Download Secondary Hypertension: Diagnosis and Management

CASE-BASED REVIEW
Secondary Hypertension: Diagnosis and
Management of an Adrenal Adenoma
Case Study and Commentary, Debbie L. Cohen, MD, and Raymond R. Townsend, MD
INSTRUCTIONS
The following article, “Secondary Hypertension:
Diagnosis and Management of an Adrenal
Adenoma,” is a continuing medical education (CME)
article. To earn credit, read the article and complete the
CME evaluation form on page 532.
OBJECTIVES
After participating in the continuing education
activity, primary care physicians should be able to:
1. Know the renal and adrenal causes of secondary hypertension
2. Know the components of the clinical examination of a
hypertensive patient
3. Be familiar with laboratory tests used to assess an incidentally discovered adrenal mass
4. Know the usual findings in primary aldosterone excess
(Conn’s syndrome)
5. Understand the approach to follow-up in patients with
secondary hypertension
A
pproximately 42.3 million adults in the United
States have hypertension, according to the National
Health and Nutrition Examination Surveys III
(NHANES). The NHANES survey defined hypertensive patients as those with a systolic blood pressure
of 140 mm Hg or greater, a diastolic blood pressure of
90 mm Hg or greater, or those taking hypertension medication [1]. Because an estimated 7.7 million adults with hypertension had adopted lifestyle changes that reduced their
blood pressure to normal levels prior to the NHANES survey, it can be assumed that there are approximately 50 million adults with hypertension in the United States [2].
Although 3 out of 4 patients with hypertension are aware of
their diagnosis of hypertension, blood pressure control
remains poor. Many patients are untreated or inadequately
treated. Only 29% of patients have their blood pressure controlled to below 140/90 mm Hg [2].
Intensive efforts have been made to improve blood pressure control by increasing both physician and patient education. Despite these efforts, blood pressure control and aware-
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ness have remained low [2]. Poor outcomes have been
blamed on patient noncompliance with medications [3], limited access to medical care, financial barriers to obtaining
medications, and, more recently, an insufficiently aggressive
approach to blood pressure lowering by health care
providers [4,5].
Hypertension is an expensive disease to treat. It has been
estimated that the cost for hypertension care in the United
States in 1995 was $18.7 billion; 20% of this amount represented the costs of antihypertensive drugs [6]. Given these
costs, it is important to rule out potentially treatable causes
of hypertension in appropriately selected patients.
CASE STUDY
Initial Presentation
A 35-year-old white woman presents to a nephrology practice for enrollment in a hypertension
study testing a new medication for high blood pressure.
She feels well and when untreated has a blood pressure of
154/108 mm Hg, confirmed by several measurements.
• What is the etiology of hypertension?
Etiology of Hypertension
More than 90% of patients with hypertension have essential
(primary) hypertension [7]; the remaining 10% have hypertension attributed to secondary causes. The prevalence of
essential and secondary hypertension is shown in Table 1.
There are 2 common types of secondary hypertension:
renal and adrenal (Table 2). These 2 causes account for more
than 90% of all cases of secondary hypertension. Renal causes are the most common. Hypertension ensues from renal
parenchymal diseases (eg, acute or chronic glomerulonephritis), renovascular diseases (eg, renal artery stenosis),
and, rarely, renin-producing tumors or primary sodium
From the Renal-Electrolyte and Hypertension Division, University of
Pennsylvania, Philadelphia, PA.
Vol. 9, No. 9 September 2002 JCOM 525
SECONDARY HYPERTENSION
Table 1. Frequency of Diagnoses in Patients Attending a
Hypertension Clinic
Diagnosis
Essential hypertension
Chronic renal disease
Renovascular disease
Primary aldosteronism
Cushing’s syndrome
Pheochromocytoma
Coarctation of the aorta
Oral contraceptive use
Frequency
92.1
5.6
0.7
0.3
0.1
0.1
0
1.0
Data from Sinclair AM, Isles CG, Brown I, et al. Secondary hypertension in a blood pressure clinic. Arch Intern Med 1987;147:1289–93.
retention disorders (eg, Liddle’s syndrome) [8]. Adrenal
causes are divided into cortical and medullary types.
