Manejo Dental
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Transcript of Manejo Dental
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VOLUME 39 NUMBER 2 FEBRUARY 2008 139
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Thyroid activity is controlled by the hypothal-
amic-pituitary-thyroid axis. Thyroid-releasing
hormone (TRH), secreted by the hypothala-
mus, induces the secretion of thyroid stimu-
lating hormone (TSH) by the anterior pitu-
itary, which in turn stimulates thyroid hor-
mone synthesis and secretion by the thyroid
gland.13 The thyroid gland is a bilobular
structure that lies on either side of the tra-
chea.1 Its functional unit is the thyroid follicle
made up of thyroid follicular cells (TFCs).4
TFCs selectively remove iodine from the
blood and synthesize iodothyronines (thyrox-
ine [T4], triiodothyroxine [T3], and reverse
triiodothyronine [rT3]).1 The enzyme respon-
sible for the synthesis of iodothyronines is
thyroid peroxidase (TPO). The approximate
proportions of T4, T3, and rT3 produced are
90%, 10%, and less than 1%, respectively. rT3appears to have no biologic function.5 Once
secreted into the bloodstream, approximately
70% of T4 and T3 binds to thyroxine-binding
globulin (TBG), while the remaining 30%
binds to transthyretin, albumin, and lipopro-
teins.1 A small percentage of T3 and T4(< 0.2%) circulates in an unbound, free state
and acts to maintain physiological hormone
levels by negative feedback mechanisms
involving the hypothalamus, pituitary, and
thyroid glands.6
Risk stratification and dental management of the patient with thyroid dysfunctionMichaell A. Huber, DDS1/Gza T. Terzhalmy, DDS, MA2
The thyroid gland produces hormones critical to the maintenance of the cellular metabolic
rate. The actions of these hormones are far-reaching, affecting thermoregulation and
calorigenesis; the metabolism of carbohydrates, fats, and proteins; and oxygen utilization.
Thyroid hormones also appear to act synergistically with epinephrine and enhance tissue
sensitivity to catecholamines. Signs and symptoms of hypothyroidism include listlessness,
fatigue, cold intolerance, dry skin, hair loss, constipation, weight gain, muscle soreness,
and slow heart rate. Signs and symptoms of hyperthyroidism include irritability, heat intol-
erance, tremors, increased sweating, frequent bowel movements, and quickened heart
rate. The effect of inadequately treated or undiagnosed hyperthyroidism on the heart car-
ries perioperative risks. To provide competent dental care to patients with thyroid dysfunc-
tion, clinicians must understand the disease, its treatment, and the impact the disease and
its treatment may have on the patients ability to undergo and respond to dental care.
(Quintessence Int 2008;39:139150)
Key words: dental care, hyperthyroid, hypothyroid, thyroid dysfunction
1Associate Professor and Head, Division of Oral Medicine,
Department of Dental Diagnostic Science, The University of
Texas Health Science Center at San Antonio, Dental School, San
Antonio, Texas.
2Endowed Professor in Clinical Dentistry, Dental School, and
Professor, Department of Pharmacology, Graduate School of
Biomedical Sciences, The University of Texas Health Science
Center at San Antonio, San Antonio, Texas.
Correspondence: Dr Michaell A. Huber, Division of Oral
Medicine, Department of Dental Diagnostic Science, The
University of Texas Health Science Center at San Antonio, Dental
School, Mail Code 7919, 7703 Floyd Curl Drive, San Antonio,
Texas, 78229-3900. Fax: 210-567-6348. E-mail: huberm@
uthscsa.edu
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ETIOLOGY AND EPIDEMIOLOGY
T4 serves as a prohormone for the extrathy-
roidal production of T3, which, in its free form,
accounts for most of the biological activity of
thyroid hormones.6 T3 stimulates RNA poly-
merase and phosphoprotein kinases and the
synthesis of nuclear proteins, which are
involved in the regulation of growth and
development; thermoregulation and calorige-
nesis; the metabolism of carbohydrates, pro-
teins, and lipids; and oxygen consumption.1
Thyroid hormones also appear to act syner-
gistically with epinephrine to enhance
glycogenolysis and hyperglycemia and
enhance tissue sensitivity to catecholamines.
