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Medical Society of Delaware
Officers and Trustees
2010-2011
OFFICERS
DAVID M. BERCAW, M.D. – PRESIDENT
RANDEEP S. KAHLON, M.D. – PRESIDENT-ELECT
STEPHEN J. KUSHNER, D.O. – VICE PRESIDENT
KEVIN P. SHEAHAN, M.D. – SECRETARY
JOSEPH F. HACKER III, M.D. – TREASURER
ROBERT L. MECKELNBURG, M.D. – SPEAKER OF THE HOUSE
WILLIAM H. DUNCAN, M.D. – VICE SPEAKER OF THE HOUSE
NICHOLAS O. BIASOTTO, D.O. – PAST PRESIDENT
TRUSTEES
Kent County
JACQUELINE J. CHRISTMAN, M.D.
New Castle County
JOHN DECARLI, D.O
KRISTINE B. DIEHL, M.D.
JAMES M. GILL, M.D., MPH
JOHN J. GOODILL, M.D.
DOROTHY M. MOORE, M.D.
Sussex County
MARK J. BOYTIM, M.D.
Council on Medical Specialties
CHRISTOPHER L. BALDI, D.O.
CEDRIC T. BARNES, D.O.
CHRISTIAN M. COLETTI, M.D.
ELLIOTT H. LEITMAN, M.D.
BHASKAR S. PALEKAR, M.D.
ESTELLE H. WHITNEY, M.D.
AMA Delegate
KELLY S. ESCHBACH, M.D.
DELPAC Representative
JOSEPH P. OLEKSZYK, D.O.
Legislative Chair
JOSEPH F. HACKER III, M.D.
Young Physicians Section Representative
NANCY FAN, M.D.
Resident & Fellow Section Representative
ROI ALTIT, M.D.
EDITORIAL STAFF
Editor-in-Chief, Delaware Medical Journal
PETER V. ROCCA, M.D.
EXECUTIVE STAFF
MARK A. MEISTER, SR. – EXECUTIVE DIRECTOR
Del Med J, June 2011, Vol 83 No 6
Instructions to Authors
The Delaware Medical Journal (DMJ) is owned and published
by the Medical Society of Delaware as a medium of communication, education, and expression for its members, and also
for others striving for excellence in medical practice. Articles
in the DMJ are intended to be scientific and educational and
are not intended to reflect standards of medical care. All
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Scientific articles on medical matters are especially welcomed,
including case reports, clinical experiences, observations, and
information on matters relevant to medical practice. Other
material may also be accepted if the editorial staff deems it
of interest to DMJ readers. All submissions should include a
brief summary and a brief (one to two sentence) biographical
sketch of all authors.
It is highly recommended that authors familiarize themselves
with DMJ style before submitting manuscripts for consideration.
Material for publication should be submitted on disk or CD
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(without graphs, charts, or photographs) may also be submitted electronically via e-mail. The ideal manuscript length is
750 to 5,000 words with up to 12 references, each keyed with
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Graphs, charts, and black-and-white glossy photographs are
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of each graph, chart or photo should also be submitted. Most
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Photos of patients should generally be taken in a way that
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All manuscripts are reviewed by the editor, and all scientific
articles are then sent for peer review by members of the Editorial Board and/or other appropriate physicians. The usual
processing time to publication is two to four months, though
in some circumstances this may be longer or shorter.
All materials should be submitted to: Delaware Medical Journal, The Medical Society of Delaware, 900 Prides Crossing,
Newark, Delaware 19713 or e-mailed to koj@medsocdel.org.
161
ISSN 0011-7781
VOLUME 83
DELAWARE
MEDICAL
JOURNAL
JUNE 2011
NUMBER 6
C O N T E N T S
Official Publication
of the Medical Society of Delaware
900 Prides Crossing
Newark, Delaware 19713
Editor-in-Chief
Peter V. Rocca, M.D.
Editorial Board Members
Joseph A. Lieberman III, M.D., MPH
Brian W. Little, M.D., Ph.D.
E. Wayne Martz, M.D. (Editor Emeritus)
Michael R. Zaragoza, M.D.
Publication and
Editorial Committee
Evan H. Crain, M.D.
Andrew J. Doorey, M.D.
Steven L. Edell, D.O.
Gerard J. Fulda, M.D.
Galicano F. Inguito, M.D.
Rebecca Jaffe, M.D.
Nancy Kim, M.D.
James F. Lally, M.D.
Joseph A. Lieberman III, M.D., MPH
Brian W. Little, M.D., Ph.D.
E. Wayne Martz, M.D.
Gregory A. Masters, M.D.
Hiep C. Nguyen, M.D.
Leo W. Raisis, M.D.
Peter V. Rocca, M.D.
Anthony C. Sciscione, D.O.
Udayan K. Shah, M.D.
Kevin P. Sheahan, M.D.
Sonya N. Tuerff, M.D.
Michael R. Zaragoza, M.D.
165
PRESIDENT'S PAGE
MSD's Patient-Centered Medical Home Pilot
David M. Bercaw, M.D.