Cortical adrenal disease can result in increased production of
aldosterone as seen in primary aldosteronism (Conn’s syndrome) or increased production of glucocorticoid as seen in
Cushing’s syndrome. Medullary adrenal disease can result
in increased production of norepinephrine and epinephrine
as seen in a pheochromocytoma. Although less common,
coarctation of the aorta can also cause secondary hypertension by causing downstream renal ischemia, resulting in
increased renin production.
A number of other phenomena are associated with
increased blood pressure. Exogenous hormones (including
estrogen in hormone replacement therapy, glucocorticoids,
mineralocorticoids), sympathomimetic agents (particularly
those used in over-the-counter cold preparations), and erythropoietin (administered to patients with anemia of chronic renal failure, HIV infection, and cancer) can cause increased blood pressure. Hypertension can also accompany
pregnancy, sleep apnea, acute stress situations (eg, hypoglycemia and burns), increased intravascular volume secondary to alcohol and nicotine use, or an increased cardiac
output due to thyrotoxicosis, arteriovenous fistulae, or
Paget’s disease of bone.
Table 2. Types and Causes of Hypertension
Essential hypertension
Endocrine: primary aldosteronism, Cushing’s syndrome, congenital
adrenal hyperplasia, pheochromocytoma, hyperthyroidism,
hypothyroidism, acromegaly, hypercalcemia, carcinoid tumors
Renal: acute glomerulonephritis, chronic glomerulonephritis, polycystic
kidney disease, diabetic nephropathy, interstitial renal diseases, renal
artery stenosis, vasculitis, renin-producing tumors, primary renal
sodium retentive states (Gordon’s syndrome, Liddle’s syndrome)
Coarctation of the aorta
Pregnancy-induced hypertension
Foods containing tyramine and monoamine oxidase inhibitors
Exogenous hormones: estrogen, mineralocorticoids, glucocorticoids,
sympathomimetics, erythropoietin
Acute stress situations: surgery, hypoglycemia, burns, alcohol withdrawal
Neurologic disorders: increased intracranial pressure, sleep apnea,
familial dysautonomia, lead poisoning
Increased intravascular volume
Drugs: cocaine, nicotine, cyclosporine, tacrolimus
Increased cardiac output states: thyrotoxicosis, Paget’s disease, beriberi, anemia, arteriovenous fistula, aortic valve regurgitation
Data from Kaplan NM, Lieberman E. Clinical hypertension. 7th ed.
Baltimore: Williams and Wilkins; 1998.
may be possible to cure the hypertension if it is detected
early enough.
One should suspect secondary hypertension in patients
who present with a negative family history of hypertension;
unprovoked hypokalemia; severe drug-resistant hypertension; recent worsening of or difficulty in controlling previously well-controlled essential hypertension; a triad of headache,
sweating, and palpitations; an abdominal bruit; or new onset
hypertension in a young patient (less than 20 years) or in a
patient older than 50 years (Table 3). In patients who present
with refractory hypertension, however, only 10% will have a
secondary cause for their hypertension. Other causes of refractory hypertension are shown in Table 4.
• What are the minimal diagnostic tests for evaluating a
new hypertensive?
• When should one suspect secondary hypertension?
When treating patients with hypertension, it is important to
keep in mind that the likelihood of finding secondary hypertension is low. Doing so can help one avoid a costly workup
in patients with essential hypertension. However, this caveat
must be balanced by understanding the possibility of finding a treatable underlying cause of hypertension. Because
patients with secondary hypertension are often young, it
526 JCOM September 2002 Vol. 9, No. 9
Evaluation of the Hypertensive Patient
The clinical examination should include an examination of
the fundi to assess for changes seen with hypertensive
retinopathy. The peripheral pulses and radiofemoral delay
should be assessed to exclude coarctation of the aorta and
presence of an epigastric bruit. The latter finding is highly
specific, although not sensitive, for renal artery stenosis.