Yet, there appears to be a paradoxical
inverse relationship between circulating nor-
epinephrine and thyroid hormone levels.710
While the myocardial effects of excess thy-
roid hormone mimic a hyperadrenergic state,
the levels of circulating catecholamines, in
these scenarios, are actually low or normal. It
is postulated that the increased sympath-
omimetic response may be due to thyroid
hormone-induced increase in myocardial
sensitivity, increased responsiveness to !-
adrenergic receptor activation or possibly an
up-regulation of adrenergic receptors.7 The
reduced peripheral resistance observed in
thyroid excess may be associated with a
reduced contractile response to norepineph-
rine (possibly through !1-adrenergic and/or
!2-adrenergic receptor modulation) and
enhanced acetylcholine-induced vasodilata-
tion.11 However, others postulate that
increased endothelial production of nitric
oxide (NO), observed in thyroid excess,
underlies the reduced peripheral resistance
observed.9
Patients with thyroid dysfunction may be
characterized as euthyroid, hypothyroid, or
hyperthyroid to reflect normal, inadequate, or
excessive hormonal secretion, respectively
(Table 1).12 Some thyroid disorders manifest
polar clinical progressions, whereby initial
glandular hypersecretion evolves into a state of
hyposecretion. Many of the more common thy-
roid disorders (Graves disease, Hashimotos
thyroiditis, postpartum thyroid dysfunction,
and painless sporadic thyroiditis) represent
autoimmune phenomenas.13,14 In addition to
genetic predisposition, numerous environ-
mental factors, such as low birth weight, iodine
deficiency or excess, selenium deficiency, the
use of oral contraceptives and other medica-
tions, stress, allergy, smoking, ionizing radia-
tion, and bacterial or viral infection, have been
postulated to contribute to etiopathogenesis of
autoimmune thyroid disease.14
Disorders characterized by euthyroidismEuthyroid goiter (diffuse, nodular, multinodular)Benign tumorsMalignant tumors
Differentiated (papillary, follicular)Undifferentiated (small cell, giant cell)Medullary
ThyroiditisAcuteSubacute thyroiditis (de Quervains)Chronic autoimmune (Hashimotos disease)PostpartumReidels thyroiditis
Disorders characterized by hypothyroidismWith hypothyroidism
Primary hypothyroidismChronic autoimmune thyroiditis Iatrogenic (surgery, 131I [radioiodine] therapy)Diffuse and nodular goiterSevere iodine deficiency
Neonatal congenital hypothyroidismSecondary hypothyroidism
Pituitary hypothyroidismTertiary hypothyroidism
Hypothalamic hypothyroidismWithout hypothyroidism
Generalized and peripheral resistance to thyroidhormones
Transient hypothyroidism (iodinedeficiency/excess, druginduced, postpartum)
Disorders characterized by hyperthyroidismGlandular hyperfunction
Diffuse hyperthyroid goiter with thyroid associatedophthalmopathy (Graves disease)
Multinodular hyperthyroid goiter or Plummersdisease
Autonomous noduleThyrotoxicosis (without thyroid gland hyperfunction)
Excessive exogenous thyroid hormonesPost-inflammatory or from glandular destructionAmiodarone induced
Transient hyperthyroidism
Table 1 Common thyroid disorders12
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The actual prevalence of thyroid disorders
is unknown. The Thyroid Foundation of
America estimates that 10 million Americans
suffer from a hypothyroid disorder and 4.5
million Americans suffer from a hyperthyroid
disorder, of whom 8 million and 600,000,
respectively, are undiagnosed.15 As is the
case with most autoimmune diseases, there
is a clear female preponderance, with a
female-to-male ratio of about 5 to 10:1.14 An
estimated 5% of individuals in the United
States have palpable thyroid nodules, of
which 95% are benign (roughly 85% hyper-
plastic nodules, 15% adenomas, and less
than 1% cysts).16 In 2006, an estimated
30,180 cases of thyroid carcinoma were diag-
nosed in the United States (7,590 men and
22,590 women).17 Thyroid carcinoma is most
frequently papillary (81%), followed by follicu-
lar and Hrthle-cell (14%), medullary (3%),
and anaplastic (2%) forms.16
CLINICAL MANIFESTATIONS
It must be emphasized that, in many cases,
the natural history of a thyroid disorder may
be marked by subtle periods of remission
and exacerbations.12 Conversely, either
extreme hypothyroidism or extreme hyper-
thyroidism may evolve into a life-threatening
medical emergency.