167
NATIONAL CANCER INSTITUTE
CLINICAL TRIAL OF THE MONTH
169
CASE STUDY
Drug Overdose with Refractory Bradycardia and Hypotension
Shyamkrishnan Ramdas, M.B.B.S., Lee Ann Riesenberg, PhD,
RN, and Neil Jasani, M.D., MBA, FACEP
175
SCIENTIFIC ARTICLE
What is the Best Operative Practice for Small Benign Parotid Pleomorphic
Adenoma?
Robert L. Witt, M.D., FACS
179
HEALTH AND LAW
The “Casual” Patient is Still Your Patient
Brandy A. Boone, JD
183
NEWSMAKERS
CORRECTION: The May 2011 President's Page stated that the Delaware
Medical Care Advisory Committee (MCAC) proposed a cost containment
strategy for Medicaid. This was incorrect. The article should be stated that
the strategies were proposed by the Delaware Division of Medicaid and
Medical Assistance.
Former Editors
Robert B. Flinn, M.D.
Bernadine Z. Paulshock, M.D.
G. Stephen DeCherney, M.D., MPH
E. Wayne Martz, M.D.
On the Cover: “Best of Greece” by Carlo Viola, photograph, Station Gallery,
Greenville, Del.
The Delaware Medical Journal (ISSN 0011-7781, USPS 152140) is published monthly by the Medical Society of Delaware at 900 Prides Crossing, Newark, DE 19713.
Periodicals postage paid at Newark, Delaware, 19711 and additional entry offices. Copyright 2010 by the Medical Society of Delaware. Indexed in "Hospital Literature Index" and "Index Medicus." Available through University Microfilms. The Delaware Medical Journal does not hold itself responsible for statements made by
any contributor or advertiser. Annual subscription rates are $30 for domestic and $45 for overseas. Single copies are $2.50. Advertising copy is accepted, subject
to the approval of the Publication and Editorial Committee of the Medical Society of Delaware. For information about advertising, call the Journal office at (302)
366-1400. POSTMASTER: Address changes to 900 Prides Crossing, Newark, DE 19713.
President's Page
PRESIDENT'S PAGE
MSD’s Patient-Centered Medical Home Pilot
David M. Bercaw, M.D.
So what’s all the buzz about Patient-Centered
Medical Homes (PCMH)? It’s more than just a
“feel-good” moniker. Multiple pilot programs
throughout the country have demonstrated positive outcomes – including decreased emergency
department visits and hospital admissions, improvements in diabetes and heart disease care,
and enhanced patient and provider satisfaction
– while at the same curtailing cost.
In 2007, the Joint Principles of the PCMH
were agreed upon and written by the four leading
primary care groups – The American Academy of
Family Physicians, the American Academy of Pediatrics, the American College of Physicians, and the
American Osteopathic Association. In a nutshell,
the principles boil down to seven points:
MSD President David M. Bercaw, M.D., is Vice Chair of the
Christiana Care Health System Department of Family and Community Medicine and practices at the Family Medicine Center in
Wilmington, Delaware.
Del Med J, June 2011, Vol 83 No 6
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Physician-directed medical practice;
Ongoing relationship with personal physician;
Whole person orientation;
Coordinated care across the health system;
Emphasis upon quality and safety;
Enhanced access to care;
Payment recognizes the value added.
More specifically, most primary care physicians will need to dramatically transform their
practices in order to truly become a PCMH. They
will need to re-tool their office work flow, revise
their office policies, and implement new approaches to scheduling appointments. Advanced access
scheduling ensures same-day appointments at
a time convenient to the patient. Many PCMH
offices have expanded their hours, offering early
morning appointments, evening appointments,
and Saturday hours. Clinical information sys-
165
President's Page
tems, most effectively provided by health information technology, will support practice-based
improvement and quality initiatives. These will
include chronic disease registries, monitoring
patient adherence to treatment regimens, decision support at the point of service, and ready
access to lab and test results for physicians as
well as for patients.
Becoming a PCMH is a process which requires
up-front investment in time, energy, and money.
For the typical doctor in a small group, such
transformation can seem daunting, if not impossible. That’s exactly why the MSD is developing
its PCMH pilot.
For those of you in subspecialty practices,
be aware that the PCMH concept is expected to
broaden into the Patient-Centered Medical Neighborhood. And no, I’m not invoking Fred Rogers
and suggesting that we all put on a cardigan and
lace up our tennies. But we are, indeed, fortunate
in Delaware that a statewide multispecialty physician organization already exists in the form of
166
MedNet’s Physician Organizations. We already
have a viable substrate upon which to build a
coordinated network of physicians providing
high quality, effective, and efficient care for our
patients.
In the meantime, involvement in the MSD
PCMH pilot will allow primary care practices
to use the expertise of others who are in the
process of implementing most, if not all, of the
above-mentioned practice changes. Then add in
the expertise of Quality Insights of Delaware’s
Regional Extension Center to assist in achieving
the CMS incentives for meaningful use. Finally,
mix in the incentives for e-prescribing and quality
reporting and you now have the perfect recipe for
change. Preheat your ovens. The time is right.
David M. Bercaw, M.D.
