Document 134708

B R I A N G. D O N L E Y , M D
Department of Orthopaedic Surgery,
Cleveland Clinic
Department of Orthopaedic Surgery,
Cleveland Clinic
Department of Orthopaedic Surgery,
Cleveland Clinic
Diagnosing and treating
plantar fasciitis: A conservative
approach to plantar heel pain
Plantar fasciitis is the most common cause of pain at the
weight-bearing surface of the heel, and may coexist w i t h
other sources of heel pain. This has led to a confusing array
of treatment strategies, including surgery. We offer a simple,
effective diagnostic and treatment algorithm that
emphasizes nonsurgical treatment options for this often
frustrating condition.
Plantar fasciitis, the most common cause of plantar heel
pain, is an overuse injury causing inflammation at the
attachment of the plantar fascia to the medial tubercle of
the calcaneus.
Physical examination of a patient w i t h plantar heel pain
often reveals a tight Achilles tendon, as noted by limited
ankle dorsiflexion w i t h the knee in extension. Swelling of
the heel is not common and, when associated w i t h painful
medial-lateral compression of the calcaneus, may suggest a
stress fracture.
Regular stretching of the Achilles tendon and plantar fascia
is the critical part of any treatment program for plantar
fasciitis. Stretching three to five times a day eventually
rehabilitates the tight, chronically inflamed fascia.
LTHOUGH CLINICIANS TRY many different approaches to relieve heel pain
associated with plantar fasciitis, the most common cause of plantar heel pain in adults, we
encourage a conservative treatment approach
in these patients, one that emphasizes protection and rehabilitation of the affected tissue in
the heel.
Surgery is a treatment option in plantar
fasciitis; however, it is usually not necessary
because of the success of nonsurgical techniques. W e have found that offering a safe and
effective treatment scheme to an informed
patient commonly resolves this frustrating
condition without surgery.
Plantar heel pain has many potential causes, 1 - 5 including:
• Plantar fasciitis
• Calcaneal stress fracture
• Fat pad atrophy
• Compressive and metabolic neuropathy
• Infection
• Ischemia
• Tumors.
P l a n t a r fasciitis
T h e most common cause of heel pain is plantar fasciitis, an overuse injury causing inflammation. It occurs at the attachment of the
plantar fascia to the medial tubercle of the calcaneus ( F I G U R E 1 ) and has been associated with
excessive walking or running, as well as with
middle age, obesity, and biomechanical disorders such as pes cavus, pes planus, and tight
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2 3 1
Achilles tendon. Repeated stress to the plantar fascia origin leads to micro-tears and
chronic inflammatory changes (necrosis,
fibrosis, chondroid metaplasia).2'5 The normally resilient fascia becomes stiffened and
prone to re-injury, thus setting up a vicious circle of persistent pain.
Plantar fasciitis
is usually an
overuse injury
Other causes of plantar heel pain
N e r v e i n p i n g e m e n t . The nerve to the
abductor digitorum quinti muscle, which
courses just superior to the origin of the plantar fascia, may become impinged. This can
lead to pain that is often mistaken for plantar
fasciitis. However, complicating the differential diagnosis, nerve impingement can also
coexist with plantar fasciitis.4-6
Fat pad atrophy. Atrophy of the plantar
heel fat pad, secondary to aging or to overzealous corticosteroid use, can produce a more
central heel pain, often a separate entity from
plantar fasciitis.
Bone spur. Many patients visit their
physician complaining of pain caused by a
"bone spur" (calcaneal osteophyte), and many
physicians presume that bone spurs are the
cause of plantar heel pain. However, this is
misleading: 50% of patients with heel pain do
not have a bone spur, and 15% of non-painful
adult heels do have a spur.
Although rarely the cause of plantar heel
pain, a bone spur within the flexor digitorum
brevis muscle dorsal to the plantar fascia ( F I G U R E
1) is present radiographically in about 5 0 % of
patients with heel pain.2'5 Pathologic changes
have been observed at the origin of the plantar
fascia from surgical specimens, located just
plantar to the region of spur formation.2-5
However, even if a bone spur is present, it
should not influence the treatment protocol.