HypothyroidismHypothyroidism is a clinical disease state
occurring when there is insufficient thyroid
hormone available to target tissues (Table 1).
Classification (cretinism versus myxedema)
by age of onset is important because the
clinical presentations will vary substantially.
CretinismCongenital hypothyroidism occurs at an over-
all incidence of approximately 1:3,000 to
4,000 births, with a slightly higher prevalence
in the Hispanic population and a decreased
prevalence in African-Americans.18 About
85% of the cases are likely due to sporadic
thyroid dysgenesis (agenesis), while the
other 15% are due to an autosomal recessive
mode of inheritance.19 Congenital hypothy-
roidism (cretinism) is a recognized cause of
mental retardation. The clinical manifesta-
tions of hypothyroidism are difficult to recog-
nize at birth, and it isnt usually until the third
month of life that symptoms begin to appear.
By this time, substantial neurological and
mental retardation may have occurred.
MyxedemaMyxedema usually develops gradually over a
period of months or years (Fig 1). Signs and
symptoms include coarse facial features
(such as thick lips, puffy eyelids, and a sad
expression), dry hair, slow speech, lethargy,
memory impairment (depression), cardiovas-
cular abnormalities (including slow pulse
rate, hypotension, cardiomegaly, low-ampli-
tude QRS, and inverted T waves), increased
sensitivity to cold, decreased sweating, dry
and cold skin, muscle weakness, and
reduced respiratory rate. A characteristic
nonpitting tissue edema is frequently ob-
Fig 1 Myxedema is characterized by coarse facialfeatures,accented by thick lips,macroglossia,puffy eye-lids, dry hair and skin, and a lethargic sad expression.
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served.8,20 It is postulated to be a conse-
quence of the deposition of mucopolysac-
charides and a viscid proteinaceous fluid
within tissues.21,22 The tongue and laryngeal
tissues are often affected, resulting in slurred
speech, hoarseness, and impaired sleep pat-
terns.21,23 A rather characteristic loss of the
outer third of the eyebrow is frequently
observed.20,21,24 Laboratory abnormalities
may include evidence of anemia and elevat-
ed levels of aspartate transaminase, alanine
transaminase, lactate dehydrogenase, creati-
nine, and cholesterol.5
Myxedema coma is an extreme life-threat-
ening complication of hypothyroidism.
Typically, the patient is elderly and has a his-
tory of hypothyroidism.3,25 Most cases are
preceded by precipitating factors such as
infection, exposure to cold, sedative drug
therapy, lung disease, stroke, congestive
heart failure, gastrointestinal bleeding, acute
trauma, or noncompliance with thyroid sup-
plementation.26 The patient manifests wors-
ening alveolar hypoventilation, hypothermia,
bradycardia and decreased cardiac contrac-
tility, hyponatremia and decreased glomeru-
lar filtration, and rarely coma.27 Management
requires prompt administration of thyroid
hormone and supportive measures (ie, venti-
latory support, fluid restoration, glucose
administration, and glucocorticoid adminis-
tration) to stabilize and reverse the down-
ward spiral. Mortality rates of 20% to 60%
have been reported. 27
HyperthyroidismHyperthyroidism is a clinical disease state
produced by the effects of excessive thyroid
hormone on peripheral tissues (Table 1). The
severity of the illness caused by thyrotoxico-
sis is related to the severity and duration of
the hormone excess, the age of the patient,
and the presence or absence of other disease.
Hyperthyroidism occurs most frequently in
women of childbearing age and may mani-
fest as a goiter, tremor, excitability, emotional
instability, rapid pulse rate (tachycardia, atrial
fibrillation), heart murmur, hypertension,
rapid respiration, facial flushing, warm and
moist skin, increased appetite with weight
loss, muscle wasting, enlarged palpable
lymph nodes, and exophthalmos often asso-
ciated with symptoms of a gritty sensation,
light sensitivity, increased tearing, double
vision, and a feeling of retroocular pressure
(Figs 2 and 3).28 Laboratory abnormalities
may include hypercalcemia and elevated lev-
els of alkaline phosphatase, aspartate
transaminase, and alanine transaminase.5
Osteoporosis typically affects cortical (hip
and forearm) rather than trabecular bone
(spine). 29
142 VOLUME 39 NUMBER 2 FEBRUARY 2008
Figs 2 and 3 Common signs and symptoms ofhyperthyroidism include a goiter and exophthalmosoften associated with symptoms of a gritty sensa-tion, light sensitivity, increased tearing, doublevision, and a feeling of retroocular pressure.
