Volume 4 issue 2 - Andrew John Publishing Inc.

Transcription

Volume 4, Issue 2 • May 2009
Publications Agreement Number 40025049 | 1911-1606
Cardiopulmonary
Resuscitation in Pregnancy
Francine Morin
Angiodysplasia of the
Gastrointestinal Tract
Narmin Kassam
www.csimonline.com
96.
CONTENTS
Volume 4, Issue 2
2009
Volume 4, Issue 2 • 2009
EDITOR-IN-CHIEF
Hector Baillie
EDITORIAL BOARD
Pat Bergin, Peter Brindley
Benjamin Chen, Kaberi Dasgupta
Don Echenberg, Don Farquhar
Bill Ghali, Bert Govig, Kerri Johannson
Luc Lanthier, Suzanne Morin, Jock Murray
Kathryn Myers, Louise Pilote
Colin Powell, Margot Roach
Linda Snell, George Veenhuyzen
Message from the President •
Message du président
57 Which Glass?
Bert Govig, MD
59 Quel verre choisirons-nous?
Bert Govig, MD
Women’s GIM
62 Cardiopulmonary Resuscitation and
Critical Care in Pregnancy
Francine Morin, MD
C S I M S TA F F
Ms. Domenica Utano
Ms. Alexi Campbell
MANAGING EDITOR
Susan Harrison
ART DIRECTOR
Binda Traver
PROOFREADER
Practice of GIM
64 Angiodysplasia of the
Gastrointestinal Tract and Bleeding:
An Overview
Narmin Kassam, MD, Anca Tapardal, MD, Alan
Thomson, MD
Scott Bryant
T R A N S L AT O R S
Marie Dumont, Victor Loewen
ADVERTISING
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 Robinson
[email protected]
ACCOUNTING
Susan McClung
GROUP PUBLISHER
John D. Birkby
Perioperative Medicine •
Médecine périopératoire
68 Complication rare d’une procédure
courante : pneumomédiastin
secondaire à un tube naso-gastrique
Luc Lanthier, MD, François Lamontagne, MD,
Catherine St-Pierre, MD
68 Rare Complication of a Common
Procedure: Pneumomediastinum
Secondary to the Insertion of a
Nasogastric Tube
Luc Lanthier, MD, François Lamontagne, MD,
Catherine St-Pierre, MD
70 Perioperative Considerations in
Frail Older Adults
Canadian Journal of General Internal Medicine is published
four times a year by Andrew John Publishing Inc., with
offices located at 115 King Street West, Suite 220, Dundas,
ON L9H 1V1.
We welcome editorial submissions but cannot assume
responsibility or commitment for unsolicited material.Any editorial material, including photographs that are accepted from
an unsolicited contributor, will become the property of
Andrew John Publishing Inc.
The publisher and the Canadian Society of Internal Medicine
shall not be liable for any of the views expressed by the
authors published in Canadian Journal of General Internal
Medicine, nor shall these opinions necessarily reflect those of
the publisher.
Roger Y. Wong, MD, Joy Liao, MD, Anson Li,
MD, Naaz Parmar, MD
Medical Humanities
75 Sabbaticals: Why Every Physician
Needs a “Braindusting”
T. Jock Murray, MD
Case Reviews • Réexamen des cas
77 Eponyms in Medicine
Hector M. Baillie, MD
79 Une lipase qui induit en erreur…
Dominique Martineau-Beaulieu, MD, JeanDaniel Baillargeon, MD
82 Post-device Chest Pain:
A Cause for Concern
Clarence Khoo, MD, Jason Andrade, MD
86 Pseudopheochromocytoma in
Black Africans: A Case Report
from Senegal
Seck Sidy Mohamed, MD, Ka Elhadj Fary, MD,
Ba Sidy, Niang Abdou, MD, Diouf Boucar, MD
88 Superinfected Pulmonary Bulla
in a Freebase Cocaine User
Jeffrey Segal, MD, Barbara Young, MD
MedEd
80 Multiple Mentoring:
A New Paradigm?
Michelle Elizov, MD
Health Promotion
85 Health Promotion:
A New Mandate for CSIM
Norm Campbell, MD, Don Echenberg, MD, Bert
Govig, MD, Akbar Panju, MBChB
EKG & U
73 Electrocardiographic Neurology
George Veenhuyzen, MD
For Instructions to Authors, please visit
www.andrewjohnpublishing.com/
CGJIM/instructionstoauthors.html
•••••
Every effort has been made to ensure that the information
provided herein is accurate and in accord with standards
accepted at the time of printing. However, readers are
advised to check the most current product information provided by the manufacturer of each drug to verify the recommended dose, the method and duration of administration,
and contraindications. It is the responsibility of the licensed
prescriber to determine the dosages and best treatment for
each patient. Neither the publisher nor the editor assumes
any liability for any injury and/or damage to persons or
property arising from this publication.
ABOUT THE COVER
This photo was taken near Cabri, Saskatchewan. It was shot during the Labour Day long weekend in 2008. The photographer writes, “I am originally from Newfoundland, now living in Calgary, and I’d never been to Saskatchewan.
Friends of mine took me to their respective home towns – Swift Current and Cabri – to give me a taste of
Saskatchewan life.” Matt Greer is 26 years old and an amateur photographer. He works for the Energy Resources
Conservation Board in Calgary, where he has lived since June of 2007.
Canadian Journal of General Internal Medicine
Volume 4, Issue 2, May 2009
55
CSIM Members of Council
Dr. Bert Govig
President, Québec Region Representative
Amos, QC | [email protected]
Dr. Finlay McAlister
President Elect, Vice-President,
Research/Awards Committee
Edmonton, AB | [email protected]
Dr. Hector Baillie
Editor-in-Chief,
Nanaimo, BC | [email protected]
Message from the President
Which Glass?
Bert Govig, MD
About the Author
Bert Govig is with the Department of Internal Medicine at CSSS Les Eskers
de L’Abitibi, Amos; is physician in chief with Coalition pour L’Acquisition de
Saines Habitudes (CASH); and is with the Department of Internal
Medicine at McGill University, Montréal, Québec.
Dr. Neil Gibson
Western Region Representative
St. Albert, AB | [email protected]
Dr. Benjamin Chen
Secretary-Treasurer,
Ontario Region Representative
Kingston, ON | [email protected]
Dr. Patrick Bergin
Eastern Region Representative
Charlottetown, PEI | [email protected]
Dr. Donald Echenberg
Québec Region Representative, CPD SubCommittee Chair, CMA Representative
Sherbrooke, QC | [email protected]
Dr. Mahesh K. Raju
Eastern Region Representative
Saint John, NB | [email protected]
Dr. Jim Nishikawa
Ontario Region Representative, RCPSC Specialty
Committee in Internal Medicine Representative
Ottawa, ON | [email protected]
Dr. Lucie Opatrny
Québec Region Representative
Montreal, QC | [email protected]
Dr. Nadine Lahoud
Québec Region Representative
LaSalle, QC | [email protected]
Dr. Maria Bacchus
Western Region Representative, Vice-President,
Education Committee | Calgary, AB
[email protected]
Dr. Barry O. Kassen
Vancouver, BC |
[email protected]
Dr. Amy Hendricks
Yellowknife, NT | [email protected]
Dr. Neil Maharaj
Vice-President, Membership Affairs
Milton, ON | [email protected]
Dr. Kerri Johannson
Resident Representative
Calgary, AB | [email protected]
Dr. Ann Colbourne
Vice-President,
Annual Scientific Meeting Representative
Edmonton, AB | [email protected]
Dr. Anthony Weinberg
2009 Annual Meeting Committee Chair
Ottawa, ON | [email protected]
Dr. Akbar Panju
Vice-President, Health Promotion Committee
Hamilton, ON | [email protected]
eneral internal medicine (GIM) plays a
core role in the Canadian health care
system. In every province in Canada, internists
are leaders and workhorses in research,
teaching, administration, clinical care, and
health promotion. Admittedly, I am preaching
to the choir in this journal, but there is growing
recognition throughout the Canadian health
care system of the value of generalism that GIM
brings. The Canadian Society of Internal
Medicine and other bodies have explored and
promoted the roles of the generalist for over a
decade. We have learned that we are remarkably
united in the vision stated above, and
remarkably different in many other ways.
GIM is, by definition, the most diverse of all
specialties. But perhaps the biggest divide is
between those that practise in university and in
community settings. Speaking for community
internists, most of us have a pretty good feeling
of what goes on in university settings – we are,
after all, products of that system. In contrast,
many academics cannot fathom the nature or
the needs of the community internists; but,
happily, this is changing. Many internal
medicine programs routinely send residents
out to community settings to train, links
between the communities and the universities
are becoming formalized along corridors of
care, and some centres are recognizing
community internists with academic
appointments. All of this helps us to better
understand the larger role of the general
internist and to promote a unified vision of our
specialty.
Such a vision cannot evolve without
confronting major resistance from many
sources and for many reasons. Internists are, by
and large, conservative creatures. Most of us
probably fit the criteria for what industry
analysts call “late adopters.” We have been
brainwashed to look not just for the evidence
but for the bias that gave rise to that evidence;
and we have all seen more than one new
wonder drug pulled from the market in the
early years of its use. We know that drugs must
not only be efficacious and effective, they must
G
be safe, and that meaningful time frames are
usually intermediate to long term rather than
short term. One of our edicts is to “do no
harm,” and so, to a practising internist, the glass
of a new wonder drug may be half empty at
best or toxic at worst. In the absence of very
strong evidence or large treatment effects, the
element of unknown risk looms high in our
collective consciousness, and we often conclude
that maintaining the status quo is the most
prudent move. Such is the mindset of the
typical “conservative” internist.
Our specialty faces some interesting choices
and challenges at the present time. Five to 10
years ago, our discipline was on a doomsday
trajectory, with an aging practitioner base, low
recruitment, and dwindling numbers. GIM was
not recognized by the Royal College or by the
vast majority of universities in our country. In
recent years, we have promoted a vision of GIM
as a distinct clinical specialty with core values
and knowledge that unite a very diverse group
of professionals across academic and
community settings. Where this vision has
taken hold, GIM has flourished.
It is clear that the recognition of GIM as a
valid specialty will be good for our patients,
and our health care system. The time is upon us
to focus on our commonalities rather than our
differences and be true advocates for our
discipline and for the health care system in
general. Despite our conservative natures, we
must see the choices before us for what they
are. Failure to gain recognition for GIM is a
glass half full – this is the status quo – a
tempered poison that we have taken for over 20
years, and we know that it leads to a slow death.
The option for GIM recognition also
represents a glass half full, but with a solid
theoretical foundation and empirical evidence
that this is indeed very good for the growth and
development of our specialty. We need to
continue to bring internists and other
stakeholders to the table as we flush out this
option – but time is not on our side.
Our discipline is on the stretcher; which glass
will you reach for?
57
Sanofi-aventis and Bristol-Myers Squibb
Canada are proud to be Platinum
Sponsors of the 2009 Canadian Society
of Internal Medicine
Sanofi-aventis, a leading global pharmaceutical
company, discovers, develops and distributes therapeutic
solutions to improve the lives of everyone. Backed by a
world-class R&D organization, the company is
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the central nervous system, internal medicine and
vaccines. Sanofi-aventis is represented in Canada by
the pharmaceutical company sanofi-aventis Canada Inc.,
based in Laval, Quebec, and by the vaccines company
Sanofi Pasteur Limited, based in Toronto, Ontario.
Together they employ more than 2,000 people across the
country.
Sanofi-aventis est un leader mondial de l’industrie
pharmaceutique qui recherche, développe et diffuse des
solutions thérapeutiques pour améliorer la vie de chacun.
Sanofi-aventis s’appuie sur une recherche internationale
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la médecine interne et les vaccins.
Sanofi-aventis est représentée au Canada par sanofiaventis Canada Inc., entreprise pharmaceutique établie à
Laval, au Québec, et par Sanofi Pasteur Limitée,
producteur de vaccins établi à Toronto, Ontario. Ces
deux entreprises comptent plus de 2 000 employés un
peu partout au pays.
Bristol-Myers Squibb Canada is an indirect whollyowned subsidiary of Bristol-Myers Squibb Company, a
global pharmaceutical and related health care products
company whose mission is to extend and enhance
human life. Bristol-Myers Squibb Canada is a leading
provider of medicines to fight cancer, cardiovascular and
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Bristol-Myers
Squibb
Canada’s
operations
are
headquartered in Montréal, Québec.
Bristol-Myers Squibb Canada est une filiale indirecte
détenue en propriété exclusive de Bristol-Myers Squibb,
une société d’envergure mondiale spécialisée dans les
produits pharmaceutiques et les produits de santé
connexes et dont la mission est de prolonger et
d’améliorer la vie humaine.
Bristol-Myers Squibb
Canada est un chef de file dans la fabrication de
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contre
le
cancer,
les
troubles
cardiovasculaires et métaboliques, les maladies
infectieuses (dont le VIH/sida), les maladies du système
nerveux et les maladies mentales graves. Bristol-Myers
Squibb est cotée à la bourse de New York sous le
symbole BMY. Le siège social de Bristol-Myers Squibb
Canada est à Montréal, au Québec.
An agreement between sanofi-aventis and Bristol-Myers Squibb for the codevelopment and marketing of clopidogrel and irbesartan, two compounds from sanofi-aventis research
Un accord entre sanofi-aventis et Bristol-Myers Squibb pour le développement et la commercialisation de clopidogrel et d’irbésartan, molécules issues de la recherche de sanofi-aventis
Message du président
Quel verre choisirons-nous?
Bert Govig, MD
Au sujet de l’auteur
Bert Govig œuvre au sein du Service de médecine interne au CSSS Les Eskers de l’Abitibi à Amos; il est médecin en chef de la
Coalition pour l’acquisition de saines habitudes (CASH); il enseigne au Département de médecine interne de l’Université
McGill à Montréal (Québec).
a médecine interne générale occupe une place centrale dans le
système de santé au Canada. Dans toutes les provinces du pays, les
internistes participent à la recherche, à l’enseignement, à
l’administration, à la prestation des services de santé et à la promotion
de la santé, que ce soit à titre de chefs de file ou d’artisans. Certes, je
prêche à des convertis dans les pages de cette revue, n’empêche que la
médecine interne générale est en voie de redorer le blason du
généralisme à la grandeur du système de santé au pays. Voilà plus de 10
ans que la Société canadienne de médecine interne et d’autres
organismes et instances se penchent sur la question de la place du
généraliste et en font la promotion. Au fil des ans, nous avons découvert
à quel point nous avons la même vision et à quel point nous sommes
différents à bien des égards.
La médecine interne générale est essentiellement la spécialité la plus
diverse de toutes. Mais sans doute que la démarcation la plus franche est
celle qui sépare les praticiens des milieux universitaires et les praticiens
des milieux communautaires. Étant du camp des internistes
communautaires, je peux dire que nous avons une bonne idée de ce qui
se passe dans les milieux universitaires – ne sommes-nous pas, après
tout, des produits de ce système? Par contre, les praticiens universitaires
sont nombreux à ne pas avoir la moindre idée de la pratique ou des
besoins des internistes communautaires; heureusement, la situation
change. Nombre de programmes de médecine interne prévoient des
stages en milieu communautaire, les liens entre les collectivités et les
universités s’officialisent dans le cadre des corridors de soins, et certains
établissements, conscients de la valeur des internistes communautaires,
leur offrent des postes universitaires. Ce mouvement contribue à mieux
faire connaître le vaste rôle de l’interniste généraliste et favorise
l’unification de notre spécialité.
Cette unification ne saurait s’imposer sans provoquer de résistance
majeure de bien des sources et pour bien des motifs. L’interniste se
caractérise par sa nature conservatrice. À telle enseigne que l’expression
« adopteur tardif », issue du monde de la commercialisation, nous irait
bien, à la plupart d’entre nous. Nous avons été conditionnés à ne pas
nous en tenir aux données probantes, mais à déceler les biais sousjacents; sans compter que nous avons été témoins à plus d’une reprise
du retrait du marché d’un médicament miracle après quelques années
d’utilisation. Nous savons pertinemment que les médicaments doivent
être efficaces et efficients, mais que cela n’est rien s’ils ne sont pas sûrs,
L
et que leur mise à l’épreuve ne se limite pas au court terme mais qu’elle
s’étire à moyen et à long terme. Conformément à l’un de nos principes,
celui de « ne pas causer de préjudices », l’interniste considère que le
verre que représente le nouveau médicament prodigieux est à moitié
vide au mieux ou que son contenu est toxique au pire. Sans données
probantes solidement concluantes ou effet thérapeutique de grande
ampleur, les risques l’emportent sur les avantages incertains dans notre
conscience collective, et par prudence, nous préférons la situation telle
qu’elle est aux promesses du médicament qui nous paraissent vaines.
C’est ainsi que fonctionne l’esprit de l’interniste conservateur type !