President, Medical Society of Delaware
Del Med J, June 2011, Vol 83 No 6
NATIONAL CANCER INSTITUTE CLINICAL TRIAL OF THE MONTH
GOG 0207:
A Randomized Double-Blind Phase II Trial of Celecoxib, A Cox-2
Inhibitor, in the treatment of patients with Cervical Intraepithelial Neoplasia 2/3 or 3 (CIN 2/3 or 3) (IND #69,656, Sponsor – GOG)
The Objectives of the Trial are:
Primary Objectives:
• To determine the efficacy of Celecoxib to induce complete remission (or partial regression to
•
CIN 1) of CIN 2/3 or CIN 3 as evaluated in the post-treatment excisional biopsy.
To determine the toxicity of Celecoxib (400 mg once daily) as assessed by Common
Terminology Criteria for Adverse Events in this patient population of women with CIN 2/3 or
CIN 3.
Exploratory Objectives:
• To assess whether treatment with Celecoxib changes the number of quadrants containing
aceto-white lesions as determined through colposcopic examination.
• To determine the efficacy of Celecoxib treatment in changing HPV viral load in cervical cells.
• To examine the association of histologic response; HPV viral load; lesion size; proliferation
index (Ki67), apoptosis index (TUNEL assay), angiogenesis (VEGF), and COX-2 in tissue; the
amount of VEGF and bFGF in serum before and after treatment; and the amount of Celecoxib
present in serum during treatment. Cervical cytology karyometry will be assessed as a
potential marker for regression.
• To determine the feasibility of digital imaging, web-based review of histopathology in a GOG
study.
• To compare the diagnoses of the web-based review of histopathology with the diagnoses of
GOG’s standard procedure.
Eligibility:
•
•
•
•
Patients must have histologically proven CIN 2/3 or CIN 3 diagnosed by cervical biopsy
between 2 and 8 weeks prior to enrollment.
Patients must have a satisfactory (readable, good quality) colposcopic evaluation at least 14
days after diagnostic biopsy.
Patients must have colposcopically visible cervical lesion at entry consistent with biopsy.
Patients must agree to refrain from using NSAIDS and aspirin during the time they are taking
the study medication.
Treatment:
All patients randomized to the study will receive either Celecoxib at 400 mg PO once daily or
placebo once daily. Patient and investigator will be blinded to the treatment.
Treatment will continue for 14-18 weeks or until disease progression or unacceptable toxicity.
For information regarding this clinical trial
or if you would like to have the list of open protocols e-mailed to you,
please call the Cancer Research Office at (302) 623-4450 or e-mail akee@christianacare.org.
Del Med J, June 2011, Vol 83 No 6
167
Case Study
CASE STUDY
Drug Overdose with
Refractory Bradycardia and Hypotension
Shyamkrishnan Ramdas, M.B.B.S.,1 Lee Ann Riesenberg, PhD, RN,2
and Neil Jasani, M.D., MBA, FACEP3
Abstract
Background: In the emergency department physicians are often called upon to make decisions with limited information. Often
the correct diagnosis and treatment hinge on one piece of information, which may be the key to the entire presentation.
Objective: We present a case report of a patient who presented with refractory bradycardia and hypotension who had overdosed on calcium channel blockers as well as beta blockers. The underlying cause however was myxedema. Were it not
for the presence of hypothermia, the correct diagnosis of myxedema secondary to severe hypothyroidism could have been
missed. We also briefly review the pathophysiology and treatment of myxedema.
Conclusion: We present a case of refractory bradycardia and hypotension in a patient who had overdosed on calcium channel blockers as well as beta blockers. Paying close attention to all the details of the case eventually uncovered the underlying
severe hypothyroidism and myxedema. In the emergency department we are always called upon to make decisions with
limited information. It is also paying close attention to all of the information presented that allows one to not miss any key
pieces central to the final diagnosis.
Key words: Refractory Bradycardia, Hypotension, Overdose, Hypothyroid
INTRODUCTION
CASE REPORT
Critically ill patients often present to the Emergency Department (ED) with no previous medical
history available. In this case, a 49-year-old female
presented having ingested anti-hypertensive (Diltiazem, Metoprolol) and anti-depressant (Clonazepam) medications. We describe the diagnostic and
therapeutic issues faced by the ED physician when
caring for a patient with suspected overdose whose
symptoms are refractory. Despite conventional treatment, she had continued refractory bradycardia and
hypotension. This led to a search for other causes,
including hypothyroidism.
A 49-year-old woman presented to the ED
with loss of consciousness subsequent to consuming large doses of Diltiazem (Cardizem),
Metoprolol (Toprol) and Clonazepam (Klonopin).
The patient was known to have Type 1 diabetes
mellitus, coronary artery disease, breast cancer, and depression. On initial evaluation by
Emergency Medical Services (EMS), her mental
status was waxing and waning with an average
Glasgow Coma Score (GCS) of 14. Her vital signs
were: pulse 44, respirations 20, O2 saturation
80 percent, BP 110/50 mm Hg, and accu-check
revealed a blood glucose level of 18 mg/dL. The
patient regained consciousness after 50 percent
dextrose was administered, and her blood glucose
level rose to 130 mg/dL. At this point, she complained of chest pain and shortness of breath, for
which she was given sublingual nitroglycerine.