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Thyroid storm is the extreme manifesta-
tion of hyperthyroidism. Its uncommon and
occurs most frequently in patients with
Graves disease, toxic adenomas, toxic
multinodular goiters, and hypersecretory thy-
roid carcinoma.26 Predisposing factors
include infection, nonthyroid trauma, psy-
chosis, parturition, myocardial infarction,
intake of radioiodine and high doses of
iodine-containing compounds, thyroid trau-
ma, the discontinuation of antithyroid drug
therapy, and the recent institution of amio-
darone therapy.25 Cardinal clinical findings
include fever (greater than 101.3F), tachy-
cardia, CNS dysfunction (including agitation,
confusion, and delirium), and gastrointestinal
dysfunction (such as nausea, vomiting, and
diarrhea).25,26 Other potential findings include
diaphoresis, atrial fibrillation, and congestive
heart failure.3,26 Management in an intensive
care unit includes the administration of !-
adrenergic blocking agents, propylthiouracil,
and supportive measures (such as external
cooling and careful fluid resuscitation). 25
DIAGNOSIS
Patients with a suspected thyroid disorder
should undergo a thorough physical evalua-
tion, including an exhaustive medical history,
physical examination, and appropriate labo-
ratory testing. A thyroid disorder may develop
insidiously over time, and the suspect signs
and symptoms are easy to overlook. This
fact, combined with the dynamic nature of
some thyroid disorders and the limited sensi-
tivity/specificity of available tests, can chal-
lenge the diagnostic acumen of even the
most experienced clinician.
CretinismMandatory screening of TSH levels in new-
borns allows for the early identification of con-
genital hypothyroidism and the prompt institu-
tion of management strategies aimed at reduc-
ing neurological impairment (cretinism).30,31
Adult Hypo- or HyperthyroidismSerum TSH concentrations represent the
most reliable indicator of thyroid status.26 The
American Thyroid Association recommends
that all patients obtain a serum TSH determi-
nation at age 35 and every 5 years there-
after.32 In general, results demonstrating a
high TSH and low free T4 (FT4) are indicative
of hypothyroidism, while results demonstrat-
ing a low TSH and a high FT4 are indicative
of hyperthyroidism.6 Following initial TSH
measurements, specialized testing may be
performed.33 For nodular disease, this may
include a needle-aspiration biopsy to rule out
malignancy.34,35 For cases of suspected
autoimmune thyroid disease, antithyroid anti-
body testing (antithyroglobulin antibody
[TgAb], anti-TPO antibody [TPOAb], antithy-
roid receptor antibody [TRAb], and thyroid
stimulating antibody) may prove valuable.6
Scintigraphy may be useful in determining
nodular functional status in hyperthyroidism
(Graves disease or multinodular goiter), fol-
licular neoplasm, and multinodular goiter.36,37
PRINCIPLES OF MEDICALMANAGEMENT
HypothyroidismWith early detection and medical manage-
ment, permanent mental retardation may be
avoided in the young. Purified or synthetic
thyroid preparations are available for replace-
ment therapy. Thyroxine, in the form of
levothyroxine, is the most widely prescribed
treatment for hypothyroidism in the United
States (Table 2).38 The amount of thyroid hor-
mone given to restore the euthyroid state
varies, but for adults, it usually lies between
0.05 to 0.15 mg (50 to 150 micrograms) of
levothyroxine or its equivalent daily. Patients
usually notice an improvement two to three
weeks after the start of treatment. Reductions
in weight and puffiness and increases in the
pulse rate and pulse pressure occur early in
treatment, but other signs and symptoms
may take months to resolve. The need for thy-
roid hormone may decrease slightly with age
and increase somewhat with stress and
infection. Inadequate thyroxine-replacement
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therapy is associated with continued clinical
features of hypothyroidism. Substantial over-
treatment with thyroxine results in clinical
manifestations of hyperthyroidism.