Notre spécialité est à la croisée des chemins, devant des possibilités et
des défis multiples. Il y a 10 ans ou même cinq, les perspectives
n’étaient pas trop réjouissantes pour notre discipline : un effectif
vieillissant, le recrutement peu fructueux, des chiffres à la baisse. Le
Collège royal, ainsi que la grande majorité des universités du pays, ne
reconnaissaient pas la médecine interne générale. Ces années, nous les
avons consacrées à promouvoir cette spécialité clinique distincte à nos
yeux avec ses connaissances et ses valeurs propres, qui rassemble des
professionnels d’horizons variés, universitaires ou communautaires. Là
où cette vision s’est ancrée, la médecine interne générale s’est épanouie.
À n’en pas douter, la reconnaissance de la médicine interne générale
en tant que spécialité en bonne et due forme sera bénéfique autant pour
nos patients que pour le système de santé. Il nous revient de mettre
l’accent sur ce que nous avons en commun et de faire abstraction de nos
différences, pour devenir d’ardents défenseurs de notre discipline et du
système de santé en général. Malgré notre nature conservatrice, nous
devons considérer les choix qui s’offrent à nous pour ce qu’ils sont. Ne
pas obtenir la reconnaissance de la médecine interne générale, c’est le
verre à moitié plein – rien ne change, en fait – un poison insidieux que
l’on nous sert depuis 20 ans et qui, nous le savons, nous fera mourir à
petit feu.
La reconnaissance de la médecine interne générale prend la forme elle
aussi d’un verre à moitié plein, mais son contenu favorisera la croissance
et l’expansion de notre spécialité, comme en témoignent un rigoureux
fondement théorique et des données probantes empiriques. Il nous faut
continuer de convaincre internistes et intervenants du bien-fondé de
cette option – mais le temps risque de manquer. La discipline est sur une
civière : quel verre prendrez-vous?
59
91.
Wo m e n ’s G I M
Cardiopulmonary Resuscitation and Critical Care in Pregnancy
Francine Morin, MD
About the Author
Francine Morin is a member of the Division of Obstetric Medicine, Department of Obstetrics and Gynecology, CHU SainteJustine, Montreal, Quebec. Correspondence may be directed to [email protected].
ardiopulmonary arrest in the pregnant woman is a rare event, with
an estimated incidence of 1 in 30,000 pregnancies.1 Therefore,
most health care providers have no experience and little knowledge of
its management. The admission of a pregnant woman to the intensive
care unit (ICU) is also an uncommon event that triggers highly
emotional reactions and, when combined with lack of experience, can
put the parturient at risk.
This article reviews the pertinent physiological changes of
pregnancy and the current knowledge and recommendations
regarding the management of a pregnant woman in cardiac arrest. It
also briefly presents the basic principles of care in a pregnant patient
admitted to the ICU.
Table 1. Common Changes in Laboratory and Cardiac
Evaluations in Pregnancy
C
Substance or Test
Units or Notes
Leukocytes
10,000–15,000
Hemoglobin
110–120 g/L
Pco2
Creatinine
28–32 mm Hg
Osmolarity
Decreased
280 mmol/kg
Alkaline phosphatase
Increased
Placental origin
Fibrinogen
Increased by 50%
3–6 g/L
Physiological Changes in Pregnancy
EKG
Left axis deviation
Cardiac output increases by as much as 50% by 32 weeks’ gestation. At
20 weeks, significant aortocaval compression compromises venous
return, and 30% of women have a significant drop in blood pressure
when lying supine.2 In late pregnancy, the vena cava may be
completely obstructed and cardiac output can be increased by as
much as 25–30% simply by moving the patient in a left lateral
decubitus position.1 Uterine blood flow accounts for 10–30% of the
cardiac output at the end of pregnancy.3
The pregnant uterus and increased breast size lead to a decrease in
functional residual capacity and a 45% decrease in chest compliance.
With such limited reserve and increased oxygen consumption, there
can be a rapid decline in oxygen saturation following hypoventilation.
Moreover, the presence of mucosal edema and friability, increased
secretions, and weight gain all contribute to a more difficult airway
intubation. There is also a greater risk of aspiration due to the
relaxation of the esophageal sphincter.2 Additional physiological
changes are listed in Table 1.
Echocardiogram
Increased left atrial and ventricular end-diastolic
dimensions
Increased left ventricular wall thickness
Cardiac Arrest in Pregnancy
Thoracic, respiratory, and circulatory changes impair the
management of a pregnant woman in cardiac arrest. Chest
compression is less efficient because of decreased chest compliance.
Cardiac output is further compromised by aortocaval compression.
Advanced Cardiac Life Support (ACLS) algorithms remain the same
in the pregnant woman. However, the following modifications are
necessary: (1) earlier definitive airway control, (2) left lateral
displacement of the uterus, (3) consideration of an early Caesarean
delivery, and (4) the use of adhesive pads for defibrillation and the
62
40–60 µmol/L
EKG = electrocardiogram; Pco2 = partial pressure of carbon dioxide.
removal of the fetal monitor to avoid electrical arcing.4
Early intubation is mandatory, with attention to the use of a smaller
endotracheal tube (0.5–1 mm smaller) and the avoidance of nasal
intubation because of the increased mucosal friability.4 Good
positioning is critical. A laryngoscope with a shorter handle is useful as
the presence of large breasts may interfere with access.
To relieve the aortocaval compression, one person is dedicated to
manually displacing the uterus upward and to the left. A pillow can be
placed under the right buttock. I do not recommend the use of devices
such as the Cardiff wedge, which, by putting the mother in the left
lateral decubitus position, decreases the force of manual compression.5
After 4 minutes of unsuccessful resuscitation, the team leader must
act to expedite Caesarean delivery. This recommendation follows two
reviews by Katz et al. In 1986, Katz looked at all published cases of
perimortem Caesarean delivery between 1900 and 1986.6 Among the
188 surviving babies, there was information on 61, of whom 70% were
delivered within 5 minutes of arrest and all of whom were
neurologically intact. At that time, the recommendation became to
initiate a Caesarean delivery at 4 minutes so that the baby would be
born at 5 minutes. The aim is to increase the survival of an intact infant
but also to improve the survival of the mother.
In 2005, Katz et al. reviewed subsequent cases published between
Morin
1985 and 2004.7 He found 38 reported perimortem Caesarean
deliveries, of which 28 resulted in 34 surviving infants. Among the 20
women with a potentially reversible cause of arrest, 13 survived; 12 had
a return of pulse when the uterus was emptied. The author concluded
that this report supports the 4-minute rule. As already mentioned,
resuscitation is difficult in a pregnant woman. There is only an
estimated 10% of a normal cardiac output generated by manual
compression. The Caesarean delivery increases the venous return by
freeing aortocaval compression. Chest compressions are mechanically
easier and generate a higher cardiac output. Following arrest, the
obstetrical and pediatric teams must be notified immediately. However,
with such short notice, the team leader may become responsible for the
Caesarean delivery.
At most institutions, a fetus is considered viable at 24 weeks’ gestation
and aortocaval compression becomes significant at about 20–24 weeks.
Therefore, a Caesarean section is indicated as of 20–24 weeks’ gestation
when there is a potentially reversible cause of arrest. If there is no
chance of maternal survival, the decision to perform a Caesarean
delivery will depend on the local ability to care for the baby and the
judgment of the team leader. Fundal height at the level of the umbilicus
corresponds to 20 weeks’ gestation, and 4 centimetres above the
umbilicus to 24 weeks.
There is insufficient time to transfer the patient or to wait for
ultrasonography. The Caesarean is performed through a vertical
incision between the umbilicus and pubis. Rapid action is of the utmost
importance. Can one do harm by proceeding too early or by a lack of
surgical experience? The response is no. After all, a patient in cardiac
arrest is, by definition, dead. A Caesarean delivery can only improve her
chance of survival by improving hemodynamics, regardless of the cause
of arrest. The longer any patients are in cardiac arrest, the less likely they
are to survive. Therefore, all personnel on the resuscitation team must
be familiar with the preceding guidelines and essential equipment
needed to perform a Caesarean delivery should be stocked on all
resuscitation carts.
Thirdly, any choice of medication must be dictated by the medical
condition; the dose must not be modified for fear of fetal harm. Although
benzodiazepines, narcotics, and nondepolarizing neuromuscular
blockers cross the placenta (the latter in very small quantities), they can
be used. If the fetus is delivered shortly after the administration of these
agents, it will need respiratory support.2 Renal clearance is increased,
and care must be taken to adjust the medication dosing (e.g., with
aminoglycosides). Use of the U.S. Food and Drug Administration
(FDA) classification for medication use in pregnancy is not sufficient,
and it is recommended to consult knowledgeable pharmacists or
physicians.9 Table 2 lists medications to avoid.
Fourthly, radiological examinations must be done when clinically
indicated. An exposure <1 rad is safe. Teratogenesis occurs at exposures
of more than 10–20 rad. For each additional rad (above 1 rad), there is
the potential risk of one additional cancer death per 1,700 fetal
exposures, based on theoretical projections.10 An exaggerated fear of
radiation is likely to cause greater harm to the pregnant patient than the
radiation itself. Table 3 lists fetal radiation doses from common
radiological examinations.
Indications for early goal therapy, activated protein C, thrombolysis,
and the use of corticosteroids remain the same.11 Strict glycemic control
is probably more important in pregnancy to reduce the metabolic stress
Pregnant Woman in the ICU
NSAIDs = nonsteroidal anti-inflammatory drugs.
Admission of an obstetrical patient to an ICU occurs in 2–4 per 1,000
deliveries. The two most common reasons for admission are
preeclampsia-related complications and postpartum hemorrhage.8 The
majority of admissions occur during the postpartum period. Thus,
admitting a pregnant woman is an uncommon occurrence. Physicians
tend to withhold investigations and medications because of an
exaggerated fear of harming the fetus. A full review is beyond the scope
of this article. However, some basic principles are worthwhile.
Firstly, early definitive airway management is important, as well as
the maintenance of oxygen saturation >95% and the avoidance of
alkalosis (which can impair uteroplacental flow).
Secondly, attention to the left lateral displacement of the uterus is
critical to alleviate aortocaval compression and reduce the risk of
hypotension. All vasopressor agents have a theoretical risk of decreasing
uterine flow; however, if hypotension persists despite left lateral
positioning and adequate and aggressive volume replacement, one must
use the most appropriate agent.
Table 2. Medications to Avoid
Medication
Notes
NSAIDs
After 26 weeks’ gestation: risk of premature
closure of ductus arteriosus
Before 26 weeks: can be used but small risk of
reversible oligohydramnios
Quinolone
Relative contraindication
Deposition in fetal cartilage
Restricted use in pediatrics
Tetracycline
Discoloration of deciduous teeth
Warfarin
Exposition 6–9 weeks: embryopathy
Throughout pregnancy: central nervous system
bleeding/neurological anomalies
Table 3. Approximate Fetal Doses from Common
Radiological Examinations
Examination
Approximate Fetal Dose (rad)
Chest radiography
0.001–0.008
Abdomen radiography
0.14–0.42
CT scan of head
<0.0005
CT scan of thorax
0.006–0.096
CT scan of abdomen
0.8–4.9
Pulmonary angiography
Via brachial artery
<0.05
Via femoral artery
0.220–0.37
Perfusion scan
0.04–0.08
Ventilation scan
0.01–0.03
CT = computed tomography.
63
Cardiopulmonary Resuscitation and Critical Care in Pregnancy
of hyperglycemia in the fetus. Thromboprophylaxis must be considered
because of the increased risk of venous thrombosis in pregnancy.
Lastly, delivery of the fetus is indicated if it will improve the survival
or hemodynamic and respiratory status of the mother. It is also
indicated if there is fetal distress, but only after the mother has been
stabilized.
3. Mallampalli A, Guy E. Cardiac arrest in pregnancy and somatic
support after brain death. Crit Care Med 2005;33(10
Suppl):S325–31.
4. European Resuscitation Council. European Resuscitation Council
Guidelines for Resuscitation 2005. Resuscitation 2005;67(Suppl
1):S159–70.
5. Kiss G. Remarks on guidelines ERC 2000: cardiac arrest associated
Summary
In summary, when taking care of a pregnant woman, one must not
forget that her well-being has priority over that of her fetus. We must
take particular care with regard to left lateral positioning and early
definitive airway management. We must initiate Caesarean delivery at 4
minutes into cardiac arrest to improve the chance of survival of a
neurologically intact mother and baby. Lastly, we must integrate the
care of the parturient in ACLS and ICU protocols in spite of inadequate
research, and we must not be afraid to investigate and properly treat an
acutely ill pregnant woman.
with pregnancy. Resuscitation 2004;61:367–9.
6. Katz VL, Dotters DJ, Droegemueller W. Perimortem cesarean
delivery. Obstet Gynecol 1986;68:571–6.
7. Katz V, Balderston K, DeFreest M. Perimortem cesarean delivery:
were our assumptions correct? Am J Obstet Gynecol
2005;192:1916–22.
8. Zeeman GG. Obstetric critical care: a blueprint for improved
outcomes. Crit Care Med 2006;34(9 Suppl):S208–14.
9. Briggs GG, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation,
8th edition. Lippincott Williams & Wilkins; 2008.
References
1. Atta E, Gardner M. Cardiopulmonary resuscitation in pregnancy.
Obstet Gynecol Clin North Am 2007;34:585–97.
2. Lapinsky SE, Kruczynski K, Slutsky AS. Critical care in the pregnant
patient. Am J Respir Crit Care Med 1995;152:427–55.
10. Lowe SA. Diagnostic radiography in pregnancy: risks and reality.
Aust N Z J Obstet Gynaecol 2004;44:191–6.
11. Shapiro JM. Critical care of the obstetric patient. J Intensive Care
Med 2006;21:278–87.
Practice of GIM
Angiodysplasia of the Gastrointestinal Tract and Bleeding: An Overview
Narmin Kassam, MD, Anca Tapardal, MD, Alan Thomson, MD
About the Authors
Narmin Kassam and Alan Thomson are members of the Division of General Internal Medicine, University of Alberta,
Edmonton, Alberta. Anca Tapardal (left) is a fourth-year internal medicine resident.
ngiodysplasia is the most common vascular abnormality of the
gastrointestinal (GI) tract and the second leading cause of lower GI
bleeding in patients older than 60 years, after diverticulosis.1 Phillips
first described a vascular abnormality that caused bleeding from the
large bowel in a letter to the London Medical Gazette in 1839. Galdabini
first used the name angiodysplasia in 1974. However, confusion about
the exact nature of these lesions resulted in a multitude of terms that
included arteriovenous malformation, hemangioma, telangiectasia, and
vascular ectasia. These terms have varying pathophysiologies that all
present with GI bleeding.
A
64
Pathophysiology
Angiodysplasia is a degenerative lesion of previously healthy blood
vessels found most commonly in the cecum and proximal ascending
colon. Lesions typically are nonpalpable and small (<5 mm). Seventyseven percent of angiodysplasias are located in the cecum and ascending
colon, 15% are located in the jejunum and ileum, and the remainder are
distributed throughout the alimentary tract. Angiodysplasia may
present as an isolated lesion but more commonly as multiple vascular
lesions. It is not associated with angiomatous lesions of the skin or other
viscera.
Kassam et al.
The exact mechanism of development of angiodysplasia is not
known. Chronic venous obstruction may play a role. This hypothesis
accounts for the high prevalence of these lesions in the right colon and
is based on the Law of Laplace. Wall tension is highest in bowel
segments with the greatest diameter, such as the right colon. Dilated
submucosal veins are the most consistent histological findings and may
represent the earliest abnormality in colonic angiodysplasia, supporting
the theory of chronic venous obstruction in the genesis of lesions.
more patients having aortic sclerosis than aortic stenosis.5 Bleeding
from angiodysplastic lesions in the upper and lower GI tracts has been
reported in patients with von Willebrand’s disease.6 Because factor VIII
complex is synthesized partly in vascular endothelial cells, patients with
von Willebrand’s disease and angiodysplasia have been proposed to
have an underlying endothelial defect that may be related to the
subsequent development of the two disorders. Finally, bleeding
angiodysplastic lesions in the upper GI tract have been found with a
high prevalence in patients with chronic renal failure requiring dialysis.7
Epidemiology
Differential Diagnosis
Angiodysplasia may account for approximately 6% of cases of lower
GI bleeding. It may be observed incidentally at colonoscopy in as many
as 0.8% of patients older than 50 years.2 Small bowel angiodysplasia
may account for 30–40% of cases of GI bleeding of obscure origin. Most
patients found to have angiodysplasia are older than 60 years; many are
over 70. However, case reports exist of angiodysplasia in young people.
Angiodysplasia occurs with equal frequency in men and women, and
there is no racial predilection.
The differential diagnosis for patients presenting with GI bleeding in
a pattern similar to that expected in angiodysplasia includes colon
and rectal cancers, colonic polyps, ischemic colitis, diverticulosis,
hemorrhoids, metastatic cancer with an unknown primary, portal
hypertension, enterocolitis, and other rare conditions. Figure 1 outlines
an algorithm for approaching the work-up of patients presenting with
GI bleeding.
Diagnosis
Clinical Presentation
The clinical presentation of angiodysplasia is related to GI bleeding or
its consequences. However, because these lesions may be located
throughout the GI tract and because the rate of bleeding may be
variable, presentations range from hematemesis or hematochezia to
occult anemia. Bleeding is usually chronic or recurrent and, in most
cases, low grade and painless because of the venous source. The
estimated incidence of active, ongoing GI bleeding in patients with
angiodysplasia is less than 10%.
