patient are at the core of all the steps that enter into the process. Frail

elders, at whatever level of dependency, should be confident that their

well-being will be ensured through the respect and duties of care held

by health care providers and their surrogate decision makers.

References1. Marsh FH. Informed consent and the elderly patient. Clin Geriatr

Med 1986;2:501–10.

2. Gillon R. Ethics needs principles – four can encompass the rest –

and respect for autonomy should be “first among equals.” J Med

Ethics 2003;29:307–12.

3. Dickens BM. Legal aspects of the dementias. Lancet

1997;349:949–50.

4. Gordon M. CPR in long-term care: mythical benefits or necessary

ritual? Ann Long-Term Care: Clin Care Aging 2003;11:41–9.

5. Ditillo BA. Should there be a choice for cardiopulmonary

resuscitation when death is expected? Revisiting an old idea whose

time is yet to come. J Palliat Med 2002;5:107–16.

6. Buhler DA. Informed consent and the elderly: an ethical challenge

for critical care nursing. Crit Care Nurs Clin North Am

1990;2:461–71.

7. Gordon M, Singer PA. Decisions and care at the end of life. Lancet

1995;346:163–6.

P h a r m - G I M

Case PresentationA 72-year-old woman with type 2 diabetes saw her family physician for

irritative voiding symptoms. A urinalysis revealed leukocytes and

nitrites, and she was treated with Septra DS (sulfamethoxazole and

trimethoprim), one double-strength tablet b.i.d. Her other medications

included glyburide 7.5 mg b.i.d. and metformin 500 mg t.i.d. Although

her urinary tract symptoms improved, on the third day of antibiotic

therapy, her husband awoke to find her rambling incoherently. Am

ambulance was summoned, and paramedics found her capillary blood

glucose level to be 1.9 mmol/L. The patient improved promptly with

intravenous dextrose and was brought to hospital, where she remained

on a D10W infusion for 18 hours.

QuestionsWhy did this happen? What alternate antidote could have been

considered in this woman’s case?

DiscussionSulfonylureas such as glyburide improve glycemic control primarily by

promoting the release of insulin from the pancreas. This effect is dose

dependent and can be prolonged, particularly following overdose or in

patients with renal dysfunction. Glyburide and other sulfonylureas are

metabolized by the hepatic cytochrome P450 (CYP) enzyme 2C9.1

Sulfamethoxazole and trimethoprim both inhibit this enzyme, resulting

in higher sulfonylurea levels and, consequently, enhanced insulin

secretion.2 In patients taking glyburide, the use of sulfamethoxazole-

trimethoprim increases the risk of hospital admission for hypoglycemia

roughly sixfold, as compared with amoxicillin.3

It is interesting to note that unlike many other CYP enzymes such as

CYP 3A4 (the dominant CYP enzyme in man), CYP 2C9 activity is

polymorphic, meaning that some people have a far less active enzyme

than others.2,4 The reason for this lies, not surprisingly, in genetics.

Roughly one third of Caucasian subjects have at least one variant allele

(e.g., *1/*2 or *1/*3), whereas these polymorphisms are far less

common in Blacks and Asians. The *2 and *3 alleles yield

functionally deficient CYP 2C9, and patients who are heterozygous

or homozygous for these variants typically need much lower doses

of drugs that are metabolized by CYP 2C9. Common drugs that are

metabolized by CYP 2C9, as well as others than can modulate its

activity, are shown in Table 1.

Table 1. Some Common Substrates, Inhibitors, andInducers of Cytochrome P450 2C9

Substrates Inhibitors InducersSulfonylureas (e.g., glyburide) Sulfamethoxazole Rifampin

Warfarin Trimethoprim Secobarbital

Fluvastatin Amiodarone

Most nonsteroidal anti-inflammatory drugs Fluconazole

Losartan Fluvastatin

Irbesartan Fenofibrate

Phenytoin Fluvoxamine

Tamoxifen Zafirlukast

The treatment of patients with sulfonylurea-induced hypoglycemia

should include supplemental dextrose, but this is primarily indicated

for the treatment of symptomatic patients. Although dextrose infusions

are often continued for prolonged periods in asymptomatic patients,

this practice is inadvisable and even potentially dangerous because of

glucose-stimulated pancreatic insulin release, which is more

pronounced in the setting of sulfonylurea therapy.

Once the symptoms of hypoglycemia have resolved, clinicians should

consider using octreotide to maintain euglycemia.5 Octreotide is a

somatostatin analogue that directly inhibits the release of insulin from

the pancreas. In an experimental sulfonylurea overdose, the drug

substantially reduces insulin levels and glucose requirement, as

compared with glucagon and diazoxide.6 Moreover, at doses used for

this indication (typically 50–100 mcg subcutaneously every 8 hours for

adult patients), the drug is relatively inexpensive and extremely well

tolerated.

In summary, many seemingly innocuous drugs can precipitate

hypoglycemia in patients receiving sulfonylureas. Depending on the

clinical circumstance, these drugs could be avoided in favour of an

alternate agent, or a dose reduction considered for the sulfonylurea. For

patients who develop hypoglycemia during sulfonylurea therapy,

octreotide is a safe, inexpensive, and pharmacologically elegant antidote

that can minimize the need for parenteral dextrose.

About the AuthorDavid Juurlink is a staff physician in the Division of General Internal Medicine and head of the Division of Clinical Pharmacology

and Toxicology at Sunnybrook Health Sciences Centre. He is also a medical toxicologist at the Ontario Regional Poison

Information Centre at the Hospital for Sick Children.

Sulfonylurea-Induced Hypoglycemia: Avoidance and TreatmentDavid Juurlink, MD


References1. Niemi M, Cascorbi I, Timm R, et al. Glyburide and glimepiride

pharmacokinetics in subjects with different CYP2C9 genotypes. Clin

Pharmacol Ther 2002;72:326–32.

2. Kirchheiner J, Brockmoller J. Clinical consequences of cytochrome

P450 2C9 polymorphisms. Clin Pharmacol Ther 2005;77(1):1–16.

3. Juurlink DN, Mamdani M, Kopp A, et al. Drug-drug interactions

among elderly patients hospitalized for drug toxicity. JAMA

2003;289:1652–8.

4. Lee CR, Goldstein JA, Pieper JA. Cytochrome P450 2C9

polymorphisms: a comprehensive review of the in-vitro and human

data. Pharmacogenetics 2002;12:251–63.

5. McLaughlin SA, Crandall CS, McKinney PE. Octreotide: an antidote

for sulfonylurea-induced hypoglycemia. Ann Emerg Med

2000;36:133–8.

6. Boyle PJ, Justice K, Krentz AJ, et al. Octreotide reverses

hyperinsulinemia and prevents hypoglycemia induced by

sulfonylurea overdoses. J Clin Endocrinol Metab 1993;76:752–6.

S u l f o n y l u r e a - I n d u c e d H y p o g l y c e m i a


D a n s l a p r a t i q u e d e l a m é d e c i n e i n t e r n e g é n é r a l e e n f r a n ç a i s

Voici une nouvelle chronique sur la bonne utilisation du français

médical. Cette chronique est adressée aux personnes qui désirent

obtenir une meilleure connaissance des difficultés d’usage du français

dans le contexte de la pratique médicale nord-américaine.Fellow :On entend souvent dire :

Il a terminé sa résidence et il est parti en fellow. Il est en train

de faire son fellowship en hémodynamie.

Il s’agit bien sûr d’un anglicisme : Les termes fellow, fellowship sont à

éviter en français.1

Comment peut-on traduire ces termes en français ?Ils peuvent avoir plusieurs sens :1. D’abord le sens commun de camarade ou compagnon ; le terme

a good fellow peut se traduire comme un bon gars.2

2. Dans le sens de membre d’une société savante on peut direassocié : associé du Collège royal des médecins et chirurgiens duCanada.3

3. Dans le sens boursier d’une organisation de subvention on peutdire, par exemple, boursier du Conseil de la recherche médicaledu Canada.3

4. On peut également employer le terme bourse de recherche pourdésigner une somme accordée par un organisme pour qu’unepersonne poursuive sa formation en participant à des recherchesau sein d’une équipe de chercheurs, le plus souvent en milieuuniversitaire.4

5. Le plus difficile à traduire est fellow ou fellowship pour désignerune période de formation supplémentaire à la fin d’un doctoratou d’une résidence. La consultation des ouvrages de terminologiene permet pas de trouver un terme parfaitement équivalent, maison peut utiliser les termes suivants : post doctorat, étudespostdoctorales ou stage postdoctoral.1

Donc : Il est parti faire son post doctorat en hémodynamie.

