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The Art and Science of Infusion Nursing
The Art and Science of Infusion Nursing
Angela M. Leung, MD, MSc
Thyroid Emergencies
ABSTRACT
Myxedema coma and thyroid storm are thyroid
emergencies associated with increased mortality.
Prompt recognition of these states-which repre
sent the severe, life-threatening conditions of
extremely reduced or elevated circulating thyroid
hormone concentrations, respectively-is neces
sary to initiate treatment. Management of myxe
dema coma and thyroid storm requires both med
ical and supportive therapies and should be treated
in an intensive care unit setting.
Key words: hypothyroidism, hyperthyroidism,
ICU, myxedema coma, thyroid emergencies,
thyroid storm
T
he thyroid is a 15- to 20-gram gland located
in the anterior neck. It is responsible for the
production of the thyroid hormones T4 (thy
roxine) and T3 (triiodothyronine). Various
factors can affect thyroid hormone synthesis,
including acute illness, coexisting morbidities, and certain
medications. Both the states of low thyroid hormone con
centrations (hypothyroidism) and thyroid hormone excess
(thyrotoxicosis) can be transient or permanent. The
decompensated, severe forms of hypothyroidism and
hyperthyroidism, termed myxedema coma and thyroid
storm, are associated with increased morbidity and mor
tality. Prompt recognition of both conditions is necessary
to initiate treatment and supportive measures. This
review will summarize the essential principles of the clini-
Author Affiliations: Division of Endocrinology, David Geffen
School of Medicine at UCLA, and the VA Greater Los Angeles
Healthcare System, Los Angeles, California.
Angela M. Leung, MD, MSc, is an assistant clinical professor of
medicine in the Division of Endocrinology at the David Geffen
School of Medicine at the University of California, Los Angeles,
and the VA Greater Los Angeles Healthcare System, both in Los
Angeles, California.
The author received funding from the National Institutes of Health,
NIH 7K23HD068552. The author has no other potential conflicts of
interest to disclose.
Corresponding Author: Angela M. Leung, MD, MSc, VA Greater
Los Angeles Healthcare Sysem, Divison of Endocrinology (111D),
11301 Wilshire Blvd, Los Angeles, CA 90073 (AMLeung@mednet.
ucla.edu).
DOI: 10.1097/NAN.0000000000000186
cal manifestations, diagnostic methods, and treatments of
hypothyroidism and hyperthyroidism, both in the
nonacute and life-threatening forms of these diseases.
THYROID HORMONE PRODUCTION
AND METABOLISM
The normal physiology of the hypothalamic-pituitary
thyroid axis involves the production of T4 and T3 by the
thyroid gland, a process that is regulated by thyroid-
stimulating hormone (TSH) secreted by the pituitary,
which is, in turn, regulated by thyrotropin-releasing hor
mone (TRH) secreted by the hypothalamus. Both serum
T4 and T3 concentrations act as negative feedback regu
lators of TSH and TRH secretion, but can be altered by
environmental conditions-including food availability
and temperature-and disease states, such as infection.1
Thyroid hormone synthesis is achieved first through
active transport of circulating iodide, which is taken in
from the diet, by the sodium/iodide symporter located at
the basolateral membrane of the thyroid follicular cell.2
Iodide then becomes oxidized by thyroid peroxidase
(TPO) and hydrogen peroxide at the apical membrane,
which then attaches to the tyrosyl residues on thyroglob
ulin (Tg) to produce monoiodotyrosine (MIT) and diio
dotyrosine (DIT). MIT and DIT are the precursors to the
thyroid hormones, which are produced by the linkage of
2 DIT molecules to form T4 and the linkage of MIT and
DIT to produce T3. Release of T4 and T3 into the circu
lation results from the digestion of Tg in MIT and DIT
by endosomal and lysosomal proteases.
The metabolic effects of thyroid hormone action result
from the binding of the thyroid hormone to thyroid hor
mone transporters located in specific target tissues, which
is mediated by the thyroid hormone nuclear receptor (TR)
that is encoded by the genes TR and TR. 3 While the
sole source of T4 is the thyroid gland, the majority
(approximately 80%) of T3 is produced from the
extrathyroidal conversion of T4 to T3 by the action of the
5 -deiodinase enzymes-D1 or D2-located in the liver,
brain, brown adipose tissue, and muscles.4 T4 can also be
converted to the inactive thyroid hormones, reverse T3 or
T2, by the 5 -deiodinase D3. The activity and expression
of the deiodinases are specific to different tissues and envi
ronmental conditions.
