18
Thyroid Gland Dysfunction
The thyroid gland is one of the largest endocrine organs,
weighing approximately 15 to 20 g in North American
adults. The potential for growth of the thyroid gland is tre-
mendous. An enlarged thyroid gland, commonly termed a
goiter, can weigh several hundred grams. The thyroid gland
is composed of two elongated lobes on either side of the
trachea joined by a thin isthmus of thyroid tissue located
at or below the level of the thyroid cartilage.1 Viewed from
the front, the thyroid gland is a butterfly-shaped organ that
wraps around the anterior and lateral portions of the larynx
and trachea (Fig. 18.1). The thyroid gland produces and
secretes three hormones that are vital for regulating the level
of biochemical activity in most body tissues. These hor-
mones include thyroxine (T4), triiodothyronine (T3), and
calcitonin. Thyroid hormones influence cell metabolism by
increasing their basal metabolic rate. Proper functioning of
the thyroid gland at birth is vital for normal growth and
metabolism.
Because there are so many generalized effects of a thyroid
hormone excess, it has been said, “To know thyroid disease
is to know medicine.”
Thyroid dysfunction can occur through either an overpro-
duction (hyperthyroidism, thyrotoxicosis) or underproduction
(hypothyroidism) of thyroid hormones. In both instances the
observed clinical manifestations can encompass a broad spec-
trum, ranging from subclinical dysfunction to an acutely life-
threatening situation. Most patients with thyroid dysfunction
exhibit milder forms of the disease.
Like adrenal insufficiency, thyroid dysfunction initially
presents as a slow, insidious process during which nonspe-
cific signs and symptoms, developing over months or years,
can be acutely exacerbated by intercurrent stress. Thyroid
dysfunction is relatively uncommon, and its characteristic
symptoms are difficult to recognize. Both hyper- and hypo-
thyroidism are potentially fatal if untreated and both con-
stitute medical emergencies in their most extreme stages.2
This chapter focuses primarily on the detection of the clin-
ical signs and symptoms of thyroid dysfunction. In addition,
parts of the discussion focus on the life-threatening situations
associated with this dysfunction—myxedema coma and thy-
roid “storm,” or crisis—both of which are extremely rare.
Hypothyroidism is a clinical condition in which the
body’s tissues do not receive an adequate supply of thyroid
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hormones. Clinical signs and symptoms of hypothyroidism
are related to the age of the patient at the time of onset and
to the degree and duration of the hormonal deficiency. A
deficiency of thyroid hormone during fetal or early life can
produce the clinical syndrome of congenital hypothyroid-
ism—previously known as cretinism—in infants and chil-
dren.3 Severe hypothyroidism that develops in an adult is
called myxedema and refers to the appearance of nonpitting,
gelatinous, mucinous infiltrates beneath the skin.4 Severe,
unmanaged hypothyroidism ultimately can induce a loss of
consciousness, a condition known as myxedema coma. The
mortality rate for myxedema coma is high (up to 50%),
even with optimal treatment.5,6 Focal or generalized seizures
occur in up to 25% of patients with this condition, and
status epilepticus has also been reported.7
Hyperthyroidism is also known by several other names,
including thyrotoxicosis, toxic goiter (diffuse or nodular), Basedow’s
disease,8 Graves’ disease,9 Parry’s disease, and Plummer’s disease.
Hyperthyroidism involves a state of heightened thyroid gland
activity associated with the production of excessive quantities
of the thyroid hormones, T4 and T3. Because thyroid hormones
affect the cellular metabolism of virtually all organ systems,
signs and symptoms of hyperthyroidism can be noted in all
parts of the body. Left untreated, hyperthyroidism can lead
to an acute, life-threatening situation known as thyroid storm,
which manifests as severe hypermetabolism; a high fever; and
cardiovascular, neurological, and gastrointestinal dysfunc-
tion.5,10 Although uncommon today, thyroid storm still has a
high mortality rate, even with treatment.11
Predisposing Factors
Excluding diabetes mellitus, which is the most common
endocrine disorder, thyroid dysfunction accounts for 80%
of all other endocrine disorders.
Hypothyroidism
A reduced production of thyroid hormones is a central
feature of this clinical state, termed hypothyroidism. Hypo-
thyroidism usually occurs as a result of thyroid gland dis-
ease or dysfunction (primary hypothyroidism), pituitary
disease or dysfunction (secondary), or hypothalamic disease
275
276 PA RT 4 Altered Consciousness

• BOX 18.1 Causes of Hypothyroidism

Primary Hypothyroidism
Autoimmune Hypothyroidism
• Hashimoto’s thyroiditis (chronic-atrophic thyroid, acute with
goiter)
• Graves’ disease (end stage)
Iatrogenic
• Radioactive iodine therapy for Graves’ disease
• Thyroidectomy for Graves’ disease, nodular goiter, or
thyroid cancer
• External neck irradiation for lymphoma or head and neck
cancer
Iodine-related
• Iodine deficiency (common worldwide but rare in North
America)
• Excess iodine (inhibition of hormone release can unmask
autoimmune thyroid disease; see under Drug-related)
Drug-related
• Lithium (inhibits hormone release)
• Figure 18.1  The thyroid gland. (Adapted from Patton K, Thibodeau G. • Amiodarone (destructive thyroiditis or iodine excess)
Anatomy and Physiology. 8th edition. St. Louis, MO: Elsevier Inc; 2014.) • Interferon-α (precipitates Hashimoto’s thyroiditis)
• Iodine excess (iodinated contrast media, kelp, amiodarone)
• Propylthiouracil, methimazole
• Interference with thyroid hormone absorption in patients on
or dysfunction (tertiary).2 The permanent loss or destruc- replacement therapy (iron, calcium, chromium, phosphate
tion of the thyroid gland through processes like autoim- binders, cholestyramine, colestipol)
mune destruction—autoimmune thyroiditis (Hashimoto’s Thyroiditis
disease)—or an irradiation injury is termed primary hypo- • Subacute
thyroidism. Autoimmunity is responsible for over 90% of • Silent
noniatrogenic hypothyroidism in countries with iodine suffi- • (Sporadic)
• Postpartum
ciency. Primary hypothyroidism is the cause of approximately • Amiodarone
99% of cases of hypothyroidism, with less than 1% due to a
thyroid-stimulating hormone deficiency or other causes.12,13 Congenital Defect in Thyroid Hormone Synthesis
Other causes of hypothyroidism in adults include a prior Central Hypothyroidism
ablative treatment for hyperthyroidism (radioactive iodine ther-
apy), surgical hypothyroidism, prior external beam radiation Euthyroid Sick Syndrome
therapy to the head or neck region, environmental radiation Pituitary Disease
exposure (e.g., nuclear disasters in Japan14 and Chernobyl15), • Pituitary adenoma
postpartum thyroiditis (occurs in 7% of pregnancies), iodine • Hemorrhage
deficiency (the most common cause of congenital hypothy- • Infiltrative (amyloid, sarcoid)
roidism worldwide), and congenital abnormalities.16 Hypothalamic Disease##
Thyroid hypofunction can develop at any age; how-
ever, its peak incidence occurs between 30 and 50 years of
age.17 This condition affects approximately 6% of females
and approximately 2.5% of males older than 60 years of etiologies of hypothyroidism. Several factors can predis-
age.18 Hypothyroidism occurs significantly more frequently pose a patient to developing myxedema coma, including
in females (1.5%–2%) than males (0.2%).17 The annual cold, infection, trauma, and exposure to central nervous
incidence of autoimmune hypothyroidism is around 80 per system (CNS) depressants and anesthetics.23
100,000 males and 350 per 100,000 females.19 Hashimoto’s The dentist should be aware of patients who may be
disease is eight times more common in females.12 hypothyroid because they are at an increased risk during
Myxedema coma is the ultimate stage of severe, long- dental treatment if medically untreated or inadequately
standing hypothyroidism.20,21 This condition develops managed. Patients who are clinically hypothyroid are
most often in older patients and is associated with a very unusually sensitive (hyperresponders on the “bell-shaped
high mortality rate.11 It is also associated with severe hypo- curve”) to most CNS depressants, including the sedatives,
thermia,11 with temperatures as low as 23°C (73.4°F) opioids, and antianxiety drugs commonly used in den-
having been recorded. Clinical manifestations of myx- tistry, such as nitrous oxide-oxygen (N2O-O2). Therefore,
edema coma include hypoventilation, hypoxia, hyper- commonly employed sedative doses (“average” doses) of these
capnia, and hypotension.22 Box 18.1 lists the potential drugs can result in an extreme overreaction in clinically