Références1. Le Grand dictionnaire terminologique de l’Office québécois de la

langue français (site Web).2. Harraps Shorter.3. Quérin, Serge; Dictionnaire des difficultés du français médical;

Québec 1998.4. Termium Plus; site Web de la bibliothèque de l’Université de

Sherbrooke.

Êtes-vous à jour en français médical ?Donald Echenberg, MD

Au sujet de l’auteurDon Echenberg est président de la Société canadienne de médecine interne et son représentant régional au Québec. Il pratique

et enseigne la médecine interne au Centre hospitalier universitaire de Sherbrooke depuis plusieurs années .

Adalat® XL®

(Nifedipine Extended Release Tablets 20, 30 and 60 mg)

THERAPEUTIC CLASSIFICATIONAntianginal/Antihypertensive Agent

INDICATIONS AND CLINICAL USEChronic Stable Angina ADALAT® XL® (nifedipine) is indicated in the managementof chronic stable angina (effort-associated angina) without evidence ofvasospasm in patients who remain symptomatic despite adequate doses of betablockers and/or nitrates, or who cannot tolerate these agents. ADALAT® XL® maybe used in combination with beta blocking drugs in patients with chronic stableangina. However, available information is not sufficient to predict with confidencethe effects of concurrent treatment, especially in patients with compromised leftventricular function or cardiac conduction abnormalities. When introducing suchconcomitant therapy, care must be taken to monitor blood pressure closely, sincesevere hypotension can occur from the combined effects of the drugs (seeWARNINGS). Hypertension ADALAT® XL® is indicated in the management ofmild to moderate essential hypertension. ADALAT® XL® should normally be usedin those patients in whom treatment with diuretics or beta blocker has beenineffective, or has been associated with unacceptable adverse effects. ADALAT®

XL® can be tried as an initial agent in those patients in whom the use of diureticsand/or beta blockers is contraindicated, or in patients with medical conditions inwhich these drugs frequently cause serious adverse effects. Combination ofADALAT® XL® with a diuretic has been found compatible and has shown addedantihypertensive effect. Concurrent administration of low doses of ADALAT® XL®

and enalapril has been shown to produce an enhanced antihypertensive effectwith no additional safety concerns when compared to that observed with eitherof the monotherapies. Safety of concurrent use of ADALAT® XL® with otherantihypertensive agents has not been established.

CONTRAINDICATIONSADALAT® XL® (nifedipine) is contraindicated in pregnancy, during lactation, and inwomen of childbearing potential. Fetal malformations and adverse effects onpregnancy have been reported in animals. An increase in the number of fetalmortalities and resorptions occurred after the administration of 30 and100 mg/kg nifedipine to pregnant mice, rats, and rabbits. Fetal malformationsoccurred after the administration of 30 and 100 mg/kg nifedipine topregnant mice and 100 mg/kg to pregnant rats. In patients withhypersensitivity to ADALAT®. In patients with severe hypotension orcardiovascular shock. Nifedipine must not be used in combination with rifampicinbecause insufficient plasma levels of nifedipine may result due to enzymeinduction.

WARNINGSExcessive Hypotension in Patients with Angina Since ADALAT® XL®

(nifedipine) lowers peripheral vascular resistance and blood pressure,ADALAT® XL® should be used cautiously in patients with angina who are prone todevelop hypotension and those with a history of cerebrovascular insufficiency.Occasional patients have had excessive and poorly tolerated hypotension.Syncope has been reported (see ADVERSE REACTIONS). These responses haveusually occurred during initial titration or at the time of subsequent upwarddosage adjustment, and may be more likely in patients on concomitant betablockers. If excessive hypotension occurs, dosage should be lowered or the drugshould be discontinued (see CONTRAINDICATIONS). Severe hypotension and/orincreased fluid volume requirements have been reported in patients receivingnifedipine, with a beta blocker, who underwent coronary artery bypass surgeryusing high dose fentanyl anesthesia. The interaction with high dose fentanylappears to be due to the combination of nifedipine and a beta blocker, but thepossibility that it may occur with nifedipine alone, with low doses of fentanyl inother surgical procedures, or with other narcotic analgesics cannot be ruled out.In nifedipine-treated patients where surgery using high dose fentanyl anesthesiais contemplated, the physician should be aware of these potential problems andif the patient’s condition permits, sufficient time (at least 36 hours), should beallowed for nifedipine to be washed out of the body prior to surgery. The followinginformation should be taken into account in those patients who are being treatedfor hypertension as well as angina. Increased Angina and/or MyocardialInfarction Rarely, patients, particularly those who have severe obstructivecoronary artery disease have developed well-documented increased frequency,duration and/or severity of angina or acute myocardial infarction on startingnifedipine or at the time of dosage increase. The mechanism of the response isnot established. Since there has not been a study of ADALAT® XL® in acutemyocardial infarction reported, similar effects of ADALAT® XL® to that ofimmediate-release nifedipine cannot be excluded. Immediate-release nifedipineis contraindicated in acute myocardial infarction. Beta Blocker WithdrawalPatients with angina recently withdrawn from beta blockers may develop awithdrawal syndrome with increased angina, probably related to increasedsensitivity to catecholamines. Initiation of treatment with ADALAT® XL® will notprevent this occurrence and might be expected to exacerbate it by provokingreflex catecholamine release. There have been occasional reports of increasedangina in a setting of beta blocker withdrawal and initiation of nifedipine. It isimportant to taper beta blockers if possible, rather than stopping them abruptlybefore beginning ADALAT® XL®. Patients with Heart Failure There have beenisolated reports of severe hypotension and lowering of cardiac output followingadministration of nifedipine to patients with severe heart failure. Thus, ADALAT®

XL® should be used cautiously in patients with severe heart failure. Rarely,patients usually receiving a beta blocker, have developed heart failure afterbeginning nifedipine therapy. In patients with severe aortic stenosis, nifedipinewill not produce its usual afterload reducing effects and there is a possibility thatan unopposed negative inotropic action of the drug may produce heart failure ifthe end-diastolic pressure is raised. Caution should therefore be exercised whenusing ADALAT® XL® in patients with these conditions. Patients with Pre-Existing Gastrointestinal Narrowing Since the ADALAT® XL® delivery systemcontains a non-deformable material, caution should be used when administeringADALAT® XL® in patients with pre-existing severe gastrointestinal narrowing(pathologic or iatrogenic). There have been rare reports of obstructive symptomsin patients with known strictures in association with the ingestion of ADALAT®

XL® tablets. In single cases, obstructive symptoms have been described withoutknown history of gastrointestinal disorders. Bezoars can occur in very rare casesand may require surgical intervention. ADALAT® XL® must not be used in patientswith a Kock pouch (ileostomy after proctocolectomy).When doing barium contrast X-ray, ADALAT® XL® may cause false positive effects (e.g., filling defectsinterpreted as polyp).