Electrocardiography should be performed to assess for left
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CASE-BASED REVIEW
Table 3. Findings That Should Increase Suspicion of
Secondary Hypertension
Negative family history for hypertension
Unprovoked hypokalemia
Unusually severe hypertension or recent dramatic worsening of
hypertension
Triad of symptoms: headache, sweating, and palpitations
New-onset hypertension in patient younger than 20 years or older
than 50 years
Epigastric bruit
Different blood pressure measurements in the arms and legs or
radiofemoral pulse delay
Drug-resistant hypertension
ventricular hypertrophy (LVH). It is important to document
the presence of LVH because it is an independent risk factor
for increased cardiovascular morbidity and mortality [9,10].
An echocardiogram is the procedure of choice, however,
since the sensitivity of the electrocardiographic criteria for
detecting LVH may be as low as 7% to 35% with mild LVH
and 10% to 50% with moderate to severe LVH [11].
Electrocardiographic evidence of reversal of LVH is associated with decreased cardiovascular morbidity [12].
Laboratory tests should include urinalysis, a chemistry
panel including measurement of serum creatinine, potassium, and glucose, and a lipid panel [1]. Urinalysis is done to
assess whether proteinuria or hematuria are present, since
either of these may indicate a renal cause for hypertension.
Measurement of glucose in the urine is also helpful to screen
for diabetes. A chemistry panel is used to assess renal function; a high serum potassium concentration may indicate
renal failure or renal tubular acidosis, and a low concentration may indicate a state of aldosterone excess. A lipid panel
is important to assess for hyperlipidemia. Hyperlipidemia
increases the patient’s cardiovascular risk profile and should
be treated according to the National Cholesterol Education
Program (NCEP) guidelines [13].
History and Physical Examination
The patient was first noted to be hypertensive after the
birth of her second child approximately 6 years ago.
Her family history is positive for hypertension in her mother.
Current medications are amiloride/hydrochlorothiazide
5/50 mg once daily, verapamil SR 240 mg daily, and a potassium supplement 20 mEq twice daily.
Her height is 5′3″ and her weight is 114 lb. Examination of
her fundi reveals evidence of arteriolar narrowing (grade 1
hypertensive changes). Heart and lung examinations are normal. The abdomen is without bruits. Examination of the
extremities shows good peripheral pulses.
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Table 4. Causes of Refractory Hypertension
Cause
Proportion of Cases, %
Secondary hypertension
Exogenous substances
Biologic factors
Inadequate or inappropriate treatment
Noncompliance
10
15–30
25–40
25
10
Data from Setaro JF, Black HR. Refractory hypertension. N Engl J Med
1992;327:543–7.
Laboratory Testing
A 12-lead electrocardiogram is normal. Results of urinalysis
are normal. Her blood glucose level is 78 mg/dL. Serum
concentrations of electrolytes are as follows: sodium,
141 mEq/L (normal, 136–144); potassium, 4.4 mEq/L (normal, 3.5–5.3); chloride, 102 mEq/L (normal, 96–108); and
bicarbonate, 29 mEq/L (normal, 24–29). The creatinine concentration is 0.9 mg/dL (normal, 0.7–1.3 mg/dL).
• Which diagnoses related to high blood pressure have
been excluded at this point?
• Is there reason to be concerned about a secondary cause
or component to the patient’s elevated blood pressure?
The patient has normal pedal pulses and no unusual murmurs, which excludes coarctation of the aorta. The patient is
not overweight, which excludes obesity-associated hypertension. The normal blood glucose level excludes diabetesassociated hypertension. The absence of abdominal bruits
decreases the likelihood of renovascular disease.
Because of the young age and normal weight of the
patient at the time of diagnosis and the potassium supplement usage, a secondary form of hypertension should at
least be considered.
Further History
On further questioning, the patient reports that
she had developed right sided flank/back pain,
which was thought to be job-related. However, the urinalysis ordered by her primary care physician revealed
microscopic hematuria, which was a new finding. It is not
known whether she was menstruating at the time the
urine sample was obtained. Her primary care physician
ordered an ultrasonographic evaluation of her right upper
quadrant to exclude the possibility of renal stones or a
renal tumor. The kidney was found to be normal, but an
incidental right adrenal mass was detected. Computed
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tomography (CT) confirmed the presence of a right adrenal mass.
• How frequently do adrenal masses incidentally occur?
• What tests are included in the workup of an adrenal
mass?