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SERUM THYROID FUNCTION AND
ANTIBODIES
Serum TSH is the most sensitive test to suggest thyroid
dysfunction, because of the logarithmic-linear relation
ship between serum TSH and thyroid hormone levels.
Overt thyroid dysfunction, whether referring to hypo
thyroidism or hyperthyroidism, is defined by the sole
abnormality of an elevated serum TSH concentration,
while subclinical thyroid dysfunction refers to both
elevated serum TSH and decreased T3 and/or T4 con
centrations. The range of subclinical to overt thyroid
dysfunction can be regarded as a continuum of increas
ingly severe biochemical thyroid disease, which inciden
tally may or may not correlate to the severity of any
corresponding symptoms, if present.
HYPOTHYROIDISM
Hypothyroidism refers to the state of low circulating
thyroid hormones. In 2 large US population-based stud
ies of data collected in the 1980s to the 1990s, the preva
lence of overt hypothyroidism ranged from 0.3% to
0.4%, while that of subclinical hypothyroidism ranged
from 4.3% to 8.5%, among the general population.5,6
The most common etiology of hypothyroidism in the
United States is Hashimoto's thyroiditis, an autoimmune
disease that is more prevalent among older women;
nutritional iodine deficiency is the most common etiology
worldwide. Additional etiologies of hypothyroidism
include a history of thyroidectomy, radioactive iodine
therapy, and, less commonly, decreased TSH production
by the pituitary. Predisposition factors for the develop
ment of hypothyroidism include thyroid autoimmunity
(which can be assessed by the determination of serum
thyroid autoantibodies, such as TPO and [Tg] antibody
titers), the use of certain medications (ie, lithium, ami
odarone, interferon-alpha), and excess iodine exposure
(ie, from iodinated contrast radiographic studies), in
which individuals with a history of thyroid disease are at
higher risk of iodine-induced hypothyroidism.7
Thyroid hormone is important for the metabolic func
tions of many major organs, including the heart, brain,
liver, and muscle. Signs and symptoms of hypothyroidism
are widely variable ( Table 1 ), often subtle, and may
include fatigue, malaise, weight gain, dry and puffy skin,
constipation, cold intolerance, altered cognition, and
hyporeflexia. In children, there may be stunted growth,
and in women, menstrual abnormalities may be present.
Hypothyroidism Among Women of
Reproductive Age and in Children
Normal thyroid function is particularly important
among pregnant and lactating women, the developing
TABLE 1
Signs and Symptoms
of Hypothyroidism
General
Fatigue
Lethargy
 Weight gain
Sleepiness
 Cold intolerance
Skin and hair
Dry, thick skin
 Coarse hair
 Eyebrow thinning
 Brittle nails
 Decreased perspiration
Cardiovascular system
Bradycardia
Elevation of blood pressure
Hyperlipidemia
Respiratory system
Shortness of breath
 Hoarse voice
 Sleep apnea
Gastrointestinal system
Constipation
 Decreased appetite
Reproductive system
Menstrual cycle irregularities
Infertility
Musculoskeletal system
Arthralgia
Neurological system
Paresthesia
Depression
 Mental impairment
 Slow movements
Hyporeflexia
fetus, and young children. As thyroid hormone is cru
cial for the complex processes of neurodevelopment and
growth,8 which begins in the first trimester of pregnan
cy and continues into the first few years of infancy,
these groups are especially susceptible to the effects of
even mild thyroid dysfunction. Several studies have
demonstrated that low thyroid hormone levels among
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Page 3
pregnant women are associated with increased risks of
preterm delivery, spontaneous miscarriage, fetal death,
and cognitive deficits,9 including a decrement in intelli
gence quotient and memory scores of the offspring,
compared with euthyroid women.10-13 Neuroimaging
studies also show abnormalities of hippocampal and
corpus callosum size, and of gray matter, among chil
dren with a form of low thyroid hormone levels at birth
14,15
termed congenital hypothyroidism.
Myxedema Coma
Myxedema coma refers to the state of severe, life-
threatening, and decompensated hypothyroidism in
which thyroid hormone levels are dangerously low. The
diagnosis appears to be more common in elderly women
with long-standing preexisting hypothyroidism. Triggers
may include cold temperature (thus, it is more common
during winter months); precipitating comorbidities,
such as infection, stroke, and heart failure; or the use of
sedative, analgesic, antidepressant, hypnotic, antipsy
chotic, or anesthetic medications.16 Patients with preex
isting hypothyroidism may also present with myxedema
coma following a period of prolonged noncompliance
with thyroid hormone replacement.