PRECAUTIONSHypotension/Heart Rate Because ADALAT® XL® (nifedipine) is an arterial andarteriolar vasodilator, hypotension, and a compensatory increase in heart ratemay occur. Thus, blood pressure and heart rate should be monitored carefullyduring nifedipine therapy. Close monitoring is especially recommended forpatients who are prone to develop hypotension, those with a history ofcerebrovascular insufficiency, and those who are taking medications that areknown to lower blood pressure (see WARNINGS). Peripheral Edema Mild tomoderate peripheral edema, typically associated with arterial vasodilation andnot due to left ventricular dysfunction, has been reported to occur in patientstreated with ADALAT® XL® (see ADVERSE REACTIONS). This edema occursprimarily in the lower extremities and may respond to diuretic therapy. Withpatients whose angina or hypertension is complicated by congestive heartfailure, care should be taken to differentiate this peripheral edema from theeffects of increasing left ventricular dysfunction. Male Fertility In some casesof in vitro fertilization, nifedipine has been associated with reversiblespermatozoal biochemical changes. in vitro studies have shown that nifedipinemay inhibit expression of mannose-ligand receptors, thus preventing thespermatozoa from attaching to the zona pellucida and impairing sperm function.In those men who are repeatedly unsuccessful in fathering a child by in vitrofertilization, and where no other explanation could be found, nifedipine should beconsidered as a possible cause. Use in Elderly ADALAT® XL® should beadministered cautiously to elderly patients, especially to those with a history ofhypotension or cerebral vascular insufficiency. Use in Diabetic Patient The useof ADALAT® XL® in diabetic patients may require adjustment for their control. Usein Patients with Impaired Liver Function ADALAT® XL® should be used withcaution in patients with impaired liver function (see CLINICAL PHARMACOLOGY). Adose reduction, particularly in severe cases, may be required. Close monitoringof response and metabolic effect should apply. Ability to Drive and UseMachines Reactions to the drug, which vary in intensity from individual toindividual, can impair the ability to drive or to operate machinery, particularly atthe start of the treatment, upon changing the medication, or in combination withalcohol. Interaction with Grapefruit Juice Published data indicate thatthrough inhibition of cytochrome P450, flavonoids present in the grapefruit juicecan increase plasma levels and augment pharmacodynamic effects of somedihydropyridine calcium channel blockers, including nifedipine (see ACTION ANDCLINICAL PHARMACOLOGY). Therefore, the administration of nifedipine withgrapefruit juice should be avoided. Drug Interactions As with all drugs, careshould be exercised when treating patients with multiple medications.Dihydrophyridine calcium channel blockers undergo biotransformation by thecytochrome P450 system, mainly via the CYP3A4 isoenzyme. Coadministrationof nifedipine with other drugs which follow the same route of biotransformationmay result in altered bioavailability. Dosages of similarly metabolized drugs,particularly those of low therapeutic ratio, and especially in patients with renaland/or hepatic impairment, may require adjustment when starting or stoppingconcomitantly administered nifedipine to maintain optimum therapeutic bloodlevels. If necessary, a reduction in the dose of nifedipine may be considered.Drugs known to be inhibitors of the cytochrome P450 system include: azoleantifungals, cimetidine, cyclosporine, erythromycin, quinidine, terfenadine, andwarfarin. Drugs known to be inducers of the cytochrome P450 system include:phenobarbital, phenytoin, and rifampicin. Drugs known to be biotransformed viacytochrome P450 include: benzodiazepines, flecainide, theophylline, imipramineand propafenone. Beta Adrenergic Blocking Agents Concomitant administrationof nifedipine and beta blocking agents is usually well tolerated, but there havebeen occasional literature reports suggesting that the combination may increasethe likelihood of congestive heart failure, severe hypotension, or exacerbation ofangina. Therefore, caution and careful monitoring of patients on concomitanttherapy is recommended (see INDICATION AND CLINICAL USE and WARNINGS).Diltiazem Diltiazem decreases the clearance of nifedipine. The combination ofboth drugs should be administered with caution, and a reduction of thenifedipine dose may be considered. Long Acting Nitrates: Nifedipine may besafely co-administered with nitrates, but there have been no controlled studiesto evaluate the antianginal effectiveness of this combination. Digoxin:Administration of nifedipine with digoxin may lead to reduced digoxin clearance,and therefore, an increase in the plasma digoxin level. It is recommended thatdigoxin levels be monitored when initiating, adjusting and discontinuingnifedipine to avoid possible “under-” or “over-”dosing with digitalis. CoumarinAnticoagulants: There have been rare reports of increased prothrombin timein patients taking coumarin anticoagulants to whom nifedipine wasadministered. However, the relationship to nifedipine therapy is uncertain.Carbamazepine No formal studies have been performed to investigate thepotential interaction between nifedipine and carbamazepine. As carbamazepinehas been shown to reduce the plasma concentrations of the structurally similarcalcium channel blocker nimodipine due to enzyme induction, a decrease innifedipine plasma concentrations and hence a decrease in efficacy cannot beexcluded. Quinidine: The addition of nifedipine to a stable quinidine regimenmay reduce the quinidine by 50%, an enhanced response to nifedipine may alsooccur. The addition of quinidine to a stable nifedipine regimen may result inelevated nifedipine concentrations and a reduced response to quinidine. Somepatients have experienced elevated quinidine levels when nifedipine wasdiscontinued. Therefore, patients receiving concomitant therapy of nifedipine andquinidine, or those who had their nifedipine discontinued while still receivingquinidine,should be closely monitored, including determination of plasma levelsof quinidine. Consideration should be given to dosage adjustment.Quinupristin/Dalfopristin Simultaneous administration ofquinupristin/dalfopristin and nifedipine may lead to increased plasmaconcentrations of nifedipine. Upon co-administration of both drugs, bloodpressure should be monitored and, if necessary, a reduction of the nifedipinedose should be considered. Cimetidine and Ranitidine: Pharmacokineticstudies have shown that concurrent administration of cimetidine or ranitidinewith nifedipine results in significant increases in nifedipine plasma levels (ca.80% with cimetidine, and 70% with ranitidine). Patients receiving either of thesedrugs concomitantly with nifedipine should be monitored carefully for thepossible exacerbation of effects of nifedipine, such as hypotension. Adjustment ofnifedipine dosage may be necessary. Cisapride Simultaneous administration ofcisapride and nifedipine may lead to increased plasma concentrations ofnifedipine. Upon co-administration of both drugs, the blood pressure should bemonitored and, if necessary, a reduction of the nifedipine dose considered.Valproic acid No formal studies have been performed to investigate the potentialinteraction between nifedipine and valproic acid. As valproic acid has beenshown to increase the plasma concentrations of the structurally similar calciumchannel blocker nimodipine due to enzyme inhibition, an increase in nifedipineplasma concentrations and hence an increase in efficacy cannot be excluded.

INFORMATION FOR PATIENTSADALAT® XL®(nifedipine) tablets must be swallowed whole. Patients should beadvised to not chew, divide or crush the tablet as this can result in a massiveimmediate release of the drug. In ADALAT® XL®, the medication is packed withina nonabsorbable shell that has been specially designed to slowly release thedrug so the body can absorb it. When this is completed, the empty tablet iseliminated in the stool. Administration of nifedipine with grapefruit juice shouldbe avoided.

ADVERSE REACTIONSAngina: In 257 chronic stable angina patients treated in controlled and longterm open studies with ADALAT® XL®, adverse effects were reported in 30.0% ofpatients and required discontinuation of therapy in 8.5% of patients. The mostcommon adverse effects were: edema (10.1%), headache (3.1%), anginapectoris (3.1%). The following adverse effects were also reported. Incidencesgreater than 1% are given in parenthesis: Cardiovascular: Palpitation (2.3%),tachycardia, myocardial infarction, ventricular arrhythmia, extrasystoles,dyspnea, chest pain. In patients with angina, rarely, and possibly due totachycardia, nifedipine has been reported to have precipitated an angina pectorisattack. In addition, more serious events were occasionally observed, not readilydistinguishable from the natural history of the disease in these patients. Itremains possible, however, that some or many of these events were drugrelated. These events include myocardial infarction, congestive heart failure orpulmonary edema, and ventricular arrhythmias or conduction disturbances.Central Nervous System: Dizziness (2.3%), hypoesthesia (1.2%),confusion, insomnia, somnolence, nervousness, asthenia, hyperkinesia.Gastrointestinal: Constipation (1.9%), dyspepsia (1.2%), abdominal pain(1.2%), diarrhea, nausea, melena. Genito-urinary: Impotence, hematuria,polyuria, dysuria. Musculo-skeletal: Leg cramps, paresthesia, myalgia,arthralgia. Dermatologic: Rash, pruritus. Other: Fatigue (1.2%), pain, periorbitaledema. Hypertension: In 661 hypertensive patients treated in controlled trialswith ADALAT® XL®, adverse effects were reported in 54.0% of patients andrequired discontinuation of therapy in 11.9% of patients. The majority of adverseeffects reported occurred within the first three months of therapy. The mostcommon adverse effects reported with ADALAT® XL® were edema, which wasdose related and ranged in frequency from approximately 10 to 30% in the 30to 120 mg dose range, headache (16.6%), fatigue (6.2%), dizziness(4.4%), constipation (3.5%), nausea (3.5%). The following adverse effects werealso reported. Incidences greater than 1% are given in parenthesis:Cardiovascular: Flushing (2.4%), palpitation (2.3%), tachycardia (1.2%), chestpain (1.1%), ventricular arrhythmia, hypotension, syncope. Central NervousSystem: Insomnia (1.8%), nervousness (1.8%), somnolence (1.5%), depression,tremor, decreased libido, migraine, vertigo, amnesia, anxiety, impairedconcentration, twitching, ataxia, hypertonia, paresthesia, hypoesthesia.Gastrointestinal: Dyspepsia (1.5%), flatulence (1.5%), abdominal pain (1.4%),dry mouth (1.1%), diarrhea, vomiting, thirst, melena, eructation, weight increase.Genito-urinary: Impotence (1.5%), polyuria (1.5%), dysuria, nocturia, oliguria,urinary incontinence, urinary frequency, menstrual disorder. Musculo-skeletal:Arthralgia, back pain, myalgia. Special Senses: Abnormal vision, abnormallacrimation, taste disturbance, conjuctivitis, tinnitus. Dermatologic: Rash (2.3%),pruritus (1.1%), erythematous rash, alopecia. Respiratory: Dyspnea (1.7%),bronchospasm, pharyngitis, upper respiratory tract infection, epistaxis. Other:Leg cramps (2.7%), pain (2.7%), asthenia (2.0%), face edema, gout, allergy,fever, breast pain.