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 CHAPTER 18  Thyroid Gland Dysfunction 277

hypothyroid individuals. As a result, the use of titratable Patients who are clinically hyperthyroid tend to be
sedation techniques, such as N2O-O2 and intravenous seda- unusually sensitive (hyperresponders) to catecholamines
tion, are recommended. like epinephrine and respond to their administration with
hypertensive episodes, tachycardia, and significant dys-
Hyperthyroidism/Thyrotoxicosis rhythmias. In addition, hyperthyroid patients may seem
quite apprehensive, which implies the need for sedation
Hyperthyroidism is a clinical state induced by the exces-
sive production and secretion of thyroid hormones by an
overactive thyroid gland. Thyrotoxicosis is a more broadly
• BOX 18.2 Causes of Hyperthyroidism
encompassing term referring to both hyperthyroidism and
an excessive level of circulating thyroid hormones due to • Graves’ disease (toxic diffuse goiter)
glandular destruction or ingestion of exogenous thyroid • Toxic multinodular goiter
• Toxic adenoma (single hot nodule)
hormones.24 Both terms, hyperthyroidism and thyrotoxico- • Factitious thyrotoxicosis
sis, are used interchangeably today and refer to the classic or • Thyrotoxicosis associated with thyroiditis
subtle physiological manifestations of an excessive quantity • Hashimoto’s thyroiditis
of thyroid hormones characteristic of this condition.24 • Subacute (de Quervain’s) thyroiditis
Like hypothyroidism, hyperthyroidism begins insidiously • Postpartum thyroiditis
• Sporadic thyroiditis
and, if left untreated, can progress, resulting in the acute and • Amiodarone thyroiditis
life-threatening form of this disorder, thyroid storm. Thyroid • Iodine-induced hyperthyroidism (areas of iodine deficiency)
storm has a mortality rate of 10% or higher with treatment.10 • Amiodarone
Hyperthyroidism has a peak occurrence between the • Radiocontrast media
ages of 20 and 50 years.25 Approximately 3 in 10,000 adults • Metastatic follicular thyroid carcinoma
• hCG-mediated thyrotoxicosis
develop thyroid gland hyperfunction each year, with the • Hydatidiform mole
diagnosis being made in eight females for every male.26 The • Metastatic choriocarcinoma
prevalence of hyperthyroid disease is 1% to 2% in females • Hyperemesis gravidarum
and 0.1% to 0.2% in males. Black and Asian populations • TSH-producing pituitary tumors
are more likely than White populations to develop Graves’ • Struma ovarii
disease,25 while White populations have a greater risk of hCG, Human chorionic gonadotropin; TSH, thyroid-stimulating hormone.
Sharma AN, Levy DL. Thyroid and adrenal disorders. From: Marx JA,
developing Hashimoto’s disease. Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and
The most common etiologies of an overactive thyroid Clinical Practice. 8th edition. St. Louis, MO: Mosby; 2014.
gland are Graves’ disease and toxic multinodular goiter.
Graves’ disease is a multisystem autoimmune disor-
der. Graves’ disease (Basedow’s disease in Europe and Latin
America) 8,9,27 has a genetic predisposition. Box 18.2 lists
other causes of thyrotoxicosis.
Toxic multinodular goiter is the second leading cause
of hyperthyroidism in the United States. Characterized
by multiple autonomously functioning nodules, it usually
occurs in females older than 50 years of age (Fig. 18.2).28
Although rare, thyroid storm most commonly occurs in
patients with untreated or incompletely treated thyrotoxi-
cosis. Only about 1% to 2% of patients with thyrotoxicosis
progress to thyroid storm.29,30 However, on rare occasions,
thyroid storm can occur suddenly in a patient who has not
previously been diagnosed with thyrotoxicosis. More com-
monly, however, thyroid storm follows a long history of
uncomplicated thyrotoxicosis. The patient usually experi-
ences 6 to 8 months of milder symptoms and may even have
developed thyrotoxicosis up to 2.5 to 5 years previously.29,30
Thyroid storm represents a sudden and severe exacerba-
tion of the signs and symptoms of thyrotoxicosis, usually
accompanied by hyperpyrexia (typically >40°C [>104°F])
and tachydysrhythmias (tachycardia or atrial fibrillation).
Thyroid storm can be precipitated by radioiodine therapy, the
• Figure 18.2  Patient with Graves’ disease demonstrating diffuse thy-
administration of iodinated intravenous (IV) contrast agents, romegaly. (Fig. 9.6 from Swartz MH. The Head and Neck. In: Swartz
diabetic ketoacidosis, surgical stress, infection, trauma, acute MH. Textbook of Physical Diagnosis: History and Examination. 8th edi-
coronary syndrome, and labor.31 tion. Philadelphia, PA: Elsevier; 2021.)

