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456
M. Sakr
catecholamines. However, it does not explain
why β-blockers fail to decrease thyroid hormone levels in thyrotoxicosis.
– Another theory suggests a rapid rise of free
hormone levels as the pathogenic source due
to post-operative drop in binding protein levels [20]. In addition, hormone levels may rise
rapidly due to vigorous palpation during
examination or rough manipulation during
surgery, or from damaged follicles following
RAI therapy.
– Other proposed theories include alterations
in tissue tolerance to thyroid hormones [21],
the presence of a unique catecholamine-like
substance in thyrotoxicosis, and a direct
sympathomimetic effect of thyroid hormone
owing to its structural similarity to catecholamines [20].
16.2.5 Clinical Presentation
Thyroid storm is usually acute in onset, with
intensied clinical manifestations of thyrotoxicosis. Hyper-metabolism contributes to the
development of high fever that may exceed
40°C and is usually considered a major factor in
differentiating thyroid storm from non-storm
thyrotoxicosis [2]. Without therapy, fever may
progressively increase to lethal levels within
24–48h. Patients with thyroid storm have warm
skin and are ushed, with profuse sweating.
However, goiter and exophthalmos may or may
not be present.
Tachycardia—often exceeding 140 beats/
min—and atrial brillation are rather common,
and tachypnea is frequently seen. Ventricular
dysfunction and acute pulmonary edema or congestive heart failure (CHF) may also develop.
Fine tremors and severe agitation are characteristic of thyrotoxic storm. Emotional lability,
restlessness, confusion, and delirium are common and may progress to frank psychosis, stupor,
and coma. Severe diarrhea is the most common
gastrointestinal (GI) symptom, but nausea, vomiting, and abdominal pain also occur and may be
misdiagnosed as an acute abdominal emergency.
Hepatomegaly, with mild jaundice and abnormal
liver function tests (LFTs) suggestive of hepatocellular dysfunction are sometimes present.
Diagnosis of thyrotoxic storm is mainly a
clinical one. Characteristic features such as
Bayley’s symptom complex of insomnia,
anorexia, vomiting, diarrhea, marked sweating,
and great emotional instability are reliable in
predicting impending storm [22]. A temperature>38°C, marked tachycardia, accentuated
symptoms and signs of thyrotoxicosis, and
central nervous system (CNS), cardiovascular,
or gastrointestinal system dysfunction indicate
a thyrotoxic storm [23, 24]. Symptoms and
signs of thyrotoxic storm are listed in
Table16.2.
Complications of thyrotoxic storm include
high output cardiac failure, arrhythmias, delirium, seizures, coma, abdominal pain, diarrhea,
vomiting, jaundice, and elevation of transami-
Table 16.2 Symptoms and signs of thyrotoxic storm
Symptoms Physical signs
General symptoms
– Fever
– Profuse sweating
– Poor feeding and
weight loss
– Fatigue
Gastro-intestinal
symptoms
– Nausea and
vomiting
– Diarrhea
– Abdominal pain
– Yellowish
discoloration of
skin and sclera
[25]
Neurologic symptoms
– Anxiety (more
common in older
adolescents)
– Altered behavior
– Seizures
– Coma
Respiratory symptoms
– Dyspnea
– Respiratory
distress
General signs
– Fever (temperature
consistently exceeds
38.5°C and frequently
exceeds 41°C).
– Excessive sweating
– Jaundice [25]
Cardio-vascular signs
– Hypertension with wide
pulse pressure
– Hypotension in later
stages with shock
– Tachycardia
disproportionate to fever
– Signs of high-output
heart failure
– Cardiac arrhythmia (e.g.,
atrial utter and
brillation, ventricular
tachycardia)
Neurological signs
– Agitation and confusion
– Hyper-reexia and
transient pyramidal signs
– Tremors
– Seizures
– Coma
Signs of thyrotoxicosis
– Orbital signs
– Goiter
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16 Thyroid andParathyroid Endocrine Emergencies
457
nases. In 2017, Mohananey et al. reported that
out of 41,835 patients with thyrotoxic storm, 1%
developed cardiogenic shock. The highest likelihood of cardiogenic shock was in male patients
with preexisting atherosclerotic or structural
heart disease [26].
Burch and Wartofsky (1993) have published
precise criteria and a scoring system for the
diagnosis of thyrotoxic storm based on clinical
features (Table 16.3) [27]. Accordingly, a score
of 25–44 is “suggestive” of an impending storm,
and a score of ≥45 is “highly suggestive” of
Table 16.3 Diagnostic criteria of thyroid storm by Burch
and Wartofsky [27]
Factor Score
Thermoregulatory dysfunction [temperature
(°F)]
– 99–99.9
– 100–100.9
– 101–101.9
– 102–102.9
– 103–103.9
– ≥104
Central nervous system effects
– Absent
– Mild (agitation)
– Moderate (delirium—psychosis—extreme
lethargy)
– Severe (coma)
Gastrointestinal-hepatic dysfunction
– Absent
– Moderate (diarrhea—nausea and
vomiting—abdominal pain)
– Severe (unexplained jaundice)
Cardiovascular dysfunction
Tachycardia (beats/min)
– 90–109
– 110–119
– 120–129
– 130–139
– ≥104
Congestive heart failure
– Absent
– Mild (pedal edema)
– Moderate (bibasilar rales)
– Severe (pulmonary edema)
Atrial brillation
– Absent
– Present
Precipitant history
– Negative
– Positive
5
10
15
20
25
30
0
10
20
30
0
10
20
5
10
15
20
25
0
5
10
15
0
10
0
10
storm. Bennett and Huston (1984) reported that
patients rarely have a thyroid storm and apathetic thyrotoxicosis, coma, cerebral infarction,
status epilepticus, and acute renal failure [28].