Signs and symptoms usually are exacerbations of the
usual manifestations of hypothyroidism and may include
extreme lethargy, which can progress to stupor or coma,
hypothermia, respiratory depression, bradycardia,
hyponatremia, and renal impairment. The diagnosis of
myxedema coma is made with the confirmation of a
biochemical thyroid profile consistent with hypothyroid
ism and corresponding clinical manifestations. A diag
nostic scoring system has been proposed to guide the
clinician toward a diagnosis of myxedema coma based
on body temperature, central nervous system signs, gas
trointestinal symptoms, precipitating events, cardiovas
cular dysfunction, and metabolic disturbances.17
Treatment of myxedema coma should be considered
as quickly as possible, given the increased mortality of
the disease (25%-60% despite treatment),18 and can be
started even before confirmation of laboratory results
demonstrating abnormal serum TSH and T4 concentra
tions. The management of myxedema coma should be
in an intensive care unit (ICU) setting. The central ten
ets of treatment are thyroid hormone replacement,
stress-dose corticosteroids if concomitant adrenal insuf
ficiency is suspected, supportive care, and the treatment
of any underlying and coexisting conditions ( Table 2 ).
Supportive care may include the administration of
intravenous (IV) fluids, sodium replacement if hypona
tremia is present, and the use of warming blankets
(although aggressive rewarming should be avoided,
given the risks of vasodilation).19
Thyroid hormone replacement should be adminis
tered as T4 and/or T3, often intravenously, given the
impaired state of the patient. Suggested regimens for the
initial and maintenance doses of thyroid hormone in a
patient with myxedema coma are provided in Table 2 .
In general, a loading dose of 200 to 400 microg IV levothy
roxine (T4) is to be followed by a maintenance dose of
1.6 microg/kg/d when given orally or 75% of this when
given intravenously; consideration can also be made for
the coadministration of liothyronine (T3), since T4 to
T3 conversion may be impaired in patients with myxe
dema coma.20 It is important to note that IV thyroid
hormone replacement should be administered only as a
push through a syringe, rather than through infusion
tubing, in which up to 40% of the starting concentra
tion may be lost from adherence to polypropylene tub
ing.21 Improvements in serum T3 and T4 concentra
tions may be seen before the normalization of serum
TSH concentrations, and measurement of serum thy
roid function tests every 1 to 2 days during treatment is
reasonable.20 Improvements in clinical cardiovascular,
renal, pulmonary, and metabolic parameters may take
as much as a week to be observed.20

THYROTOXICOSIS
Thyrotoxicosis refers to the state of thyroid hormone
excess arising from either overproduction from the thyroid
gland (termed hyperthyroidism) or extrathyroidal,
including exogenous, sources. Of the etiologies attributable
to hyperthyroidism, the most common cause worldwide
is Graves' disease, resulting from the autoimmune
TABLE 2
Management of
Myxedema Coma
Thyroid hormone replacement
 Levothyroxine (T4)
Loading dose of 200-400 microg IV once
Maintenance dose of 1.6 micro g/kg/d IV/PO
 Liothyronine (T3)
Loading dose of 5-20 microg IV/NG once
Maintenance dose of 2.5-10 every 8 hours IV/PO
Supportive measures
IV fluids containing electrolytes and glucose
Passive rewarming with a blanket
Treatment of any underlying comorbidities, including infection
Glucocorticoids
Hydrocortisone 100 mg IV every 8 hours if adrenal insufficiency
is suspected
Abbreviations: IV, intravenous; NG, nasogastric; PO, per oral.
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Page 4
stimulation of the thyroid by serum thyroid-stimulating
immunoglobulin, followed by toxic multinodular goiter
and toxic adenoma. In the United States, the prevalence
of hyperthyroidism from all causes is approximately
1.2%, of which 0.5% is overt and 0.7% is subclinical.22
Other causes of thyrotoxicosis include overproduction of
TSH from a pituitary adenoma, thyroiditis, exogenous
thyroid hormone ingestion, ectopic hyperthyroidism
(such as from struma ovarii or metastatic thyroid
cancer), or human chorionic gonadotropin-mediated
hyperthyroidism (such as from hyperemesis gravidarum
or a molar pregnancy).