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278 PA RT 4 Altered Consciousness
during dental treatment. However, it is important to note
that sedation can prove to be a futile exercise in these
patients, whose “anxiety” is hormonally induced rather
than psychological.
Both thyrotoxicosis and hypothyroidism are associated
with an increased incidence of cardiovascular disease.32–34
Milder forms of both types of thyroid dysfunction
can be asymptomatic. Although both thyrotoxicosis and
hypothyroidism can potentially create increased risks dur-
ing dental treatment, patients with more severe, undiag-
nosed, or untreated disease present the greatest risks. The
doctor must be able to recognize each form of thyroid
dysfunction and take the necessary steps to decrease
potential risks.
Prevention
Two goals are essential in the management of patients with
thyroid dysfunction:
1. Prevention of the life-threatening situations of myx-
edema coma and thyroid storm
2. Prevention of an exacerbation of the complications
associated with thyroid dysfunction, most notably
cardiovascular disease
MEDICAL HISTORY QUESTIONNAIRE
Question 49 on the University of the Pacific School of
Dentistry’s medical history questionnaire refers specifically
to thyroid disease. However, other questions may also
provide important information about potential thyroid gland
dysfunction.
Section III, Do You Have, or Have You Had:
Question 49: Thyroid, adrenal disease?
Section I, Questions 1 to 4
Question 1. Is your general health good?
Question 2. Has there been a change in your health within the
last year?
Question 3. Have you been hospitalized or had a serious
illness in the last three years? If YES, why?
Question 4. Yes/No: Are you being treated by a physician
now? For what? Date of last medical exam?
Comment: Patients with a known history of thyroid
dysfunction will most often mention this problem in one or
more of these questions.
Section II, Have You Experienced:
Question 10: Recent weight loss, fever, night sweats?
Comment: Unexplained weight loss in a patient with an
increase in appetite should alert the doctor to the possible
presence of thyrotoxicosis. Conversely, an unexplained
increase in weight accompanied by other clinical signs and
symptoms may indicate hypothyroidism.
Section IV, Have You Experienced:
Question 52: Radiation treatments?
Question 10: Recent weight loss, fever, night sweats?
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Question 58: Surgeries?
Comment: Thyroid hyperfunction is commonly discovered
during the routine palpation of a patient’s neck, since the
condition often manifests itself as a lump or bump (Fig. 18.2).
Question 58 prompts the individual to explain the type of
thyroid dysfunction and the mode of treatment.
A total or subtotal thyroidectomy are common surgical
treatments for thyroid hyperfunction in patients with Graves’
disease, while a subtotal thyroidectomy is most commonly
employed for patients with toxic multinodular goiter.35 There
are three treatment options for hyperthyroidism associated
with an increased radioiodine uptake: (1) antithyroid
medications, (2) radioiodine therapy with iodine I-131, and
(3) surgery.36
Section V, Are You Taking:
Question 62: Drugs, medications, over-the-counter medicines
(including aspirin), natural remedies?
Comment: Hypothyroidism is gratifying to treat because of
the ease and completeness with which it responds to the
administration of thyroid hormone.37 The current standard
of care for patients with thyroid hypofunction is to receive
thyroid hormone replacement with levothyroxine (T4)
monotherapy.38,39 More than a dozen clinical trials comparing
the outcomes of T4 monotherapy versus a combination
of T3 and T4 therapy have failed to demonstrate any
superiority or preference for combination therapy.40
The goal of the management of thyroid hypofunction is
to maintain normal thyroid hormone blood levels to bring
the patient back to what is known as the euthyroid state.
Drug therapy for thyrotoxicosis includes antithyroid
drugs:41,42 thioamides, which are used to treat causes of
hyperthyroidism attributable to the overproduction and
oversecretion of thyroid hormones. Methimazole is most
frequently prescribed because of its longer duration of action
and lower incidence of adverse effects. Propylthiouracil
was also a first-line drug but, due to reports of severe
hepatotoxicity (fulminant hepatic failure and death), is now
only recommended during the first trimester of pregnancy
(because of the potential teratogenicity of methimazole).43
Other drugs used for symptomatic relief in
hyperthyroidism include41,42 β-adrenergic blockers, such
as propranolol and atenolol, to control the heart rate;
nonsteroidal antiinflammatory drugs (NSAIDs), which are
first-line drugs for pain relief in patients with subacute
thyroiditis; corticosteroids, which are a second-line therapy
for pain relief and are also used to reduce inflammation in
thyroiditis; and inorganic iodine, which is useful in the short-
term management of thyrotoxicosis when administered
prior to methimazole or propylthiouracil (Table 18.1).
Dialogue History
If the patient indicates a positive history of thyroid disease on
Question 49 of the health history questionnaire, an in-depth
dialogue history is indicated.
Question: What is the nature of the thyroid dysfunction—
hypofunction or hyperfunction?
Question: How do you manage the disorder?
Comment: These questions prompt the individual to disclose
general information about their thyroid problems.