DOSAGE AND ADMINISTRATIONDosage should be individualized depending on patient tolerance and response.ADALAT® XL® (nifedipine) tablets must be swallowed whole and should not bebitten or divided. In general, titration steps should proceed over a 7-14 dayperiod so that the physician can assess the response to each dose level beforeproceeding to higher doses. Since steady-state plasma levels are achieved onthe second day of dosing, if symptoms so warrant, titration may proceed morerapidly provided that the patient is closely monitored. Angina Therapy withADALAT® XL® should normally be initiated with 30 mg once daily. Experience withdoses greater than 90 mg daily in patients with angina is limited, therefore,doses greater than 90 mg daily are not recommended. Angina patientscontrolled on ADALAT® capsules alone or in combination with beta blockers maybe safely switched to ADALAT® XL® tablets at the nearest equivalent daily dose.Subsequent titration to higher or lower doses may be necessary and should beinitiated as clinically warranted. Hypertension Therapy should normally beinitiated with 20 or 30 mg once daily. The usual maintenance dose is 30 to 60mg once daily. Doses greater than 90 mg daily are not recommended. Patientsswitched from ADALAT® PA 10 or 20 to ADALAT® XL® therapy should receive aninitial dosage of ADALAT® XL® no higher than 30 mg once daily, based onpreviously prescribed dosing regimen. If clinically warranted, the dosage ofADALAT® XL® should be increased to 60 mg once daily. Blood pressure andpatient symptoms should be monitored closely following the switch fromADALAT® PA to ADALAT® XL®. No “rebound effect” has been observed upondiscontinuation of ADALAT® XL®. However, if discontinuation of nifedipine isnecessary, sound clinical practice suggests that the dosage should be decreasedgradually under close physician supervision.

PHARMACEUTICAL INFORMATIONCompositionADALAT® XL® is supplied as 20, 30 and 60 mg tablets for oral administration.ADALAT® XL® 20, 30 and 60 mg tablets, in addition to the active ingredientnifedipine, contain the following inactive ingredients: polyethylene oxide,cellulose acetate, sodium chloride, hydroxypropyl methylcellulose 2910,magnesium stearate, hydroxypropyl cellulose, titanium dioxide, polyethyleneglycol 3350, red ferric oxide, pharmaceutical shellac, synthetic black iron oxide.

AVAILABILITY OF DOSAGE FORMSADALAT® XL® (nifedipine) extended release tablets contain nifedipine in strengthsof 20 mg, 30 mg and 60 mg.ADALAT® XL® 20 mg is a dusty rose tablet imprinted with “ADALAT 20” on one side.ADALAT® XL® 20 mg is available in blister packs of 28 and 98 tablets.ADALAT® XL® 30 mg is a dusty rose tablet imprinted with “ADALAT 30” on oneside.ADALAT® XL® 30 mg is now available in blisters of 28 and 98 tablets.ADALAT® XL® 60 mg is a dusty rose tablet imprinted with “ADALAT 60” on oneside.ADALAT® XL® 60 mg is now available in blisters of 28 and 98 tablets.

PRODUCT MONOGRAPH IS AVAILABLE UPON REQUEST®Adalat, Bayer and Bayer Cross are registered trade-marks of Bayer AG usedunder licence by Bayer Inc. XL is a registered trade-mark of Bayer Inc., denotingits once-daily nifedipine.

Reference: Product Monograph Adalat® XL®, revised August 12th, 2004.Bayer Healthcare Inc.

Bayer Inc.77 Belfield Road, Toronto, Ontario M9W 1G6

XL1253AE

E x a m i n a t i o n S k i l l s

Arterial disease is common and tends to increase with age. Multiple

arteries are often involved, so a detailed examination (including

examining for the presence or absence of pulses, phase lags between

regions, and bruits) should be done. Blood pressures should be

measured in both arms and both legs if vascular disease is suspected.

Remember to use a large enough cuff that the inflated bag surrounds

the circumference. (In very obese patients, this may mean using the

forearm and calf for the cuff.) If symptoms occur with exercise, the

examination should be repeated after enough exercise to produce the

symptoms.

The major symptoms from arterial disease are tied to tissue hypoxia

and so occur primarily with very severe disease (beyond 80% occlusion

by area, in most cases), while intermittent symptoms such as angina and

claudication occur with moderate (60–80%) to severe disease. The

former alter the pulse characteristics and so are detected by palpation,

whereas the latter alter the flow patterns and so are detected mainly with

auscultation. The history gives you important clues.

Arterial pulsation can be detected normally in the aorta (suprasternal

notch and the abdomen), carotids (supraclavicular and neck), axillary,

brachial, radial, femoral, popliteal, dorsalis pedis, and temporal arteries

in most patients.

The amplitude of the pulse is not a good guide to blood pressure, and

the rate of rise and fall is more indicative aortic valvular disease than of

arterial disease (a slow rise with aortic stenosis, and a collapsing pulse

with aortic insufficiency). The systolic pressure is determined by the left

ventricular output and the elastic properties of the aorta. The diastolic

pressure is determined by the systolic pressure and the peripheral

resistance, which depends on the arterioles.

The elastic properties of the arteries play a major role in what one

feels, and change dramatically with age1 (Figures 1 and 2). The youngest

arteries double in diameter between 0 and 150 mm Hg, while the oldest

arteries increase by just over 20% between 0 and 200 mm Hg, and most

of this change is below the diastolic pressure. This causes the systolic

hypertension of old age, but also means the pressure drops more

precipitously with blood loss. Older arteries are often longer and so

more tortuous.

The change in size is palpable (and occasionally visible) and the

vibration from the travelling pressure wave in the wall of the artery

palpable. This wave is much faster than the flow wave, and will stop and

start again if something like a coarctation, atherosclerotic lesion, or

aneurysm encircles the whole circumference, or most of it; therefore, it

About the AuthorMargot Roach trained in mathematics/physics in New Brunswick, medicine at McGill, and biophysics at UWO. She obtained

her FRCPC in 1965 and did postdoctoral studies at Oxford before taking appointments in medicine and biophysics at UWO.

She has published research on the elastic properties of arteries and the consequent changes seen in arteriosclerosis and

aneurysmal disease. A pioneer in medical biophysics, she has won many prestigious teaching and research awards and is now

happily retired in Tatamagouche, Nova Scotia.

Arterial ExaminationMargot R. Roach, MD


Figure 1. An elastic diagram modified from Roach and Burton1 to show howthe mean curves change with age in human external iliac arteries obtainedat autopsy. Note the dramatic decrease in distensibility after age 20 years.

Figure 2. Unpublished data from Roach as part of the study in Figure 1 onsingle male patients age 30 and 60 years. The diameter is expressed as thepercent of that at zero pressure. Note the dramatic difference with age. Thebiggest changes in diameter occur at low pressures at all ages, and sopulsation is greater at low pressures than at high ones.


R o a c h

increases the normal pulse lag between locations. This may be palpable

between the brachial and radial pulses in the same arm up to about age

25 years but is palpable in older patients between the arm and leg pulses

only with disease. It is useful to feel radial and posterior tibial pulses on

each side simultaneously in all patients (the leg pulses are delayed in the

young, with coarctations of the aorta below the arch, and with

abdominal aortic aneurysms or severe atherosclerosis proximal to the

femoral) and dorsalis pedis pulses bilaterally in those who may have

disease in the iliac or femoral arteries. The pulse wave travels fastest in

the stiffest arteries and so increases toward the periphery,2 which

decreases the lag. The same phenomenon explains why a tap is

transmitted faster along a metal pipe than along a soft latex tube.

Practice is needed to make this test useful.

Dissecting aortic aneurysms can close off almost any of the arteries

arising from the aorta or its branches if the dissection extends into or

around them. These change as the dissection progresses, so pressure in

both the arms and legs should be checked several times a day, as well as

examining for pulses and pulse lags. It is easiest to follow these if they

are recorded on a flow chart.

Arterial bruits are produced by turbulent blood flow and are usually

loudest with moderate stenoses.3 If the stenosis becomes severe, then the

blood flow is decreased and the bruit decreases in amplitude.

Experimentally, flow and pressure decrease rapidly with stenoses greater

than 80% by area at rest, and more slowly beyond 60% stenosis with

exercise.4 An increase in a dimensionless parameter known as the

Reynolds number (Re) increases the risk of turbulence.5 It depends on

the diameter of the tube times the velocity of flow in it, divided by the

viscosity of the fluid. The viscosity of blood is dependent on hematocrit

and doubles between 20 and 60% hematocrit.6 Thus, bruits (and heart

murmurs) are louder in large vessels with high velocity and in anemic

patients. They are rare beyond the carotids and femorals in the absence

of arteriovenous fistulas, which have a very high velocity of flow. Blood

velocity also increases in high-output states such as exercise,

hyperthyroidism, and pregnancy, so bruits are more common with

them.