Hyperthyroidism Antithyroid drugs are the cornerstones in the
management of hyperthyroidism (Table 3). 39,40
They may be used as primary treatment for
hyperthyroidism or preparative therapy before
surgery or radioiodine therapy. Antithyroid
drugs are usually discontinued or tapered
after 12 to 18 months of therapy. Lifelong fol-
low-up is required for patients in remission,
since spontaneous hypothyroidism may devel-
op decades later. Iodine or iodide prepara-
tions may be prescribed as adjunctive therapy
for short-term benefits and to decrease the
size and vascularity of the thyroid gland in
preparation for surgery. Radioactive iodine,
given orally in the treatment of older patients
with thyrotoxicosis, accumulates in the storage
follicles and emits beta rays with a half-life of 5
days, which destroys a portion of the hyperac-
tive gland. Beta-adrenergic antagonists may
be used to suppress some of the symptoms of
hyperthyroidism, such as tremor, anxiety, and
tachycardia.
ORAL MANIFESTATIONSOF THYROID DYSFUNCTION
With few exceptions, the oral manifestations
attributable to thyroid dysfunction are neither
well-established nor consistent and are large-
ly based on anecdotal case reports. The age
of onset, severity, and duration of any thyroid
dysfunction directly affects the likelihood of
any potential oral manifestations. Thus, the
presence of associated oral manifestations is
more likely to occur at either end of the thy-
roid dysfunction spectrum (ie, extreme
hypothyroidism or extreme hyperthyroidism).
HypothyroidismCretinism. The oral complications of undiag-nosed and untreated congenital thyroid hypo-
function include the characteristic facies of
cretinism (puffy face, disproportionately large
Adverse drug Drug Mechanisms of action Indication effects (ADEs)
Levothyroxin T4 and T3 replacement (T4 is Drug of choice No ADEs at therapeuticconverted to T3 in plasma) dosages
Hyperthyroidism at overdose
Liothyronine T3 replacement Used when levothyroxin is notabsorbed adequately
Liotrix T4 and T3 replacement Used when the conversion of levothyroxin from T4 to T3 is abnormal
Table 2 Drugs used to treat hypothyroidism
Adverse drug Drug Mechanisms of action Indication effects (ADEs)
Methimazole Inhibits the transformation of Long-term thyroxin suppression Agranulocytosis, hepatotoxicity,inorganic iodine to organic or in preparation for surgery urticarial or macular reactions,iodine or 131I therapy arthralgia, sialadenitis (rarely)
with methimazolePropylthiouracil Inhibits the transformation
of inorganic iodine to organic iodine and blocks the conversion of T4 to T3
Iodine or iodide Short term inhibition of Adjunctive therapy to the drugsthyroxin release above and in preparation for
surgery
Table 3 Drugs used to treat hyperthyroidism
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cranium, dull expression, flat and broad nose,
macroglossia, malocclusion, thick everted
lips, and an open mouth). 41 There are con-
flicting reports of altered tooth morphology
(hypoplastic versus unaltered) and eruptive
patterns (delayed versus normal). 4144
Myxedema. The principal oral findingassociated with chronic hypothyroidism in
adults is macroglossia (Fig 1).21,4446 The
nose, eyelids, and lips may be edematous.
Caries risk has been variably reported as
increased, normal, or decreased.41 Impaired
periodontal health has been reported, but it
is unclear whether this finding is related to a
lack of adequate patient compliance with
hygiene procedures, altered bone metabo-
lism, or both.41,47 Some patients may experi-
ence dysgeusia. Salivary gland enlargement,
especially of the parotid and sublingual
glands, has been reported.48
HyperthyroidismChildren with hyperthyroidism may experi-
ence early loss of deciduous teeth and early
eruption of the permanent dentition.5,42 Other
potential findings in either the child or adult
hyperthyroid patient include tremor of the
lips and tongue, increased caries risk, accel-
erated alveolar ridge atrophy, and increased
incidence of mucosal erosions (burning
mouth syndrome).5,42 The characteristic
exophthalmos often observed in Graves dis-
ease might be striking. Lid retraction with
exposure of the white sclera above the lim-
bus produces a characteristic stare.24 Other
findings include lid lag, proptosis, diplopia,
and decreased visual acuity.