TABLE
Medications Used to Manage Hypothyroidism and Thyrotoxicosis (Hyperthyroidism)
18.1
Hypothyroidism
Generic Proprietary
Thyroid USP (desiccated) Armour Thyroid, Nature-Throid, NP
Thyroid, Westhroid
Levothyroxine (T4) Euthyrox, Levothyroid, Levoxyl,
Synthroid, Tirosint, Unithroid
Liothyronine (T3) Cytomel, Triostat
NSAIDS, Nonsteroidal antiinflammatory drugs.
A physical examination should be performed to uncover
any clinical evidence of thyroid dysfunction. In many
instances the patient will be euthyroid and will therefore
represent a normal risk during dental treatment. According
to the American Society of Anesthesiologists (ASA)
Physical Classification System, patients with an underlying
thyroid disorder who are currently euthyroid represent an
ASA 2 risk.
However, if no history of thyroid dysfunction is
disclosed, clinical evidence can lead to a suspicion of its
presence, and the following dialogue history is warranted.
Question: Have you unexpectedly gained or lost weight
recently?
Comment: A recent weight gain (2–5 kg [4.4–11 pounds])
is commonly noted in clinically hypothyroid individuals,44
whereas persons who are hyperthyroid frequently lose
weight despite an increase in the appetite.41 Note, however,
that many other medical conditions, including diabetes,
heart failure, and malignancy, can also induce weight gain
or loss.
Question: Are you unusually sensitive to cold temperatures or
pain-relieving medications?
Comment: Cold intolerance is frequently observed in
hypothyroid individuals.
Question: Are you unusually sensitive to heat?
Question: Have you become increasingly irritable or tense?
Comment: Heat intolerance is observed in hyperthyroid
individuals. Patients might be more aware of their
sensitivity to temperature but may be less aware
of changes in their temperament, whereas a close
acquaintance (e.g., a spouse) is more likely to notice
subtle changes in temperament.
Physical Examination
In most cases in which patients report a history of thy-
roid gland dysfunction, they have received or are currently
receiving treatment. These individuals are usually in a
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CHAPTER 18  Thyroid Gland Dysfunction 279
Thyrotoxicosis
Generic Proprietary
Methimazole Tapazole
Propylthiouracil None
Propranolol Inderal
Atenolol Tenormin
NSAIDs Advil, Caldolor, Motrin
Ibuprofen
Corticosteroids Rayos, Sterapred
Prednisone
Inorganic iodine
euthyroid state and do not represent an increased risk dur-
ing dental treatment.
In contrast, patients with previously undetected thyroid
dysfunction may be at an increased risk during dental treat-
ment. Fortunately, the presence of clinical signs and symp-
toms can allow the doctor to recognize thyroid dysfunction
and modify the treatment plan accordingly.
Clinically, hypothyroid patients may have an enlarged,
thick tongue with atrophic papillae and thick, edematous
skin with puffy hands and face. Their skin is dry, rough,
thick, and cool, and their nails are rough. The blood pres-
sure is close to normal (for the patient), with a slight eleva-
tion in the diastolic pressure and a slowing of the heart rate
(bradycardia).45 A hypothyroid patient may appear lethargic
and speak slowly (Table 18.2).
A significant proportion of hypothyroid patients are
asymptomatic.46
Hyperthyroid patients often appear nervous, with
warm, sweaty hands and a possible slight tremor. In these
patients, the blood pressure is elevated (systolic more than
diastolic, with a widened pulse pressure), and the heart
rate is increased (tachycardia).31 It can be quite difficult
to distinguish between thyrotoxicosis and acute anxiety in
patients. However, one clue to this differential diagnosis is
that patients with thyrotoxicosis often have warm, sweaty
palms, whereas the palms of an acutely anxious individual
are frequently cold and clammy (Table 18.3ab).
Dental Therapy Considerations
Euthyroid
Patients with thyroid dysfunction who are receiving or
have received therapy to treat the condition (e.g., surgery,
oral medication, irradiation) and who have normal levels
280 PA RT 4 Altered Consciousness

TABLE Reproductive
Signs and Symptoms of Hypothyroidism
18.2
Oligomenorrhea or amenorrhea
Vital Signs Menorrhagia
Decreased fertility
Systolic blood pressure, normal or low Early abortions
Diastolic blood pressure, normal or elevated Decreased libido
Slow pulse to sinus bradycardia Erectile dysfunction
Respirations, normal or slow, shallow
Temperature, normal, but prone to hypothermia with stress Rheumatic
Hypometabolic Complaints Polyarthralgias
Joint effusions
Cold intolerance Acute gout or pseudogout
Fatigue
Weight gain but decreased appetite Head, Ear, Eyes, Nose, and Throat
Cutaneous Hoarseness
Deep husky voice
Coarse, brittle hair Macroglossia
Alopecia Hearing loss
Dry skin, decreased perspiration Periorbital swelling
Pallor, cool hands and feet Broad nose
Coarse, rough skin Swollen lips
Yellow tinge from carotenemia Goiter
Thin, brittle nails Modified from Thiessen MEW. Thyroid and Adrenal Disorders. In: Walls RM,
Lateral thinning of the eyebrows Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Con-
cepts and Clinical Practice. 9th edition. Philadelphia, PA: Elsevier; 2018, pp.
Neurologic 1557-1571. (Reference # 2)

Slow mentation and speech

Impaired concentration and attention span
Lethargy
Decreased short-term memory
Agitation, psychosis TABLE
Seizures Symptoms of Hyperthyroidism
18.3A
Ataxia, dysmetria
Mononeuropathy Constitutional
Carpal tunnel syndrome Weight loss despite hyperphagia
Sensorineural hearing loss Fatigue
Peripheral neuropathy, paresthesias Generalized weakness
Muscular Hypermetabolic
Proximal myopathy Heat intolerance
Pseudohypertrophy Cold preference
Delayed relaxation of reflexes Excessive perspiration
Cardiac Cardiorespiratory
Decreased exercise capacity Palpitations
Dyspnea on exertion Dyspnea
Sinus bradycardia Dyspnea on exertion
Long QT with increased ventricular dysrhythmia Chest pains
Chest pain, accelerated coronary disease Poor exercise tolerance
Diastolic heart failure (delayed ventricular relaxation) Gastrointestinal
Pericardial effusion (asymptomatic)
Peripheral edema Nausea
Vomiting
Respiratory Diarrhea
Dyspnea on exertion Dysphagia
Obstructive sleep apnea Neuropsychiatric
Primary pulmonary hypertension
Anxiety
Gastrointestinal Restlessness
Constipation Hyperkinesis
Emotional lability
Ileus
Confusion
Gastric atrophy Insomnia
Poor attention
Continued
Continued

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 CHAPTER 18  Thyroid Gland Dysfunction 281

TABLE Ophthalmologic
Symptoms of Hyperthyroidism (cont'd)
18.3A
Widened palpebral fissures (stare)
Neuromuscular Lid lag
Globe lag
Myopathy Conjunctival injection
Myalgias Periorbital edema
Tremor Proptosis
Proximal muscle weakness (e.g., difficulty getting out of a Limitation of superior gaze
chair or brushing hair)
Neurologic
Ophthalmologic
Fine tremor
Tearing Hyperreflexia
Irritation Proximal muscle weakness
Wind sensitivity
Diplopia Psychiatric
Foreign body sensation Fidgety
Thyroid Gland Emotionally labile
Poor concentration
Neck fullness
Dysphagia Dermatologic
Dysphonia Warm, moist skin
Dermatologic Rosy cheeks, blushing face
Fine brittle hair
Flushed feeling Alopecia
Hair loss Flushed facies
Pretibial swelling Palmar erythema
Reproductive Onycholysis (separation of the distal portion of the
fingernail from the nail bed)
Oligomenorrhea
Amenorrhea Neck
Menometrorrhagia Diffuse symmetric thyroid enlargement
Decreased libido Thyroid with multiple irregular nodules or a prominent
Gynecomastia single nodule
Erectile dysfunction Racheal deviation
Infertility Venous prominence with arm elevation
Modified from Thiessen MEW. Thyroid and Adrenal Disorders. In: Walls RM, Modified from Thiessen MEW. Thyroid and Adrenal Disorders. In: Walls RM,
Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Con- Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Con-
cepts and Clinical Practice. 9th edition. Philadelphia, PA: Elsevier; 2018, pp. cepts and Clinical Practice. 9th edition. Philadelphia, PA: Elsevier; 2018, pp.
1557–1571. (Reference # 2) 1557–1571. (Reference # 2)