The signs and symptoms of thyrotoxicosis are reflec
tive of the excess concentrations of thyroid hormone
present ( Table 3 ) and can include anxiety, fatigue, dia
phoresis, heat intolerance, tremors, palpitations, tachy
cardia, weight loss, hyperreflexia, and warm and moist
skin. In women, menstrual abnormalities may be seen.
In patients in whom the thyrotoxicosis is due to Graves'
disease, specific clinical manifestations may also include
thyroid eye disease (ie, exophthalmos, lid lag), a diffuse
goiter with a bruit, localized dermopathy, thyroid
acropachy (ie, digital clubbing and swelling), and the
coexistence of other autoimmune diseases in the patient
or the patient's family.
Thyroid Storm
Thyroid storm is the clinical manifestation of elevated
serum thyroid hormone concentrations, resulting in the
extreme alteration of usual hyperthyroid symptoms.
The diagnosis can occur in patients with or without
preexisting hyperthyroidism. It is a rare diagnosis and
usually triggered by precipitants such as trauma, myo
cardial infarction, surgery (including thyroid surgery
for hyperthyroidism or other surgeries in general), or
infection. In some cases, acute exposure to excess
iodine (ie, administration of iodinated contrast radio
graphic scan) may result in iodine-induced hyperthy
roidism to trigger thyroid storm.23 Patients with known
severe hyperthyroidism who are noncompliant with
prescribed antithyroid medications may also develop
thyroid storm.
Prompt recognition of thyroid storm is essential to
initiate treatment, which should be performed in an
ICU setting. Clinical manifestations of thyroid storm
can be quite varied and may include fever, cardiac
arrhythmias, vomiting, and impaired mental status.
Patients with thyroid storm have increased inpatient
mortality rate, overall hospital and ICU length of stay,
and ventilation requirements compared with those with
compensated thyrotoxicosis.24 The mortality rate of
thyroid storm ranges from 10% to 20%.25,26
Diagnosis of thyroid storm is made using a combi
nation of biochemical laboratory tests confirming
thyrotoxicosis in a patient displaying the severe,
TABLE 3
Signs and Symptoms
of Thyrotoxicosis
General
Fatigue
 Weight loss
Insomnia
 Heat intolerance
Eyes
Exophthalmos, lid lag, or periorbital/conjunctival edema, if
thyrotoxicosis is due to Graves' disease
Skin and hair
Warm, moist skin
Thin, fine hair
 Brittle nails
Diaphoresis
Thyroid acropachy if due to Graves' disease
Localized dermopathy, if due to Graves' disease
Cardiovascular system
 Tachycardia
Palpitations
 Atrial arrhythmias
 Systolic hypertension
 Hyperdynamic precordium
Respiratory system
Shortness of breath
Gastrointestinal system
Loose stools or hyperdefecation
 Increased appetite
Reproductive system
Menstrual cycle irregularities
Infertility
Musculoskeletal system
Muscle weakness, especially of proximal muscles
Neurological system
Nervousness
Anxiety
 Tremor
Hyperactivity
Hyperreflexia
life-threatening symptoms of hyperthyroidism. Several
diagnostic scoring systems have been proposed that
can be used to assess the likelihood of thyroid storm in
patients. The Burch-Wartofsky scoring system is based
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Page 5
on factors related to temperature, central nervous sys
tem effects, gastrointestinal/hepatic dysfunction, car
diovascular dysfunction, heart failure, and any pre
cipitant history. 27 The Akamizu criteria are similar
and have also been proposed as another diagnostic
scoring system in the assessment of thyroid storm.28
Treatment usually consists of multiple measures
and medications aimed to target the various causes
and effects of thyrotoxicosis, as summarized in
Table 4 . 19,22 Symptomatic improvement of tachycar
dia and clinical manifestations reflecting the increased
adrenergic tone can be achieved with beta-blocker
therapy. Methimazole or propylthiouracil should be
initiated to decrease production of thyroid hormone.