The patient denied suicidal ideation or attempt,
stating that she had accidentally consumed the
pills while dreaming she was eating candy.
1. Shyamkrishnan Ramdas, M.B.B.S. is a resident in the
Department of Internal Medicine at Christiana Care Health
System in Newark, Del.
2. Lee Ann Riesenberg, PhD, RN is the Director of Medical
Education Research and Outcomes at Christiana Care
Health System in Newark, Del., and a research Assistant
Professor at Jefferson School of Population Health at Thomas
Jefferson University in Philadelphia.
3. Neil Jasani, M.D., MBA, FACEP is the Program Director for
the Emergency Medicine Residency Program at Christiana
Care Health System in Newark, Del.
Del Med J, June 2011, Vol 83 No 6
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Case Study
In the ED her vital signs were: pulse 33,
BP 88/40 mm Hg, temperature 33.5° C. She was
started on intravenous (IV) fluids, Atropine 0.5
mg IV, Glucagon 1 mg IV, and Calcium Gluconate
1 ampoule. The Cardiology consultant ordered
Epinephrine 1mg, which produced a transient
increase in her heart rate and BP. She was then
placed on a continuous IV Epinephrine infusion.
Despite rigorous treatment, her bradycardia and
hypotension remained refractory leading to a
continued search for ancillary causes. Her initial lab chemistries included Sodium 133mM/L,
BUN 44mg/dL, Creatinine 3.2mg/dL, Chloride
95mM/L, and Phosphorous 5.7 mM/dL. Urinalysis
was normal, but the urine toxicology screen was
positive for benzodiazepines. Blood gas levels were
pH 7.28, PCO2 33 mm Hg, and PO2 127mm Hg.
Electrocardiogram (ECG) demonstrated junctional bradycardia and first degree AV block with
a rate of 33 beats per minute. Chest radiograph
was normal. Thyroid function tests were ordered
due to her severe hypothermia.
She remained persistently bradycardic and
hypotensive. IV Dopamine was initiated and a
temporary pacemaker placed. Three hours later
her TSH level was found to be >100 MIU/L (Normal: 0.27 – 4.2) suggesting severe hypothyroidism. She was then promptly started on 300 μg
IV Levothyroxine and 100 mg IV hydrocortisone.
Later family members arrived and provided the
history of hypothyroidism, with poor compliance
with prescribed thyroid medications.
The patient was admitted to the MICU, where
she was intubated to secure her airway as a result
of her deteriorating mental status. She improved
over the course of a few days and was gradually
taken off the ventilator, IV pressors, and the
temporary pacemaker. Upon discharge, she was
transferred to a psychiatric in-patient facility.
DISCUSSION
ED physicians are called upon to make rapid
decisions with limited and sometimes inaccurate information. This case illustrates how one
symptom, hypothermia, was obscured by a host
of other seemingly more acute symptoms. The
combination of known overdose and the lack of
knowledge of this patient’s hypothyroidism could
170
have been fatal. However, persistence in identifying the cause of her hypothermia resulted in a
diagnosis and appropriate treatment plan.
Drug overdose, cold temperature, infection,
hypoglycemia, hyponatremia, and beta blockers
are some of the well-documented causes of myxedema coma, a challenging and potentially fatal
manifestation of hypothyroidism. Myxedema
coma, though rare, is mostly found in elderly
women with a history of longstanding, undertreated or undiagnosed hypothyroidism. It has
a very high mortality rate if not diagnosed and
treated rapidly. This requires the ED physician
to be extremely vigilant in identifying subtle
clues and in initiating prompt treatment once
the diagnosis is made.1
The fundamental triad that should arouse
suspicion for Myxedema is: altered mental status,
defective thermoregulation, and a precipitating
event(s).2 Usually, in long standing hypothyroidism, the body’s metabolic rate and oxygen consumption are decreased, which causes peripheral
vasoconstriction and central shunting thereby
maintaining the core temperature. Also seen is an
imbalance between the alpha and beta adrenergic
receptors where the numbers of beta receptors are
reduced with preservation of the alpha receptors
resulting in diastolic hypertension and reduced
total blood volume.3 Myxedema coma represents
the most severe form of hypothyroidism in which
the physiological adaptations are no longer sufficient to maintain homeostasis.
The pathophysiology involves three features:4
1. CO2 retention and hypoxia – Due to a
blunted response to decreased O2 tension and
hypercapnia. Other factors that contribute
include obesity, central nervous system depression, heart failure, and immobilization.
The impairment of ventilatory drive is often
severe and patients almost always need assisted respiration.
2. Fluid and electrolyte balance – Due to
free water intoxication, due to reduced renal
perfusion and impaired free water clearance
resulting in hyponatremia.
3. Hypothermia – Due to the resetting of the
body’s ‘thermostat’ resulting in decreased core
temperature sometimes as low as 80° F. This
sign may not be picked up because ordinary
Del Med J, June 2011, Vol 83 No 6
Case Study
clinical thermometers do not go below 34°C.
Hence, thermometers with broader scales or
electronic ones must be used.