TABLE of circulating thyroid hormones are asymptomatic. These

Signs of Hyperthyroidism patients represent ASA 2 risks and may be managed nor-
18.3B
mally during dental treatment. In addition, if mild clini-
Vital Signs
cal manifestations of either hyper- or hypothyroidism are
Tachycardia present, elective dental treatment can still proceed, although
Widened pulse pressure
Bounding pulses
certain treatment modifications should be considered. These
Fever patients represent ASA 3 risks.
Cardiac Hypothyroid
Hyperdynamic precordium If clinical hypothyroidism is suspected, certain precautions
Systolic flow murmur
are recommended. A medical consultation with the patient’s
Prominent heart sounds
Systolic rub primary care physician should be considered prior to the
Tricuspid valve regurgitation start of dental treatment. In addition, caution should be
Atrial fibrillation exercised when prescribing CNS depressants. Of particu-
Evidence of heart failure lar concern are the sedative-hypnotics, opioid analgesics,
and other antianxiety drugs. Because clinically hypothy-
Continued roid patients demonstrate an increased sensitivity to CNS
depressants, the administration of an “average” dose may

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282 PA RT 4 Altered Consciousness
actually produce an overresponse (known as a relative
overdose), leading to respiratory and/or cardiovascular
depression.47 A history of thyroid hypofunction should
also direct the doctor to look for signs and symptoms of
cardiovascular disease. In individuals with more intense
signs and symptoms of thyroid hypofunction (e.g., men-
tal apathy, drowsiness, or slow speech), dental treatment
should be postponed until a consultation with the patient’s
primary care physician occurs or definitive management of
the clinical disorder is achieved.
Hyperthyroid
Mild degrees of thyrotoxicosis can lead to acute anxiety,
with little increase in the clinical risk. However, various
cardiovascular disorders, primarily angina pectoris, are
exaggerated in patients with thyrotoxicosis.47,48 If, in the
course of a dental treatment, the patient develops one or
more of these cardiovascular disorders (e.g., chest pain or
palpitations), the management protocol for that specific
situation should be followed (see Part Seven: Chest Pain).
Patients exhibiting more severe signs and symptoms of
thyrotoxicosis should receive an immediate medical con-
sultation, and dental care should be postponed until the
patient’s underlying metabolic disturbance is corrected. It
is worthwhile to remember that psychological and physi-
ological stress can precipitate thyroid storm in patients with
untreated or incompletely treated hyperthyroidism.28
Furthermore, the use of atropine (i.e., which inhibits the
vagus nerve [stimulation of the vagus nerve decreases the heart
rate]) should be avoided. Atropine, a vagolytic drug, causes an
increase in the heart rate and may be a factor in precipitating
thyroid storm. In addition, epinephrine and other vasopres-
sors present in local anesthetics should be used with caution
in patients with clinical hyperthyroidism. Vasopressors stimu-
late the cardiovascular system and can precipitate cardiac dys-
rhythmias, tachycardia, and thyroid storm in poorly controlled
hyperthyroid patients whose cardiovascular systems have
already been sensitized. However, local anesthetics with vaso-
constrictors can be used with the following precautions:
• Use the least-concentrated effective solution of epi-
nephrine (1:200,000 is preferred to 1:100,000, which
is preferred to 1:50,000)
TABLE
18.4
Physical Status Classifications of Patients with Thyroid Gland Dysfunction
Degree of Thyroid Dysfunction
EUTHYROID – Hypofunctioning or hyperfunctioning
patient receiving medical therapy; no signs or
symptoms of dysfunction evident
Clinical hypofunction or hyperfunction; signs and
symptoms of dysfunction evident
ASA, American Society of Anesthesiologists; CNS, central nervous system.
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• Inject the smallest effective volume of an anesthetic/
vasopressor
• Aspirate prior to every injection (see Chapter 23)
Of greater potential risk, however, are the racemic
epinephrine-impregnated cords sometimes used for gingi-
val retraction. This form of epinephrine is more likely to
precipitate unwanted side effects, especially in the presence
of clinical thyrotoxicosis. The use of racemic epinephrine
is absolutely contraindicated in clinically hyperthyroid
patient.49,50
Patients with mild hyperthyroidism may easily be mis-
taken for those who are just apprehensive. In these patients,
use of minimal or moderate sedation is not contraindicated;
however, sedative drugs may prove to be less than effective
because the apparent nervousness of these individuals is hor-
monally induced and not related to fear (patients may require
larger than normal doses to achieve any degree of sedation).
Hypothyroid or hyperthyroid patients who have been
treated and are currently euthyroid represent an ASA 2
risk, whereas patients who exhibit clinical manifestations of
thyroid dysfunction represent an ASA 3 risk (Table 18.4).
Clinical Manifestations
Hypothyroidism
Hypothyroidism is the clinical state produced by a
reduced production of thyroid hormones.13,51 When this
deficiency occurs during childhood, the syndrome is
termed congenital hypothyroidism. (The obsolete name
is cretinism.)23 The child exhibits alterations in growth
and development, including a retardation of mental
development and growth that manifests only in later
infancy, with the former being largely irreversible.23 The
characteristic appearance of a patient with congenital
hypothyroidism includes a broad, flat nose; widely set
eyes; periorbital puffiness; a large protruding tongue;
sparse hair; rough skin; a short neck; and a protuberant
abdomen with an umbilical hernia (Fig. 18.3). The mental
deficiency of these patients is usually severe.16,23
Children with congenital hypothyroidism lack the neces-
sary thyroid hormone in utero or shortly after birth, which
retards their physical and mental development. In these
ASA
Physical Status Considerations
2 Usual ASA 2 considerations
3 Usual ASA 3 considerations, including care in the use
of vasopressors (hyperfunction) or CNS depressants
(hypofunction)
Evaluation for cardiovascular disease