Patients with colonic angiodysplasia may present with hematochezia
(0–60%), melena (0–26%), hemoccult-positive stool (4–47%), or irondeficiency anemia (0–51%). Ninety percent of angiodysplastic lesions
stop the bleeding spontaneously. Hematemesis is frequently observed in
patients with angiodysplasia of the upper GI tract: the presentation of
hemodynamically well-compensated, chronic bleeding is typical and
often suggests the diagnosis.
Hemodynamic instability may occur if bleeding is massive. This is
observed in 15% of cases. Vital signs may demonstrate tachycardia,
hypotension, and postural changes based on the amount of blood loss.
In most cases, bleeding presents as bright red blood per the rectum but
can also be maroon or melena. Stool typically is guaiac positive. Since
bleeding may be intermittent, alternating positive and negative guaiac
stools can be found. In 40–60% of patients with gastric and duodenal
angiodysplasia, multiple lesions are observed at endoscopy, and 15–20%
have accompanying colonic lesions that also tend to multiple rather
than single.
Associated Conditions
Angiodysplasia has been reported to be associated with a number of
other conditions. In 1958, Heyde first reported the combination of
calcific aortic stenosis and GI bleeding due to angiodysplasia of the
colon.3 A month later, Schwartz suggested a similar association.4 Studies
using echocardiography have indicated that only a few patients with
angiodysplastic lesions have significant valvular heart disease, with
Assessment
Approximately 10% of patients who bleed from angiodysplasia present
with anemia and iron deficiency only. As many as 15% of patients with
bleeding angiodysplasia have stool that is intermittently positive for
occult blood.
A number of imaging studies may be useful in the work-up for
angiodysplasia. Radionuclide scanning using technetium Tc
99m–labelled red blood cells or 99mTc sulphur colloid can detect
bleeding with rates as low as 0.1 mL/min. However, due to the
intermittent bleeding nature of angiodysplasia, radionuclide studies
are of limited use. Technetium has a long half-life, and repeat imaging
may detect bleeding up to 72 hours after a single injection.
Technetium Tc 99m sulphur colloid has a half-life of only 3 minutes;
therefore, this tracer is helpful only in patients with active bleeding.
Although nuclear scans are noninvasive and relatively easy to perform,
they lack the specificity of an angiogram in differentiating the nature
of bleeding lesions. Nuclear scans also do not have the therapeutic
potential of angiography. Selective mesenteric angiography is a useful
diagnostic technique, especially in patients with massive bleeding.
Active bleeding is detected in 6–20% of patients, depending on the
rate of bleeding (as low as 0.5 mL/min), the technique, and timing of
angiography in relation to the period of bleeding. The sensitivity of
detecting ectatic changes in vascular lesions is 58–86%, but this
abnormality may also be observed in other disorders, such as
malignancy. Helical computed tomography (CT) angiography can
detect extravasation from angiodysplasia and may potentially be an
important noninvasive test in patients with obscure, actively bleeding
sites. Capsule endoscopy has been reported to detect cecal
angiodysplasias in selected cases and is particularly useful to
demonstrate actively bleeding in small intestinal lesions, but its role as
a diagnostic test for the colon is still experimental.8 Finally, air contrast
barium enema is not recommended during acute lower GI bleeding
because the lesions are too small to be detected and the contrast can
obscure other diagnostic studies.
Endoscopy is the most common and reliable method of diagnosing
angiodysplasia in both the upper and lower GI tracts. The endoscopic
65
A n g i o d y s p l a s i a o f t h e G I Tr a c t a n d B l e e d i n g
History, physical examination, and stabilization
1. CBC
2. IVF/transfusions
3. EKG, chest and abdominal radiographs
4. NG tube insertion
(+) Nasogastric aspirate
(–) Nasogastric aspirate
Upper GI bleeding
Probably lower GI bleeding
Endoscopy
Sigmoidoscopy/colonoscopy
Diagnostic
Treat
Nondiagnostic
Active bleeding
Inactive bleeding
Angiography/
enteroscopy
GI series/enteroscopy
Bleeding stopped
Active bleeding
Colonoscopy
Radionuclide study
Angiography
Figure 1. Approach to acute gastrointestinal bleeding. CBC = complete blood count; EKG = electrocardiogram; GI = gastrointestinal; IVF = intravenous fluids; NG = nasogastric.
appearance of lesions typically has been described as discrete, flat, or
slightly raised (2–10 mm) and bright red with a stellate configuration
(Figure 2).9 A surrounding pale rim or halo may also characterize the
lesion. Angiodysplastic lesions encountered as incidental findings
generally are small lesions with a pale colouration compared with
lesions with recent hemorrhage, which are bright with elevated centres.
The endoscopic appearance of angiodysplasia can be confused with the
ectasias associated with systemic diseases, such as hereditary
hemorrhagic telangiectasia, as well as the CREST (calcinosis cutis,
Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, and
telangiectasia) and Ehlers-Danlos syndromes. The lack of systemic
manifestations distinguishes angiodysplasia from these syndromes.
Comparative studies using selective angiography and colonoscopy
indicate that the sensitivity of colonoscopy exceeds 80% when the
lesions are located in the area examined by colonoscopy. Most
angiodysplastic lesions are located in the right colon, so the entire colon
must be examined. It goes without saying that the colon must be very
well prepared in order for these tiny lesions to be seen. Angiography has
the advantage of detecting additional non-colonic angiodysplastic
lesions not detected by colonoscopy. Of course, upper endoscopy is
66
preferable to establish a diagnosis of gastric and duodenal
angiodysplasia. Push enteroscopy and double-balloon endoscopy are
useful to identify small bowel lesions, and retrograde double-balloon
endoscopy may allow for careful inspection of the cecum and ileocecal
valve.10 Angiodysplasia can be detected very infrequently by visual
Figure 2.
Angiodysplasia
identified on cecum
wall during
colonoscopy.
Kassam et al.
inspection of the serosal side of the bowel during laparotomy; however,
intraoperative enteroscopy can help in the localization of distal small
bowel lesions.10
Endoscopic mucosal biopsy for the purpose of diagnosis generally is
not recommended because of the low diagnostic yield and the risk of
provoking hemorrhage. Biopsy may help to differentiate angiodysplasia
from vascular tumours, lesions associated with congenital or systemic
disease, or radiation damage.
Treatment
All patients need to be assessed for hemodynamic stability, with volume
support and correction of any coagulation abnormality, as required.
Gastroenterologists or surgeons may provide specific intervention to
control hemorrhage, namely endoscopic obliteration, particularly for
angiodysplasia of the colon, stomach, or duodenum. Rebleeding after
these techniques may be due to bleeding at other sites rather than a
failure of the procedure. The techniques include monopolar
electrocautery, heater probe, sclerotherapy, band ligation, and argon
and neodymium:yttrium-aluminum-garnet (Nd:YAG) lasers. Argon
plasma coagulation is now the treatment of choice for most
angiodysplastic lesions. Fifty percent of patients with distal small bowel
lesions and no other defined GI bleeding sites benefit from enteroscopy
and lesion obliteration.
Angiodysplasia rarely presents with acute, massive hemorrhage; this
can be controlled effectively with angiographic therapy. Angiography is
appropriate in severely ill patients who are not candidates for surgical
intervention. In these patients, transcatheter embolization of selected
mesenteric arteries has been effective.11 Angiography also plays an
important role in preoperative localization.
Right hemicolectomy for angiodysplasia is second-line therapy after
endoscopic ablation, if repeated endoscopic coagulation has failed. The
mortality rate associated with surgical resection ranges from 10–50%,
depending upon the patient’s comorbidities. Surgical resection is
preferred for the acute management of severe hemorrhage or for the
management of recurrent hemorrhage over a relatively short period
accompanied by a large transfusion requirement. The risk of the left
colon becoming a source of future bleeding if left behind is relatively
low compared with the increased morbidity and mortality of subtotal
colectomy. Partial or complete gastrectomy for the management of
gastric angiodysplasia, on the other hand, is followed by rebleeding
from other lesions in as many as 50% of patients.
Presently, no medical therapy has been proven to be effective in the
management of active bleeding from angiodysplasia. Regularly
scheduled octreotide infusion has been reported to decrease the rate of
chronic bleeding and is usually well tolerated. It should be the first
choice in patients with portal hypertension. Other agents, such as
estrogen and progesterone, thalidomide, and desmopressin, are
considered experimental, with controversial results in studies, and are
used only on the basis of case reports. In the patient with chronic
bleeding from angiodysplasia despite endoscopic obliteration, the
patient may be maintained on oral iron therapy, their hemoglobin
monitored regularly, and blood transfusions given as appropriate.
Prognosis and Follow-Up
Mortality is related to the severity of bleeding, hemodynamic instability,
age, and the presence of comorbid medical conditions. Richter et al.
reviewed the clinical course of 101 patients with colonic
angiodysplasia.12 Fifteen asymptomatic individuals who had never bled
were followed up for as long as 68 months (mean 23 months), and no
patient experienced bleeding. Thirty-one patients with overt bleeding
or anemia managed with blood transfusions alone had rebleeding rates
at 1 and 3 years of 26% and 46%, respectively. The high rate of
rebleeding justifies treatment for angiodysplasia in symptomatic
individuals.
If a patient has asymptomatic angiodysplasia, a repeat colonoscopy is
not recommended. Outpatient monitoring of hemoglobin and repeated
tests for occult blood can be performed. Patients with chronic GI
bleeding may need repeated colonoscopies. No preventive methods
have been definitely identified at this time. Avoidance of nonsteroidal
anti-inflammatory drugs is recommended in patients with chronic
bleeding.
References
1. Regula J, Wronska E, Pachlewski J. Vascular lesions of the
gastrointestinal tract. Best Pract Res Clin Gastroenterol
2008;22:313–28.
2. Foutch PG, Rex DK, Lieberman DA. Prevalence and natural history
of colonic angiodysplasia among healthy asymptomatic people. Am J
Gastroenterol 1995;90:564–7.
3. Heyde EC. Gastrointestinal bleeding in aortic stenosis. N Engl J Med
1958;259:196.
4. Schwartz J, Rozenfeld V, Habot B. Cessation of recurrent bleeding
from gastrointestinal angiodysplasia, after beta blocker treatment in
a patient with hypertrophic subaortic stenosis – a case history.
Angiology 1992;43(3 Pt 1):244–8.
5. Imperiale TF, Ransohoff DF. Aortic stenosis, idiopathic
gastrointestinal bleeding, and angiodysplasia: is there an association?
A methodologic critique of the literature. Gastroenterology
1988;95:1670–6.
6. Fressinaud E, Meyer D. International survey of patients with von
Willebrand disease and angiodysplasia. Thromb Haemost
1993;70:546.
7. Kaaroud H, Fatma LB, Beji S, et al. Gastrointestinal angiodysplasia in
chronic renal failure. Saudi J Kidney Dis Transpl 2008;19:809–12.
8. Kovacs M, Pak P, Pak G, et al. Multiple angiodysplasias diagnosed by
capsule endoscopy. Orv Hetil 2007;148:2435–40.
9. Skibba RM, Hartong WA, Mantz FA, et al. Angiodysplasia of the
cecum: colonoscopic diagnosis. Gastrointest Endosc 1976;22:177–9.
10. Suzuki N, Arebi N, Saunders BP. A novel method of treating colonic
angiodysplasia. Gastrointest Endosc 2006;64:424–7.
11. Polese L, Angriman I, Pagano D, et al. Laser therapy and surgical
treatment in transfusion-dependent patients with uppergastrointestinal vascular ectasia. Lasers Med Sci 2006;21:140–6.
12. Richter JM, Hedberg SE, Athanasonlis CA, Schapiro RH.
Angiodysplasia clinical presentation and colonoscopic diagnosis. Dig
Dis Sci 1984;29:481–5.
67
Médecine périopératoire • Perioperative Medicine
Complication rare d’une procédure courante :
pneumomédiastin secondaire à un tube naso-gastrique
Rare Complication of a Common Procedure: Pneumomediastinum Secondary to the
Insertion of a Nasogastric Tube
Luc Lanthier, MD, François Lamontagne, MD, Catherine St-Pierre, MD
Au sujet des auteurs
Luc Lanthier est interniste au CHUS à Sherbrooke. François Lamontagne et Catherine St-Pierre sont internistes et intensivistes
au CHUS à Sherbrooke. Ils sont aussi professeurs à la Faculté de Médecine et des Sciences de la Santé de l’Université de
Sherbrooke.
About the Authors
Luc Lanthier is an internist at the University of Sherbrooke Hospital (CHUS) in Sherbrooke. François Lamontagne and
Catherine St-Pierre are internist-intensivists, also at CHUS. They are also professors on the university’s Faculty of Medicine
and Health Sciences.
ne femme de 91 ans consulte à l’urgence pour un tableau de
douleur abdominale depuis 3 semaines. Une distension
abdominale est notée par l’urgentologue, qui prescrit l’installation d’un
tube naso-gastrique (Levine) à la patiente. Après quelques tentatives
infructueuses, la patiente développe de l’œdème cervical ainsi qu’une
difficulté respiratoire. À l’examen physique, une tuméfaction cervicale
et de l’emphysème sous-cutané sont notés. La radiographie pulmonaire,
normale la veille (Figure 1), montre un pneumomédiastin (Figure 2),
aussi retrouvé à la tomodensitométrie (TDM) thoracique (Figure 3).
Une image compatible avec un hématome œsophagien est aussi notée à
la TDM (Figure 4). La patiente est intubée et on procède à une chirurgie
qui dure 8 heures (drainage cervical, laparotomie exploratrice,
jéjunostomie d’alimentation, thoracotomie droite et gastrostomie de
décompression). La lésion œsophagienne n’est pas identifiée.
L’évolution post-opératoire sera compliquée d’un choc septique et
d’une hypertension pulmonaire sévère et la patiente décèdera 10 jours
après son admission. En rétrospective, la douleur abdominale était
probablement secondaire à un fécalome.
Un pneumomédiastin suivant l’introduction d’un tube nasogastrique est une complication rare, surtout avec les tubes nasogastriques souples utilisés actuellement.1,2 Bien qu’exceptionnelle, cette
complication très morbide nous rappelle qu’il n’y a pas de procédure
sans risque.
U
91-year-old woman presented to the emergency room with a 3week history of abdominal pain. The emergency doctor noted an
abdominal distension and prescribed nasogastric intubation (Levine
tube). After a few unsuccessful intubation attempts, the patient
developed cervical edema and respiratory difficulty. A physical
examination revealed cervical swelling and a subcutaneous emphysema.
The chest radiograph, normal the evening before (Figure 1), showed a
pneumomediastinum (Figure 2), confirmed by a computed
tomography (CT) of the thorax (Figure 3). An image compatible with
an esophageal hematoma was also observed on the CT (Figure 4). The
patient was intubated and underwent 8 hours of surgery (cervical
drainage, exploratory laparotomy, feeding jejunostomy, right
thoracotomy and decompression gastrostomy). The esophageal injury
was not identified. Postoperative changes were complicated by septic
shock and severe pulmonary hypertension, and the patient died 10 days
after admission. A retrospective analysis indicated that the abdominal
pain was probably secondary to a fecal impaction.
Pneumomediastinum secondary to nasogastric intubation is a rare
complication, especially if the currently available flexible nasogastric
tubes are used.1,2 Although exceptional, this morbid complication
reminds us that there is no such thing as a risk-free procedure.
A
Références
1. Ahmed A, Aggarwal M, Watson E. Esophageal perforation: a complication of nasogastric tube placement. Am J Emerg Med 1998;16:64–6.
2. Coronel MJ, Sideridis K, Bank S. Intramucosal esophageal perforation with nasogastric tube. Pract Gastroenterol 2006;30:82–5.
68
Médecine périopératoire • Perioperative Medicine
Figure 3.
Figure 1.
Figure 4.
Figure 2.
69
Perioperative Medicine
Perioperative Considerations in Frail Older Adults
Roger Y. Wong, MD, Joy Liao, MD, Anson Li, MD, Naaz Parmar, MD
About the Authors
Roger Wong (left) and Joy Liao are members of the Division of Geriatric Medicine, Department of Medicine, at the University
of British Columbia, Vancouver, British Columbia. Anson Li and Naaz Parmar are members of the Department of Medicine
at the University of British Columbia. Correspondence may be directed to [email protected].
erioperative care for frail older adults is complex and challenging.
Frailty refers to the vulnerability to functional and cognitive decline
that results in increased dependency and institutionalization. Surgery in
this cohort is associated with high complication and death rates1 due to
medical comorbidities and loss of physiological reserves. Currently,
there are no comprehensive guidelines on the evaluation of frail older
individuals undergoing surgery.2 In this article, we outline a
multifaceted framework to the geriatric perioperative assessment
(Figure 1).