Workup of Adrenal Mass
Adrenal masses, or incidentalomas, occur in approximately
2% to 3% of the general population, and many are nonfunctional [14]. All patients with an incidentally discovered
adrenal mass must be evaluated for malignancy and subtle
hormonal overproduction and to determine whether surgical treatment is needed [15]. Because the case patient has
hypertension, an adrenal workup should be done to exclude
an aldosterone-secreting adenoma and pheochromocytoma
as secondary causes.
To pursue a diagnosis of primary aldosterone excess, one
needs to demonstrate suppressed plasma renin activity and
show that aldosterone excretion is elevated, either by plasma
levels or by a 24-hour urine collection [16–18]. Urine aldosterone levels need to be interpreted in the setting of a normal
plasma volume and a urine sodium level of greater than
50 mEq/day [19]. The plasma aldosterone-to-renin ratio can
also be suggestive of primary aldosterone excess. This ratio
should be greater than 30:1 in patients with primary aldosteronism, and the plasma aldosterone level should be greater
than 15 ng/dL [18].
Testing of a 24-hour urine sample for metanephrines and
catecholamines is used as a screening test for a pheochromocytoma. A workup is not necessary to evaluate cortisol function because a patient with hypertension and cortisol excess
would have clinical manifestations of Cushing’s syndrome.
Testing and Diagnosis
Testing of a 24-hour urine sample for metanephrines
reveals normal excretion: 97 µg of metanephrines per
24 hours (normal < 150) and 176 µg of normetanephrines per
24 hours (normal < 450). The plasma renin activity (off medications) is < 0.1 ng/mL/hr (normal, 2–4). The 24-hour urinary aldosterone excretion is 52 µg (normal, 4–19). The physician makes a diagnosis of primary aldosteronism (Conn’s
syndrome). Therapy is initiated with spironolactone, which is
and titrated over 2 months to 200 mg daily.
• What are the usual findings in Conn’s syndrome?
528 JCOM September 2002 Vol. 9, No. 9
Conn’s Syndrome
Conn described a syndrome of hypertension with hypokalemia and tumor of the adrenal cortex that secretes aldosterone. Metabolic alkalosis is frequently present. Conn’s
syndrome is thought to cause less than 1% of cases of hypertension [20], although newer series suggest that the incidence may be higher, especially in drug refractory hypertension [21].
In summary, primary aldosterone excess should be suspected if there is evidence of the following: a low potassium
level in blood, suppression of plasma renin activity with evidence of aldosterone excess either by elevated plasma aldosterone blood levels or an increase in 24-hour urinary excretion of aldosterone [20], elevated plasma aldosterone-to-renin
ratio [18], and an increase in serum bicarbonate level due to
loss of hydrogen (and potassium) ions in urine. It is also reasonable to consider aldosterone excess in a hypertensive
patient with an incidentally discovered adrenal mass, in a
patient with a need for potassium supplements on modest
doses of diuretics, and in patients taking 3 or 4 antihypertensive agents who still have difficulty in controlling their blood
pressure.
• Was there anything in the patient’s history to raise suspicion of an aldosterone problem?
The need for 40 mEq of potassium supplement is unusual in
a patient on a potassium-sparing diuretic such as amiloride.
Patient Response to Spironolactone
The patient’s blood pressure 3 months after starting
spironolactone is 116/78 mm Hg.
• What are the management options in this patient?
There are 2 options: surgery in the form of a right adrenalectomy [22] or medical management of the patient [23] controlling her blood pressure as needed.
• What factors predict a good response to surgery?
• Do any factors suggest that surgery might not “cure”
her high blood pressure?
The patient’s young age suggests that she should have a
good response to surgery; however, the length of time she
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CASE-BASED REVIEW
has been hypertensive reduces the likelihood of a cure with
surgery. The positive family history of hypertension in her
mother also raises the possibility that she has essential (or
primary) hypertension and that the aldosterone excess is a
component, not the sole cause, of her hypertension.