• Figure 18.3  A clinical picture of an individual with congenital hypo-
thyroidism demonstrating the characteristic flat nose and broad, puffy
face. (From Little J, Miller C, Rhodus N. Little and Falace’s Dental Man-
agement of the Medically Compromised Patient. 9th edition. St. Louis,
MO: Elsevier; 2018.)
patients, the ossification of bone is delayed, tooth develop-
ment is poor, and tooth eruption is delayed. Permanent neu-
rological damage is also observed. Clinically, the infant will
appear dull and apathetic, with a body temperature usually
below normal. In infants with congenital hypothyroidism,
the determining factor for eventual intellectual attainment
is the age at which adequate treatment with thyroid hor-
mone is initiated.52,53
When hypothyroidism develops in adults, the onset is
usually insidious, with a significant proportion of patients
being asymptomatic. Frequently, a friend or spouse will per-
suade the individual to seek medical assistance because of
a noticeable increase in their weakness or fatigue, a sudden
weight gain (2–5 kg [4.4–11 pounds]) not associated with
an increased appetite,43 or cold intolerance (present in half
of cases). Frequently, patients are unaware of these changes
themselves.
As hypothyroidism progresses, the patient may dem-
onstrate slowing of the speech, hoarseness, an absence of
sweating, moderate weight gain, constipation (in 25% of
cases), a decreased sense of taste and smell, peripheral non-
pitting edema, dyspnea, and anginal pain. Clinical signs
include a puffiness of the face and eyelids;21 a carotenemic
(orange-red) skin color and rosy cheeks; a thickened tongue;
and thickened, edematous skin (nonpitting). The blood
pressure remains approximately normal, though sometimes
with a slight elevation in the diastolic pressure.54 However,
the heart rate is decreased (sinus bradycardia is the most
common dysrhythmia in individuals with a hypofunction-
ing thyroid). Patients with severe, untreated hypothyroid-
ism can develop heart failure with pulmonary congestion.
Pseudomyotonic deep tendon reflexes and paresthesias
are also extremely common (almost 100% occurrence) in
patients with hypothyroidism. Pseudomyotonic deep tendon
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CHAPTER 18  Thyroid Gland Dysfunction 283
reflexes are characterized by a prolonged relaxation phase,
which can be confirmed through testing of the Achilles
tendon reflex while the patient kneels on a chair. In these
patients, the relaxation phase is at least twice as long as the
contraction phase.55 About 80% of cases have paresthesias,55
of which the median nerve (carpal tunnel syndrome) is the
most common.
The most severe complication of hypothyroidism, how-
ever, is myxedema coma.21,56 This condition has a high mor-
tality rate (between 30%–60% with management57) and is
marked by hypothermia (temperatures commonly between
29.5°C–30°C but temperatures as low as 23°C have been
recorded), bradycardia, severe hypotension, and intense
cerebral obtundation (loss of consciousness).
Myxedema coma is rare, occurring in only 0.1% of
all patients with hypothyroidism, and is extremely rare
in patients younger than 50 years. It is most common in
older women with a history of primary hypothyroidism.11,21
Approximately 80% of patients with myxedema coma expe-
rience hypothermia.11
Essential symptoms for the diagnosis of hypothyroid-
ism include cold intolerance, fatigue, lethargy, generalized
weakness, anorexia, constipation, depression, weight gain,
menstrual irregularities or amenorrhea, and infertility.45
Signs that are necessary for the diagnosis include dry,
rough, thick, cool skin; brittle, dry, coarse hair; a loss of
eyebrow hair; alopecia; a thickened tongue; periorbital
edema; thick, slow-moving lips; and hoarseness. The thy-
roid gland may also be palpable depending on whether a
goiter is present (Fig. 18.2). The patient may also exhibit
cardiac manifestations, including bradycardia and an
elevated diastolic pressure, and neurologic abnormalities,
such as hearing impairment, peripheral neuropathies with
paresthesias, skeletal muscle weakness, and delayed deep
tendon reflexes (Table 18.2).45,58,59
Thyrotoxicosis
Similarly to hypothyroidism, patients with hyperthyroidism
generally have manifestations for months prior to diagnosis.
In most cases, questioning of the patient will reveal clinical
evidence of dysfunction occurring over a period of months
before its “discovery.” As with thyroid hypofunction, the
individual who actually discovers the disease is often a
spouse, friend, or someone else who is able to notice subtle
changes in the habits and personality of the patient.
Patients with thyrotoxicosis due to thyroiditis can
frequently date the onset of their signs and symptoms pre-
cisely, as might be expected from the effects of releasing the
equivalent of 30 to 60 days’ supply of thyroid hormone into
the circulation over a few days or weeks.24
The classic symptoms of hyperthyroidism include31,41,42
weight loss despite an increased appetite and hyperphagia;
palpitations; tremulousness; heat intolerance; increased
frequency of formed bowel movements; hyperhidrosis (a
marked increase in sweating); overactivity, including quick,
uncoordinated movements that range from mild to gross
284 PA RT 4 Altered Consciousness
tremors; and rapid speech. Nonspecific symptoms include
fatigue, generalized weakness, emotional lability, edema of
the legs, and menstrual abnormalities. Anorexia, depression,
and lethargy are frequently noted in elderly patients,60 while
patients with Graves’ disease have additional symptoms,
including ophthalmopathy, a skin rash, and swelling.31,61
Nervousness, increased irritability, and insomnia are
often the first clinical signs to be noted in patients with
hyperthyroidism. An unexplained weight loss accompanied
by an increased appetite is another important signal. Up to
half of all patients seen in an emergency department with
thyroid storm have lost more than 40 pounds.30
Clinical signs include excessive sweating, with the skin
of a hyperthyroid individual feeling warm and moist to the
touch. The extremities, especially the hands, exhibit varying
degrees of tremulousness. Cardiovascular manifestations of
thyrotoxicosis vary from an increase in the blood pressure
(systolic pressure increasing more than diastolic pressure)
and a widening of the pulse pressure to sinus tachycardia
(more common during sleep), paroxysmal atrial fibrillation,
and heart failure. In addition, hyperthyroid individuals
experience mitral valve prolapse significantly more fre-
quently than the general population.28
When thyrotoxicosis results from Graves’ disease, oph-
thalmopathy may be noted, the severity of which does not
parallel the intensity of the thyroid gland dysfunction.
Graves ophthalmopathy (GO) is also known as Graves orbi-
topathy, thyroid-associated ophthalmopathy, and thyroid
eye disease. Graves hyperthyroidism is present in approxi-
mately 90% of patients with GO, whereas 5% to 10% of
patients with GO are euthyroid or hypothyroid.24,59 GO
appears at an average age of 49 years. Like most thyroid
diseases, GO is much more common in females but is more
severe in males and the elderly.24 GO is typically a bilateral
and symmetrical eye disease; however, approximately 10%
of patients have unilateral GO.
The clinical manifestations of GO include upper eyelid
retraction (occurs in approximately 90% of Graves’ disease
patients), proptosis (exophthalmos), extraocular muscle
dysfunction (in about 40% of GO patients), a tendency to
stare, lid lag, and conjunctival erythema (Fig. 18.4).62
• Figure 18.4  Hyperthyroid patient exhibiting exophthalmos. (From
Lewis S, Bucher L, Heitkemper M. Medical-Surgical Nursing. 9th edi-
tion. St. Louis, MO: Mosby; 2014.)
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Approximately 10% of patients with Graves’ disease
develop Graves’ dermopathy, presenting with myxedema
(raised, red, edematous skin), predominantly of the hands
and lower extremities, and thyroid acropachy (soft tissue
enlargement of the fingers with clubbing) (Fig. 18.5).31,63
Untreated thyrotoxicosis may eventually result in thyroid
storm, an acutely life-threatening situation. Thyroid storm
is extremely rare and represents an acute exacerbation of the
signs and symptoms of thyrotoxicosis, manifested by signs
of severe hypermetabolism. Clinical manifestations include
hyperpyrexia, excessive sweating, nausea, vomiting, abdom-
inal pain, cardiovascular disturbances (such as tachycardia
and atrial fibrillation), and heart failure with possible pul-
monary edema. CNS manifestations usually start as a mild
tremulousness, with the patient then becoming severely
agitated and disorientated, which next leads to psychotic
behavior, stupor (partial unconsciousness), and eventually
coma. Thyroid storm is associated with a high mortality rate
(10%64–20%65), even with proper management.
Symptoms and signs of thyrotoxicosis are presented in
Tables 18.3a and 18.3b.
Pathophysiology
T4 is a prohormone with mild biological activity. It is con-
verted to T3, a biologically active hormone, through deio-
dination. More than 99.5% of the thyroid hormones are
bound to protein in the serum, rendering them metaboli-
cally inactive. Only free T4 and T3 are clinically relevant.
• Figure 18.5  Infiltrativedermopathy of Graves’ disease. (From
Melmed S, Auchus RJ, Goldfine AB, et al. (eds.). Williams Textbook of
Endocrinology. 14th edition. Elsevier; 2020.