Rare cases of rhabdomyolysis have been reported
following a diagnosis of thyroid storm in adults
[28, 29].
16.2.6 Pathophysiology
Thyroid storm is a decompensated state of thyroid hormone-induced, severe hyper-metabolism
involving multiple systems and is the most
extreme state of thyrotoxicosis. The mechanism
underlying the pathogenesis of thyrotoxic storm
is not yet completely understood. A dramatic
increase in serum FT4 level is commonly
observed and may precipitate its onset. Additional
factors such as poor nutrition and complicating
medical, surgical, and emotional effects on thyroid hormone binding, metabolic clearance, general physiologic reserve, and increased
catecholamines are other important contributing
factors [27]. In addition, in a patient with a thyroid storm combined with primary hyperparathyroidism (PHPT), a markedly elevated serum
calcium level has been reported to possibly augment the action of T4 via its role as a second messenger [28].
The clinical picture relates to severely exaggerated effects of thyroid hormones due to
increased release (with or without increased synthesis) or, rarely, increased intake of thyroid hormones. Heat intolerance and diaphoresis are
common in simple thyrotoxicosis, but manifest
as hyperpyrexia in thyrotoxic storm. Extremely
high metabolism also increases oxygen and
energy consumption. Cardiac manifestations of
mild-to-moderate sinus tachycardia in thyrotoxicosis intensify to accelerated tachycardia, hypertension, high-output cardiac failure, and the risk
of developing cardiac arrhythmias. Similarly,
irritability and restlessness in thyrotoxicosis
progress to severe agitation, delirium, seizures,
and coma [30]. Gastrointestinal manifestations of
thyroid storm include diarrhea, vomiting, jaundice, and abdominal pain, in contrast to only mild
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458
M. Sakr
elevations of transaminases and simple enhancement of intestinal transport in thyrotoxicosis.
16.2.7 Diagnosis: Work-Up
inThyrotoxic Storm
16.2.7.1 Approach Considerations
Early diagnosis and prompt adequate treatment are
the most important determinants in the successful
management of thyrotoxic storm and minimizing
the risk of its potential fatal outcome. The diagnosis of thyroid storm is based on clinical features,
not on laboratory test ndings. If the patient’s clinical picture is consistent with thyroid storm, treatment should not be delayed by waiting for pending
laboratory conrmation of thyrotoxicosis.
16.2.7.2 Laboratory Studies
– Thyroid function tests: Laboratory tests of
serum tri-iodothyronine (T3), thyroxin (T4),
or free T4 (FT4) are essential for diagnosis,
although these tests are similar in patients
with storm and non-storm thyrotoxicosis.
They are useful only if the patient has not been
previously diagnosed. Test results may not
come back quickly and are usually unhelpful
for immediate management [31, 32]. Usual
ndings include elevated T3, T4, and FT4 levels; increased T3 resin-uptake; suppressed
thyroid-stimulating hormone (TSH) levels;
and an elevated 24-h iodine uptake. TSH levels are not suppressed in the rare instances of
excess TSH secretion.
– Complete blood count (CBC): Leukocytosis is
occasionally present, particularly in patients
with co-existent infections.
– Liver function tests (LFTs): The LFTs com-
monly reveal nonspecic abnormalities such
as elevated levels of alanine aminotransferase
(ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatinine kinase,
alkaline phosphatase, and serum bilirubin.
– Arterial blood gases (ABG) and urinalysis:
Measurement of ABC and electrolyte levels
and urinalysis testing may be performed to
assess and monitor short-term management.
– Serum Calcium: Hypercalcemia may also
occur from thyrotoxicosis.
16.2.7.3 Imaging Studies
Chest radiography may reveal cardiac enlargement due to CHF.It may also reveal pulmonary
edema caused by heart failure and/or evidence
of pulmonary infection. Computed tomography
(CT) scan of the head may be necessary to
exclude other neurological conditions if diagnosis is uncertain after the initial stabilization
of a patient who presents with altered mental
status.
16.2.7.4 Other Tests
Electro-cardiogram (ECG) is useful in monitoring of cardiac arrhythmias. Atrial brillation is
the most common cardiac arrhythmia associated
with thyroid storm. Other arrhythmias such as
atrial utter and, less commonly, ventricular
tachycardia may also occur.