D e t a i l e d history
A detailed history will often provide enough
information to make the diagnosis of plantar
fasciitis, and physical examination will confirm it. A complete description of the pain is
essential. Patients typically describe their
plantar heel pain in the following ways:
• Deep aching pain (like a "bruise")
under the heel brought on by standing or
walking and relieved with rest.
• "Start-up pain," ie, pain exacerbation
with initial weight-bearing in the morning or
when rising from a chair, is typical of plantar
fasciitis. Start-up pain is improved after a few
minutes of walking, but pain will worsen again
with prolonged standing.
• Pain of gradual onset. Patients often
describe a gradual onset of pain, present for
weeks to months prior to seeking attention.
• Acute trauma or swelling is not common; however, further questioning may indicate a change of activity level or a change of
shoe wear preceding pain onset. Pain associated
with significant swelling, occurring primarily at
rest or without "start-up" qualities, is not suggestive of plantar fasciitis. A complete history
may elicit conditions associated with heel pain,
such as diabetes, inflammatory arthropathies,
and spinal disorders.1-3-7
Examination of t h e f o o t a n d ankle:
seeking sources of pain
The physical examination in suspected plantar
fasciitis begins with observing the exposed foot
and ankle during gait and stance. Record any
deviations from a normal foot type and gait.
In the directed foot examination of
patients with plantar heel pain, the clinician
can elicit pain by palpating the origin of the
plantar fascia ( F I G U R E 1 ) . Pain may be exacerbated by dorsiflexing the ankle and the
metatarsal phalangeal joints, which stretches
the plantar fascia. Pain may also be noted
more medially, near the origin of the abductor
hallucis muscle, and may extend distally along
the plantar fascia.
A tight Achilles tendon, as noted by limited ankle dorsiflexion with the knee in extension, is commonly seen with this condition. 1-3
Swelling is not common and, when associated with painful medial-lateral compression
of the calcaneus, suggests a stress fracture.
Pain posterior to the origin of the plantar
fascia is more likely secondary to fat pad atrophy or periostitis.
A complete foot and ankle examination
that includes neurovascular assessment should
rule out most other causes of heel pain. An
exam of other organ systems (ie, eyes, mouth,
spine, joints) is appropriate when other pain
etiologies are suspected.
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Plantar fasciitis: A n a t o m y , diagnosis, t r e a t m e n t
stress f r a c t u r e
( b o n e spur)
r heel
fat pad atrophy
Pain f r o m
p l a n t a r fasciitis
Pain f r o m
fat pad atrophy
A N A T O M Y Heel p a i n has m a n y possible causes, i n c l u d i n g
c a l c a n e a l b o n e spurs, stress f r a c t u r e s , a n d a t r o p h y o f t h e calc a n e a l f a t pad. H o w e v e r , t h e m o s t c o m m o n cause is p l a n t a r
fasciitis, a c o m b i n a t i o n o f o v e r u s e i n j u r y a n d a n i n f l a m m a t o ry process, o c c u r r i n g a t t h e a t t a c h m e n t o f t h e p l a n t a r fascia
t o t h e m e d i a l t u b e r c l e o f t h e calcaneus ( a r r o w ) .
DIAGNOSIS P a l p a t i o n o f t h e o r i g i n o f t h e
p l a n t a r fascia elicits t h e p a i n o f p l a n t a r
fasciitis; d o r s i f l e x i o n o f t h e a n k l e a n d t h e
m e t a t a r s a l p h a l a n g e a l j o i n t s m a y exacerb a t e t h e p a i n . Pain p o s t e r i o r t o t h e o r i g i n
o f t h e p l a n t a r fascia is m o r e l i k e l y secondary t o fat pad a t r o p h y or periostitis.