Hypothyroidism
Insufficient levels of circulating thyroid hormones produce
signs and symptoms of hypothyroidism. All the body’s
functions are slowed down. In addition, mucopolysaccha-
rides and mucoproteins progressively infiltrate the skin of
individuals with chronic hypofunction, lending the skin
its characteristic puffy appearance. This hard, nonpitting,
mucinous edema, called myxedema, is a characteristic of
hypothyroidism.66,67 Initially, this edema does not appear in
dependent areas.31
Myxedema may also cause significant cardiac enlarge-
ment leading to pericardial and pleural effusions and to the
cardiovascular and respiratory difficulties associated with hypo-
thyroidism.68 Hypothyroid patients have a higher prevalence
of coronary heart disease and a higher severity of coronary
lesions.69 Thyroid hormone increases the heart’s rate and con-
tractility, leading to an increased myocardial oxygen demand.
Myxedema coma is the endpoint of severe, long-standing
hypothyroidism.20,21 The loss of consciousness may be
caused by hypothermia, hypoglycemia, or carbon dioxide
retention, all of which are present in this clinical condition.
Other presenting signs of myxedema coma include severe
mental changes, including hallucinations and disorienta-
tion; seizures; deep coma; body edema; swollen eyes and
tongue; labored breathing; pleural and/or pericardial effu-
sions; and dysrhythmias.45
Hyperthyroidism and Thyrotoxicosis
Hyperthyroidism results from the excessive production of
endogenous thyroid hormone by the thyroid gland, while
thyrotoxicosis results from the excessive administration of
exogenous thyroid hormone (as in the treatment of hypo-
thyroid states). Clinically observed signs and symptoms are
related to the levels of these hormones in the blood. Thyroid
hormones increase the body’s energy consumption and
elevate the basal metabolic rate. This increased energy use
results in fatigue and weight loss. Thyrotoxicosis is a more
broadly encompassing term referring to both hyperthyroid-
ism and an excessive level of circulating thyroid hormones
caused by a destruction of the thyroid gland or by the inges-
tion of exogenous thyroid hormones.31
Cardiovascular findings in thyrotoxicosis are related to
the direct action of thyroid hormones on the myocardium.
These are characterized by a hyperdynamic, electrically
excitable state. These findings include an elevated heart rate
and an increase in myocardial irritability. The increased inci-
dence of cardiac problems (e.g., angina pectoris and heart
failure) and cardiac symptoms (e.g., palpitations, dyspnea,
chest pain) in hyperthyroid individuals is most likely related
to an increase in the cardiac workload.29,33 Subclinical car-
diac disease may have been present prior to the onset of the
hyperthyroid state or in the hypothyroid state before the
start of therapy. However, clinically significant cardiac dis-
ease becomes evident with the addition of thyroid hormone,
which creates an increase in the heart’s workload and the
myocardial oxygen requirement.
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CHAPTER 18  Thyroid Gland Dysfunction 285
Because of the effects of atropine and epinephrine on the
heart and cardiovascular systems, their use is relatively con-
traindicated in severely hyperthyroid individuals.
In addition, thyrotoxicosis decreases liver function. Jaun-
dice may appear but is readily eliminated through the treat-
ment of thyrotoxicosis.70 Because of the variable degree of
liver dysfunction associated with thyrotoxicosis, all drugs
and medications metabolized primarily in the liver should be
administered judiciously and in smaller than normal doses.
Thyroid storm represents the endpoint of untreated thy-
rotoxicosis. The primary difference between thyroid storm
and severe thyrotoxicosis is the presence of hyperpyrexia.
If left untreated, the body’s temperature can reach a lethal
level (40.5°C [105°F] or higher) within 24 to 48 h. In this
severely hypermetabolic state, the body’s demand for energy
overtaxes the cardiovascular system, leading to cardiac
dysrhythmias, heart failure, and acute pulmonary edema.
Thyroid storm also causes a profound delirium, vomiting,
diarrhea, and dehydration.
Management
Acute thyroid-related emergencies are unlikely to develop
during the dental treatment of patients with thyroid disease.
If a loss of consciousness does occur, the immediate man-
agement is supportive in nature.
Hypothyroidism
No specific management is necessary for most patients who
exhibit clinical evidence of thyroid hypofunction. If the
doctor has doubts or concerns after a complete medical and
dental evaluation, a medical consultation with the patient’s
primary care physician is warranted before treatment begins.
It is worth noting that hypothyroid patients may be
unusually sensitive to the following categories of drugs:
• Sedatives and anxiolytics (e.g., benzodiazepines)
• Opioids (e.g., meperidine, fentanyl, codeine, hydromor-
phone, oxycodone)
• Most other CNS depressants, such as histamine-blockers
(antihistamines)
Moderate to severe overdose reactions can develop following
the administration of “normal” doses of these drugs.
The effective management of hypothyroid patients is
achieved through the oral administration of desiccated thyroid
hormone. In almost all cases, therapy continues for the remain-
der of the patient’s life. Within 30 days of the start of therapy,
the patient usually returns to a normal body weight, with all
clinical signs and symptoms disappearing. Overall, the prog-
nosis for treated hypothyroidism is a return to normal health.
Diagnostic clues to the presence of hypothyroidism
include:
• Cold intolerance
• Weakness
• Fatigue
• Dry, cold, yellow, puffy skin
• Thick tongue
286 PA RT 4 Altered Consciousness