P
•
•
•
•
•
Cardiovascular
Pulmonary
Endocarditis Prophylaxis
Anticoagulation
Stress Steroids
Medical Risks
•
•
•
•
Diabetes
Hypertension
Renal Dysfunction
Other
Other
Conditions
Geriatric
Syndromes
•
•
•
•
Delerium
Mobility & Function
Nutrition & Wound Healing
Discharge Disposition
Figure 1. Medical preoperative assessment in the geriatric patient:
a comprehensive approach.
Medical Risk Assessment
Cardiovascular Risk
Heart disease is common in older individuals because of aging-related
changes to the vascular system and the high prevalence of comorbid
illnesses that increase the risk of coronary artery disease (CAD). Various
guidelines exist for perioperative cardiac risk assessment,3,4 although
most are extrapolated from younger patients. The commonly used
modified cardiac risk index3 focuses on six parameters, each adding one
point to the risk score: history of CAD, congestive heart failure,
cerebrovascular disease, diabetes mellitus requiring insulin treatment,
raised serum creatinine >176.8 µmol/L, and high-risk surgery (thoracic,
abdominal, suprainguinal vascular surgeries). There is no definitive
evidence that confirms a benefit from the use of such an index on
perioperative outcomes in the elderly. Specifically, the classification
system of patients into the various risk classes (i.e., 0 points carries 0.4%
risk of adverse cardiac events, 1 point carries 0.9% risk, 2 points carry
70
6.6% risk, and 3 points or higher carry 11% risk) has not been validated
in frail older adults.
The use of noninvasive cardiac testing for preoperative screening is
controversial. There is no evidence to support routine 12-lead or
continuous/Holter electrocardiography. Many frail older patients are
limited in their baseline exercise endurance, and most are not
appropriate subjects for exercise tolerance testing due to comorbidities
such as arthritis. Nuclear medicine perfusion imaging and
echocardiography done with pharmacological stressing are reasonable
options to look for reversible myocardial ischemia for patients who are
potential candidates for revascularization, although the evidence is
unclear in terms of the long-term benefits of percutaneous coronary
intervention preoperatively.
The evidence for perioperative beta-blocker use is evolving, with the
primary concern of reducing the myocardial infarction risk at the
expense of increasing overall mortality and stroke risk.5 Its use in the
frail elderly should be individualized, especially considering that the
side effects, such as weakness and delirium, are more common.
Pulmonary Risk
The aging-related changes of diminished cough, decreased lung
elasticity/recoil, and increased chest wall stiffness all contribute to
potentially poor respiratory outcomes perioperatively.6 The focus of a
pulmonary risk assessment is to identify and determine the severity of
existing lung disease such as chronic obstructive pulmonary disease
(COPD) or interstitial lung disease. Risk factors for poor outcomes
include age over 60 years, COPD, congestive heart failure, a history of
cigarette smoking, and poor preoperative function.6 Recent studies
suggest no increased pulmonary risk attributable to asthma or
underlying obesity.6,7
Preoperative chest radiography for screening is not mandatory. Pulse
oximetry is preferred over arterial blood gases in evaluating
desaturation. Spirometry may be useful for evaluating frail patients
with respiratory complaints but without definitive diagnoses. Smoking
cessation is encouraged at least 8 weeks prior to surgery. Pre-existing
COPD should be optimized medically prior to surgery. There is no
evidence to support blanket oxygen supplementation except in
desaturation. Chest physiotherapy and early mobilization may reduce
postoperative aspiration risk,6,7 although their usefulness in frail
individuals with nonmodifiable risk factors (e.g., dementia, delirium,
stroke, Parkinson’s disease) remains uncertain.
Wong et al.
Endocarditis Prophylaxis
Recent evidence recommends antimicrobial prophylaxis only for
patients with prosthetic heart valves, previous endocarditis, or
congenital heart disease and for cardiac transplant recipients with
valvulopathy.8 Cardiac conditions prevalent in the elderly – such as a
bicuspid aortic valve, acquired aortic or mitral valve disease, and
hypertrophic cardiomyopathy – do not require routine prophylaxis.
Antibiotics are not indicated for genitourinary or gastrointestinal
procedures, both commonly performed in the elderly.8
Anticoagulation
Frail older patients often have multiple risk factors (poor baseline
function, limited mobility, prolonged hospitalization) for venous
thromboembolic events (VTEs) in the perioperative period. The choice
of prophylactic anticoagulation depends on patient risk factors, the
type of surgery, and the length of postoperative immobilization.
Patients on warfarin may continue therapy, interrupt and resume
treatment, or bridge anticoagulation over the perioperative period.
Careful consideration of the risks of a VTE versus bleeding will
determine the most appropriate strategy. The guidelines for VTE
prevention in the perioperative period are often extrapolated from
younger populations for use in the frail elderly.9 Decisions surrounding
anticoagulation should be discussed with the surgeon to ensure
collaborative management.
Stress Corticosteroids
Older patients on long-term corticosteroids preoperatively may be at
risk of hypothalamic-pituitary-adrenal (HPA) suppression, which can
manifest as delirium, obtundation, hypotension, and shock. The
cosyntropin stimulation test may be helpful to evaluate
hypoadrenalism. There is low-grade evidence that recommends
prophylactic stress dose coverage for patients receiving 5 mg/d or more
of prednisone (or equivalent) for longer than 1 week in the 6–
12 months prior to surgery. This is a controversial topic, and no
conclusive evidence exists in the frail elderly population.10
Comorbid Illnesses
Diabetes Mellitus
Although high-quality studies are lacking in the area of perioperative
glycemic control, the goals are to reduce hypoglycemia, ketosis, and
marked hyperglycemia. End-organ complications (especially
nephropathy and vasculopathy) can become exacerbated
perioperatively and require careful management.
Preoperative screening with fasting or random serum glucose and
glycosylated hemoglobin is optional. In the event of preoperative longacting insulin use, consider switching to intermediate-acting insulin
1–2 days prior. Multiple clinical protocols exist to direct glycemic
perioperative management in frail older patients, although most are
borrowed from younger cohorts. Preprinted physician orders, including
insulin sliding scales, can help to reduce medication-related errors in
hospital. The glycemic targets in frail older patients remain
controversial.
Hypertension
Hypertension is common in the elderly, and uncontrolled hypertension
preoperatively is associated with increased cardiovascular lability under
anesthesia. Recent guidelines suggest stage 3 hypertension (blood
pressure [BP] ≥180/110 mm Hg) may be an indication to delay elective
surgery until adequate control is attained.2 The possibility of secondary
hypertension should be considered in patients with severe or refractory
hypertension.
Oral hypertensive medications may be taken until the time of
surgery. To avoid intraoperative hypotension and the risk renal
dysfunction, diuretics and angiotensin-converting enzyme (ACE)
inhibitors may be held the morning of the surgery and restarted when
the patient is euvolemic in the postoperative period.2 The BP targets in
the frail elderly are also controversial, especially in the very elderly.11
Most guidelines suggest 140–160/90 or lower for nondiabetic patients
and 120–130/80 or lower for those with diabetes.
Renal Dysfunction
Postoperative renal failure is associated with increased morbidity and
mortality, and risk factors include pre-existing renal dysfunction,
diabetes, and left ventricular dysfunction, all commonly seen in the frail
elderly. Preoperative serum electrolytes, urea, creatinine, and urine
microscopy are recommended, and, if abnormal, serial monitoring is
important. Strategies to minimize the risk of worsening renal function
include preventing volume depletion as well as avoiding nonsteroidal
anti-inflammatory drugs and ACE inhibitors in the perioperative period.
Other Diseases
Patients with a history of obstructive sleep apnea are at risk for difficult
intubation and require a preoperative anesthesia consultation. Cervical
spine radiography should be considered in patients with rheumatoid
arthritis and severe osteoporosis, both prevalent in the frail elderly.
Geriatric Syndromes
Delirium
In frail older patients, delirium is underdiagnosed and undertreated,
despite its high prevalence.12 The diagnostic features of delirium (acute
confusion that fluctuates with time, disturbance in consciousness, poor
attention and disorganized thinking, cognitive deficits and perceptual
disturbances, and altered sleep-wake cycles) are commonly
misinterpreted as normal responses in older patients. The etiology of
delirium is often multifactorial, and active identification of
predisposing risk factors (e.g., underlying dementia, previous delirium,
brain injury, poor premorbid function, visual and hearing
impairments, poor nutrition) in the preoperative history is helpful.13
There is no single validated scoring system for calculating delirium risk
in the perioperative setting; however, generally the more baseline risks a
patient has, the higher the risk for delirium. Common precipitating
factors are summarized by the mnemonic DIMS, which stands for
drugs, infections, metabolic anomalies, and structural brain diseases.
Urinary or fecal retention and suboptimal pain control may also induce
and exacerbate delirium.14
A preoperative Mini-Mental State Examination (MMSE) is helpful to
quantitatively document baseline cognitive status. The Confusion
Assessment Method (CAM) can be done by nursing and allied health
staff to screen for delirium postoperatively. Structural and functional
neuroimaging or electroencephalography is not required for routine
preoperative screening.12
71
Perioperative Considerations in Frail Older Adults
There is strong evidence that supports a multipronged approach for
the primary prevention of delirium,15 reducing the frequency and
duration of delirium. Components include the use of orientating aids
and cognitive activities, corrective lenses and hearing aids, good sleep
hygiene, early mobilization, the removal of restraints and bladder
catheters, vigilant monitoring or correction of volume status, and the
avoidance of opioids and benzodiazepines.
Once delirium has occurred, no treatment has been proven to alter its
course. The approaches then are to identify and treat reversible
precipitants and treat the behavioural symptoms. Not all cases of
perioperative delirium in the frail elderly are reversible, and refractory
cases are associated with prolonged hospitalization, poor functional
recovery, institutionalization, and death.16
Mobility and Function
Preoperative assessment of function and mobility is important because
postoperative decline is common in frail older patients. Impairment
may be due to underlying medical illnesses such as osteoarthritis,
stroke, heart or lung disease, reduced vision, and so on. A physical
examination of gait and balance is helpful, especially when a
standardized physical performance measure such as the Timed Up and
Go (TUG) is used.17 An abnormal result on the TUG test predicts poor
activities of daily living. Early mobilization may prevent physical
deconditioning, although the details of the exercise prescription
(nature, intensity, and frequency) are unclear. Consultation with
physiotherapy and occupational therapy is the standard of care in many
postoperative settings.
Wound Healing and Nutrition
Malnutrition is associated with poor surgical outcomes, functional
decline, institutionalization, and death.18 Risk factors for malnutrition
include inadequate food intake, illnesses that increase metabolic
requirements, and malabsorption. Preoperative blood tests are
nonspecific and of limited value. Recognizing malnutrition in the
preoperative period is important as wound healing and immune
function may be compromised. There is variable opinion on how
rapidly the resumption of nutrition in the postoperative period should
occur, especially with the concern of refeeding syndrome. Consultation
with a nutritionist is recommended.
Discharge Disposition
Returning frail older patients to their original residence following
surgery can be challenging. While risk calculators exist to estimate the
degree of frailty, there is no easy method to translate the risk to actual
probabilities of discharge disposition. The question of whether geriatric
rehabilitation is indicated can be addressed by considering the burden
of medical illness, premorbid disability, the extent of cognitive
impairment, the patient’s motivation, and psychosocial supports. Other
venues for convalescence include subacute medical care and transitional
care. Consultation with social work can be helpful.
Conclusion
Frail older adults undergoing surgery present unique management
challenges. A comprehensive, multicomponent framework such as that
presented in this paper can be useful.
72
References
1. Polanczyk CA, Marcantonio E, Goldman L, et al. Impact of age on
perioperative complications and length of stay in patients
undergoing noncardiac surgery. Ann Intern Med 2001;134:637–43.
2. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007
guidelines on perioperative cardiovascular evaluation and care for
noncardiac surgery: an executive summary. Circulation
2007;116:1971–96.
3. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and
prospective validation of a simple index for prediction of cardiac
risk of major noncardiac surgery. Circulation 1999;100:1043–9.
4. Almanaseer Y, Mukherjee D, Kline-Rogers EM, et al. Implementation
of the ACC/AHA guidelines for preoperative cardiac risk assessment
in a general medicine preoperative clinic: improving efficiency and
preserving outcomes. Cardiology 2005;103(1):24–9.
5. POISE Study Group. Effects of extended-release metoprolol
succinate in patients undergoing non-cardiac surgery (POISE trial):
a randomized controlled trial. Lancet 2008;371(9627):1839–47.
6. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med
1999;340:937–44.
7. Qaseem A, Snow V, Fitterman N, et al. for the Clinical Efficacy
Assessment Subcommittee of the American College of Physicians.
Risk assessment for and strategies to reduce perioperative
pulmonary complications for patients undergoing non
cardiothoracic surgery: a guideline from the ACP. Ann Intern Med
2006;144:575–80.
8. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective
endocarditis: guidelines from the American Heart Association.
Circulation 2007;116:1736–54.
9. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous
thromboembolism. The Seventh ACCP Conference on
Antithrombotic and Thrombolytic Therapy. Chest
2004;126:338–400S.
10. Axelrod L. Perioperative management of patients treated with
glucocorticoids. Endocrinol Metab Clin North Am 2003;32:367–83.
11. Beckett NS, Peters R, Fletcher AE, et al.; HYVET Study Group.
Treatment of hypertension in patients 80 years of age or older. N
Engl J Med 2008;358:1887–98.
12. Inouye SK. Delirium in older persons. N Engl J Med
2006;354:1157–65.
13. Freter SH, Dunbar MJ, MacKnight C, et al. Predicting post-operative
delirium in elective orthopaedic patients: the Delirium Elderly AtRisk (DEAR) instrument. Age Ageing 2005;34:169–84.
14. Lynch EP, Lazor MA, Marcantonio ER, et al. The impact of
postoperative pain on the development of postoperative delirium.
Anesth Analg 1998;86:781–5.
15. Inouye SK, Bogardus ST, Charpentier PA, et al. A multicomponent
intervention to prevent delirium in hospitalized older patients. N
Engl J Med 1999;340:669–76.
16. Dasgupta M, Dumbrell AC. Preoperative risk assessment for
delirium after noncardiac surgery: a systematic review. J Am Geriatr
Soc 2006;54:1578–89.
17. Podsiadlo D, Richardson S. The timed “Up & Go”: a test of basic
functional mobility for frail elderly persons. J Am Geriatr Soc
1991;39:142–8.
18. Covinsky KE, Covinsky MH, Palmer RM, Sehgal AR. Serum albumin
concentration and clinical assessments of nutritional status in
hospitalized older people: different sides of different coins? J Am
Geriatr Soc 2002;50:631–7.
EKG & U
Electrocardiographic Neurology
George Veenhuyzen, MD
About the Author
George 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. Correspondence
may be directed to [email protected].
egarding the 12-lead electrocardiograms (EKGs) recorded over a
5-minute time period and shown in Figures 1 through 3, where is
the lesion?
R
Discussion
The EKG in Figure 1 reveals normal sinus rhythm with marked
ST-segment elevation in all the anterior and lateral leads. There is also
marked ST-segment depression in the inferior leads. The degree of
ST-segment elevation is so pronounced as to make the ST-T component
of the QRS complex resemble the headstone marking a burial site;
hence, the term “tombstone ST elevation.” Note that the QRS duration
is not prolonged in any of the 12 EKG leads.
ST-segment elevation in leads V1–V4 should raise suspicion of an
acute coronary syndrome caused by a ruptured plaque in the left
anterior descending coronary artery (LAD), which is usually the largest
coronary artery, supplying the anterior, septal, lateral, and, in 70% of
humans, inferoapical segment of the left ventricle (LV). The prognosis
is related to the size of the area at risk, which is in turn related to the site
of the occlusion in the LAD.
The EKG is often able to discriminate between the following LAD
locations, listed from distal to proximal: (1) after the first diagonal
branch (mid- to distal LAD, supplying the apical and inferoapical LV);
Figure 1. Where is the lesion?
(2) between the first septal perforator branch and the first diagonal
branch (the latter supplies the anterolateral LV); and (3) at or before the
first septal perforator branch (which supplies the basoseptal LV,
including the right bundle and left anterior fascicle).
An occlusion at the most proximal of these three locations portends
the greatest risk because the entire LAD distribution (described above)
is jeopardized, resulting in an ST-segment spatial vector directed
superiorly (often, this is not appreciated) and to the left. This results in
ST-segment elevation in leads V1–V4, I, aVL, and often aVR. There is
also reciprocal ST-segment depression in leads whose positive pole is
directed inferiorly, namely, II, III, and aVF. This ST-segment depression
is reciprocal to the superiorly direct ST-segment spatial vector caused by
involvement of the basal LV (though, in this particular case, it may also
be reciprocal to the ST segment elevation in leads I and aVL). There
ought to be more ST-segment elevation in aVL than aVR because the
ST-segment spatial vector is directed more to the left than right. For the
same reason, there ought to be more reciprocal ST-segment depression
in lead III than lead II. These features are displayed in the EKG shown
in Figure 1.