Silicone o r plastic heel p a d
or cup adds comfort t o
w a l k i n g a n d j o g g i n g shoes
Night splint w o r n
t o b e d stretches
t h e p l a n t a r fascia
K e e p leg
foot flat
on the
TREATMENT O p t i o n s f o r p l a n t a r fasciitis are p r i m a r i l y c o n s e r v a t i v e a n d i n c l u d e plastic heel pads o r cups, a
s p l i n t t o b e w o r n a t n i g h t , a n d s t r e t c h i n g exercises t o be d o n e t h r e e t o f i v e t i m e s a day.
233 C L E V E L A N D C L I N I C J O U R N A L OF M E D I C I N E
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injections of
may cause fat
pad atrophy or
plantar fascia
Diagnostic studies:
W h e n is further investigation a p p r o p r i a t e ?
Plantar fasciitis is a diagnosis made by the history and physical examination. When other
sources of pain are possible, ancillary tests may
be appropriate. Lateral and axial radiographs
of the heel are typically normal but may be
used to rule out fractures, rheumatologic conditions, or tumors.8
Bone scan. When patients present with
atypical or chronic symptoms, a triple-phase
bone scan may provide useful information.
Plantar fasciitis is confirmed by uptake at the
origin of the fascia. 1-3 Calcaneal stress fractures will reveal intense uptake throughout
the bone. A negative scan may suggest neurogenic or other extraskeletal pain sources.
Blood work may be helpful when considering inflammatory arthropathies or infection.
A standard rheumatoid panel that includes a
complete blood count with differential, erythrocyte sedimentation rate, antinuclear antibodies, and rheumatoid factor can supplement
findings of the history and examination.
Electromyelography and nerve conduction studies can provide objective information
regarding nerve involvement when dysesthesias are prominent; however, these tests can be
uncomfortable and are often negative until
late nerve pathology develops.4
Treatment options for plantar fasciitis vary
widely, but treatment should always begin
with a combination of nonsurgical modalities.
Treatment guidelines are available, based on
recent studies that asked patients to rate various techniques.2,7,9,10 W
recommend the
lowing treatment scheme, which usually
resolves pain in 2 to 6 months. 2 ' 7 - 10
Initial conservative strategies
Inform the patient. Begin treatment by
educating the patient as to the cause of plantar heel pain and how he or she can actively
participate in its cure, such as performing specific exercises ( F I G U R E 1 ) .
Supportive shoes. First, emphasize a
change to more supportive shoes (eg, walking
or jogging shoes) for routine activities.
Patients can insert over-the-counter soft, pli234
V O L U M E 6 6 • NUMBER 4
able plastic (Silastic) heel pads or protective
heel cups into these shoes for more comfort
( F I G U R E 1 ) . Walking barefoot or in slippers
should be avoided.
Non-weight-bearing exercise. Suggest
that patients change their activities to avoid
aggravating factors until the pain resolves.
Switching from weight-bearing activities (eg,
walking, jogging) to non-weight-bearing aerobic exercise (eg, biking, swimming) can be
Stretching. We believe stretching is the
critical part of any treatment program for
plantar fasciitis. Regularly stretching the
Achilles tendon and plantar fascia eventually
rehabilitates the tight, chronically inflamed
fascia. Prescribe patients a simple stretching
routine, which they should do three to five
times a day (FIGURE 1 ) . 2 . 1 0 Be sure to warn
patients that stretching may exacerbate symptoms for 1 to 3 weeks, but encourage them to
continue until the pain resolves.
Nonsteroidal anti-inflammatory drugs
often help speed pain relief. The patient may
need to take the medication for several weeks
or months until pain resolves, so monitoring
against side effects (eg, gastritis, peptic ulcers)
is important.
Nighttime splint. If morning start-up pain
is significant or resistant to the above treatments, a splint can be worn to bed to maintain
plantar fascia stretch ( F I G U R E 1 ) .
W h a t t o do if initial t r e a t m e n t fails
Corticosteroid injection. For patients slow
to improve, a corticosteroid injection near the
plantar fascia origin may provide adequate
pain relief. However, multiple injections are
discouraged as they may cause fat pad atrophy
or plantar fascia rupture.11 In recalcitrant
cases, patients may need to take time off work
or use a walking cast for 4 to 6 weeks,10 or both.