Bruits are rare in normal arteries but develop in the presence of

stenoses or aneurysms as turbulence develops distal to the stenosis as

the velocity in the stenosis increases and then is slowed distally. In an

aneurysm, the blood swirls to fill up the larger diameter and, again,

creates turbulence. In most arteries, and with normal hematocrit, bruits

are heard at rest with stenoses of about 40–90% by area and at exercise

with stenoses of about 30–80%. This means that bruits get louder with

exercise with moderate stenoses but get softer or disappear with severe

stenoses in the limbs where the peripheral arterioles dilate with exercise.

Only when the resistance of the stenosis approaches that of the

arterioles will the stenosis alter the flow and pressure distally. This

explains why bruits increase with exercise with moderate stenoses but

decrease with exercise with tight stenoses. Carotid and renal bruits do

not change with exercise as their arterioles do not dilate with exercise.

Abdominal aortic aneurysms (AAA) are readily palpable with the hips

and knees flexed in thin people or those with poor abdominal

musculature. They are prone to thrombosis and, if so, have no bruit. If

there is no thrombosis, there is usually a bruit over the aneurysm. If a

bruit was present but disappears, usually a thrombus has developed

and, with it, the risk of peripheral emboli.

Renal artery bruits may be audible either anteriorly or posteriorly. It

is easy to hear them in thin people but hard in obese ones. To my

knowledge, there have been no quantitative studies to determine the

usefulness of a renal arterial bruit in determining if the stenosis is

hemodynamically significant. Exercise causes no change.

Arteriovenous fistulas produce very loud bruits that occur in both

systole and diastole and are over both the artery and the vein.

Temporal arteries dilate with migraines. They do not dilate with

tension headaches, so this is a useful clue if the diagnosis is not obvious.

Sometimes pressure on them will decrease the severity of the migraine.

Arteritis, whether in the temporals in association with temporal arteritis

or peripherally with Takayasu’s disease, are firm, often tender, and may

have decreased pulsation. Because the lumen is narrowed by the wall

thickening, bruits are rare.

Ophthalmic arteries can be seen pulsing with an ophthalmoscope,

and occasionally cerebral aneurysms or arteriovenous fistulas in the

region can produce bruits over the eye.

References1. Roach MR, Burton AC. The effects of age on the elasticity of human

iliac arteries. Can J Biochem Physiol 1959;37:557–70.2. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries. 6th

edition. Philadelphia: Lea & Febiger; 1990:102–14.3. Roach MR. Poststenotic dilatation in arteries. In: Bergel DH, ed.

Cardiovascular Fluid Dynamics, Volume 2. London: Academic Press;1972:111–39.

4. May AG, van den Berg L, de Weese JA, Rob CG. Critical arterialstenosis. Surgery 1963;54;250–8.

5. Reynolds O. An experimental investigation of the circumstanceswhich determine whether the motion of water shall be direct orsinuous and the law of resistance in parallel channels. Phil Trans RoySoc London 1883;174:935–82.

6. Burton AC. Physiology and Biophysics of the Circulation. 2ndedition. Chicago: Year Book; 1972:39–43.

R e s i d e n t G I M


Canadian postgraduate residents currently beginning their third

year of core internal medicine will soon be expected to participate

in the annual R4 match. Unfortunately, it can be a source of anxiety,

stress, and confusion among residents of all years of training. To help

alleviate this, we’ve chosen to outline the match process so that future

applicants will be better informed.

Subspecialty and Program SelectionChoosing a career path is an important and difficult process. Arguably,

one of the most important factors in choosing a career is to choose

something that you enjoy. This decision is usually reached from sound

mentorship as well as positive elective and research experience over the

first 2 years of residency. For those residents who remain undecided

about their career plans, faculty mentors and fellows can act as excellent

resources.

Once the decision is made, visiting individual programs in person is

the key. The chance to see the program and engage in discussions with

current fellows provides invaluable information. This will give you a

much needed and honest perspective on the merits and weaknesses of a

given program. Furthermore, it provides a chance to discuss

employment opportunities with fellows nearing the completion of their

training. This is important to new trainees in planning their eventual

career paths.

Although all accredited programs provide residents with quality

training, there are important differences among them. The amount of

time devoted to a specific area of expertise, elective time, and teaching

rounds varies considerably. Some may wish to pursue additional

training with a master’s thesis or attain competency in a specific skill.

Certain programs may offer these options with relative ease and

funding, but it may be more difficult with others. Consider this in your

decision. Be clear about your goals and the feasibility of achieving them.

Your life outside of medicine also needs to be part of this decision.

Your fellowship years are a transition, both personally and

professionally. Family, friends, and social situation need to enter this

process through careful discussion. Incorporating all these factors will

take time, but it can make this important transition in your life a

relatively smooth one.

Required Documentation Subspecialty programs across Canada all have different application

deadlines, varying between mid-July and September 1. Most

universities require completion of a generic postgraduate application

form, an updated curriculum vitae (CV), and three reference letters.

Some require additional documentation such as personal letters and

copies of publications. As this can be a time-consuming task, junior

residents are strongly encouraged to begin updating their CV early on

in residency. Keep track of academic activities such as rounds

presentations, journal clubs, research activities, memberships, and

undergraduate teaching. Frequently updating your CV will save you

time when you apply.

Most programs have their application packages available to

download online. Some, however, continue to use regular mail. Contact

information for individual accredited residency programs and their

program directors can be accessed via the Royal College of Physicians

and Surgeons of Canada website at http://rcpsc.medical.org/

information/index.php.

Selecting RefereesYour referees should be able to attest to your academic strengths and

personal character, so choose them wisely! One of your referees is

usually your core IM program director. When choosing the others, try

to choose people with whom you’ve had a good longitudinal working

relationship. Meeting in person to discuss the content of the letter is

important, and providing a copy of your CV will help. Unforeseen

circumstances can arise, so make sure you request your letter early to

avoid problems. Letters should generally be sent directly to the program

from the referee. For residents requesting reference letters for more than

one program, providing referees with the exact coordinates of the

programs as well as preaddressed and prestamped envelopes can

increase the likelihood that the letters will get there on time. It also gives

you a means by which to track them if they are sent by registered mail.

A thank you card sent to the referee after the letters have been mailed is

an appreciated gesture.

The Interview PeriodInterviews not only allow for programs to better select prospective

fellows, they also provide another opportunity for candidates to inquire

further. During a given interview, you will likely be asked about career

choices and reasons for applying to a particular centre. If you’ve done

an elective at the centre of choice, highlight this, as it strengthens your

application. Don’t forget, this is your opportunity to interview the

program as well, so you should have a list of your questions to help you

About the AuthorsDr. Angèle Brabant is currently a PGY-4 in general internal medicine at the University of Ottawa.

Dr. Karim Abou-Nassar is currently a PGY-4 in hematology at the University of Ottawa.

The R4 Match: Demystifying the ProcessAngèle Brabant, MD, Karim Abou-Nassar, MD

B r a b a n t a n d A b o u - N a s s a r


make the most out of the interview process.

Programs are encouraged to offer interviews during a set period in

the early fall (i.e., September and October), with a deadline prior to the

actual start of the match. Certain subspecialties, such as cardiology,

coordinate their interviews at one specific location and on one specific

date to facilitate the process. However, this is not the case for most

programs. Careful planning of your interview schedule can minimize

the associated travel time and costs.

The MatchThe match lasts for a 2-week period beginning annually on the first

Monday in November. On this date, university programs begin

contacting prospective candidates with offers in writing, via e-mail or

via their core postgraduate program office. Residents can then choose to

reject, accept, or hold an offer. A maximum of two offers can be held

simultaneously for up to a maximum of 2 working days each.

Candidates have the option of holding only one offer for the duration

of the match period. Rejected offers are subsequently offered to other

potential candidates. Following this 2-week period, a second iteration

match is held for unfilled positions.

In order to track offers and remaining available positions from each

school, the University of Alberta annually hosts a website for the

duration of the match (http://www.departmentofmedicine.

ualberta.ca/r4match/). Although it does describe guidelines and offer

various links, it does not provide a centralized database or resource for

candidates. It is useful once the match has officially begun.

Ombudspersons for both residents and program directors,

representing the Canadian Association of Interns and Residents and the

Canadian Association of Internal Medicine Program Directors,

respectively, are available throughout the match. Their contact

information can also be found on the University of Alberta R4 match

website.

Overall, the outcome of the match is a positive one. Most residents

enrolled in the 2006 match are currently training in their specialty of

choice. Early electives in subspecialties, general internal medicine,

academia, and the community are strongly recommended in order to

facilitate your selection. After all, this is perhaps one of the most

important decisions of your career. Careful planning can make a

significant difference in your eventual career goals.