Surgery is generally recommended after 2 localizing
procedures have been performed to confirm that the adrenal gland with the tumor is the source of the aldosterone
excess. In the case patient, the CT scan is considered as one
localizing procedure; 2 other procedures are available. One
is sampling the adrenal veins for aldosterone and demonstrating lateralization [24–26] with interventional radiology. The other is a nuclear study in which radioactivelabeled cholesterol is administered and its uptake in the
adrenal gland is evaluated (cholesterol is a precursor to
aldosterone synthesis) [27]. In our institution, the preference is to demonstrate lateralization using adrenal vein
sampling.
Adrenalectomy and Follow-up
The physician discusses the treatment options with
the patient, but she does not want to undergo a lateralizing procedure and declines the option of surgery as
well. The physician follows her clinically on the spironolactone.
Three months later the patient reports to the physician
with complaints of amenorrhea and nausea, which are side
effects of the spironolactone. The physician recommends
that she have adrenal surgery despite not having a lateralizing procedure. She undergoes an uneventful right adrenalectomy and recovers. Two months postoperatively, her
blood pressure untreated is 118/80 mm Hg.
• How specific is a blood pressure response to spironolactone as a diagnostic tool for aldosterone excess?
Spironolactone is a competitive inhibitor of the binding of
aldosterone to the mineralocorticoid receptor. Spironolactone
is very effective at reducing blood pressure and restoring
potassium balance to normal in states of aldosterone excess
[23,28]; however, it is also an effective antihypertensive drug
in patients with suppressed renin activity whose aldosterone
production is normal. Therefore, the blood pressure response
is suggestive but nonspecific for primary aldosteronism. The
case patient’s clear response to the spironolactone led the primary care physician to refer the patient for surgery. In general, despite such a response to spironolactone, we still recommend a second localizing procedure before recommending
surgery.
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• What potential electrolyte problem can occur postoperatively following adrenalectomy for Conn’s syndrome?
Hyperkalemia can occur postoperatively. Occasionally, unilateral aldosterone release suppresses the aldosterone synthesis on the contralateral side, and the loss of aldosterone
production following adrenalectomy can produce a state of
“hypoaldosteronism” characterized by hyperkalemia and
possibly some salt wasting with low blood pressures. It can
take several months to recover full activity in the remaining
adrenal gland.
• What is the approach to follow-up of patients with secondary hypertension?
Monitoring Hypertensive Patients
In patients whose blood pressure is restored to normal (without the need for medication) by an intervention, current
guidelines suggest yearly blood pressure checks [7]. In the
long-term management of secondary hypertension, when
patients are not or cannot be cured by surgery or another
intervention, follow-up depends on the severity of the
hypertension and presence of comorbidities. In general, we
recommend follow-up visits every 6 to 12 months for monitoring of stable patients. We typically do annual routine
blood testing (measurement of potassium, creatinine, glucose, lipids), unless medication adjustments are made or
progression (eg, further loss of renal function) is suspected.
Managing hypertension in general prompts one to check for
potassium abnormalities that would occur with diuretic and
angiotensin-converting enzyme inhibitor/angiotensin II
receptor blocker therapy or intercurrent drug use such as
nonsteroidal anti-inflammatory agents or steroids. Routine
glucose testing and measurement of lipid fractions should be
done to screen for diabetes and determine concurrent cardiovascular risk. Creatinine should be measured to monitor
kidney function.
Repeat angiograms after a renal angioplasty have not
been shown, to our knowledge, to be of value outside of
research protocols; therefore, we follow patients clinically
and do not routinely schedule follow-up renovascular studies unless blood pressure increases or creatinine changes
prompt reevaluation. It could be argued that renal Doppler
evaluations are a relatively inexpensive and noninvasive
maneuver to monitor renal artery status after renal vessel
angioplasty. However, they are also observer/technician
Vol. 9, No. 9 September 2002 JCOM 529
SECONDARY HYPERTENSION
dependent and time-consuming for patients, and in our
experience they have a low yield. However, the experience
of others has been much more gratifying [29].
In patients with diabetes and those with renal failure with
or without renovascular disease, progressive loss of renal
function is an unfortunate fact of medical life. The question
of when to refer these patients to a nephrologist often arises.