PRINCIPLES OF DENTALMANAGEMENT
GoalsWhen treating patients with thyroid dysfunc-
tion in the oral healthcare setting, the goals
are to develop and implement timely preven-
tive and therapeutic strategies compatible
with the patients physical and emotional
ability to undergo and respond to dental
care, as well as the patients social and psy-
chological needs and desires.
Patient assessmentThe first priority for the dental practitioner is
to obtain a meticulous medical history and
perform a thorough head and neck examina-
tion. The presence of signs and symptoms of
a potential thyroid dysfunction mandate a
medical consultation for further evaluation.5,24
Medical historyFor patients with an acknowledged thyroid
dysfunction, it is essential to assess the
patients current status and identify potential
comorbidities, which may necessitate a mod-
ification to the delivery of dental care.
Identifiable risk factors for thyroid dysfunc-
tion from the medical history include previ-
ous thyroid dysfunction; goiter; surgery or
radiotherapy of the thyroid gland; diabetes
mellitus (DM); vitiligo; pernicious anemia;
leukotrichia; medications such as lithium car-
bonate and iodine-containing drugs; and a
family history of diabetes mellitus, pernicious
anemia, thyroid disease, or primary adrenal
insufficiency.32 Clinicians should also seek to
determine the presence or absence of car-
diovascular diseases (such as angina pec-
toris, coronary artery disease, arrhythmias,
and congestive heart failure). There is some
evidence that patients with hyperlipidemia
associated with overt hypothyroidism have
an increased incidence of coronary artery
disease and associated angina pectoris.38,49
Furthermore, some patients with hypothy-
roidism cannot tolerate full replacement
therapy because of angina pectoris and
increased incidence of myocardial infarction
and sudden death.38 There is also evidence
that patients treated for thyroid disease
(Graves disease, toxic multinodular goiter,
Hashimotos thyroiditis) have an increased
long-term cardiovascular risk despite restora-
tion of euthyroidism.50
Functional capacity. Since T4 and T3exert direct inotropic and chronotropic
effects on cardiac muscle and appear to act
synergistically with epinephrine, the history
should also seek to determine the patients
functional capacity. Functional capacity,
which is expressed in terms of metabolic
equivalents (METs), is a measure of an indi-
viduals ability to perform a spectrum of com-
mon daily tasks (physical stressors). Cardiac
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risk in association with noncardiac proce-
dures is increased in patients unable to meet
a 4-MET demand during normal daily activi-
ties. 5153 Four METs is approximately equiva-
lent to the physiological stress produced by
doing light yard work (such as raking leaves,
weeding, or pushing a power mower), paint-
ing, doing light carpentry, or climbing a flight
of stairs. The hemodynamic effects of 4
METs is equivalent to that produced by 0.045
mg of epinephrine.54
Physical examinationGeneral appearance. The hypothyroidpatient may present with coarse facial fea-
tures (thick lips, puffy eyelids, sad expression),
dry hair, and dry and cold skin. The hyperthy-
roid patient may manifest tremor, excitability,
warm and moist skin, and exophthalmos.
Vital signs. Thyroid hormones appear toact synergistically with epinephrine affecting
cardiac contractility, vascular tone, and blood
pressure. As a result of this increased sym-
pathomimetic activity, heart rate, blood pres-
sure, and the rate of respiration are increased
in the hyperthyroid and decreased in the
hypothyroid patient. Myxedema coma is an
extreme life-threatening complication of
hypothyroidism. It is characterized by
hypoventilation, hypotension, and bradycar-
dia. A blood pressure of < 90/50 mm Hg is a
reliable sign of shock. Thyroid storm is the
extreme manifestation of hyperthyroidism. It
is characterized by an elevated temperature,
tachycardia, and high blood pressure. A
blood pressure in excess of 180/110 mm Hg
represents a hypertensive crisis. A resting
pulse rate below 60 or above 100 beats per
minute in adults, if symptomatic (sweating,
weakness, dyspnea, and/or chest pain),
should be considered a cardiac risk in
association with noncardiac procedures.
Respiratory rates less than 10 or greater that
20 breaths per minute may indicate respira-
tory distress.