With more distal LAD lesions, basoseptal involvement is reduced
(leading to less or no ST-segment elevation in leads V1, aVR, and aVL
and less or no reciprocal ST-segment depression in the inferior leads)
and the ST-segment spatial vector is
directed progressively more inferiorly
(possibly even causing ST-segment
elevation in the inferior leads due to
involvement of the inferoapical
segments). More detail on how EKG
changes reflect more distal LAD lesions,
and on the ability of the EKG to localize
the lesion in general, can be found in a
recent issue of the Journal of the
American College of Cardiology1 and a
terrific short book by one of the world’s
foremost experts on this topic,
Professor Hein J. J. Wellens.2
The EKG shown in Figure 2,
recorded only 3 minutes after the EKG
shown in Figure 1, reveals normal sinus
rhythm with new complete right
bundle branch block (now the QRS
73
Electrocardiographic Neurology
The rapidity with which the EKG
changes resolved suggest that coronary
vasospasm was the etiology. So, if you
guessed that the therapy administered was
sublingual nitro-glycerine, you guessed
correctly.
This series of EKGs displays the changes
associated with occlusion of the proximal
LAD (the highest-risk anterior infarct
site) and the sensitivity of the proximal
His-Purkinje system to acute ischemia.
It is worth remembering that in the
setting of anterior transmural ischemia,
ST-segment depression in the inferior
leads is due to a superiorly direct
ST-segment spatial vector from basoseptal
LV involvement, indicating a high-risk
occlusion of the proximal LAD at or
before the first septal perforator branch.
Figure 2. This 12-lead EKG was recorded 3 minutes after the EKG shown in Figure 1.
complex duration is prolonged, best appreciated in leads V1 and aVR)
and left axis deviation. In this setting, acute left axis deviation is
invariably due to new left anterior fascicular block (i.e., bifascicular
block). As described above, acute ischemia of the right bundle branch
(with or without concomitant ischemia of the left anterior fascicle) is
further evidence that the LAD occlusion is at or before the first septal
perforator branch of the LAD. Note that the ST segment changes
remain fully interpretable despite the bifascicular block.
The ST-segment changes and conduction disturbances nearly
completely resolved 2 minutes later, when the EKG in Figure 3 was
recorded. Can you surmise what therapy was administered between the
recording of the EKGs in Figures 2 and 3?
References
1. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS
recommendations for the standardization and interpretation of the
electrocardiogram. Part VI: acute ischemia/infarction. A scientific
statement from the American Heart Association Electrocardiography
and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm
Society endorsed by the International Society for Computerized
Electrocardiology. J Am Coll Cardiol 2009;53:1003–11. DOI:
10.1016/j.jacc2008.12.016.
2. Wellens HJJ, Gorgels APM, Doevendans PA, eds. The EKG in Acute
Myocardial Infarction and Unstable Angina. Diagnosis and Risk
Stratification. Kluwer Academic Publishers; 2003.
Figure 3. This 12-lead EKG was recorded 2 minutes after the EKG shown in Figure 2.
74
Humanities
Sabbaticals: Why Every Physician Needs a “Braindusting”
T. Jock Murray, MD
About the Author
Jock Murray is a former dean of Dalhousie Medical School and professor of medicine (neurology) and founding director of the
Dalhousie Multiple Sclerosis Research Unit. He has appointments in medicine, the Division of Medical Education, and medical
humanities at Dalhousie University, Halifax, Nova Scotia. Correspondence may be directed to [email protected].
ir William Osler said there were three things to maintain a
physician’s education – a notebook, a library and a quinquennial
braindusting.1 He recognized that the “braindusting,” a period of study
and experience away from the dailiness of practice, was the hardest to
manage but was essential for “renovation, rehabilitation, rejuvenation,
reintegration, resuscitation.” He encouraged practicing physicians to
begin saving years ahead for a period away. He thought the rural doctor,
John Y. Bassett, who spent a year in Paris, to be a heroic figure for
making the sacrifices necessary to improve his knowledge and skill.2
I suspect everyone has pondered, especially when practice is getting
hectic, the possibility of a time away from the constant responsibilities,
the endless requests, the interruptions, the sea of paper, the multiplying
e-mails, the dreary meetings, the sameness of it all. Wouldn’t it be
rewarding to take time off to learn something new, take a new direction,
experience something totally different?
This was well expressed by Dr. Walter Channing of Boston, who after
40 years of practice, took 1856 as a sabbatical year3:
S
I was desirest to get out of the harness with a whole ocean between me
and work – to feel as free as in my earliest days of conscious liberty, –
to go when and where I pleased – to be conscious of an entire new
mode of life; of one especially which was not to be daily determined
by the variety of professional calls, – the different phases of disease, –
to see life, health, and countries in their beauty, power, truth, – and
to find everywhere, and in everything, opportunities of varied
observation, thought, and pleasure, and to enjoy them. And I did
enjoy them all.
Historic Basis of Sabbaticals
A sabbatical (Latin sabbaticus, Greek sabbatikos, Hebrew shabbathon)
refers to a period of rest from work, a hiatus. Our understanding of the
sabbatical relates to a Jewish concept but may date even further back to
the Babylonian festival of “sapattu,” which corresponds to the cycles of
the full moon.4 The Jews celebrate the Sabbath as a day of rest and
prayer on the seventh day of the week, while Christians have adopted
the Sabbath on the first day of the week, and Muslims have Yaum alJum’ah (the Day of Assembly) on Fridays.
A number of rules and laws became associated with the Sabbath. In
Babylonian times, people were prohibited from eating salted meats
cooked over embers, wearing white, changing clothes, offering
sacrifices, and making wishes. Physicians were not permitted to touch
the sick on these days unless this avoidance would be life threatening. In
the Jewish tradition every seventh year, “the land must rest so the poor
and wild animals may eat the fruits of the earth” (Ezekiel 23:10, 11). In
the sabbatical year, laws also referred to the release of slaves, cancellation
of debts, and the sharing of goods, but the longest lasting tradition was
the rule to let the land lie fallow every seventh year.3
It seems that the first academic sabbatical was in the late 1880s,
negotiated by philologist Charles Lanman as part of the agreement for
him to leave Johns Hopkins University for Harvard. By the turn of the
twentieth century, 10 American universities had adopted the idea of the
sabbatical, and now all universities have a policy regarding sabbaticals,
as well as paid and unpaid leave.3
In recent years, sabbaticals have been adopted by individuals and
organizations as a way to encourage creativity, learn, or experience
something new and to ward off burnout. After a growth period in the
1990s, there has been some decline as physicians have become busier
and practices more complicated, and as the business world has
undergone cutbacks, downsizing, and layoffs. When the atmosphere
was focused on creativity, sabbaticals flourished as an important catalyst
to innovation. When the scene changed to time pressures, efficiency,
and cost cutting, sabbaticals were regarded as a costly frill. In the current
economic downturn, it is likely that fewer will seek or be granted
sabbaticals, but I would argue they are even more important in difficult
times when people feel more strained and pressured. When an
organization cannot bring in new blood, it is even more important to
keep people rejuvenated and vibrant.4
In the academic world, a sabbatical is a period of leave after 6 years of
employment. Implied are certain concepts: that the person will be paid
80–100% of the usual pay, sometimes supplemented by travel or
research grants; that the activity will be beneficial not only to the
individual but to the institution; and that the person will return to the
institution following the sabbatical and report on the activities. Each
institution has differing arrangements, rules, and support, so read the
regulations of your organization first and seek discussion of any
unanswered questions. In medical practice groups, there can be an
arrangement to share income, defer costs and on-call duties, and make
other arrangements to permit periods away, usually for months.
Who Should Have a Sabbatical?
Everyone needs a sabbatical. One could argue that the farmer, the single
parent, the housewife, the minimum wage worker all need a sabbatical
more than the academician or the professional, who have ways to vary
75
Sabbaticals: Why Every Physician Needs a “Braindusting”
their lives. Impractical as it may sound, everyone would benefit from a
period away from the predictable routine of work to revise priorities,
learn a new skill, or carry out a project, and to redirect the next period
of life. Although originally for those in academic life, sabbaticals are
now arranged by community physicians, corporate executives, lawyers,
writers, musicians, and actors, all seeking to “recharge the batteries.”
Beneficial as this might be, only a small number of people who are
allowed sabbaticals take advantage of the opportunity, especially
physicians. There are many reasons for this. Some are comfortable
staying in fixed settings and responsibilities. Others have difficulty
seeing how they could manage the pressures of their finances, mortgage,
children’s schooling, added costs, disruption of life, and covering
responsibilities to get away for an extended period. The idea of
interrupting patient care, teaching, and research projects, arranging for
others to cover these responsibilities, taking the kids out of school,
renting out the house, disrupting the spouse’s work and life all seems
too daunting. And all of this has to be balanced while developing the
sabbatical projects with unfamiliar people in unfamiliar places. Many
think it is better to stay home and go to work. But those who do go on
sabbatical usually say it was the most life-changing event they
experienced in their professional lives.
Sabbaticals for Physicians
Community physicians have taken sabbaticals to experience practice
and teaching in an academic centre, write a book, volunteer in a
developing country, experience a new culture and language, or learn a
new skill. There is no limit to the possibilities. Rarely do we hear of a
physician lounging on the beach for months. A cynical friend, when he
heard I was going on sabbatical, stated, “How do you spell sabbatical?
H-o-l-i-d-a-y?” Those who write about their sabbaticals talk not about
relaxation but how productive and busy they were.5
No matter what the activity, almost all speak of re-evaluating life and
practice and of important family experiences. There has been a lot of
discussion of having sabbaticals to reduce the possibility of burnout,
but those who take sabbaticals are usually busy, productive, and
successful individuals in their current lives. An American study of
medical school sabbaticals noted that most found the time away very
productive, culturally enriching, and strengthening for family
relationships. The small number who found the experience less
rewarding had inadequate preplanning, were not very productive prior
to sabbatical, and had unrealistic expectations that the time away would
result in substantial career change.5
The greatest benefits of a sabbatical come to the physician and the
family. A sabbatical is certainly expected to benefit the individual but
also the group or institution that supports the period away. In almost all
cases this is achieved. The physician can access resources, libraries, and
colleagues beyond the experiences available at home. The institutions
also benefit from visiting physicians and the positive effect new blood
has in a group. The visiting physician brings new ideas and projects and
establishes creative collaborations that last long after the sabbatical is
over.
Almost all sabbaticals are successful, but they take effort, sacrifice,
and cooperation. I believe the major secret of arranging a sabbatical,
beyond the decision to do it, is to decide long enough in advance so that
76
there is time to make everything fall in place. Preplanning is the secret
to a successful experience. Seldom can someone arrange the complex
nature of professional and family lives in less than a year or two, and I
would recommend planning at least 2 years in advance.
The impact on the whole department must be assessed. Are there
enough professors to take up the slack? Will courses be interrupted or
ongoing research disrupted? Normally, it is not a problem because, as
Vinet explains, McGill generally assumes, for planning purposes, that
one-seventh of its professors are away on sabbaticals or other forms of
leave at any given time.
It is always challenging to make arrangements for the aspirations and
lives of other family members. Often the spouse has commitments and
responsibilities that are equally difficult to suspend. The children have
their lives and their friends and often feel more pull from their peer
group than the call of far-off lands. I am reminded of the comment of
Dr. Samuel Johnson who responded to a man who wished to see the
Great Wall of China but felt he could not as he had children. Johnson
said: “Sir, (said he) by doing so, you would do what would be of
importance in raising your children to eminence. There would be a
lustre reflected upon them from your spirit and curiosity. They would
be at all times regarded as the children of a man who had gone to view
the wall of China. I am serious, Sir.”
During my career I had three 6-month sabbaticals in London and six
or seven shorter ones in London and South Carolina to work, research,
and write. Janet was always very supportive and did much of the
background planning. Our four children initially found it hard to leave
their friends and school but were great travellers and adventurers. They
now say the sabbaticals were one of the most formative adventures in
their lives, and they are now taking sabbaticals with their children.
When times are tough it may be even more important to have
sabbaticals available to physicians. When work is more pressured and
recruitment is increasingly limited, it is even more important to have
opportunities to become renewed, stimulated, and rejuvenated.6
Share Your Experiences
I’m sure many of you have had sabbatical experiences involving creative
ways to combine a period of study, exploration, or travel with your busy
lives and practice. Write to me about your experiences: Dr. T. Jock
Murray, 16 Bobolink St., Halifax, NS, B3M 1W3 [email protected]. In
a later issue, we will publish excerpts to help others plan their sabbatical
experience.
References
1. Murray TJ. President’s message: Osler’s braindusting. Oslerian
2006;7:1–2.
2. Osler WO. An Alabama Student. London, England: Henry Froude;
1909.
3. Channing W. A physician’s vacation: or, a summer in Europe.
Boston: Ticknor and Fields; 1856:87–90.
4. Kimball BA. The origin of the sabbatical and its legacy to the
modern sabbatical. J Higher Educ 1978;49:305–15.
5. Jarecky RK, Sandifer MG. Faculty members’ evaluation of
sabbaticals. J Med Educ 1986;61:803–7.
6. Murray TJ. Sabbaticals for physicians. Ann R Coll Physicians Surg
Can 1987;20:125–8.
Case Review
Eponyms in Medicine
Hector M. Baillie, MD
ILLUSTRATION: BINDA TRAVER
About the Author
Hector Baillie is a specialist in complex adult medicine in Nanaimo, British Columbia.
Figure 1. The patient exhibited a small right pupil with partial ptosis.
Case Report
R. J., a 65-year-old woman, presented to the emergency room with right
shoulder pain. She also described weakness of the right arm and hand.
She had lost 18 kg in weight during the preceding 3 months. She was
a 1–2 ppd smoker and had chronic obstructive pulmonary disease. A
physical examination revealed bronchial sounds at the right apex,
weakness and wasting of the right arm and hand muscles, and a small
right pupil with partial ptosis (Figure 1). A chest radiograph and
computed tomography were performed (Figures 2 and 3).
Figure 2. Chest radiograph: Large right apical “Pancoast” tumour resulting in
destruction of the right first and second ribs. Associated mediastinal and
right hilar lymphadenopathy. The increased interstitial markings in both
lungs suggest obstruction of the lymphatics. (Courtesy of Dr R. Johnson,
Radiology, Nanaimo Regional General Hospital)
Figure 3. Computed tomography of the chest: Destruction of the right first
and second ribs is noted. The findings are in keeping with a large Pancoast
tumour. Some coarsening of the interstitial markings is seen in the right midand lower lung zones suggesting interstitial edema or peripheral lymphatic
involvement. The cardiac silhouette is normal. No focal abnormality is seen
in the left lung. ((Courtesy of Dr R. Johnson, Radiology, Nanaimo Regional
General Hospital)
Horner Syndrome (Miosis, Ptosis, and Anhidrosis)
Johann Friedrich Horner was born
in Zurich in March 1831, his father
a doctor, his mother a linguist. He
completed his medical studies in
1854, his thesis being on spinal
curvature, and moved on to Vienna.
There he was introduced to
ophthalmology by Dr. von Jaxtthal,
leading to his subsequent association with his mentor, Dr. von
Graefe, in Berlin. He studied the
use of fundoscopy in the diagnosis
of systemic disease under the Paris
surgeon Louis-August Demarres,
before returning to Zurich in 1856
to an academic career in ophthalJohann Friedrich Horner
mology. He published over
40 papers on various diseases of the eye, one of which described the
x-linked transmission of red-green colour blindness. He was
instrumental on insisting that schoolchildren have regular eye
77
Eponyms in Medicine
examinations. He died of a stroke at the young age of 55.
The clinical features of Horner syndrome are caused by a lesion in the
sympathetic tracts that originate in the hypothalamus and travel
through the pons and medulla to reach the ciliospinal centre in the
cervical cord (C8, T1, T2). Second-order neurons travel with the
brachial plexus, traverse the apex of the lung, and then rise to the
superior cervical ganglion (near the carotid bifurcation). Third-order
post-ganglionic fibres ascend within the adventitiae of the internal
carotid artery to the ophthalmic division of the trigeminal nerve, before
supplying the long ciliary nerve (the papillary dilator muscle) and
giving sympathetic input to Müller’s muscle of the eyelids (Figure 4).
Hypothalamus
Ophthalmic division
of trigeminal nerve
Long ciliary nerve
To sweat glands of forehead
To smooth muscle of eyelid
To pupil
Internal carotid artery
To sweat glands of face
External carotid artery
G2
Superior cervical ganglion
First neuron
T1
Second neuron
Spinal cord
ILLUSTRATION: BINDA TRAVER
Third neuron
Figure 4. Nerves affected in Horner syndrome.
The degree of ptosis associated with paresis of Müller’s muscle is mild
(less dramatic than that seen in third cranial nerve lesions) and can be
noted to affect both superior and inferior lids. The pupil is small, due to
loss of iris dilatation, and is slow to enlarge in darkness. Because
sympathetic vasomotor fibres branch off soon after the superior
ganglion, anhidrosis is not seen with third-order lesions.