We gratefully acknowledge supportof our scientific program by

unrestricted educational grants from:

We gratefully acknowledge supportof our scientific program by

unrestricted educational grants from:

We gratefully acknowledge support of our 2007 Annual Scientific Meeting

by unrestricted educational grants from:

MICARDIS® (telmisartan)40 mg and 80 mg Tablets THERAPEUTIC CLASSIFICATION: Angiotensin II AT1 Receptor BlockerINDICATIONS AND CLINICAL USEMICARDIS® (telmisartan) is indicated for the treatment of mild to moderate essentialhypertension. MICARDIS® may be used alone or in combination with thiazide diuretics. Thesafety and efficacy of concurrent use with angiotensin converting enzyme inhibitors havenot been established. Information on the use of telmisartan in combination with betablockers is not available.CONTRAINDICATIONSMICARDIS® (telmisartan) is contraindicated in patients who are hypersensitive to anycomponents of this product (see Composition).WARNINGSPregnancy: Drugs that act directly on the renin-angiotensin system can cause fetal andneonatal morbidity and mortality when administered to pregnant women. If pregnancy isdetected, MICARDIS® (telmisartan) should be discontinued as soon as possible. The useof drugs that act directly on the renin-angiotensin system during the second and thirdtrimesters of pregnancy has been associated with fetal and nonnatal injury, includinghypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, anddeath. Oligohydramnios has also been reported, presumably resulting from decreasedfetal renal function; oligohydramnios in this setting has been associated with fetal limbcontractures, craniofacial deformation, and hypoplastic lung development. Prematurity,intrauterine growth retardation, and patent ductus arteriosus have also been reported,although it is not clear whether these occurrences were due to exposure to the drug.These adverse effects do not appear to have resulted from intrauterine drug exposure thathas been limited to the first trimester. Mothers whose embryos and fetuses are exposedto an angiotensin II receptor antagonist only during the first trimester should be soinformed. Nonetheless, when patients become pregnant, physicians should have thepatient discontinue the use of MICARDIS® as soon as possible unless it is considered life-saving for the mother. Rarely, probably less often than once in every thousandpregnancies, no alternative to an angiotensin II AT1 receptor antagonist will be found. Inthese rare cases, the physician should apprise mothers of the potential hazards to theirfetuses, and serial ultrasound examinations should be performed to assess the intraamniotic environment. If oligohydramnios is observed, contraction stress testing (CST), anon-stress test (NST), or biophysical profiling (BPP) may be appropriate, depending uponthe week of pregnancy. Patients and physicians should be aware, however, thatoligohydramnios may not appear until after the fetus has sustained irreversible injury.Infants with histories of in utero exposure to an angiotensin II AT1 receptor antagonistshould be closely observed for hypotension, oliguria, and hyperkalemia. If oliguria occurs,attention should be directed toward support of blood pressure and renal perfusion.Exchange transfusion may be required as a means of reversing hypertension and/orsubstituting for disordered renal function. Telmisartan is not removed from plasma byhemodialysis. No teratogenic effects were observed when telmisartan was administeredto pregnant rats at oral doses of up to 50 mg/kg/day and to pregnant rabbits at oral dosesof up to 45 mg/kg/day with saline supplementation. In rabbits, fetotoxicity (totalresorptions) associated with maternal toxicity (reduced body weight gain, mortality) wasobserved at the highest dose level (45 mg/kg/day). In rats, maternally toxic (reduction inbody weight gain and food consumption) telmisartan doses of 50 mg/kg/day in lategestation and during lactation were observed to produce adverse effects in rat fetusesand neonates, including reduced viability, low birth weight, delayed maturation, anddecreased weight gain. Significant levels of telmisartan were present in rat milk and ratfetuses’ blood during late gestation. Hypotension: In patients who are volume-depletedby diuretic therapy, dietary salt restriction, dialysis, diarrhea or vomiting, symptomatichypotension may occur after initiation of therapy with MICARDIS®. Such conditions,especially volume and/or sodium depletion, should be corrected prior to administration ofMICARDIS®. In these patients, because of the potential fall in blood pressure, therapyshould be started under close medical supervision. Similar considerations apply topatients with ischemic heart or cerebrovascular disease, in whom an excessive fall inblood pressure could result in myocardial infarction or cerebrovascular accident.PRECAUTIONSGeneral: Due to the sorbitol content in MICARDIS® (telmisartan) tablets, MICARDIS® isunsuitable for patients with hereditary fructose intolerance. Hepatic Impairment: As themajority of telmisartan is eliminated by biliary excretion, patients with biliary obstructivedisorders or hepatic insufficiency have reduced clearance of telmisartan. Three-to four-foldincreases in Cmax and AUC were observed in patients with liver impairment as comparedto healthy subjects. MICARDIS® (telmisartan) should be used with caution in these patients(see DOSAGE AND ADMINISTRATION). Renal Impairment: As a consequence of inhibitingthe renin-angiotensin-aldosterone system, changes in renal function may be anticipated insusceptible individuals. In patients whose renal function may depend on the activity of therenin-angiotensin-aldosterone system, such as patients with bilateral renal artery stenosis,unilateral renal artery stenosis to a solitary kidney, or severe congestive heart failure,treatment with agents that inhibit this system has been associated with oliguria,progressive azotemia, and rarely acute renal failure and/or death. There is no experiencewith long-term use of MICARDIS® (telmisartan) in patients with unilateral or bilateral renalartery stenosis, but an effect similar to that seen with ACE inhibitors should be anticipated.In susceptible patients, concomitant diuretic use may further increase the risk. Use oftelmisartan should include appropriate assessment of renal function in these types ofpatients. There is no experience regarding the administration of MICARDIS® (telmisartan)in patients with a recent kidney transplant. Valvular Stenosis: There is concern ontheoretical grounds that patients with aortic stenosis might be at a particular risk ofdecreased coronary perfusion, because they do not develop as much afterload reduction.Hyperkalemia: Drugs such as MICARDIS® that affect the renin-angiotensin-aldosteronesystem can cause hyperkalemia. Monitoring of serum potassium in patients at risk isrecommended. Based on experience with the use of drugs that affect the renin-angiotensinsystem, concomitant use with potassium-sparing diuretics, potassium supplements, saltsubstitutes containing potassium or other medicinal products that may increase thepotassium level (heparin, etc.) may lead to a greater risk of an increase in serumpotassium. Use in Nursing Mothers: It is not known whether telmisartan is excreted inhuman milk, but telmisartan was shown to be present in the milk of lactating rats. Becauseof the potential for adverse effects on the nursing infant, a decision should be madewhether to discontinue nursing or discontinue the drug, taking into account the importanceof the drug to the mother. Use in Children: Safety and effectiveness in pediatric patientshave not been established. Use in the Elderly: Of the total number of patients receivingMICARDIS® (telmisartan) in clinical studies, 551 (18.6%) were 65 to 74 years of age and130 (4.4%) were 75 years or older. No overall age-related differences were seen in theadverse effect profile, but greater sensitivity in some older patients cannot be ruled out.Effects on Ability to Drive and Use Machines: No studies on the effect on the abilityto drive and use machines have been performed. However, when driving vehicles oroperating machinery, it must be borne in mind that dizziness or drowsiness mayoccasionally occur when taking antihypertensive therapy. Drug Interactions: Warfarin:MICARDIS® (telmisartan) administered for 10 days slightly decreased the mean warfarintrough plasma concentration; this decrease did not result in a change in International