Unconscious Patient with History • BOX 18.3 Management of an Unconscious

of Hypothyroidism Patient with Thyroid Disease
The possibility that an undiagnosed, untreated, clinically
hypothyroid patient will lose consciousness and not respond HYPOTHYROID PATIENT (MYXEDEMA COMA)
to resuscitative measures is extremely unlikely. It is more HYPERTHYROID PATIENT (THYROID STORM)
probable that a patient will lose consciousness because of
Recognize problem
a fear of dental treatment. In this situation the individual
generally regains consciousness after the usual steps in the ↓
management protocol of any unconscious patient. Discontinue dental treatment

Step 1: Termination of the Dental Procedure ↓

Step 2: P (Position) Activate office emergency team

The unconscious patient is placed in the supine position ↓
with the feet slightly elevated.
P—Position patient supine with feet elevated
Step 3: C → A → B (Circulation-Airway-Breathing), ↓
Basic Life Support (BLS), as Needed C → A → B—Assess and perform basic
If a hypothyroid patient loses consciousness, the possibil- life support as needed
ity of myxedema coma must be considered. Management ↓
of this situation includes an assessment of the adequacy of
circulation, establishment of a patent airway (head tilt–chin D—Definitive management:
Activate emergency medical service if
lift maneuver), assessment of breathing, and administration recovery not immediate
of O2. The blood pressure and heart rate are usually within Establish IV access, if possible
the low-normal range, and effective breathing (exchange of Administer O2
air) is present (airway management may be necessary). ↓
Step 4: D (Definitive Care) Discharge or hospitalization of patient as per
emergency medical technicians
Step 4a: Summoning of Medical Assistance. Because the
underlying cause of unconsciousness is not a lack of cerebral A, airway; B, breathing; C, circulation; D, definitive care; IV, intravenous; P,
blood flow or O2, an unconscious hypothyroid patient will not position.

regain consciousness after the initiation of BLS. Medical assis-

tance should be sought immediately whenever a patient does
not regain consciousness after the implementation of BLS.
Step 4b: Establishment of an IV Line (If Available).  If avail-
able, an IV infusion of 5% dextrose and water, lactated Ringer’s
solution, or normal saline can be started prior to the arrival of
emergency personnel. The availability of a patent vein will also
facilitate subsequent medical management of the patient.
Step 4c: Administration of O2. O2 may be administered
at any time during the emergency. Although O2 administra-
tion does not lead to a recovery of consciousness, no harm
can result.
Step 4d: Definitive Management.  Definitive management
of myxedema coma includes transport of the individual to a
hospital emergency department, IV administration of appro-
priate doses of thyroid hormones (e.g., T3 or T4) for several
days, and the reversal of hypothermia. Additional therapy
may vary according to the patient’s clinical state. The mortal-
ity rate associated with myxedema coma is high (40%), even
with proper and rigorous management (Box 18.3).
Thyrotoxicosis
Patients with hyperthyroidism often appear nervous and
apprehensive. If clinical symptoms are so intense that the
doctor remains doubtful about the nature of the patient’s
problem, a medical consultation is indicated before the start
of dental treatment. Although the risk of thyroid storm
is minimal, undue stress can induce this life-threatening
situation. In addition, the use of certain drugs, particu-
larly atropine and epinephrine, can precipitate a thyroid
crisis. Therefore, these drugs should not be administered
or should be administered with extreme caution to clini-
cally hyperthyroid individuals.
The following are diagnostic clues that may prompt a
suspicion of thyrotoxicosis:
• Sweating
• Heat intolerance
• Tachycardia
• Warm, thin, soft, moist skin
• Exophthalmos
• Tremor
Unconscious Patient With History of
Thyrotoxicosis
As with hypothyroid patients, undiagnosed, untreated,
clinically hyperthyroid patients are unlikely to lose con-
sciousness to the point at which resuscitation is impos-
sible. Vasodepressor syncope is a much more likely cause
of unconsciousness. In this situation the patient should
regain consciousness rapidly after the implementation

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of the basic steps in the management of an unconscious
patient.
Step 1: Termination of the Dental Procedure
Step 2: P (Position)
The patient is placed in the supine position with the feet
slightly elevated.
Step 3: C → A → B (BLS As Needed)
If a hyperthyroid patient loses consciousness, the possibility
of thyroid storm must be seriously considered, especially if
the body temperature is elevated. Management of this situ-
ation includes implementing the steps of BLS, including an
assessment of the circulation, establishing a patent airway,
assessing breathing, and administering O2, as needed. The
blood pressure and heart rate are elevated, sometimes dra-
matically. Spontaneous respirations are usually present, but
airway management may be necessary to affect a patent air-
way.
Step 4: D (Definitive Care)
Step 4a: Summoning of Medical Assistance.  Because the
underlying cause of unconsciousness is not a lack of cerebral
blood flow or O2, a hyperthyroid patient will not regain
consciousness after these basic procedures are implemented.
Medical assistance should be sought immediately whenever
a patient does not regain consciousness after BLS has been
performed.
Step 4b: Establishment of an IV Line (If Available). An
IV infusion of a 5% solution of dextrose and water, lac-
tated Ringer’s solution, or normal saline may be established
before emergency personnel arrive. The availability of a pat-
ent vein will also facilitate the subsequent medical manage-
ment of this patient.
Step 4c: Administration of O2. O2 may be administered at
any time during this emergency. Although its administration
will not lead to recovery, O2 cannot harm the individual.
Step 4d: Definitive Management.  Definitive management
of thyroid storm includes transport of the patient to a hos-
pital emergency department and administration of large
doses of antithyroid drugs (e.g., methimazole and propyl-
thiouracil). Additional therapy includes the administration
of propranolol to control the heart rate and large doses of
glucocorticosteroids to prevent acute adrenal insufficiency.
Other measures may include O2, cooling blankets to atten-
uate hyperthermia, sedation, and careful monitoring of
hydration and electrolyte balance.28 The prognosis is poor
for individuals with thyroid storm.
Box 18.3 outlines the management of an unconscious
patient with thyroid disease. In addition, the following
information may prove useful:
• Drugs used in management: No drugs are used to man-
age thyroid diseases in the dental office.
• Medical assistance required: If a hyperthyroid or hypo-
thyroid individual loses consciousness, medical assistance
should be sought immediately.
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CHAPTER 18  Thyroid Gland Dysfunction 287
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