Custom orthotic. If the patient has coexisting biomechanical foot problems such as pes
planus or cavus, a custom foot orthotic may be
beneficial. We recommend a semirigid orthotic that supports the longitudinal arch, takes
some of the weight-bearing load away from
the plantar calcaneus, and absorbs weightbearing stresses. However, only very few
patients with plantar fasciitis require custom
orthotics. 10
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Surgical options. Nonsurgical techniques
are successful in over 9 0 % of our patients. If
pain persists after 6 to 12 months of an
exhaustive conservative program,
surgery may be recommended.
W h e n indicated, a partial release of the
medial plantar fascia, along with decompression of the nerve to the abductor digiti quinti
may effect a cure. Advise the patient that a
prolonged recovery after surgery may be
expected, with cure rates in the 8 0 % to 9 0 %
range 1-3,5
Bordelon RL. Heel pain. In: Mann RA, Coughlin MJ, editors. Surgery of the Foot and Ankle, 6th ed. St. Louis:
Mosby-Year Book, Vol 2, 1993:837-857.
Gill LH. Plantar fasciitis: Diagnosis and conservative management. J A m Acad Orthopaed Surg 1997; 5:109-117.
Schepsis A A , Leach RE, Gorzyca J. Plantar fasciitis.
Etiology, treatment, surgical results and review of literature Clin Orthop 1991; 266:185-196.
Let us hear your opinions about the Cleveland
Schon LC, Glennon TP, Baxter DE. Heel pain syndrome:
Electrodiagnostic support for nerve entrapment. Foot
A n k l e 1993; 14:129-135.
Tountas A A , Fornasier VL. Operative treatment of subcalcaneal pain. Clin Orthop 1996; 332:170-178.
Baxter DE, Pfeffer GB. Treatment of chronic heel pain by
surgical release of the first branch of the lateral plantar
nerve. Clin Orthop 1992; 279:229-236.
Wolgin M, Cook C, Graham C, Mauldin D. Conservative
treatment of plantar heel pain: Long term follow-up.
Foot A n k l e Int 1994; 15:97-102.
Amis J, Jennings L, Graham D, Graham CE. Painful heel
syndrome: Radiographic and treatment assessment. Foot
A n k l e 1988; 9:91-95.
Tisdel CL, Harper MC. Chronic plantar heel pain:
Treatment w i t h a short leg walking cast. Foot Ankle Int
1996; 17:41-42.
Pfeffer G. AO FAS Heel Pain Study Group. Paper presented
at: W i n t e r Meeting of the American Orthopaedic Foot
and A n k l e Society; March 1997; San Francisco.
Clinic Journal of Medicine.
Do you like current articles and sections?
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can we make the Journal
more useful to you?
PHONE 216.444.2661
FAX 216.444.9385
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The Cleveland Clinic Foundation
9500 Euclid Avenue, EE37
Cleveland, Ohio 44195
Sellman JR. Plantar fascia rupture associated w i t h corticosteroid injection. Foot Ankle Int 1994; 15(7):376-381.
ADDRESS: Christopher L Tisdel, MD, Department
Orthopaedic Surgery, A41, The Cleveland Clinic
9500 Euclid Avenue, Cleveland, OH 44195.
V O L U M E 6 6 • NUMBER 4
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In hypertension or angina...
once-daily dosing
The usual starting dose is 5 mg in
hypertension or angina
— In hypertension, small, fragile, or elderly individuals or
patients with hepatic insufficiency may be started on
2.5 m g once dally
Titration can proceed to 10 mg
— Most angina patients will require 10 m g
Can be taken with or without food
An excellent side-effect profile
NORVASC 5 mg(%)
NORVASC 10 mg (%)
5-mg and 10-mg tablets
(amlodipine besylate)
The #1 Branded Cardiovascular
Agent Worldwide 1
References: 1. IMS Midas sales data, 1Q98; and IMS America prescription data, April 1998.2. Neaton
JD, Grimm RH Jr. Prineas RJ, et al, for the Treatment of Mild Hypertension Study Research Group. Treatment of
Mild Hypertension Study: final results. JAMA. 1993;270:713-724.3. Hayduk K, Sauerbrey-Wullkopf N, Leverkus