Saturated solution of potassium iodide can be used to
inhibit thyroid hormone release from the thyroid
gland. Glucocorticoids decrease the conversion of T4
to T3, which can also be accomplished by the use of
propylthiouracil.29 Supportive measures include IV
fluids, oxygen, cooling, and treatment of any precipi
tating causes. Finally, if necessary when the above
treatments cannot be used or are unsuccessful, plas
mapheresis can be attempted to decrease thyroid hor
mone excess, as well as cytokines and putative anti
bodies, in the circulation.30
TABLE 4
Management of
Thyroid Storm
Antithyroidal drugs
Propylthiouracil
Loading dose of 600 mg PO/NG/PR once
Maintenance dose of 200-300 mg every 6 hours PO/NG/PR
Methimazole
Loading dose of 20 mg PO every 6 hours
Saturated solution of potassium iodide
5 drops PO every 6 hours; must be started after antithyroid drug
therapy is initiated to avoid potential worsening of
hyperthyroidism
Glucocorticoids
Hydrocortisone 100 mg IV every 8 hours
Beta-blocker therapy
Propranolol 40-80 mg PO every 4 hours or 2 mg IV every 4 hours
Supportive measures
 IV fluids
Oxygen
Cooling
Treatment of any precipitating causes
Abbreviations: IV, intravenous; NG, nasogastric; PO, per oral; PR, per rectum.
CONCLUSION
Hypothyroidism and thyrotoxicosis are common endo
crine disorders, each with a variety of etiologies, and
most patients with thyroid dysfunction are easily man
aged. However, in certain patients, severe, life-threatening
forms of these states, representing rare thyroid emergen
cies, can develop on exposure to precipitating triggers or
among patients with preexisting thyroid dysfunction or
noncompliance with medical treatment. Both myxedema
coma, corresponding to extremely low serum thyroid
hormone concentrations, and thyroid storm, correspond
ing to extremely elevated thyroid hormone concentra
tions, are associated with increased mortality and must
be recognized promptly. Treatment of myxedema coma
and thyroid storm is multifaceted and should be man
aged by the interdisciplinary team of an ICU setting.
REFERENCES
1. Fekete C , Lechan RM .  Central regulation of hypothalamic-
pituitary-thyroid axis under physiological and pathophysiological
conditions .  Endocr Rev. 2014 ; 35 ( 2 ): 159-194 .
2. Zimmermann MB , Boelaert K .  Iodine deficiency and thyroid
disorders .  Lancet Diabetes Endocrinol. 2015 ; 3 ( 4 ): 286-295 .
3. Brent GA .  Mechanisms of thyroid hormone action .  J Clin Invest.
2012 ; 122 ( 9 ): 3035-3043 .
4. Gereben B , Zavacki AM , Ribich S , et al. Cellular and molecular
basis of deiodinase-regulated thyroid hormone signaling .  Endocr
Rev. 2008 ; 29 ( 7 ): 898-938 .
5. Hollowell JG , Staehling NW, Flanders WD , et al. Serum TSH,
T(4), and thyroid antibodies in the United States population
(1988 to 1994): National Health and Nutrition Examination
Survey (NHANES III) .  J Clin Endocrinol Metab. 2002 ; 87 ( 2 ): 489-499 .
6. Canaris GJ , Manowitz NR , Mayor G , Ridgway EC .  The
Colorado thyroid disease prevalence study.  Arch Intern Med.
2000 ; 160 ( 4 ): 526-534 .
7. Leung AM , Braverman LE .  Consequences of excess iodine .  Nat
Rev Endocrinol. 2014 ; 10 ( 3 ): 136-142 .
8. Zoeller RT, Rovet J .  Timing of thyroid hormone action in the
developing brain: clinical observations and experimental findings .
J Neuroendocrinol. 2004 ; 16 ( 10 ): 809-818 .
9. Lazarus JH .  Thyroid disorders associated with pregnancy: etiol
ogy, diagnosis, and management .  Treat Endocrinol. 2005 ; 4 ( 1 ):
31-41 .
10. Haddow JE , Palomaki GE , Allan WC , et al. Maternal thyroid
deficiency during pregnancy and subsequent neuropsychological
development of the child .  N Engl J Med. 1999 ; 341 ( 8 ): 549-555 .
11. Pop VJ , Kuijpens JL , van Baar AL , et al. Low maternal free thy
roxine concentrations during early pregnancy are associated with
impaired psychomotor development in infancy.  Clin Endocrinol
(Oxf). 1999 ; 50 ( 2 ): 149-155 .
12. Pop VJ , Brouwers EP, Vader HL , Vulsma T , van Baar AL , de
Vijlder JJ .  Maternal hypothyroxinaemia during early pregnancy
and subsequent child development: a 3-year follow-up study.  Clin
Endocrinol (Oxf). 2003 ; 59 ( 3 ): 282-288 .