Localization of the lesion responsible for Horner syndrome can be
made with the help of accompanying symptoms. First-order lesions in
the brainstem might be accompanied by vertigo, ataxia, hemicorpus
weakness, or diplopia. This may be seen in association with a posterior
inferior cerebellar artery stroke (Wallenberg syndrome) or in the
presence of demyelinating or tumour disease. In the cord, long tract
signs with sensory level, bowel, and bladder dysfunction may point to
neck pathology. A Pancoast tumour in the apex of the lung can cause
78
local rib destruction, with arm pain and weakness, and thus give rise to
preganglionic Horner syndrome. Head and neck pain, particularly in
the setting of recent trauma, should suggest a dissection of the internal
carotid artery, with its attendant high risk of stroke. Other compressive
etiologies in the head and neck exist.
Neuroimaging with computed tomography, or more effectively
magnetic resonance imaging, should be guided by clinical suspicion of
the potential causative etiology.
Pancoast’s Syndrome
Pancoast’s syndrome is characterized by a malignant neoplasm of the
lung apex (usually squamous or adeno-carcinoma) and is relatively
uncommon. It causes local
destruction of the thoracic
inlet and involves the brachial
plexus and cervical sympathetic nerves. Shoulder pain,
weakness and wasting of the
arm and hand muscles, and
venous congestion of the limb
may be expected. Interestingly, the syndrome was
first described by the British
surgeon Edward Hare in 1838,
then by Ciuffini in 1911,
before Pancoast published his
three-case series of “superior
pulmonary sulcus tumours”
in 1932.
Henry Khunrath Pancoast. (Reproduced
Henry Khunrath Pancoast
with permission from the Collections of
was also a doctor’s son. He
the University of Pennsylvania Archives)
graduated from the University
of Pennsylvania in 1898, moving from surgery to anesthesia before
settling on a career in radiology. He was appointed America’s first
professor of this new specialty in 1912, pioneering x-ray therapy for
cancer, gastrointestinal radiology, and occupational health.
Bibliography
Bardoff CM, Van Stavern GP, Garcia-Valenzuela E. Horner syndrome.
Omaha (NE): emedicine, 2008; http://www.emedicine.com/OPH/
topic336.htm.
Horner JF. Über eine Form von Ptosis. Klin Monatsbl Augenheilk
1869;7:193–8.
Meyers DS. Pancoast’s syndrome. N Engl J Med 1998;338:765–66.
Pancoast HK. Superior pulmonary sulcus tumor: tumor characterized by
pain, Horner’s syndrome, destruction of bone and atrophy of hand
muscles. JAMA 1932;99:1391–6.
Whonamedit.com. Johann Friedrich Horner. Oslo, Norway:
Whonamedit.com, 2009; http://www.whonamedit.com/doctor.cfm/
1044.html.
Réexamen d’un cas
Une lipase qui induit en erreur …
Dominique Martineau-Beaulieu, MD, Jean-Daniel Baillargeon, MD
Au sujet des auteurs
Dominique Martineau-Beaulieu est résident 1 du programme de Médecine interne tronc commun à l’Université de
Sherbrooke, Sherbrooke, Québec. Jean-Daniel Baillargeon est gastro-entérologue au CHUS et directeur du programme de
Médecine interne tronc commun à l’Université de Sherbrooke.
Rapport de cas
Un homme de 53 ans consulte à l’urgence en raison de douleur
abdominale, diarrhée et déshydratation. Il a fait une dépression
majeure et a subi une cholécystectomie dans le passé. Il n’a pas
d’allergie, fume vingt-cinq cigarettes et un joint de cannabis par jour
depuis plusieurs années, et consomme de l’alcool occasionnellement.
Sur le plan de la médication, il prend de la venlafaxine et du
pantoprazole.
Initialement, le patient se présente à l’urgence pour un épisode aigu
de douleurs abdominales diffuses crampiformes et de constipation
depuis quelques jours, qu’il a tenté de soulager avec des laxatifs. Des
nausées et des efforts de vomissements font aussi partie du tableau
clinique et il accuse une diarrhée. Il note par ailleurs une perte d’appétit,
mais son poids demeure stable. Il n’a pas de fièvre ni de frisson, et il n’a
pas de rectorragie ou de méléna. Le patient affirme spontanément que
la seule chose qui soulage ses douleurs et ses nausées est la prise d’un
bain très chaud. Dans la dernière année, il décrit quatre épisodes
similaires. La revue des systèmes est par ailleurs négative.
L’examen physique est sans particularité à l’exception de la présence
de signes cliniques de déshydratation. L’abdomen est souple et les signes
de péritonisme sont absents.
Les bilans sanguins initiaux démontrent une hémoconcentration
importante avec des globules blancs à 20,9 x 109/L, une hémoglobine à
196 g/L et des plaquettes à 248 x 109/L. La créatinine et l’urée sont
initialement à 521 µmol/L et 18,7 µmol/L. La créatine kinase est à
4000 U/L. Sur le plan radiologique, une plaque simple et une
échographie de l’abdomen sont sans grande particularité.
L’impression clinique initiale de l’équipe est la suivante : diarrhée
induite par laxatifs entraînant une déshydratation sévère accompagnée
d’une insuffisance rénale aiguë pré-rénale. Le patient est donc admis
pour être hydraté agressivement. Rapidement, sa condition s’améliore
et ses symptômes s’estompent. Toutefois, lors d’un bilan de contrôle, la
lipase qui était initialement normale est augmentée à 585 U/L (normale
100-300 U/L). Une consultation en gastro-entérologie est donc
demandée pour investiguer ce changement.
Initialement, avec les résultats des tests de laboratoire disponibles et
l’histoire clinique, le diagnostic différentiel inclue une pancréatite aiguë,
une pancréatite chronique, une gastro-entérite virale, une subocclusion intestinale, un ulcère peptique et un syndrome des
vomissements cycliques secondaire au cannabis.
Le bilan a été complété pour éliminer les pathologies mentionnées ciCanadian Journal of General Internal Medicine
haut. Une tomographie axiale de l’abdomen a été faite malgré
l’échographie abdominale normale et a démontré un pancréas d’aspect
entièrement sain. Une oesophago-gastro-duodénoscopie a démontré
l’absence d’ulcère peptique. Par ailleurs, le dosage de la lipase du
lendemain était de 382 U/L.
Devant le bilan paraclinique normal et la récurrence des
symptômes dans la derniére année, le diagnostic retenu a été le
syndrome de vomissements cycliques (SVC) secondaire à la
consommation chronique de cannabis. L’insuffisance rénale aiguë a
été mise sur le compte de la diarrhée induite par les laxatifs.
Finalement, l’augmentation de la lipase a été expliquée par
l’insuffisance rénale et les vomissements. Le traitement offert au
patient, outre la réhydratation intraveineuse, a été la cessation de sa
consommation de cannabis.
Discussion
Le syndrome de vomissements cycliques est une pathologie bien
connue chez l’enfant qui est de plus en plus diagnostiquée chez l’adulte.
Décrite pour la première fois au 19e siècle, cette entité clinique se
présente par des épisodes stéréotypés de nausées et de vomissements
intraitables entraînant une déshydratation sévère pouvant durer de
quelques heures à quelques jours. Une douleur abdominale est présente
chez environ 60% des patients.1
Pour établir le diagnostic, le patient doit présenter depuis trois mois
des épisodes stéréotypés durant au moins une semaine, ayant débuté il
y a au moins 6 mois et étant entrecoupés de périodes complètement
asymptomatiques. Il doit par ailleurs avoir eu au moins trois épisodes
dans la dernière année.
Le syndrome de vomissements cycliques est un diagnostic
d’exclusion et plusieurs examens sont souvent effectués pour éliminer
des pathologies organiques faisant partie du diagnostic différentiel et
pouvant entraîner des complications si elles ne sont pas traitées. Les
patients sont donc sujets à subir une gastroscopie et/ou une
tomographie abdominale, comme dans le cas décrit ci-haut, qui ne
feront que confirmer l’absence d’anomalie.
Lorsque le diagnostic de syndrome de vomissements cycliques est
retenu, le traitement consiste à donner des anti-émétiques dans la phase
aiguë et à administrer hydratation intra-veineuse à bon débit tant que le
patient ne peut pas s’alimenter par lui-même. Entre les épisodes, le
patient doit éviter les facteurs précipitants qui sont le plus souvent le
stress, les infections, la migraine et parfois certains aliments.
79
Une lipase qui induit en erreur
En ce qui concerne le syndrome de vomissements cycliques
secondaire au cannabis, il s’agit d’une pathologie rare caractérisée par
les mêmes critères diagnostiques évoqués précédemment se retrouvant
chez des patients dont la consommation de cannabis précède
clairement le début des symptômes.
Allen et coll2 ont publié une série de cas de neuf patients en 2004 qui
décrit ce phénomène. Dans cette étude, tous les patients retenus pour
leur SVC accompagné de consommation de cannabis chronique ont été
encouragés à cesser leur consommation pour des raisons légales. Pour
sept des neuf patients, les symptômes se sont amendés. Trois des sept
patients ont repris leur consommation par la suite ayant pour
conséquence un retour des symptômes de SVC. Deux de ces trois
patients ont cessé la consommation à nouveau et ont noté une
disparition des symptômes. L’auteur note que ces patients avaient une
habitude d’hygiène particulière, soit la prise de bains chauds pour
soulager leurs symptômes. De plus, la température était directement
proportionnelle au soulagement observé. Ce phénomène a aussi été
décrit dans un rapport de cas de Wallace et coll3 en 2007. Le traitement
recommandé par Allen consiste en l’arrêt de la consommation de
cannabis. Il a d’ailleurs observé que la prise d’anti-émétiques était peu
efficace chez ces patients.
Conclusion
Le syndrome de vomissements cycliques est une pathologie importante
à reconnaître, car elle nécessite une prise en charge rapide afin d’en
minimiser les conséquences. Les patients présentant ce syndrome
clinique auront souvent une investigation extensive qui se révèlera
normale la plupart du temps. Lorsqu’un patient soulève la
consommation de cannabis ainsi que la prise de bains chauds pour
soulager ses symptômes, il est important d’évoquer le diagnostic de SVC
secondaire à cette drogue, car le traitement le plus efficace chez ces
patients est l’arrêt de la consommation.
Remerciements
Je voudrais remercier le Dr Luc Lanthier pour la révision du manuscrit.
Références
1. Fleisher DR, Gomowicz B, Adams K, et al. Cyclic vomiting syndrome
in 41 adults: the illness, the patients, and problems of management.
BMC Med 2005;3:20.
2. Allen JH, Moora GM, Heddle R, et al. Cannabinoid hyperemesis:
cyclical hyperemesis in association with chronic cannabis abuse. Gut
2004;53:1566–70.
3. Wallace D, Martin AL, Park B. Cannabinoid hyperemesis: marijuana
puts patients in hot water. Australas Psychiatry 2007;15:156–8.
MedEd
Multiple Mentoring: A New Paradigm?
Michelle Elizov, MD
About the Author
Michelle Elizov is a general internist at the Jewish General Hospital in Montreal, Quebec. She is a member of the Centre for
Medical Education at the Faculty of Medicine, McGill University. Correspondence may be directed to [email protected].
t all goes back to Hippocrates: the senior physician nurtures a young,
promising student, guiding him, moulding him, and grooming him
to be the senior’s successor. Until very recently, mentoring in many
fields, including medicine, followed this model. The mentor would take
on a very paternalistic role for the “protégé”: identifying a bright
student, taking the student under the mentor’s wing, directing the
student to the mentor’s own field of study, and moving from
supervising the student to collaborating with him or her. Eventually, the
student would take over the practice or field of study and become
himself a mentor to a new and promising student. This apprenticeship-
I
80
like relationship would be predominantly focused on the professional
aspect of the student’s life and might last an entire career; like the king
in Alice and Wonderland said, “Begin at the beginning and go on till you
come to the end: then stop.”1 However, with the changing scope and
practice opportunities in medicine, that model no longer seems
adequate, and many people have moved to the idea of multiple
mentoring, even if they haven’t attached that label to it.
The realities of modern practice are what drive the need for a change
in how we view, and find, suitable mentors. As a result of social,
economic, or academic pressures, physicians are increasingly mobile.
Elizov
Also, physicians are taking on a variety of roles in teaching, research, or
administration, in addition to clinical practice, and these roles may
change with time. The requirement to “produce” early on after gaining
a position is of an intensity few of our predecessors had to face so early
in their careers. On the positive side, there is a relatively new emphasis
on a work-life balance and on psychological and emotional well-being,
which many of our predecessors did not consider as they structured
their own careers.
For these and many other reasons, having multiple “mentors of the
moment”2 – people who can guide you in specific areas, at specific times
– becomes a useful idea. The relationship then becomes almost project
or competency based as opposed to the linear one described above.2
Physicians with a new staff appointment may be frustrated by the lack
of guidance and mentoring available to them, compared with their
residency days. They often waste precious time and energy figuring out
what they need to know to succeed: this is illustrated by the following
quotation from de Janasz: “Not one of them has offered to help. This
system would be considered madness in industry. They wouldn’t …
recruit a doctoral-level specialist and then watch him or her fail.”2
Having a mentor, or several, has definitely been shown to ease the
transition for new staff, providing the support and guidance they need
to do the job at hand, and increasing both their job satisfaction and
productivity. It’s a win-win situation for physicians and the institutions
they work for.
So how do you go about finding these mentors? First, you need to
identify your own goals and priorities – if you don’t know what you
want, even the best mentor in the world can’t help you. In the words of
Lewis Carroll, “If you don’t know where you are going, any road will
take you there.”1
Then you must recognize the enormous value of talking to the people
who have “been there, done that.” Look around at people who, in
different spheres, seem to be “doing it right,” remembering that that the
right way may be different for different people based on factors like
personality, stage in career, and available resources. Rather than asking
yourself, “How do they do that?” go and ask them directly: “How do you
do that?” Whether or not you find a mentor, take the time to speak to
your department chair or division chief. These individuals will have
valuable insights and can direct you to people outside of your
department or institution, or even your country, depending on the
needs you have expressed. Keep in mind that local mentors will have the
advantage of knowing the lay of the land, whereas more distant mentors
can sometimes provide a broader perspective. It depends what you need
and want. The bottom line, though, is that most people who are
approached to provide mentorship are sincere in their desire to help, are
willing to share their experience and their pearls, and are happy to spare
you some of the trouble they went through.
On the flip side, how does one become a mentor? First, recognize that
any help you provide is valued and appreciated. This may simply be to
identify the person to go to for specific advice. Identify your “new”
colleagues, introduce yourself and let them know in what areas you
could be of assistance if needed. These new colleagues could be junior
faculty just hired, new in the institution, or even new to a particular
career path. Be open and honest, not only in the guidance you can
provide but also in the magnitude of your commitment to this goal.
Recognize that expertise is not always age defined: even junior faculty
have knowledge and skills that would be valuable in a mentorship role.
And finally, remember that you were once the new physician too.
The concept of multiple mentoring has grown out of our practice
realities. The person we look to when getting started in research may
not be the same person we look to when taking on the role of principal
investigator in a multicentre trial. Our clinical skills mentor may well be
different from the individual who counsels when we feel down. These
multiple mentors of the moment provide us with rich and focused
guidance at the individual level. The whole process of give and take at
all levels encourages a spirit of respect and collegiality within the
organization, and this benefits everyone.
References
1. Carroll, L. Alice’s Adventures in Wonderland. England: Macmillan;
1865.
2. de Janasz SC, Sullivan SE. Multiple mentoring in academe:
developing the professional network. J Vocat Behav 2004;64:263–83.
81
Case Review
Post-device Chest Pain: A Cause for Concern
Clarence Khoo, MD, Jason Andrade, MD
About the Authors
Clarence Khoo (left) and Jason Andrade are cardiology fellows in the Department of Medicine, Division of
Cardiology, University of British Columbia, Vancouver, British Columbia. Correspondence may be directed to
[email protected].
Case Presentation
A 73-year-old woman with a longstanding history of anthracyclinerelated dilated cardiomyopathy (left ventricular ejection fraction of
20%) sustained an out-of-hospital cardiac arrest. She was successfully
resuscitated and underwent subsequent implantation of an implantable
cardioverter-defibrillator (ICD) for secondary prevention.
One week following ICD implantation, she returned to the hospital
with pleuritic chest pain. An electrocardiogram (EKG) tracing showed
diffuse ST elevation. Her serum troponin was not elevated. A
provisional diagnosis of pericarditis was made, and after 24 hours of inhospital monitoring, she was discharged home on high-dose
acetylsalicylic acid therapy.
She returned 3 days later after experiencing progressive shortness of
breath and fatigue, culminating in a syncopal episode after taking
nitroglycerin for transient neck pain. She denied any chest pain,
palpitations, orthopnea, or ankle swelling. There had been no changes
to her chronic beta-blocker, angiotensin-converting enzyme inhibitor,
or statin therapy. She was on a tapering course of prednisone for a
recent exacerbation of chronic obstructive pulmonary disease.
In the emergency room, she had a heart rate of 70 beats/minute, a
blood pressure of 66/31 mm Hg (without pulsus paradoxus), and a
normal temperature. She was tachypneic at 18 breaths/min, and her
oxygen saturation on 4 L/min of nasal prongs oxygen was 100%. The
internal jugular waveform was not visible, but the external jugular vein
was distended. Heart sounds were clear, and there were no murmurs
present. Widespread crackles were heard on auscultation of the left
chest, consistent with her known radiation-induced lung disease. There
was no pedal edema or calf asymmetry. Abdominal examination was
normal.