A recent study shows that late referral to a nephrologist (late
defined as 3 months before the first dialysis session) greatly
compromises the nephrologist-patient relationship, and in
diabetic patients leads to greater mortality in the first year on
dialysis [30]. Consequently we prefer to see male patients
when the creatinine level is 2 mg/dL or greater in diabetics
or 3 mg/dL in nondiabetics, with corresponding values of
1.7 mg/dL and 2.5 mg/dL for women. In patients with proteinuria ++ or greater by dipstick or greater than 1 g/day by
24-hour urine collection, the data on proteinuria reduction as
a therapeutic endpoint suggest that at least consultation with
nephrology should be done if the proteinuria persists on
subsequent repeat testing [31].
Last, it is important to recognize that secondary hypertension does not equal curable hypertension. It may be possible to reduce or even eliminate medications in some patients with hypertension when a remediable cause is found.
However, some patients have essential hypertension, which
is very common, with a superimposed renal artery stenosis
or an intercurrent productive adrenal lesion whose relief or
removal occurs on a background of essential hypertension.
In our, experience factors that help identify those with a
higher likelihood of remaining hypertensive after an intervention include older age, duration of hypertension greater
than 5 years, and positive family history of hypertension in
first-degree relatives.
Summary
One should suspect and pursue a workup for secondary
hypertension in patients who appear to be more susceptible
from their demographics, history, and physical findings.
Conn’s syndrome accounts for 1% of all causes of hypertension
and for about 5% of secondary hypertension cases. Patients
with Conn’s syndrome can have a normal serum potassium
level. It is important to identify patients with secondary hypertension because they may have a curable form of hypertension.
Corresponding author: Debbie Cohen, MD, Renal-Electrolyte and Hypertension Div., University of Pennsylvania, 210 White Building, 3400
Spruce St., Philadelphia, PA 19104, [email protected].
Financial disclosures: None.
Author contributions: conception and design, DC, RRT; drafting of the
article, DC, RRT; critical revision of the article for important intellectual content, DC, RRT; final approval of the article, DC, RRT; administrative, technical, or logistic support, DC, RRT.
530 JCOM September 2002 Vol. 9, No. 9
References
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19. Young DB. Quantitative analysis of aldosterone’s role in
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20. Stewart PM. Mineralocorticoid hypertension. Lancet 1999;
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Copyright 2002 by Turner White Communications Inc., Wayne, PA. All rights reserved.
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Vol. 9, No. 9 September 2002 JCOM 531
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CME
EVALUATION FORM: Secondary Hypertension: Diagnosis and Management of an Adrenal Adenoma
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Part 1. Please respond to each statement.
Strongly Agree
Strongly Disagree
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I was provided with new information pertinent to my practice.
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I reaffirmed a specific skill or knowledge.
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This article will help with clinical decision making.
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Relevant clinical outcomes are addressed.
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The case is communicated in a manner that kept my interest.
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The case presentation is realistic and effective.
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I could easily interpret the tables and figures.
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My attitude about this topic changed in some way.
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Additional comments: ______________________________________________________________________________________
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Part 2. Please complete the following sentence.
As a result of reading this case study, I . . .
❏ see no need to change my practice.
❏ will seek more information before modifying my practice.
❏ intend to change the following aspect(s) of my practice: (Briefly describe)
__________________________________________________________________________________________________________
__________________________________________________________________________________________________________
Part 3. Statement of completion: I attest to having completed the CME activity.
Signature: _________________________________________ Date: _________________________________________________
Part 4. Identifying information: Please PRINT legibly or type the following:
Name: ____________________________________________ Fax number ___________________________________________
Address: __________________________________________ Telephone number ______________________________________
__________________________________________________ Social Security number: __________________________________
(Required and confidential)
__________________________________________________
Medical specialty: __________________________________
Wayne State University School of Medicine is accredited by the Accreditation Council for Continuing
Medical Education to provide continuing medical eduSEND THE COMPLETED
cation for physicians.
CME EVALUATION FORM TO:
Wayne State University School of Medicine desigBY FAX: 313-577-7554
nates this CME activity for a maximum of 1 hour of catBY MAIL: Wayne State University
egory 1 credit toward the Physician’s Recognition
Division of CME
Award of the American Medical Association. Physicians
should claim only those hours of credit actually spent in
101 Alexandrine, Lower Level
the educational activity.
Detroit, MI 48201
532 JCOM September 2002 Vol. 9, No. 9
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