Normalized Ratio (INR). Coadministration of MICARDIS® also did not result in a clinicallysignificant interaction with acetaminophen, amlodipine, glyburide, hydrochlorothiazide oribuprofen. For digoxin, median increases in digoxin peak plasma concentration (49%) andin trough concentration (20%) were observed. It is recommended that digoxin plasmalevels be monitored when initiating, adjusting or discontinuing MICARDIS®. Lithium:Reversible increases in serum lithium concentrations and toxicity have been reportedduring concomitant administration of lithium with angiotensin converting enzymeinhibitors. Rare cases have also been reported with angiotensin II receptor antagonistsincluding MICARDIS®. Therefore, serum lithium level monitoring is advisable duringconcomitant use. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Combinations ofangiotensin-II antagonists (MICARDIS®) and NSAIDs (including ASA and COX-2 inhibitors)might have an increased risk for acute renal failure and hyperkalemia. Blood pressure andkidney function should be monitored more closely in this situation, as occasionally therecan be a substantial increase in blood pressure. NSAIDs (including ASA and COX-2inhibitors) and angiotensin-II receptor antagonists exert a synergistic effect on thedecrease of glomerular filtration. In patients with pre-existing renal impairment, this maylead to acute renal failure. Monitoring of renal function at the beginning and during thecourse of the treatment should be recommended.ADVERSE EVENTSMICARDIS® (telmisartan) has been evaluated for safety in 27 clinical trials involving 7,968patients. Of these 7,968 patients, 5,788 patients were treated with MICARDIS®

monotherapy including 1,058 patients treated for ≥1 year and 1,395 patients treated inplacebo-controlled trials. In 3,400 patients, discontinuation of therapy due to adverseevents was required in 2.8% of MICARDIS® patients and 6.1% placebo patients. Thefollowing potentially serious adverse reactions have been reported rarely with telmisartanin controlled clinical trials: syncope and hypotension. In placebo-controlled trials, noserious adverse event was reported with a frequency of greater that 0.1% in MICARDIS®-treated patients.ALL CLINICAL TRIALSThe adverse drug events listed below have been accumulated from 27 clinical trialsincluding 5,788 hypertensive patients treated with telmisartan. Adverse events have beenranked under headings of frequency using the following convention: very common(≥1/10); common (≥1/100, >1/10); uncommon (≥1/1.000, <1/100); rare (≥1/10.000,<1/1.000); very rare (<1/10.000). Body as a Whole, General: Common: Back pain (e.g.sciatica), chest pain, influenza-like symptoms, symptoms of infection (e.g. urinary tractinfections including cystitis), fatigue, conjunctivitis. Uncommon: Abnormal vision, sweatingincreased. Cardiovascular System: Common: Edema, palpitation. Central andPeripheral Nervous System: Very common: Headache. Common: Dizziness, insomnia.Uncommon: Vertigo. Gastro-Intestinal System: Common: Abdominal pain, diarrhea,dyspepsia, nausea, constipation, gastitis. Uncommon: Dry mouth, flatulence. Musculo-Skeletal System: Common: Arthralgia, cramps in legs or leg pain, myalgia, arthritis,arthrosis. Uncommon: Tendinitis like symptoms. Psychiatric System: Common: Anxiety,depression, nervousness. Respiratory System: Common: Upper respiratory tractinfections including pharyngitis and sinusitis, bronchitis, coughing, dyspnea, rhinitis. Skinand Appendages System: Common: Skin disorders like eczema, rash.CLINICAL LABORATORY FINDINGSHemoglobin: Infrequently, a decrease in hemoglobin has been observed which occursmore often during treatment with telmisartan than with placebo.PLACEBO-CONTROLLED TRIALSThe overall incidence of adverse events reported with MICARDIS® (41.4%) was usuallycomparable to placebo (43.9%) in placebo-controlled trials. Adverse events occurring in1% or more of 1,395 hypertensive patients treated with MICARDIS® monotherapy inplacebo-controlled clinical trials, regardless of drug relationship, include the following:

Disorders: rash, skin dry. Urinary System Disorders: dysuria, hematuria, micturitiondisorder, urinary tract infection. Vascular (Extracardiac) Disorders: cerebrovasculardisorder, purpura. Vision Disorders: vision abnormal. Clinical Laboratory Findings: Inplacebo-controlled clinical trials involving 1,041 patients treated with MICARDIS®

monotherapy, clinically relevant changes in standard laboratory test parameters wererarely associated with administration of MICARDIS®. Creatinine, Blood Urea Nitrogen:Increases in BUN (≥11.2 mg/dL) and creatinine (*0.5 mg/dL) were observed in 1.5% and0.6% of MICARDIS®-treated patients; the corresponding incidence was 0.3% each forplacebo-treated patients. These increases occurred primarily with MICARDIS® incombination with hydrochlorothiazide. One telmisartan-treated patient discontinuedtherapy due to increases in creatinine and blood urea nitrogen. Hemoglobin, Hematocrit:Clinically significant changes in hemoglobin and hematocrit (<10 mg/dL and <30%respectively) were rarely observed with MICARDIS® treatment and did not differ from ratesin placebo-treated patients. No patients discontinued therapy due to anemia. Serum UricAcid: An increase in serum uric acid (≥2.7 mg/dL) was reported in 1.7% of patientstreated with MICARDIS® and in 0.0% of patients treated with placebo. Clinically significanthyperuricemia (≥10 mEg/L) was observed in 2.3% of patients with MICARDIS® with 0.4%reported in patients at baseline. Increases in serum acid were primarily observed inpatients who received MICARDIS® in combination with hydrochlorothiazide. No patient wasdiscontinued from treatment due to hyperuricemia. Liver Function Tests: Clinicallysignificant elevations in AST and ALT (>3 times the upper limit of normal) occurred in 0.1%and 0.5% respectively of patients treated with MICARDIS® compared to 0.8% and 1.7% ofpatients receiving placebo. No telmisartan-treated patients discontinued therapy due toabnormal hepatic function. Serum Potassium: Marked laboratory changes in serumpotassium (≥+/-1.4 mEg/L) occurred rarely and with a lower frequency in MICARDIS®-treated patients (0.3%, 0.1%, respectively) than in placebo patients (0.6%, 0.3%,respectively). Clinically significant changes in potassium (that exceed 3 mEg/L were foundin 0.6% of MICARDIS®-treated patients, with 0.5% of these reported at baseline. Thecorresponding rates for placebo-treated patients were 0.6% and 0.8%. Cholesterol: Inplacebo-controlled trials, marked increases in serum cholesterol were reported in a totalof 6 telmisartan-treated patients (0.4%) and no placebo patients. Two of these patientswere followed over time; in both cases cholesterol values reverted to baseline levels.Serum elevations in cholesterol were reported as adverse events in 11 of 3,445 patients(0.3%) in all clinical trials. There were no reported cases of hypercholesterolemia intelmisartan-treated patients in placebo-controlled trials.POST-MARKETING EXPERIENCESince the introduction of telmisartan in the market, cases of erythema, pruritus,syncope/faint, insomnia, depression, stomach upset, vomiting, hypotension (includingorthostatic hypotension), bradycardia, tachycardia, abnormal hepatic function/liverdisorder, renal impairment including acute renal failure, hyperkalemia, dyspnoea, anaemia,eosinophilia, thrombocytopenia, weakness and lack of efficacy have been reported. Thefrequency of these effects is unknown. As with other angiotensin II antagonists rare casesof angio-oedema, pruritus, rash and urticaria have been reported. Cases of muscle pain,muscle weakness, myositis and rhabdomyolysis have been reported in patients receivingangiotensin II receptor blockers. In addition, since the introduction of telmisartan in themarket, cases with increased blood creatinine phosphokinase (CPK) have been reported.SYMPTOMS AND TREATMENT OF OVERDOSAGELimited data are available with regard to overdosage in humans. The most likelymanifestation of overdosage would be hypotension and/or tachycardia. If symptomatichypotension should occur, supportive treatment should be instituted. Telmisartan is notremoved by hemodialysis.DOSAGE AND ADMINISTRATIONThe recommended dose of MICARDIS® (telmisartan) is 80 mg once daily. Theantihypertensive effect is present within 2 weeks and maximal reduction is generallyattained after four weeks. If additional blood pressure reduction is required, a thiazidediuretic may be added. No initial dosing adjustment is necessary for elderly patients or forpatients with renal impairment, but greater sensitivity in some older individuals cannot beruled out. Markedly reduced telmisartan plasma levels were observed in patients onhemodialysis. For patients with hepatic impairment, a starting dose of 40 mg isrecommended (see PRECAUTIONS, Hepatic Impairment). MICARDIS® should be takenconsistently with or without food. Composition: MICARDIS® Tablets contain the followinginactive ingredients: sodium hydroxide, meglumine, povidone, sorbitol, and magnesiumstearate. Stability and Storage Recommendations: MICARDIS® Tablets arehygroscopic and require protection from moisture. Tablets are packaged in blisters andshould be stored at room temperature, 15-30°C (59-86°F). Tablets should not be removedfrom blisters until immediately prior to administration.AVAILABILITY OF DOSAGE FORMS MICARDIS® is available as white, oblong-shaped, uncoated tablets containing telmisartan40 mg or 80 mg. Tablets are marked with the Boehringer Ingelheim logo on one side, andon the other side, either 51H or 52H for the 40 mg and 80 mg strengths, respectively.MICARDIS® Tablets 40 mg are individually blister sealed in cartons of 28 tablets as 4 cardscontaining 7 tablets each. MICARDIS® Tablets 80 mg are individually blister sealed incartons of 28 tablets as 4 cards containing 7 tablets each.Product Monograph available upon request.References: 1. Mallion J, et al. ABPM comparison of the antihypertensive profiles ofthe selective angiotensin II receptor antagonists telmisartan and losartan in patientswith mild-to-moderate hypertension. J Hum Hypertens 1999;13:657-664. 2.Neldam S et al. Telmisartan Plus HCTZ vs. Amlodipine Plus HCTZ in Older Patients WithSystolic Hypertension: Results From a Large Ambulatory Blood Pressure MonitoringStudy. The American Journal of Geriatric Cardiology 2006:15(3):151-160. 3. WhiteWB, et al. Effects of the angiotensin II receptor blockers telmisartan versus valsartan onthe circadian variation of blood pressure: impact on the early morning period. Am JHypertens 2004;17:347-353. 4. Lacourcière Y, et al. A multicenter, 14-week study oftelmisartan and ramipril in patients with mild-to-moderate hypertension usingambulatory blood pressure monitoring. Am J Hypertens 2006;19:104-112. 5. Data onfile, Boehringer Ingelheim Canada Ltd. 6. MICARDIS® Product Monograph, BoehringerIngelheim (Canada) Ltd. August 14, 2006.