Head and neck examination. Everypatient should be clinically screened for a
thyroid abnormality as part of the routine
head and neck examination.5,37,42 Normal thy-
roid tissue is often difficult to distinguish in
the relaxed neck; however, having the patient
extend the neck to one side allows for easier
palpation of the thyroid lobule on the opposite
side. The thyroid gland should be assessed
for textural consistency, overall size, presence
of growths, and tenderness. 5,37 The presence
of multinodularity of similar consistency is
most consistent with a benign goiter, while
the presence of a midline mass that moves
up with protrusion of the tongue is likely to be
a thyroglossal duct cyst.37
Treatment strategiesAs noted earlier, both hypothyroidism and
hyperthyroidism adversely affect cardiac
function. Thyroid dysfunction may also be
associated with DM and adrenal disease
(autoimmune polyglandular syndrome, type 2).
Consequently, treatment strategies for a
patient with thyroid dysfunction (Table 4)
should take into consideration the patients
overall health as reflected by the patients
medical history and vital signs. The dental
management of patients with cardiovascular
diseases, DM, and adrenal dysfunction
has been extensively reviewed in recent
publications. 5560
The hypothyroid patientThere are no randomized, prospective studies
in dentistry or medicine looking at surgical
outcomes in hypothyroid patients versus
controls. However, two retrospective case-
matched controls can provide some guid-
ance with relevance to dentistry. In one study,
researchers reviewed anesthetic and surgical
outcomes in 59 hypothyroid patients and 59
paired euthyroid controls.61 There were no dif-
ferences between the groups in perioperative
complications, surgical outcome, or length of
hospital stay. There were also no differences
in outcome among subsets of hypothyroid
patients as determined by thyroxine levels;
however, only a few patients were severely
hypothyroid. The authors concluded that
there was no evidence to justify deferring nec-
essary surgery in patients with mild to moder-
ate hypothyroidism and not enough evidence
to make recommendations for patients with
severe hypothyroidism. A severe hypothyroid
patient is one with myxedema characterized
by delayed mentation, pericardial effusions,
heart failure, or very low levels of thyroxine.62
In the second study, investigators looked
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at perioperative complications in 40 hypothy-
roid patients compared with 80 matched con-
trols. 63 Hypothyroid patients had more intra-
operative hypotension in noncardiac surgery,
but there were no differences between the
groups in perioperative arrhythmias or dura-
tion of hospitalization.
The use of local anesthetic agents andanalgesics. A review of the literature revealedno adverse effects associated with epineph-
rine infusion in patients with hypothyroidism
without significant cardiovascular disease.58
Well-controlled, medically supervised patients
on thyroid replacement and patients with mild
to moderate symptoms of hypothyroidism
may safely undergo routine dental care under
local anesthesia. However, patients with
hypothyroidism are hyperreactive to central
nervous system depressants (opioid anal-
gesics, anxiolytic agents), which should there-
fore be administered judiciously.5
The hyperthyroid patientT4 and T3 exert direct inotropic and chrono-
tropic effects on cardiac muscle. Left ventricu-
lar ejection fraction may not increase normally
during physiological stress, and increased
cardiac output may limit cardiac reserves dur-
ing surgery in the hyperthyroid patient.65
Consequently, the effect of inadequately treat-
ed or undiagnosed hyperthyroidism on the
heart carries perioperative risks. If hyperthy-
roidism is suspected, because of either med-
ical history or clinical signs and symptoms, the
patient should be referred for evaluation by an
internist or endocrinologist. Once medical
treatment has been instituted and the patient
is euthyroid, there is no contraindication to
dental treatment.