F. Initial dose finding of amlodipine in patients with essential hypertension, Eur Heart J. 1994; 15(suppl): 194A.
4. Data on file. Pfizer Ine, New York, NY.
Pharmaceutical A m e r i c a n Heart |
Association •
Brief Summary
NORVASC® (amlodipine besylate) Tablets
For Oral Use
CONTRAINDICATIONS: NORVASC is contraindicated in patients with known sensitivity to amlodipine.
WARNINGS: Increased Angina and/or Myocardial Infarction: Rarely, patients, particularly those with severe
obstructive coronary artery disease, have developed documented increased frequency, duration and/or severity of
angina or acute myocardial infarction on starting calcium channel blocker therapy or at the time of dosage increase.
The mechanism of this effect has not been elucidated.
PRECAUTIONS: General: Since the vasodilation induced by NORVASC is gradual in onset, acute hypotension has
rarely been reported after oral administration of NORVASC. Nonetheless, caution should be exercised when administering NORVASC as with any other peripheral vasodilalor particularly in patients with severe aortic stenosis.
Use in Patients with Congestive Heart Failure: In general, calcium channel blockers should be used with caution in
patients with heart failure. NORVASC (5-10 mg per day)has been studied in a placebo-controlled trial of 1153 patients
with NYHA Class III or IV heart failure on stable doses oí ACE inhibitor, digoxin, and diuretics. Follow-up was at least
6 months, with a mean of about 14 months. There was no overall adverse effect on survival or cardiac morbidity (as
defined by life-threatening arrhythmia, acute myocardial infarction, or hospitalization for worsened heart failure).
NORVASC has been compared to placebo in four 8-12 week studies of patients with NYHA Class ll/lll heart failure,
involving a total of 697 patients. In these studies, there was no evidence of worsened heart failure based on measures of
exercise tolerance, NYHA classification, symptoms, or LVEF.
Beta-Blocker Withdrawal: NORVASC is not a beta-blocker and therefore gives no protection against the dangers of
abrupt beta-blocker withdrawal; any such withdrawal should be by gradual reduction of the dose of the beta-blocker.
Patients with Hepatic Failure: Since NORVASC is extensively metabolized by the liver and the plasma elimination halflife (t Jf) is 56 hours in patients with impaired hepatic function, caution should be exercised when administering
NORVASC to patients with severe hepatic impairment.
Drug Interactions: In vitro data in human plasma indica:e that NORVASC has no effect on the protein binding of drugs
tested (digoxin, phenytoin, warfarin, and indomethacin).Special studies have indicated that the co-administration of
NORVASC with digoxin did not change serum digoxin le/els or digoxin renal clearance in normal volunteers; that coadministration with cimetidine did not alter the pharmacckinetics of amlodipine; and that co-administration with warfarin
did not change the warfarin prothrombin response time.
In clinical trials, NORVASC has been safely adminis'ered with thiazide diuretics, beta-blockers, angiotensin
converting enzyme inhibitors, long-acting nitrates, sublingual nitroglycerin, digoxin, warfarin, non-steroidal antiinflammatory drugs, antibiotics, and oral hypoglycemic crugs.
Drug/Laboratory Test Interactions: None known.
Carcinogenesis, Mutagenesis, Impairment of Fertility: Rats and mice treated with amlodipine in the diet for two years,
at concentrations calculated to provide daily dosage levels of 0.5,1.25, and 2.5 mg/kg/day showed no evidence of
carcinogenicity. The highest dose (for mice, similar to, ard for rats twice* the maximum recommended clinical dose of
10 mg on a mg/m 2 basis), was close to the maximum tolerated dose for mice but not for rats.
Mutagenicity studies revealed no drug related effects at either the gene or chromosome levels.