13. Wheeler SM , Willoughby KA , McAndrews MP, Rovet JF.
Hippocampal size and memory functioning in children and
adolescents with congenital hypothyroidism .  J Clin Endocrinol
Metab. 2011 ; 96 ( 9 ): E1427-E1434 .
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Copyright (c) 2016 Infusion Nurses Society 285
Copyright (c) 2016 Infusion Nurses Society. Unauthorized reproduction of this article is prohibited.

Page 6
14. Samadi A , Skocic J , Rovet JF.  Children born to women treated
for hypothyroidism during pregnancy show abnormal corpus cal
losum development .  Thyroid. 2015 ; 25 ( 5 ): 494-502 .
15. Rovet JF, Skocic J , Khan S .  Grey matter reductions in children
with congenital hypothyroidism: a voxel-based morphometry
(VBM) neuroimaging study. Paper presented at: 14th International
Thyroid Congress; September 11-16, 2010 ;  Paris, France .
16. Wartofsky L .  Myxedema coma . In:  Braverman LE , Cooper DS ,
eds. Werner & Ingbar's the Thyroid: A Fundamental and Clinical
Text. 10th ed .  Philadelphia, PA:  Lippincott Williams & Wilkins ;
2012 : 600-605 .
17. Popoveniuc G , Chandra T , Sud A , et al. A diagnostic scoring
system for myxedema coma .  Endocr Pract. 2014 ; 20 ( 8 ): 808-817 .
18. Mathew V , Misgar RA , Ghosh S , et al. Myxedema coma: a new
look into an old crisis .  J Thyroid Res. 2011 ;2011:493462.
19. Hampton J .  Thyroid gland disorder emergencies: thyroid storm
and myxedema coma .  AACN Adv Crit Care. 2013 ; 24 ( 3 ): 325-332 .
20. Jonklaas J , Bianco AC , Bauer AJ , et al. Guidelines for the treat
ment of hypothyroidism: prepared by the American Thyroid
Association task force on thyroid hormone replacement .  Thyroid.
2014 ; 24 ( 12 ): 1670-1751 .
21. Golombek SG , Alpan G , Frey M , Corbi D , Lagamma EF.
Stability of thyroid hormones during continuous infusion .  J
Perinat Med. 2011 ; 39 ( 4 ): 471-475 .
22. Bahn RS , Burch HB , Cooper DS , et al. Hyperthyroidism and
other causes of thyrotoxicosis: management guidelines of the
American Thyroid Association and American Association of
Clinical Endocrinologists .  Endocr Pract. 2011 ; 17 ( 3 ): 456-520 .
23. Alkhuja S , Pyram R , Odeyemi O .  In the eye of the storm: iodi
nated contrast medium induced thyroid storm presenting as car
diopulmonary arrest .  Heart Lung. 2013 ; 42 ( 4 ): 267-269 .
24. Angell TE , Lechner MG , Nguyen CT, Salvato VL , Nicoloff JT,
LoPresti JS .  Clinical features and hospital outcomes in thyroid
storm: a retrospective cohort study.  J Clin Endocrinol Metab. 2015 ;
100 ( 2 ): 451-459 .
25. Chiha M , Samarasinghe S , Kabaker AS .  Thyroid storm: an
updated review.  J Intensive Care Med. 2015 ; 30 ( 3 ): 131-140 .
26. Karger S , Fuhrer D .  Thyroid storm-thyrotoxic crisis: an update
[in German] .  Dtsch Med Wochenschr. 2008 ; 133 ( 10 ): 479-484 .
27. Burch HB , Wartofsky L .  Life-threatening thyrotoxicosis .
Thyroid storm. Endocrinol Metab Clin North Am. 1993 ; 22 ( 2 ):
263-277 .
28. Akamizu T , Satoh T , Isozaki O , et al. Diagnostic criteria, clinical
features, and incidence of thyroid storm based on nationwide
surveys .  Thyroid. 2012 ; 22 ( 7 ): 661-679 .
29. Geffner DL , Azukizawa M , Hershman JM .  Propylthiouracil
blocks extrathyroidal conversion of thyroxine to triiodothyronine
and augments thyrotropin secretion in man .  J Clin Invest. 1975 ;
55 ( 2 ): 224-229 .
30. Muller C , Perrin P , Faller B , Richter S , Chantrel F .  Role of plasma
exchange in the thyroid storm .  Ther Apher Dial. 2011 ; 15 ( 6 ):
522-531 .
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