The use of local anesthetic agents andanalgesics. The use of local anestheticagent containing a vasoconstrictor in
patients with high concentrations of T4 and
T3 is an area of concern.5,24,42,66 Thyroid hor-
mones appear to act synergistically with epi-
nephrine by increasing tissue sensitivity to
catecholamines and possibly up-regulating
adrenergic receptors. An additional problem
associated with the use of local anesthetic
agents containing epinephrine is related to
the treatment of hyperthyroid symptoms with
a nonselective !-adrenergic antagonist. 5,67
However, these concerns must be balanced
against the value of a vasoconstrictor in
Euthyroid patient OR patient with mild to moderate thyroid dysfunction AND/OR minor clinical predictors(advanced age, atrial fibrillation, history of stroke) OR intermediate clinical predictors (stable angina pectoris, pre-vious myocardial infarction [MI], compensated heart failure renal insufficiency) of cardiovascular risk
Blood pressure less than 180/110 mm Hg; normal pulse pressure, rate and rhythm; functional capacity greaterthan 4 METsComprehensive dental careRoutine referral for medical management and risk factor modification
Blood pressure less than 180/110 mm Hg; normal pulse pressure, rate and rhythm; BUT functional capacityless than 4 METs Appropriate limited dental care*Routine referral for medical management and risk factor modification
Blood pressure greater than 180/110 mm Hg OR systolic blood pressure less than 90 mm Hg AND/OR abnor-mal pulse pressure, rate, or rhythm Appropriate emergency dental care**If patient is symptomatic, immediate referral for medical management and risk factor modification If patient is asymptomatic, routine referral for medical management and risk factor modification
Patient with severe hypothyroidism OR thyrotoxicosis AND/OR major clinical predictors (unstable coronary syn-drome, decompensated heart failure, severe valvular disease, significant arrhythmias) of cardiovascular risk
Appropriate emergency dental care**Immediate referral for medical management and risk factor modification
* Limited office care may include dental prophylaxis, restorative procedures, simple periodontal and endodontic procedures, androutine extractions.** Emergency office care under local anesthesia without a vasoconstrictor should be based on firm evidence that the benefitsachieved by therapeutic intervention outweigh the risk of complications associated with the patient's diabetic or cardiovascularstatus and may include activities related to pain relief, the treatment of infection (including simple incision and drainage), and theinduction of hemostasis (avoid the use of epinephrine to control local bleeding).
Table 4 Dental management of the patient with thyroid dysfunction
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148 VOLUME 39 NUMBER 2 FEBRUARY 2008
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inducing profound local anesthesia, which is
essential in reducing the physiologic stress
associated with pain. For the patient with
overt evidence of hyperthyroidism, the use of
vasoconstrictors should be avoided. For all
other scenarios, the cautious use of vaso-
constrictors, based on the patients function-
al capacity, should be considered. For those
patients whose functional capacity is equal
to or greater than 4 METs, 4.5 mL of a local
anesthetic agent with epinephrine 1:100,000
(or equivalent) can be administered safely.
Furthermore, combination analgesics con-
taining acetylsalicylic acid (ASA) are con-
traindicated in patients with hyperthyroidism
because ASA interferes with the protein bind-
ing of T4 and T3, thereby increasing their free
form, and can lead to thyrotoxicosis.
Preventive strategiesSome patients with hyperthyroidism may be
treated with 131I (radioiodine) for the short-
term inhibition of thyroxin release. Salivary
glands are known to concentrate iodide
selectively (up to 24% of administered 131I is
lost through the saliva). To reduce the poten-
tial for 131I-induced sialadenitis, it is recom-
mend that measures be taken to increase
salivation and thus accelerate the flow of 131I
through the glandular parenchyma.59 These
patients may benefit from simple measures
such as eating carrots or celery or chewing
sugarless or xylitol-containing gums. How-
ever, pilocarpine hydrochloride (Salagen,
MGI Pharma) and cevimeline hydrochloride
(Evoxac, Daiichi Pharmaceuticals), both mus-
carinic agonists, may more predictably
increase salivary activity. The use of the
radioprotectant agent amifostine has also
been advocated. The patient who manifests
residual salivary gland damage should be
managed in a manner similar to that estab-
lished for the patient who has received thera-
peutic head and neck radiotherapy. 60
CONCLUSIONS
When treating patients with thyroid dysfunc-
tion in the oral healthcare setting, the goals
are to develop and implement timely preven-
tive and therapeutic strategies compatible
with the patients physical and emotional
ability to undergo and respond to dental
care. There is no evidence to justify deferring
necessary dental procedures in patients with
mild to moderate hypothyroidism. However,
T4 and T3 exert direct inotropic and
chronotropic effects on cardiac muscle. Left
ventricular ejection fraction may not increase
normally during physiological stress, and
increased cardiac output may limit cardiac
reserves during stressful procedures in the
hyperthyroid patient. The effect of inade-
quately treated or undiagnosed hyperthy-
roidism on the heart may carry perioperative
risks in the oral healthcare setting.
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