There was no effect on the fertility of rats treated with amlodipine (males for 64 days and females 14 days prior to
mating) at doses up to 10 mg/kg/day (8 times* the maximum recommended human dose of 10 mg on a mg/m 2 basis).
Pregnancy Category C: No evidence of teratogenicity o* other embryo/fetal toxicity was found when pregnant rats or
rabbits were treated orally with up to 10 ma/kg amlodipine (respectively 8 times* and 23 times* the maximum recommended human dose of 10 mg on a m g / n r basis) during their respective periods of major organogenesis. However, litter
size was significantly decreased (by about 50%) and the number of intrauterine deaths was significantly increased
(about 5-fold) in rats administered 10 mg/kg amlodipine :or 14 days before mating and throughout mating and
gestation. Amlodipine has been shown to prolong both tfe gestation period and the duration of labor in rats at this dose.
There are no adequate and well-controlled studies in pregnant women. Amlodipine should be used during pregnancy
only if the potential benefit justifies the potential risk to the fetus.
Nursing Mothers: It is not known whether amlodipine is excreted in human milk. In the absence of this information, it is
recommended that nursing be discontinued while NORVASC is administered.
Pediatric Use: Safety and effectiveness of NORVASC in children have not been established.
ADVERSE REACTIONS: NORVASC has been evaluated for safety in more than 11,000 patients in U.S. and foreign
clinical trials. In general, treatment with NORVASC was vell-tolerated at doses up to 10 mg daily. Most adverse reactions
reported during therapy with NORVASC were of mild or moderate severity. In controlled clinical trials directly comparing
NORVASC (N =1730) in doses up to 10 mg to placebo (N=1250), discontinuation of NORVASC due to adverse reactions
was required in only about 1.5% of patients and was not significantly different from placebo (about 1%). The most
common side effects are headache and edema. The incidence (%) of side effects which occurred in a dose related
manner are as follows: edema (1.8% at 2.5 mg, 3.0% at i.Omg, and 10.8% at 10.0 mg, compared with 0.6% placebo);
dizziness (1.1% at 2.5 mg, 3.4% at 5.0 mg, and 3.4% at 10.0 mg, compared with 1.5% placebo); flushing (0.7% at
2.5 mg, 1.4% at 5.0 mg, and 2.6% at 10.0 mg, compared with 0.0% placebo); and palpitation (0.7% at 2.5 mg, 1.4% at
5.0 mg, and 4.5% at 10.0 mg, compared with 0.6% placebo).
Other adverse experiences which were not clearly dose related but which were reported with an incidence greater
than 1.0% in placebo-controlled clinical trials include thefollowing: headache (7.3%, compared with 7.8% placebo);
fatigue (4.5%, compared with 2.8% placebo); nausea (2.9%, compared with 1.9% placebo); abdominal pain (1.6%,
compared with 0.3% placebo); and somnolence (1.4%, compared with 0.6% placebo).
For several adverse experiences that appear to be d'ug and dose related, there was a greater incidence in women
than men associated with amlodipine treatment as follows: edema (5.6% in men, 14.6% in women, compared with a
placebo incidence in men of 1.4% and 5.1% in women); fUshing (1.5% in men, 4.5% in women, compared with a placebo
incidence of 0.3% in men and 0.9% in women); palpitations(1.4% in men, 3.3% in women, compared with a placebo
incidence of 0.9% in men and 0.9% in women); and somrolence (1.3% in men, 1.6% in women, compared with a placebo
incidence of 0.8% in men and 0.3% in women).