The incidence of adverse events was not dose-related and did not correlate with thegender, age, or race of patients. In addition, the following adverse events, with noestablished causality, were reported at an incidence of <1% in placebo-controlledclinical trials. Autonomic Nervous Systems Disorders: sweating increased. Body as aWhole: abdomen enlarged, allergy, cyst nos, fall, fever, leg pain, rigors, syncope.Cardiovascular Disorders, General: hypotension, hypotension-postural, leg edema.Central & Peripheral Nervous System Disorders: hypertonia, migraine-aggravated,muscle contraction-involuntary. Gastrointestinal System Disorders: anorexia, appetiteincreased, flatulence, gastrointestinal disorder nos, gastroenteritis, gastroesophagealreflux, melena, mouth dry, abdominal pain. Heart Rate & Rhythm Disorders: arrhythmia,tachycardia. Metabolic & Nutritional Disorders: diabetes mellitus, hypokalemia.Musculoskeletal System Disorders: arthritis, arthritis aggravated, arthrosis, bursitis,fascitis plantar, tendinitis. Myo Endo Pericardial & Valve Disorders: myocardialinfarction. Psychiatric Disorders: nervousness. Red Blood Cell Disorders: anemia.Reproductive Disorders, Female: vaginitis. Resistance Mechanism Disorders:abscess, infection, bacterial, moniliasis genital, otitis media. Respiratory SystemDisorders: bronchospasm, epistaxis, pneumonia, bronchitis. Skin & Appendage

Adverse Event, by System MICARDIS® Total Placebon=1,395 n=583

% %Body as a WholeBack pain 2.7 0.9Chest pain 1.3 1.2Fatigue 3.2 3.3Influenza-like symptoms 1.7 1.5Pain 3.5 4.3Central & Peripheral Nervous SystemDizziness 3.6 4.6Headache 8.0 15.6Somnolence 0.4 1.0Gastrointestinal SystemDiarrhea 2.6 1.0Dyspepsia 1.6 1.2Nausea 1.1 1.4Vomiting 0.4 1.0Musculoskeletal SystemMyalgia 1.1 0.7Respiratory SystemCoughing 1.6 1.7Pharyngitis 1.1 0.3Sinusitis 2.2 1.9Upper respiratory tract infection 6.5 4.6Heart Rate and Rhythm DisordersECG abnormal specific 0.2 1.0Palpitation 0.6 1.0Cardiovascular Disorders, GeneralHypertension 1.0 1.7Oedema peripheral 1.0 1.2

Boehringer Ingelheim (Canada) Ltd.5180 South Service Rd.,Burlington, Ontario L7L 5H4

MCE-PI5-GIM 5/1/07 10:15 PM Page 1


www.viha.ca

Do you want balance between your personal and professional life in a location where the outdoor living is easy? With its enviable west coast climate, stunning natural beauty and endless recreational opportunities, Campbell River offers a quality of life second to none!

The surrounding waters of Discovery Passage, and adjacent numerous lakes and rivers, offer an idyllic setting for outdoor enthusiasts. Enjoy year-round access to world-class golf courses or visit Mt. Washington Resort for spectacular winter skiing and summer mountain biking.

Campbell River & District General Hospital (5 closed ICU beds) provides services to a district population of 55,000. Enjoy a collegial and academic work group with opportunities for teaching and research. Candidates would be eligible to read echocardiograms/stress echocardiograms/holter monitors/spirometry/ECG’s and do stress tests, bronchoscopy and endoscopy.

Specialist colleagues include: ENT, plastics, general and orthopedic surgeons, anesthesiologists, obstetricians/gynecologists, pathologist, pediatricians and radiologists (on-site CT).

General Internists in Campbell River qualify for BC’s highly competitive on-call per diem and rural benefits from the Rural Retention program as well as a relocation incentive.

For more information contact:Ms. B. Warren, Coordinator Medical Administration1200 Dufferin Crescent, Nanaimo, BC V9S 2B7Fax: 250.716.7747 or email: [email protected]

oooooonnn-sn-sn-siteiteite CT CTCT)).).

Vancouver Island…the perfect climate for your future!General InternistsCampbell River, British Columbia

authors, shorten to three and add “et al.”

Col NF, Eckman MH, Karas RH, et al. Patient

specific decisions about hormone replacement

therapy in postmenopausal women. JAMA

1997;277:1140-7.

The sequence for chapters of a book should

be as follows: author(s) of chapter, chapter title,

author(s) of book, book title, edition, place of

publication, publisher, year of publication, page

numbers.

Galloway AC, Colvin SB, Grossi EA, et al.

Acquired heart disease. In: Schwartz SI, Shires

GT, Spencer FC, eds. Principles of Surgery, 6th

edition. New York: McGraw-Hill; 1994:845-99.

Tables and illustrationsEach table should be typed on a separate page,

and should have a legend at the top indicating

the information contained.

Illustrations may be sent electronically as a

TIFF or JPEG file on a disk or CD. Do not

embed images, etc., in text files. Note: Figure

reproduction cannot improve on the quality of the

originals.

Numbers, units, and abbreviationsMeasurements are to be metric. In scientific

text, physical quantities and units of time

should be expressed in numerals, for example, 2

kg, 6 mmol, 5 hours, 4°C.

Use only standard abbreviations, and avoid

using abbreviations in the title. Define all

abbreviations on their first mention.

PermissionsWritten permission must be obtained for

material that has been published in copyrighted

material; this includes tables, figures, and

quoted text that exceeds 150 words. Signed

patient release forms are required for

photographs of identifiable persons. A copy of

all permissions and patient release forms must

accompany the manuscript.

ProofsProofs for correction will be sent to authors by

e-mail as a Word file. Authors are asked to fax or

e-mail corrections back to the publisher within

72 hours. Unless otherwise indicated by the

author, manuscripts will be published as sent.

Please submit manuscripts to:

Dr. Hector Baillie

[email protected]

Copy: [email protected]

Only electronic submissions will be accepted.

The Canadian Journal of General InternalMedicine publishes concise papers, which

are subject to peer review. The Journalconsiders articles of original research, reviews,scholarly addresses, case reports, book reviews,historical interest, clinical tips, guidelines,letters to the editor, and so on. Requirementsare in accordance with “Uniform requirementsfor manuscripts submitted to biomedicaljournals” (www.icmje.org). The editorialpolicies of the journal are in line with those ofthe Council of Science Editors (www.councilscienceeditors.org/services/draft_approved.cfm).

Authors must disclose any commercialinterest in the subject of study and the source ofany support. A covering letter should state thatthe work is original and should include theaddress for correspondence, as well as thephone and fax numbers and e-mail address toensure rapid processing. Authors shouldidentify their affiliation with a hospital oruniversity department, and indicate if they arestudents, residents, fellows, or on staff. Afteracceptance of the manuscript, the author(s)must sign a copyright transfer agreement.

The Journal reserves the right to editmanuscripts to ensure conformity with theJournal’s style. Such editing will not affect thescientific content.

Manuscript PreparationManuscripts should be double-spaced andapproximately 800–1500 words. Themanuscript must be sent by e-mail attachment(Word or Rich Text Format only). An abstractof up to 150 words should be provided, and astatement that the study was approved by therelevant research ethics board should beincluded, where relevant.

The lead author should also provide a briefbio sketch and high-resolution photo ofhimself or herself (see details regardingillustrations below).

ReferencesReferences should be numbered consecutivelyin the text by superscript numerals.Corresponding references should be listed atthe end of the text. Exhaustive lists of referencesare not encouraged. Unpublished sources suchas personal communications should be citedwithin the text and not included in thereference list.

The sequence for journal references shouldbe as follows: author(s); title of paper; journalname abbreviated as in the Index Medicus; yearof publication, volume number, first and lastpage numbers. When there are more than three

Instructions to Authors

an internist in kandahar prioritizing gim through leadership · 2020. 7. 6. · 4 volume 2, issue...

Documents