Her EKG (Figure 1) showed preserved QRS voltages and evidence of
left ventricular hypertrophy with ST-segment depressions in the
inferior and lateral leads, unchanged from previously. A chest
radiograph showed caudal migration of the right ventricular AICD lead
when compared with her discharge film (Figure 2). There was no
Figure 1. Electrocardiogram demonstrating preserved QRS voltages and evidence of left ventricular hypertrophy with ST-segment depressions in the inferior
and lateral leads – unchanged from previously.
82
Khoo and Andrade
evidence of pulmonary edema, and the cardiac
silhouette and mediastinum appeared unchanged.
The patient remained hypotensive despite fluid
resuscitation, and progressive hemodynamic instability
required the use of vasopressors. An emergency
bedside echocardiographic study revealed 2 cm of
circumferential pericardial fluid with right atrial
diastolic collapse suggesting cardiac tamponade.
Urgent pericardiocentesis via a sub-xiphoid approach
was performed. Aspiration of approximately 120 cc of
non-clotting, sanguineous pericardial fluid resulted in
an immediate improvement and the return of
hemodynamic stability.
Interrogation of her AICD showed the right
ventricular lead was not sensing appropriately,
suggesting a migration of the lead. A computed
tomography (CT) scan of the chest confirmed a
perforation of the right ventricular AICD lead into the
pericardium (Figure 3). She returned to the operating
room where a new right ventricular pacing lead was
successfully implanted.
Discussion
The implantation of transvenous endocardial leads has
become increasingly commonplace in the context of
both permanent pacemakers (PPM) and implantable
cardioverter defibrillators (ICD). Despite modern
techniques and increased familiarity with PPM/ICD
insertion, complications of implantation are not
uncommon.1 Case series and reviews have suggested
that the incidence of complications associated with
PPM implantation ranges between 3 and 9%, and is
roughly twice that rate with ICDs.2,3 Complications can
be divided into those associated with the implant
procedure itself, those related to leads and venous
access, and problems associated with device function.1
Early (<2 weeks postimplantation) and late complications occur with equal frequency.3
Myocardial perforation by transvenous leads is a
rare but well-recognized complication of PPM-ICD
insertion.1 With the use of thinner, more flexible
pacing leads, the rate of acute PPM-related lead
perforations has fallen to <1%. ICD leads have
remained relatively thick and stiff to allow for the
delivery of high-energy currents.2,3 As such, although
the incidence of ICD-related lead perforation was
initially quoted at <1%, this rate may be as high as
3–5% due to the aforementioned lead characteristics.4,5
The clinical presentation of transvenous lead
perforation is variable. While the majority of cases
present within 2 weeks, this can occur as late as 16–
23 months postimplantation.3,5–10
The most common clinical presentation of
Figure 2. Chest radiograph demonstrating ventricular lead position at time of device
implantation (A) and post-migration at time of presentation with tamponade (B).
Figure 3. Computed tomography scan of the chest demonstrating perforation of the right
ventricular lead through the right ventricular myocardium into the pericardial space.
83
Po s t - d e v i c e C h e s t Pa i n
myocardial lead perforation is that of increasing shortness of breath or
pleuritic chest pain suggestive of pericarditis. The reported incidence is
0.3–2%.4,7,9 There appears to be a consistent association of pericarditis
with active lead fixation in the right atrium but not with passive fixation
in the atrium or active fixation in the right ventricle.7 Other less
common presentations include new-onset atrial fibrillation, hemoptysis
following migration of the lead into lung parenchyma, or sudden
cardiac death.8–10 Likewise, symptomatic pericardial effusions resulting
from lead perforation are reported to occur at an incidence of 1%.11
Despite the presence of pericardial pathology, a number of patients
remain asymptomatic despite lead perforation and are only diagnosed
when increased sensing or pacing thresholds are noted on device
interrogation.1
In most individuals, pericarditis or pericardial effusion post-lead
implantation appears to have a self-limited and benign course.7 A few
individuals progress to cardiac tamponade and shock. In one centre, up
to 5.4% of all cases of cardiac tamponade requiring intervention was
associated with PPM implantation.6 Possible predictors of those who
may develop symptomatic pericardial effusions post-PPM have been
derived from analysis of the Mayo Clinic database and include the use
of temporary transvenous pacemaker leads (HR 2.7), the use of helical
screws for active lead fixation (HR 2.5), and recent steroid use within
the past 7 days (HR 3.2). Weaker predictors include advanced age, a low
body mass index, and prolonged use of fluoroscopy during lead
implantation.11
Pericarditic or pleuritic chest pain following lead implantation
should alert you to the diagnosis. Other supportive findings may
include a pericardial friction rub, an alteration in the pattern of
ventricular activation by the pacemaker, loss of capture, or frank pacing
of the diaphragm.1 Various imaging modalities can be used to confirm
this diagnosis. On chest radiographs, a separation of the lead tip of
<3 mm from the radiolucent stripe of the epicardial fat pad (the
“epicardial fat-pad sign”) is suggestive of lead perforation.12
Echocardiography can be used to detect pericardial fluid and right atrial
collapse. In addition, the location of the lead tip may sometimes be
visualized by echocardiography, less commonly by CT.1,9,10
Management of cases of lead perforation undoubtedly depends on
the clinical presentation and, more specifically, the presence or absence
of cardiac tamponade and hemodynamic compromise. In cases with
mild symptoms, minimal effusion, and no clear evidence of
perforation, observation may be appropriate. Small effusions should be
followed with serial echocardiograms.1 As noted above, uncomplicated
cases of pericarditis generally have a benign self-limited course but have
been managed in some case series with nonsteroidal antiinflammatory drugs or steroids.7 It is unclear whether the clinical
improvement noted in these cases occurred due to the therapy itself or
merely as a consequence of the natural history of the pericarditis.
84
Patients with cardiac tamponade require urgent pericardiocentesis
with the placement of a pericardial drain, followed by the surgical
removal of the lead.1
Summary
Lead perforation is a rare but potentially fatal complication of
PPM/ICD implantation. It should be suspected in individuals
presenting with pleuritic or pericarditic chest pain who have had a
device recently implanted. Clinical findings of pericarditis or
deterioration in the quality of pacing are supportive, as are radiological
signs of pericardial effusion or frank lead perforation. It is imperative
that a diagnosis of lead perforation not be delayed as urgent
pericardiocentesis may be required for those with cardiac tamponade.
For those with uncomplicated cases of pericarditis, observation and
treatment with anti-inflammatory agents may suffice.
References
1. Bailey SM, Wilkoff BL. Complications of pacemakers and
defibrillators in the elderly. Am J Geriatr Cardiol 2006;15:102–7.
2. Link MS, Estes NA III, Griffin JJ, et al. Complications of dual
chamber pacemaker implantation in the elderly. Pacemaker Selection
in the Elderly (PASE) investigators. J Interv Card Electrophysiol
1998;2:175–9.
3. Kiviniemi MS, Pirnes MA, Eranen HJ, et al. Complications related to
permanent pacemaker therapy. Pacing Clin Electrophysiol
1999;22:711–20.
4. Molina JE. Perforation of the right ventricle by transvenous
defibrillator leads: prevention and treatment. Pacing Clin
Electrophysiol 1996;19:288–92.
5. Danik SB, Mansour M, Singh J, et al. Increased incidence of subacute
lead perforation noted with one implantable cardioverterdefibrillator. Heart Rhythm 2007;4:439–42.
6. Navarrete CO, Marin F, Escriva AG, et al. Cardiac tamponade
following pacemaker implantation. Int J Cardiol 2005;104:350–1.
7. Levy Y, Shovman O, Granit C, et al. Pericarditis following permanent
pacemaker insertion. Isr Med Assoc J 2004;6:599–602.
8. Garcia-Bolao I, Teijeira R, Diaz-Dorronsoro I. Late fatal right
ventricular perforation as complication of permanent pacing leads.
Pacing Clin Electrophysiol 2001;24:1036–7.
9. Ellenbogen KA, Wood MA, Shepard RK. Delayed complications
following pacemaker implantation. Pacing Clin Electrophysiol
2002;25:1155–8.
10. Haq SA, Heitner JF, Lee L, Kassotis JT. Late presentation of a lead
perforation as a complication of permanent pacemaker insertion: a
case report. Angiology 2008;59:619–21.
11. Mahapatra S, Bybee KA, Bunch TJ, et al. Incidence and predictors of
cardiac perforation after permanent pacemaker placement. Heart
Rhythm 2005;2:907–11.
12. Rubenfire M, Anbe DT, Drake EH, Ormond RS. Clinical evaluation
of myocardial perforation as a complication of permanent
transvenous pacemakers. Chest 1973;63:185–8.
Health Promotion
Health Promotion: A New Mandate for CSIM
Norm Campbell, MD, Don Echenberg, MD, Bert Govig, MD, Akbar Panju, MBChB, for the CSIM Health Promotion Committee
About the Authors
(clockwise from top left) Norm Campbell is a professor of medicine at the University of Calgary,
Calgary, Alberta, and the president of Blood Pressure Canada. Donald Echenberg is the immediate
past president of CSIM and a professor of medicine at the University of Sherbrooke, Sherbrooke,
Quebec. Bert Govig is the president of CSIM and the founder of the Coalition for the Acquisition of
Sound Habits – CASH; he practises in Amos, Quebec. Akbar Panju is a past president of CSIM and
the current vice-president of Health Promotion for CSIM. He is a professor of medicine at McMaster
University, Hamilton, Ontario.
he CSIM Health Promotion Interest Group was founded in 2005 at
our national meeting in Toronto, Ontario. It became apparent that
this struck a chord with many of our members; and in 2007, the Interest
Group was upgraded to a CSIM Committee. Here we review existing
CSIM initiatives in the domains of preventive medicine, public health,
and medical education, and we report on our progress and future plans.
T
Collaboration for Salt-Reducing Strategies
In 2007, based on advice from the Health Promotion Committee, we
signed a Blood Pressure Canada policy statement calling for the
following:
•
The food sector to reduce sodium additives to food
•
The federal government to oversee a reduction in dietary sodium
through policy and education
•
Health care professional and scientific organizations to educate
their membership and the public on the health risks of high dietary
sodium
A great deal has happened since then. Statistics Canada prioritized
the analysis of dietary sodium in the national food survey (CCHS 3.1
2005) and issued a media release stating that a large majority of
Canadians consume an unhealthy amount of salt. A National Sodium
Strategic Planning Committee (SSPC) of eight national health care
organizations was formed to develop strategies for the health care sector
to advocate for a lower intake of dietary sodium in Canada. Blood
Pressure Canada has a grant from the Public Health Agency of Canada
to support this objective. The Canadian Stroke Network has also
embraced this initiative as its major focus for stroke prevention. The
Canadian Stroke Network, the Heart and Stroke Foundation of Canada,
and the government of Canada have issued several statements to the
media on dietary sodium in an attempt to increase public awareness.
Notably, the Canadian Stroke Network has recently created a sodium
website (www.sodium101.ca), and the Heart and Stroke Foundation of
Canada has revised its Health Check program to be more stringent with
regard to the sodium content of foods eligible for the label. Several
national organizations have organized talks, workshops, or symposia on
this topic. With the support of Food and Consumer Products Canada (a
major umbrella group for food manufacturers), the government of
Canada has struck a Health Canada Multi-Sectoral Work Group to
oversee a reduction in dietary sodium to recommended levels.
What does the CSIM need to do next? While Canadian action seems
impressive, it is unlikely to have had much impact. Given that 80% of
sodium in our food is there as a result of food processing, we need to
continue to play an active advocacy role. We must encourage the Health
Canada Work Group to report in a timely fashion and to act decisively.
If successful, this effort could reduce cardiovascular events in Canada
by 13% and save about $2 billion a year in health care expenses.
Collaboration for Improving Public Nutrition
In 2008, CSIM endorsed a healthy nutrition intervention administered
by the Coalition for the Acquisition of Sound Habits (CASH), a
Canadian health promotion charity. CASH promotes community
organization for health, and favours an environmental approach to
promoting healthy lifestyles. A randomized controlled trial study design
was used to evaluate a nutrition intervention in 30 participating arenas
in Quebec, Ontario, and New Brunswick. All sites were evaluated using
pre-established criteria to assess various elements of the nutrition
environment. The results of this study are under analysis, and the
intervention has been opened up to other arenas. Currently, 47 arenas
in Quebec, Ontario, and New Brunswick participate in this project, and
more are added on a monthly basis. CASH, the sponsoring
organization of this intervention, is currently developing similar tools
for use in other settings including daycares, schools, hospitals, events,
and conferences. CSIM members can learn of opportunities to
85
Health Promotion: A New Mandate for CSIM
CSIM Healthy Meeting Commitment
participate in future interventions on our website, in our journal, and
at www.soundhabits.org.
CSIM recognizes health promotion and health advocacy as a core value
CSIM’s Healthy Meeting Policy
and skill set of general internal medicine, and we recognize the
Our annual meeting Planning Committee has made an effort over the
past 5 years to develop healthy practices. We offer more nutritious meals
and snacks, and limit unhealthy food alternatives. We incorporate time
for early morning runs and walks and understand the importance of
dedicated time for networking, socializing, and simply relaxing.
In late 2008, after 4 years of promoting a healthy meeting on an ad hoc
basis, the Health Promotion Committee created a standing policy to
underscore our commitment to these objectives. We invite your
comments on this statement (see below): tell us how you feel we are
doing.
responsibility we have to our members and to society in general to promote
In the Works
policies and practices that are environmentally sustainable and will
Our Health Promotion Committee continues to develop new initiatives
and interventions. For example, we recognize that on-call practices vary
widely across Canada and have important implications both for patient
safety and for physician health and well-being. Work has begun to create
a national dialogue on this subject. For an update, watch this space!
attempt to use electronic forms of communication and documentation to
health in every aspect of the CSIM’s activities.
CSIM commits to playing an active role in promoting healthy lifestyles
at CSIM events by working in collaboration with relevant partners to
create environments conducive to healthy choices. This commitment
includes but is not limited to promoting access to healthy food, daily
physical activity, smoke-free environments, positive social interactions,
healthy sleep patterns, and work-life balance.
Where possible and appropriate, CSIM will also work to promote
promote active transport and mass transport and to promote recycling
and the parsimonious consumption of polluting and nonrenewable
resources.
Case Review
Pseudopheochromocytoma in Black Africans: A Case Report from Senegal
Seck Sidy Mohamed, MD, Ka Elhadj Fary, MD, Ba Sidy, Niang Abdou, MD, Diouf Boucar, MD
About the Authors
Drs. Seck and Ka are postdoctoral fellows, and Drs. Abdou and Boucar are staff and head, Department of Nephrology,
Hospital Aristide LeDantec, Dakar, Senegal. Correspondence may be directed to [email protected].
Editor’s note: CJGIM welcomes this paper from Senegal describing a
patient with an unusual form of hypertension.
Case Presentation
A 42-year-old black African man presented to the emergency
department with a severe headache, dizziness, and visual disturbance.
Eight months prior, he had been diagnosed with severe hypertension,
when similar symptoms occurred on returning from a business trip. He
had been treated with atenolol 100 mg daily, amlodipine 10 mg daily, and
lisinopril 20 mg/hydrochlorothiazide 12.5 mg daily, but experienced
several episodes of hypertension and hypotension on this regimen. He
was compliant with therapy and did not use illicit or traditional herbal
drugs. He was a nonsmoker, but did drink one or two glasses of wine
after dinner. He was married and lived quietly with his wife and two
86
children. For the previous 10 years, he had worked
12 hours a day as financier for an international group at the stock
exchange. He confessed to working many additional hours recently, in
response to the international financial crisis. Nevertheless, he denied
any particular fear, anxiety, or emotional distress. His personal and
family histories were otherwise unremarkable.
His examination revealed a pulse of 70 bpm and a blood pressure (BP)
of 235/145 mm Hg. He weighed 98 kg and was 1.95 m tall, yielding a
body mass index of 25.5 kg/m2. Fundoscopic examination revealed stage
III hypertensive retinopathy. The rest of his examination was normal.
His electrocardiogram showed LVH, confirmed by echocardiography. His cardiac output was normal. Blood tests showed blood urea
nitrogen of 50 mg/100 mL (46–95 mg/100 mL); serum creatinine of
132 mmol.l–1 (53–106 mmol.l–1); Na+ =136 mmol.l–1 (134–146 mmol.l–1);
Seck et al.
K+ = 3.8 mmol.l–1 (3.5–5.4 mmol.l–1); Cl– = 97 mmol.l–1 (90–
101 mmol.l–1); Ca++ = 2.05 mmol.l–1 (1.98–2.56 mmol.l–1); CO2 =
25 mmol.l–1 (21–27 mmol.l–1). A urinalysis revealed a pH of 6.6; no
albumin, no casts, and no red or white blood cells were present. A urine
drug screen for cocaine and narcotics was negative.
Two days later, his systolic BP was still difficult to maintain below
180 mm Hg despite a combination of nicardipine IV 2–4 mg/h, atenolol
150 mg/d, lisinopril 20 mg/d, and hydrochlorothiazide 12.5 mg/d. He
was transferred to our nephrology department for further tests.