The severe bradycardia and hypotension
precipitated by these drugs impairs renal and
cerebral perfusion, disrupting electrolyte balance and psychomotor stability. Calcium channel
blocker overdose also can precipitate metabolic
acidosis. Benzodiazepine toxicity depresses the
CNS and the respiratory center. At higher doses,
benzodiazepines slightly depress alveolar ventilation and cause respiratory acidosis as the result
of a decrease in hypoxic rather than hypercapnic
drive.5-7
The combined toxicities of the drugs ingested
by our patient resulted in severe bradycardia,
hypotension, acidosis, and hypoglycemia. In
addition, her poor compliance in taking her hypothyroid medications precipitated myxedema
coma.
CLINICAL PRESENTATION
The clinical presentation of myxedema coma
is characterized by progressive weakness, stupor,
hypothermia, hypoglycemia, and hyponatremia.
If not treated promptly, shock or death may result.
Myxedema coma occurs more frequently in the
winter in older patients with underlying pulmonary and vascular disease. The patient may have
a history of thyroid disease, radio iodine/radiation therapy to the neck area, or thyroidectomy.
On examination, the patient may have clinical
features of longstanding hypothyroidism, such
as yellowish dry skin, hoarse voice, large tongue,
thin hair, puffy eyes, delayed deep tendon reflexes
(Woltman’s Sign).4,8,9
Laboratory clues pointing to myxedema
coma are markedly elevated TSH, low T4 levels,
thyroid auto antibodies (if present, suggesting
Hashimoto’s thyroiditis), high serum carotene,
elevated serum cholesterol, increased CSF protein.4 ECG will show sinus bradycardia and low
voltage.4
MANAGEMENT
Considering the severity of this condition it
is essential that the management be initiated
in the ED or intensive care setting. In addition
to vital signs, blood gases should be monitored
frequently, and the patient almost always requires intubation and mechanical ventilation in
the first 48 hours.4,10 It is imperative to give T4
intravenously, because patients with myxedema
coma have poor gastric absorption.4 A loading
dose of 300-500 μg of IV T4 is given followed
by IV maintenance doses of 50 to 100 μg daily,
which is continued until an oral regimen can be
started.2 A rise in body temperature and return
of normal cerebral and respiratory function
indicates an appropriate response to therapy.44
Caution should be maintained while administering IV T4, especially in geriatric patients. IV T4
Table 1: Conditions known to cause Myxedema Coma
Table 2: Drugs known to cause Myxedema Coma
Infection/systemic illness
Tranquilizers
Cold temperatures
Sedatives
Trauma
Anesthetics
Burns
Amiodarone
Decreased cerebral blood flow/CVA
Lithium
Decreased cardiac output/CHF
Beta-blockers
Respiratory acidosis
Phenytoin
Hypoglycemia
Analgesics/Narcotics
CO2 retention
Diuretics
GI hemorrhage
Rifampin
Del Med J, June 2011, Vol 83 No 6
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Case Study
increases cardiac workload, which increases the
risk of angina, heart failure, and arrhythmias.2,4
Hence, it would be prudent to start the treatment
slowly in such patients. If arrhythmia or angina
occurs, it is recommended that the T4 dose be
reduced immediately.4
These patients should be continuously
monitored for hyponatremia, hypoglycemia, and
hypothermia. Hyponatremia generally responds
to fluid restriction, but experts recommend hypertonic saline when serum sodium concentrations
fall below 110 mEq/L. Asymptomatic mild hyponatremia (>120 mEq/L) may be monitored without
specific therapy and can be expected to resolve
with thyroid hormone replacement therapy.1 Hypothermia should be passively treated with space
blankets. Active rewarming is avoided because
it causes significant peripheral vasodilatation,
triggering an increase in oxygen consumption
and eventual vascular collapse.2,4,8,11
The mortality associated with myxedema
coma is surprisingly high, varying between
20 to 60 percent. Persistent hypothermia and
bradycardia have been associated with poor
prognosis.2,3 With prompt institution of thyroxine
replacement therapy – as well as other general
supportive measures – to correct life-threatening
metabolic derangements, myxedema coma can be
fully reversed.1,9
CONCLUSION
We present a case of refractory bradycardia
and hypotension in a patient who had overdosed
on calcium channel blockers as well as beta
blockers. Paying close attention to all the details
of the case eventually uncovered the underlying
severe hypothyroidism and myxedema resulting
in definitive treatment for the patient. In the
172
emergency department we are always called upon
to make decisions with limited information. It is
also paying close attention to all of the information presented that allows one not to miss any
key pieces central to the final diagnosis.
REFERENCES
1. Wall CR. Myxedema coma: diagnosis and treatment. Am
Fam Physician. 2000;62:2485-2490.
2. Fliers E, Weirsinga WM. Myxedema coma. Rev Endocrinol Metab Disord. 2003;4:137-141.
3. Jordan RM. Myxedema coma: Pathophysiology, therapy,
and factors affecting prognosis. Med Clin North Amer
1995;1:185-194.
4. David S, Greenspan FS, Ladenson PW. The Thyroid
Gland. In: Gardner DG, Shoback D, Greenspan’s Basic
and Clinical Endocrinology. 8th ed. New York, NY:
McGraw Hill Co; 2007:240-248.