The following events occurred in <1% but >0.1% of patients in controlled clinical trials or under conditions of open
trials or marketing experience where a causal relationship is uncertain; they are listed to alert the physician to a possible
relationship: cardiovascular: arrhythmia (including ventricular tachycardia and atrial fibrillation), bradycardia, chest pain,
hypotension, peripheral ischemia, syncope, tachycardia, Dostural dizziness, postural hypotension; central and peripheral
nervous system: hypoesthesia, paresthesia, tremor, vertgo; gastrointestinal: anorexia, constipation, dyspepsia,**
dysphagia, diarrhea, flatulence, vomiting, gingival hyperplasia; general: asthenia,** back pain, hot flushes, malaise, pain,
rigors, weight gain; musculoskeletal system: arthralgia arthrosis, muscle cramps,** myalgia; psychiatric: sexual
dysfunction (male** and female), insomnia, nervousness, depression, abnormal dreams, anxiety, depersonalization;
respiratory system: dyspnea,** epistaxis; skin and appendages: pruritus,** rash,** rash erythematous, rash
maculopapular; special senses: abnormal vision, conjunctivitis, diplopia, eye pain, tinnitus; urinary system: micturition
frequency, micturition disorder, nocturia; autonomic nervous system: dry mouth, sweating increased; metabolic and
nutritional: thirst; hemopoietic: purpura.
The following events occurred in <0.1% of patients: cardiac failure, pulse irregularity, extrasystoles, skin discoloration,
urticaria, skin dryness, alopecia, dermatitis, muscle weakness, twitching, ataxia, hypertonia, migraine, cold and clammy
skin, apathy, agitation, amnesia, gastritis, increased appeite, loose stools, coughing, rhinitis, dysuria, polyuria, parosmia,
taste perversion, abnormal visual accommodation, and xerophthalmia.
Other reactions occurred sporadically and cannot be distinguished from medications or concurrent disease states
such as myocardial infarction and angina.
NORVASC therapy has not been associated with clinbally significant changes in routine laboratory tests. No clinically
relevant changes were noted in serum potassium, serum glucose, total triglycerides, total cholesterol, HDL cholesterol,
uric acid, blood urea nitrogen, creatinine or liver function ests.
NORVASC has been used safely in patients with chronic obstructive pulmonary disease, well compensated
congestive heart failure, peripheral vascular disease, diabetes mellitus, and abnormal lipid profiles.
OVERDOSAGE: Single oral doses of 40 mg/kg and 100 ng/kg in mice and rats, respectively, caused deaths. A single
oral dose of 4 mg/kg or higher in dogs caused a marked peripheral vasodilation and hypotension.
Overdosage might be expected to cause excessive peripheral vasodilation with marked hypotension and possibly a
reflex tachycardia. In humans, experience with intentional overdosage of NORVASC is limited. Reports of intentional
overdosage include a patient who ingested 250 mg and v»as asymptomatic and was not hospitalized; another (120 mg)
was hospitalized, underwent gastric lavage and remained normotensive; the third (105 mg) was hospitalized and had
hypotension (90/50 mmHg) which normalized following plasma expansion A patient who took 70 mg amlodipine and an
unknown quantity of benzodiazepine in a suicide attempt,developed shock which was refractory to treatment and died
the following day with abnormally high benzodiazepine plasma concentration. A case of accidental drug overdose has
been documented in a 19 month old male who ingested 30 mg amlodipine (about 2 mg/kg). During the emergency room
presentation, vital signs were stable with no evidence of hypotension, but a heart rate of 180 bpm. Ipecac was
administered 3.5 hours after ingestion and on subsequentobseivation (overnight) no sequelae were noted.
If massive overdose should occur, active cardiac and respiratory monitoring should be instituted. Frequent blood
pressure measurements are essential. Should hypotension occur, cardiovascular support including elevation of the
extremities and the judicious administration of fluids should be initiated. If hypotension remains unresponsive to these
conservative measures, administration of vasopressors (sich as phenylephrine), should be considered with attention to
circulating volume and urine output. Intravenous calcium cluconate may help to reverse the effects of calcium entry
blockade. As NORVASC is highly protein bound, hemodiáysis is not likely to be of benefit.
* Based on patient weight of 50 kg.
**These events occurred in less than 1% in placebo controlled trials, but the incidence of these side effects was between
1% and 2% in all multiple dose studies.
U.S. Pharmaceuticals
D1998, Pfizer Ine
More detailed professional information available on request.
Revised June 1996
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