Ultrasonography and computed tomographic imaging showed normalsized kidneys with good cortical indices and normal vessels.
Table 1 shows further laboratory tests performed to screen for
secondary hypertension. All tests were repeated 1 week later with
similar results.
Table 1. Biochemical Tests for Secondary Hypertension
Screening
Plasma Results
24-Hour Urine Results
Thyroid stimulating hormone
2.47 mIU/L (ref. 0.45–4.9 mIU/L)
Cortisol 430 nmol/L
(ref. 245–845 nmol/L)
Plasma renin 1.8 ng/mL
(ref. 0.25–1.9 ng/mL)
Plasma aldosterone 29 ng/100 mL
(ref. 5–32 ng/100 mL)
Plasma renin:
aldosterone ratio 0.06
Aldosterone 20.5 µg
(ref. 5–24 µg)
Free cortisol 12 µg
(ref. 0–49 µg)
5-HIAA 3 mg
(ref. 0–8 mg)
Normetanephrines 512 µg
(ref. 45–630 µg)
Metanephrines=220 µg
(ref. 35–400 µg)
Vanillylmandelic acid 4 mg
(ref. 0–7 mg)
Clinical Follow-Up
Calcium channel blockers, angiotensin-converting enzyme inhibitors,
and diuretics were discontinued. Doxazosin 1 mg/d and paroxetine
10 mg were prescribed, and the patient was seen 2 weeks later for
follow-up. His self-recorded home blood pressures were all below
140/90 mm Hg, confirmed at this clinic visit. Repeat fundoscopic
examination showed regression of previously noted papilledema, and
his renal function normalized. He continued to work long hours but
had no symptoms or side effects of note.
Two months later, we reduced atenolol to 50 mg/d to prevent episodic
hypotension. His blood pressure has remained stable, even after
exercise.
Discussion
In this case of malignant hypertension in a young man, we started by
looking for secondary causes of hypertension. The impaired renal
function noted at presentation was most likely due to his malignant
hypertension and related to a markedly activated renin angiotensin
system.1
Endocrine etiologies such as primary hyperaldosteronism,
hyperthyroidism, and hypercortisolemia were excluded. Pheochromocytoma was then considered, given the clinical presentation. Paroxysmal
hypertension with elevation of plasma or urine cathecholamines can be
seen in conditions such as obstructive sleep apnea and pre-eclampsia, or
with the use of anti-parkinsonian drugs or cocaine.2–4 In absence of
overt catecholamine excess the differential diagnosis includes panic
attack, alcohol withdrawal, and carcinoid syndrome.4 None of these
conditions was found in our patient.
The clinical, biochemical, and imaging findings in our patient are
most consistent with a diagnosis of pseudopheochromocytoma. This
condition was first described as essential paroxysmal hypertension
without biochemical evidence of catecholamine excess.5 Many cases
have been reported since 1981, but we believe our observation is the first
in a black African patient – despite the higher prevalence of malignant
hypertension in this ethnic group.6
Early reports have emphasized that emotional upset can often trigger
a precipitous elevation of blood pressure.7,8 However, this criterion is
not mandatory.4,9 Although our patient denied uncommon anxiety and
stress, it seems likely there was a causative association between his blood
pressure and work stress. His previous episode of paroxysmal
hypertension occurred after an important business trip, and the present
one with pressures at work due to uncertainties in the financial market.
In retrospect, his response to therapy confirmed our diagnosis. A
combination of alpha-1-blockers and beta-blockers, with an
antidepressant medication, is recommended for treatment of
pseudopheochromocytoma.9
Conclusion
This case proves again that etiology of hypertension in a young patient
is often elusive. Pseudopheochromocytoma should be considered in
case of paroxysmal hypertension of unknown etiology with normal
investigations. The presence of emotional disturbance is suggestive,
although an overt anxiety disorder may be absent.
References
1. van den Born BJ, Koopmans RP, van Montfrans GA. The reninangiotensin system in malignant hypertension revisited: plasma
renin activity, microangiopathic hemolysis, and renal failure in
malignant hypertension. Am J Hypertens 2007;20:900–6.
2. Shah BR, Gandhi S, Asa SL, et al. Pseudopheochromocytoma of
pregnancy. Endocr Pract 2003;9:376–9.
3. Duarte J, Sempere AP, Cabezas C, et al. Pseudopheochromocytoma
in a patient with Parkinson’s disease. Ann Pharmacother
1996;30:546.
4. Hunt J, Lin J. Paroxysmal hypertension in a 48-year-old woman.
Kidney Int 2008;74:532–5.
5. Kuchel O, Buu NT, Hamet P, et al. Essential hypertension with low
conjugated cathecholamines imitates pheochromocytoma.
Hypertension 1981;3:347–55.
6. van den Born BJ, Koopmans RP, Groeneveld JO, van Montfrans GA.
Ethnic disparities in the incidence, presentation and complications
of malignant hypertension. J Hypertens 2006;24: 2299–304.
7. Kuchel O. Increased plasma dopamine in patients presenting with
the pseudopheochromocytoma quandary: retrospective analysis of
10 years’ experience. J Hypertens 1998;16:1531–7.
8. Takabatake T, Yamamoto Y, Ohta H, et al. Blood pressure variability
and hemodynamic response to stress in patients with paroxysmal
elevation of blood pressure. Clin Exp Hypertens A 1985;7:235–42.
9. Mann SJ. Severe paroxysmal hypertension
(pseudopheochromocytoma): understanding the cause and
treatment. Arch Intern Med 1998;158:1381–2.
87
Case Review
Superinfected Pulmonary Bulla in a Freebase Cocaine User
Jeffrey Segal, MD, Barbara Young, MD
About the Author
Jeffrey Segal is a PGY2 resident, and Barbara Young is an assistant clinical professor in the Division of Internal Medicine,
Montreal General Hospital, Montreal, Quebec.
Case Report
A 54-year-old homeless man of Haitian origin presented to our hospital
with a 5-day history of right-sided pleuritic chest pain, dyspnea, and a
productive cough. The patient had no other pertinent past medical or
surgical history, and he took no prescription medications. He had a
15 pack-year smoking history and reported smoking freebase cocaine
five to 10 times per week for over 20 years. Marijuana use was not
determined.
He reported a loss of appetite and a 2.3 kg weight loss in the previous
week. His physical examination was normal, except for poor oral
hygiene and decreased air entry in the right upper lobe. In particular, he
was afebrile.
Laboratory assessment showed a white blood cell count of 10.9 x 10.6;
other laboratory parameters, including hemoglobin, electrolytes, liver
profile, and lactate dehydrogenase, were within normal limits. Screening
for human immunodeficiency virus was negative. A chest radiograph
showed moderate-sized bullae in the upper lung zones bilaterally, with
an air fluid level in the right-sided bulla (Figure 1). A computed
tomography scan of the thorax showed bilateral bullous
emphysematous changes in the apices with the largest bulla in the right
apex measuring greater than 10 cm in anteroposterior and transverse
diameter (Figure 2). An air fluid level and air bubbles were present in
this bulla, with adjacent air bronchograms.
The patient was admitted to the internal medicine ward and
prescribed ticarcillin-clavulanate for a presumed superinfected
pulmonary bulla. Blood and sputum cultures were negative.
The patient developed a low-grade fever for the first 2 days of
therapy, but this subsided. His condition improved and his antibiotic
was changed to oral moxifloxacin. The patient left hospital of his own
volition after 1 week without completing the remainder of his antibiotic
therapy.
Discussion
Cocaine use is widespread in Canada, with 0.7% of the population
15 years and over admitting to use. Among those who live on the street,
approximately 40% report frequent use.1 There are many forms of
cocaine, and the end product is dependent on the chemicals used in its
production. Cocaine hydrochloride is a salt that is derived from the
Erythroxylon coca plant; it cannot be smoked because of its high
88
Figure 1. Chest radiograph showing moderate-sized bullae in the upper lung
zones bilaterally, with an air fluid level in the right-sided bulla.
Figure 2. Computed tomography scan of the thorax showing bilateral bullous
emphysematous changes in the apices with the largest bulla in the right
apex measuring >10 cm in anteroposterior and transverse diameter.
vaporizing temperature. Freebase cocaine is made by dissolving cocaine
hydrochloride in water and then adding ammonium; the precipitant is
then dissolved in ether, which is then evaporated, leaving a vaporizable
solid, which can be smoked.2
A multitude of pulmonary complications associated with smoking
S e g a l a n d Yo u n g
cocaine have been described, and include acute respiratory distress
syndrome, airway injury, exacerbation of asthma, interstitial
pneumonititis, bronchiolitis obliterans and organizing pneumonia,
pulmonary edema, and pulmonary hemorrhage.3 Other pulmonary
pathology attributed to cocaine use includes the precocious
development of bullae with upper lobe predominance.
Van Der Klooster and Grootendorst4 reported a similar case, a
40-year-old freebase cocaine user with fever, dyspnea, and cough whose
chest radiograph showed bilateral upper-lung bullous emphysema.
Bullae are thinly walled, air-filled spaces within the lung. A
longstanding pathophysiological explanation for bulla formation and
growth was that a local deleterious process led to a focal area of alveolar
weakening, which would then act as a one-way valve, allowing air to
enter the space on inspiration but not allowing air to escape on
expiration. An expanding bulla would thereby compress adjacent
normal lung.5 This mechanism was challenged in the 1980s. Morgan
and colleagues examined the dynamic behaviour of bullae in patients
undergoing CT imaging and bullectomy. They found that gas flow into
and out of bullae was unhindered. Moreover, on histological
examination of the bullae, no one-way valvular mechanism was seen.6
They proposed a different mechanism of bulla growth. A process
leading to parenchymal weakness would still be the impetus for bulla
generation; however, since bullae are more compliant than the
surrounding normal lung, they would preferentially inflate during tidal
respiration. The maintained elastic recoil in the surrounding normal
lung tissue would lead to retraction away from the bulla, thereby leading
to bullous enlargement.
The pathogenesis of bullae with cocaine use is unknown. A common
finding in cocaine smokers is chronic alveolar hemorrhage, postulated
to be due to alterations in the pulmonary microcirculation. Baldwin
and colleagues assessed the levels of endothelin-1 (ET-1), a
vasoconstrictor, and hemosiderin-laden alveolar macrophages, a
marker of recent alveolar hemorrhage, in bronchoalveolar fluid
specimens in cocaine users. They found increased levels in cocaine
smokers compared with nonsmokers,7 suggesting that cocaine induced
ET-1 release may lead to vasoconstriction of the pulmonary
endothelium and hemorrhage into alveoli.8 Another finding is that
cocaine itself can lead directly to alveolar cell damage. Susskind and
colleagues examined the lung clearance technetium labelled
diethylenetriamine pentaacetic acid (DTPA), a marker of alveolar
epithelial permeability, in cocaine smokers versus controls.9 They found
clearance to be abnormally elevated in cocaine users,9 implying an
alteration in alveolar epithelium.8 In either case, might these changes be
the inciting factor for pulmonary bullous development? The
explanation for the apical predominance of the bullae is still elusive.
The premature formation of bullae is not unique to cocaine smoking,
however. Johnson and colleagues reported four cases of young male
tobacco and marijuana smokers who presented to hospital with
respiratory complaints and were found to have bullous changes
exclusively in the upper lobes and apices.10 Apical bullous lung disease
can also be a rare pulmonary manifestation of ankylosing spondylitis
(AS),11 sarcoidosis,12 and genetic anomalies such as Marfan syndrome
and Ehlers-Danlos syndrome.12
In the case of marijuana, the suspected etiology of bullous changes is
a combination of pulmonary toxicity from the inhaled chemicals as well
as pressure swings related to the deep inspiration and prolonged breathholding these individuals practise when smoking marijuana.10
Autoimmunity and recurrent infection might be the cause of bullae in
AS,11 while abnormal collagen fibre production leading to terminal
bronchiolar flaccidity is the presumed mechanism in the genetic
collagen disorders.13 The pathogenesis of bullae in pulmonary
sarcoidosis might involve endobronchial granulomas causing alveolar
destruction.14
In conclusion, pulmonary bullae form as a result of local areas of
alveolar weakness. They grow as a result of preferential inflation during
inspiration and elastic recoil of surrounding lung tissue. Isolated apical
bullae can be a consequence of illicit drug use, as is suspected in our
patient, or a manifestation of genetic or autoimmune diseases. In the
case of freebase cocaine smoking, we hypothesize that direct drug
toxicity – or drug-induced vasoconstriction – is the most likely cause of
bulla development.
References
1. Health Canada. Cocaine use: recommendations in treatment and
rehabilitation. Ottawa, ON: Health Canada, 2000; http://www.hcsc.gc.ca/hl-vs/alt_formats/hecs-sesc/pdf/pubs/adp-apd/cocaine_useusage_cocaine/cocaine-eng.pdf. Accessed June 20, 2008.
2. Restrepo CS, Carillo JA, Martinez S, et al. Pulmonary complications
from cocaine and cocaine-based substances: imaging manifestations.
Radiographics 2007;27:941–56.
3. Haim DY, Lippmann ML, Goldberg SK, Walkenstein MD. The
pulmonary complications of crack cocaine. Chest 1995;107:233–40.
4. Van Der Klooster JM, Grootendorst AF. Severe bullous emphysema
associated with cocaine smoking. Thorax 2001;56:982–3.
5. Greenberg JA, Singhal S, Kaiser LR. Giant bullous lung disease:
evaluation, selection, techniques, and outcomes. Chest Surg Clin
North Am 2003;13:631–49.
6. Morgan MD, Edwards CW, Morris J, Matthews HR. Origin and
behaviour of emphysematous bullae. Thorax 1989;44:533–8.
7. Baldwin GC, Choi R, Roth MD, et al. Evidence of chronic damage to
the pulmonary microcirculation in habitual users of alkaloidal
(“crack”) cocaine. Chest 2002;121:1231–8.
8. Tashkin PD. Airway effects of marijuana, cocaine, and other illicit
agents. Curr Opin Pulm Med 2001;7:43–61.
9. Susskind H, Weber DA, Volkow ND, Hitzemann R. Increased lung
permeability following long-term use of free-base cocaine (crack).
Chest 1991;100:903–9.
10. Johnson MK, Smith RP, Morrison D, et al. Large bullae in marijuana
smokers. Thorax 2000;55:340–2.
11. Lee CC, Lee SH, Chang LJ, et al. Spontaneous pneumothorax
associated with ankylosing spondylitis. Rheumatology
2005;44:1538–41.
12. Zahra MZ, Amer C. One may die from giant bullae. Heart Views
2005;8:62–5.
13. Ha HI, Seo JB, Lee SH, et al. Imaging of marfan syndrome:
multisystemic manifestations. Radiographics 2007;27:989–1004.
14. Juson MA, Strange, C. Bullous sarcoid – a report of three cases.
Chest 1998;114:1474–8.
89
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CLASSIFIEDS
Positions Available for
GENERAL INTERNISTS
in Sault Ste. Marie, Ontario
ault Ste. Marie is a northern urban centre situated on the
Canadian/U.S. border at the hub of the Great Lakes, with
both the Canadian wilderness and extraordinary vacation areas
in Michigan just minutes away. Summer and winter recreational opportunities are abundant and a strong cultural basis in the
arts exists in the community.
S
The local education system includes both French and
English primary and secondary schools, two Montessori
Schools, Algoma University and Sault College
Our community offers the opportunity for private solo practice, or group practice at the Group Health Centre with the
Algoma District Medical Group (ADMG). The Algoma District
Medical Group (ADMG) is an independent medical corporation
of over 60 physicians and associates providing healthcare services to most of the population of Sault Ste. Marie.
The Group Health Centre, located in the geographic centre of
the community, is a multi-specialty, multi-disciplinary, modern,
well-equipped ambulatory care facility, with diagnostic services
and electronic medical record. It is Ontario’s largest and longest
established membership-based organization. www.ghc.on.ca
The Sault Area Hospital (SAH) is the community hospital providing emergency, primary, secondary and tertiary hospital services for the residents of Sault Ste. Marie and surrounding area.
Sault Area Hospital serves a catchment area of 120,000 and
operates a total of 289 beds, including acute, chronic care, rehabilitation and mental health beds, and 10 Level 3 neonatal intensive care bassinets.
The anticipated completion of a new hospital in Sault Ste.
Marie in 2010 will provide significant opportunities to serve a
growing population. www.sah.on.ca
Affiliation with the new Northern Ontario School of
Medicine (NOSM) provides the opportunity to teach residents
and medical students.
Locum positions qualify for funding support from the
Ministry of Health and Long-Term Care Underserviced Area
Program, including daily honourarium and stipend plus payment
for travel and accommodation plus additional on-call stipend.
Full-time positions are eligible for MOHLTC/UAP grants as
well as a very competitive community incentive.
For further information, please contact:
Mary Jane Yorke, Manager,
SSM Physician Recruitment & Retention Program
Phone: (705) 759-3720 or E-mail: [email protected]
Visit our website: www.saultmed.com
94
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Volume 4 issue 2 - Andrew John Publishing Inc.

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