5. Westfall TC, Westfall DP. Adrenergic agonists and antagonists. In: Brunton LL, Lazo JS, Parker KL. Goodman
& Gilman's the Pharmacological Basis of Therapeutics.
11th ed. New York, NY: McGraw Hill; 2006. http://www.
accessmedicine.com/content.aspx?aID=936313. Accessed
July 27, 2009.
6. Hoffman BB. Therapy of hypertension. In: Brunton LL,
Lazo JS, Parker KL. Goodman & Gilman's the Pharmacological Basis of Therapeutics.11th ed. New York, NY:
McGraw Hill; 2006. http://www.accessmedicine.com/
content.aspx?aID=944839. Accessed July 27, 2009.
7. Charney DS, Mihic SJ, Harris RA. Hypnotics and sedatives. In: Brunton LL, Lazo JS, Parker KL. Goodman
& Gilman's the Pharmacological Basis of Therapeutics.
11th ed. New York, NY: McGraw Hill; 2006. http://www.
accessmedicine.com/content.aspx?aID=938413. Accessed
July 27, 2009.
8. Jameson JL, Weetman AP. Disorders of the thyroid
gland. In: Fauci AS, Braunwald E, Kasper DL, Hauser
SL, Longo DL, Jameson JL, Loscalzo J. Harrison's
Principles of Internal Medicine. 17th ed. New York, NY:
McGraw Hill; 2008. http://www.accessmedicine.com/
content.aspx?aID=2877285. Accessed July 27, 2009.
9. Marinella MA. Woltman’s Sign of Hypothyroidism. Hosp
Physician 2004;40:31-32.
10. Wartofsky L.Myxedema coma. Endocrinol Metab Clin
North Am. 2006;35:687-698.
11. Sarlis NJ, Gourgiotis L. Thyroid emergencies. Rev Endocrinol Metab Disord. 2003;4:129-136.
Del Med J, June 2011, Vol 83 No 6
Scientific Article
SCIENTIFIC ARTICLE
What Is the Best Operative Practice
for Small Benign Parotid Pleomorphic Adenoma?
Robert L. Witt, M.D., FACS
BACKGROUND
Superficial parotidectomy (SP) with facial
nerve dissection dramatically reduced the
high rates of tumor recurrence that occurred
with simple enucleation of parotid pleomorphic
adenoma (PPA) in the second half of the 20th
century. However, there is no agreement in the
current medical literature confirming the exact
margin of parotid tissue to be resected to avoid
recurrence and reduce morbidity. More complete
parotidectomy results in higher rates of transient
facial nerve dysfunction and Frey’s syndrome. A
better understanding of histo-pathology, the use
Robert L. Witt, M.D., FACS is Professor of Otolaryngology-Head
and Neck Surgery at Thomas Jefferson University in Philadelphia,
Penn., Adjunct Scientist in Translational Cancer Research at the
University of Delaware in Newark, Del., and Director of the Head
and Neck Multidisciplinary Clinic at the Helen F. Graham Cancer
Center at Christiana Care Health System in Newark, Del.
Del Med J, June 2011, Vol 83 No 6
of magnification, bipolar coagulation to control
hemostasis, and nerve integrity monitors have
led to less invasive surgery. Partial superficial
parotidectomy (PSP) with facial nerve dissection
and a 2 cm margin of normal parotid parenchyma,
except where the tumor abuts the facial nerve, is
the generally favored approach to small (< 3cm)
benign PPA reducing morbidity without increasing recurrence. Selected reports on Extracapsular
Dissection (ECD), mostly from Europe, but also
from North America suggest equivalent results
for recurrence and better results for morbidity.
ECD dissects a small cuff of normal parotid
parenchyma around the tumor without facial
nerve dissection. Outcomes data between PSP
with facial nerve dissection and ECD without
facial nerve dissection will be compared for the
relative risks of recurrence, permanent and transient facial nerve dysfunction, Frey’s syndrome,
and numbness.
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Scientific Article
LITERATURE REVIEW
In a publication with meta-analysis of a large
number of case series,1 recurrence of PPA with
PSP with facial nerve dissection occurs in less
than 1 percent of cases. Permanent and transient
facial nerve dysfunction occurs in less than 1
percent, and 18 percent, respectively. Frey’s
syndrome occurs in 10 percent of cases. Minimal
contour deformity, but permanent numbness of
the ear lobule are expected outcomes in most
cases.
Smith and Komisar2 reported on a highly selected series of 27 patients using ECD. There were
no recurrences, however the follow up was only
a mean of 41 months and PPA recurs at a mean
of seven years.1 There were no cases of permanent or transient facial nerve dysfunction. There
were no cases of Frey’s and there was no contour
deformity and only minimal numbness.
McGurk et al3 reported on a series of 413
cases of ECD. ECD was selected when the tumor
appeared clinically benign. Recurrence was 1.7
percent at 15 years. The rate of permanent and
transient facial nerve dysfunction was 1.6 percent
and 10 percent, respectively. Frey’s syndrome
occurred in 5 percent of cases and10 percent had
numbness. 5 percent of cases had unexpected
malignancy on final pathology.
The Erlangen group in Germany4 reported
on 377 patients who received ECD with a rate of
permanent and transient facial nerve dysfunction
of 2 percent and 6 percent respectively. Numbness
was reported in only 10 percent of cases.
Piekarski et al5 for ECD reported an unacceptable recurrence rate of 8 percent with permanent and transient facial nerve dysfunction
also unacceptable at 8 percent and 10 percent,
respectively.
Meta-analysis summary effect for recurrence
has been reported as no higher for ECD compared
to SP; permanent facial nerve dysfunction is 1.8
times higher for ECD; transient dysfunction is
2.0 times lower.1
Selection criteria for ECD and training are
variable. The hypocelluar, soft friable pleomorphic
adenoma and/or ill-defined pseudo-capsule are
relative contraindications to ECD. This cannot
176
always be determined until after rupture. The
pseudo-capsule of a PPA has a positive margin
in 25-33 percent of cases.1 ECD may be a modern
day euphemism for yester-years enucleation made
perhaps viable by magnification, nerve integrity
monitors and improved control of hemostasis with
bipolar coagulation. Malignancy, however, can be
an unexpected final pathology. Although facial
nerve dysfunction, Frey’s, and numbness can be
fairly precisely documented, recurrence data can
be more difficult to prove given that more than
half of recurrences occur beyond seven years and
the associated loss to follow up. Without initial
identification of the facial nerve, the risk of permanent facial nerve paralysis can be high for the
novice or occasional parotid surgeon.
SUMMARY
Most surgeons will reduce the risk of recurrence and permanent facial nerve dysfunction
with PSP for PPA with dissection and control of
the facial nerve. High volume, very experienced
parotid surgeons can offer ECD with the expectation of less transient facial nerve dysfunction,
Frey’s syndrome, and numbness. Long term
recurrence rates await further reports.
Level of Evidence:
One manuscript is Level 2, one is Level 3, and
three are Level 4.
REFERENCES
1. Witt R. The significance of margin in surgery for parotid
pleomorphic adenoma. Laryngoscope. 2002;112:21412154.
2. Smith SL, Komisar A. Limited parotidectomy: The role
of extracapsular dissection in parotid gland neoplasms.
Laryngoscope. 2007;117:1163-67.
3. McGurk M, Thomas BL, Renehan AG. Extracapsular
dissection for clinically benign parotid lumps: Reduced
morbidity without oncologic compromise. Br J Cancer.
2003;89:1610-13.
4. Klintworth N. Zenk J. Koch M. Iro H. Postoperative
complications after extracapsular dissection of benign
parotid lesions with particular reference to facial nerve
function. Laryngoscope. 2010;120(3):484-90.
5. Piekarski J, Nejc D, Szymczak W et al. Results of extracapsular dissection of pleomorphic adenoma of parotid
gland. J Oral Maxillofac Surg 2004;62:1198-1202.
Del Med J, June 2011, Vol 83 No 6
Health and Law
HEALTH AND LAW
The “Casual” Patient is Still Your Patient
By Brandy A. Boone, JD
Most physician practices have a specific protocol for established patients, whether the physician has seen the patient once or for 20 years.
The practice maintains a chart – either paper or
electronic – with documentation of the patient’s
history, medications, and examination notes. But
what happens when a physician provides care for
friends, family members, or employees? Physicians
may feel that because they “know” a family or staff
member – and may not provide care on a regular
basis – formalities, like histories and documentation, are not as necessary as for established
patients. This kind of thinking is risky because
the “casual” patient is still your patient.
FAMILY
The American Medical Association’s Code
of Ethics discourages self-treatment and treatment of immediate family members for several
Brandy A. Boone, JD is a Manager of Risk Resource for ProAssurance Corporation.
Del Med J, June 2011, Vol 83 No 6
reasons. These reasons include potential loss of
professional objectivity, which can interfere with
the care of the patient, and potential failure to
obtain relevant – but sensitive – information because of embarrassment or personal discomfort.
Consider this case:
Following a fertility procedure at a medical
practice, the patient experienced heavy bleeding. When her Obstetrician/Gynecologist
husband was notified, he admitted her and
operated, discovering she had lost almost 75
percent of blood volume. The patient stabilized
following surgery, and the Obstetrician/
Gynecologist had his wife transferred to a
surgical floor rather than the ICU. He stayed
in her hospital room following the procedure
and awoke at 4:00 a.m. to find his wife in
distress. She experienced respiratory distress
and died one week later.
A malpractice lawsuit was filed against the
hospital, several nurses, and the fertility specialists. The Obstetrician/Gynecologist was
179
Health and Law
sued as a third party defendant by the other
defendants in the case. A jury exonerated the
husband and rendered a $25 million verdict
against the fertility specialists. The nurses
settled the case, possibly because pre-trial discovery revealed unwillingness on the nurses’
part to intrude upon the husband’s “care” in
order to monitor the patient.
of the employee, either positively or negatively,
in the workplace?
Similar to treatment of family members, physicians may also be less likely to record histories
and maintain documentation of patient encounters
with employees. Consider this example:
A medical assistant working in an orthopedic
practice asked one of the physicians for the
hepatitis B vaccine. He agreed even though she
was not an established patient. The physician
obtained the vaccine from his drug rep and
gave her one shot. The medical assistant then
began caring for her father, who was near
death from hepatitis B. She found out later
she might have received the wrong vaccination
and blamed the physician who gave her the
shot. The physician had not documented the
encounter and had no defense for a lawsuit.
Physicians who treat family members may
also be less likely to take a thorough history,
maintain documentation, or refer to documentation prior to treatment. In another family treatment case, the patient, who happened to be the
physician’s wife’s uncle, sued the physician after
he received an injection to which the patient had
a history of being allergic. The patient suffered
anaphylactic shock and was taken to the emergency department. This patient was an established
patient of the practice, but despite the familial
relationship, a lawsuit ensued.
TIPS TO REDUCE RISK
employees
l
There are also issues for physicians who provide medical care for their employees, whether as
an established patient or by informal consultation.
Physicians examining co-workers may encounter
the same sensitivity issues or embarrassing situations as those who treat family members, such
as the awkwardness of disrobing or discussion
of personal issues. Treating employees can also
cause physicians to lose objectivity. For instance,
if an employee reveals personal information to the
physician in the context of a health discussion,
could it cause the physician to think differently
180
l
l
l
Limit care for immediate family members or
employees to emergency situations.
Document all encounters where care is rendered, regardless of relationship.
Treat “casual” patients the same as established patients (histories, documentation,
etc.).
Avoid prescribing controlled substances to
family members or employees, especially for
pain management.
This article is not intended to provide legal advice, and no
attempt is made to suggest more or less appropriate medical
conduct.
Del Med J, June 2011, Vol 83 No 6
MSD Member News
NEWSMAKERS
MSD Members
Forty MSD member physicians from A.I. duPont
Hospital for Children and Nemours were selected
for inclusion on the Best Doctors in America®
listing for 2011-2012. They include:
Michael A. Alexander, M.D.; Jeanne M. Baffa,
M.D.; Patrick C. Barth, M.D.; Louis E. Bartoshesky, M.D.; S. Charles Bean, M.D.; Abdul
Majeed Bhat, M.D.; Howard Z. Borin, M.D.;
J. Richard Bowen, M.D.; Hal Byck, M.D.;
Jeffrey W. Campbell, M.D.; Aaron Chidekel,
M.D.; Steven P. Cook, M.D.; Kathleen M.
Cronan, M.D.; Kirk W. Dabney, M.D.; Maria
Carmen Diaz, M.D.; Divya Dixit, M.D.; Stephen Dunn, M.D.; Stephen J. Falchek, M.D.;
Sandra G. Hassink, M.D.; James H. Hertzog,
M.D.; Jing Jin, M.D.; Richard Kingsley, M.D.;
Joel D. Klein, M.D.; Richard W. Kruse, D.O.;
Stephen Lawless, M.D.; Sharon S. Lehman,
M.D.; William G. Mackenzie, M.D.; Rita Meek,
M.D.; Freeman Miller, M.D.; Joseph A. Napoli, M.D.; Scott H. Penfil, M.D.; Joseph H.
Piatt Jr., M.D.; Russell C. Raphaely, M.D.;
Suken A. Shah, M.D.; Udayan K. Shah, M.D.;
Ellen A. Spurrier, M.D.; Mihir Thacker, M.D.;
Andrew W. Walter, M.D.; Rhonda S. Walter,
M.D.; and Oliver Yost, M.D.
Patricia M. Curtin, M.D. received the Christiana Care Health System 2011 Spirit of Women
Health Care Hero Award at an event held April
26 at Christiana Hospital. Dr. Curtin has been a
guiding force for many initiatives at Christiana
Care in the field of elder care. She serves on the
Senior Service Task Force for the State of Delaware and is Medical Director of the Stonegates
Retirement Community. She traveled twice to
Haiti as part of the Notre Dame Medical Group
Del Med J, June 2011, Vol 83 No 6
and recently returned from a third trip to help
families with complex medical issues.
Jeffry I. Komins, M.D. has been appointed
Chief Medical Officer of Catholic Health East
(CHE). Dr. Komins is a fellow of the American
College of Obstetricians and Gynecologists and
Senior Fellow in the Department of Health
Policy at Jefferson Medical College. CHE is a
multi-institutional Catholic health system which
includes St. Francis Hospital in Wilmington. Dr.
Komins lives in Wilmington, Delaware.
Julia M. Pillsbury, D.O. has been appointed
to the Current Procedural Terminology (CPT)
Editorial Panel of the American Medical Association. Dr. Pillsbury has represented the American
Academy of Pediatrics (AAP) on the AMA RVS
Update Committee (RUC) as the AAP Alternate
Advisor to the CPT Panel. She continues to serve
on the AAP Committee on Coding and Nomenclature. Dr. Pillsbury practices at the Center for
Pediatric and Adolescent Medicine in Dover.
Joseph Siebold, D.O. received the American
College Health Association's Ollie B. Moten
Award for Outstanding Service to One's Institution. Dr. Siebold is the Director of Student Health
Services at the University of Delaware.
Hospitals
Bayhealth Medical Center was named Large
"Business of the Year" by the Chamber of Commerce for Greater Milford at its awards dinner
on April 7.
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