16.2.8 Dierential Diagnoses
The differentials of thyrotoxic storm include a
variety of disorders such as anticholinergic or
adrenergic drug intoxication, anxiety disorders,
central nervous system (CNS) infections, heart
failure, hypertension, hypertensive encephalopathy, hyperthyroidism and thyrotoxicosis, malignant hyperthermia, panic disorder, pediatric atrial
ectopic tachycardia, pheochromocytoma, and
septic shock.
16.2.9 Prevention
Given the signicant mortality associated with
thyrotoxic storm, it would be benecial to prevent episodes completely or at least recognize
impending storm and treat it aggressively before
signicant systemic decompensation occurs. A
surgical storm has been virtually eliminated by
early treatment of thyrotoxic patients and adequate preoperative preparation. The potential for
an inter-current illness to precipitate storm in a
thyrotoxic patient needs to be recognized and
treated as well. Elective surgery should be postponed. If surgery is urgent, patients should be
properly prepared and watched closely for evidence of developing a thyroid storm.
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16 Thyroid andParathyroid Endocrine Emergencies
459
Thyroid storm following radioactive iodine
(RAI) therapy for hyperthyroidism may be
related to (1) withdrawal of anti-thyroid drugs
(ATDs) for RAI administration (usually withdrawn 5–7days before administration of RAI and
held until 5–7days after RAI therapy), (2) release
of large amounts of thyroid hormone from damaged follicles, and (3) RAI itself. Many endocrinologists believe that withdrawal of ATDs is the
cause of thyroid storm. One option is to stop
ATDs (including methimazole) only 3 days
(rather than 5–7days) before RAI therapy and to
restart ATDs 3 days after RAI administration
[33].
Testing thyroid function before operative procedures in children at high risk for hyperthyroidism (e.g. patients with McCune-Albright
syndrome) should also be considered.
16.2.10 Management Approach
It is crucial that proper treatment be instituted
promptly, without waiting for the results of serum
T4 and T3 levels [27]. In general, management is
mainly directed at blocking thyroid hormone
synthesis, secretion, and action on peripheral tissues. Supporting treatment to reverse decompensation of the normal homeostatic mechanisms,
with elimination of any known precipitating factor or concurrent illness, is essential. Patients
with thyrotoxic storm should be treated in an ICU
for close monitoring of vital signs and for access
to invasive monitoring and inotropic support, if
necessary.
The approach to treatment of thyroid storm
includes the following:
– Supportive measures.
– Thionamides (methimazole, carbimazole, and
propylthiouracil).
– Iodine preparations.
– Anti-adrenergic drugs.
– Glucocorticoids.
– Bile acid sequestrants to lower the low- density
level (LDL) cholesterol.
– Treatment of the underlying condition.
– Rarely, plasmapheresis.
Patients with contraindications to thionamides
need to be managed with supportive measures,
aggressive β-blockade, iodine preparations, glucocorticoids, and bile acid sequestrants for about
a week in preparation for a thyroidectomy.
Plasmapheresis may be attempted if other measures are not effective.
16.2.11 Medical Treatment
16.2.11.1 Anti-thyroid Drugs (ATDs)
The ATD propyl-thiouracil (PTU) is adminis-
tered orally to correct the hyperthyroid state by
blocking new hormone synthesis and reducing
the extra-thyroidal conversion of T4–T3. Propylthiouracil has also the advantage of early onset of
action as its effect begins within an hour of
administration. Burch and Wartofsky [27]
advised a loading dose of 600–1000-mg followed
by 200–250 mg every 4 h. A loading dose of
200mg followed by 200mg of PTU every 4h has
recently been reported to be equally effective [1].
Although methimazole (20 mg every 4–6 h)
decreases thyroid hormone synthesis, unlike PTU
it does not affect extra-thyroidal conversion of T4
or T3, and therefore is generally not recommended in the treatment of thyrotoxic storm.
However, a study by the taskforce committee of
the Japan Thyroid Association (JTA) and the
Japan Endocrine Society (JES) found evidence
that in severe thyrotoxic storm, T4-to-T3 conversion may have already been reduced. The taskforce also reported that disease severity and
mortality did not signicantly differ between thyroid storm patients in the study who were managed with methimazole or PTU [34]. In patients
with severe vomiting or in those who cannot tolerate oral medications, rectal administration can
be an alternative [35]. If the patient is in coma or
noncooperative, gavage via a naso-gastric tube
(NGT) is advised. Guidelines by the JTA/JES
(2016) recommended the use of IV methimazole
in severe cases of thyroid storm [34, 36].
In neonates, dosing of PTU for thyrotoxic
storm is 5–10 mg/kg/day (PO/NGT), divided
every 6–8h. In children, the recommended dose
is 15–20 mg/kg/day (PO/NGT), divided every
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460
M. Sakr
6–8 h (up to 40 mg/kg/has been used; not to
exceed 1200 mg/day). Recommendations for
methimazole dosing are variable; a suggested
starting dose is about one tenth of the PTU dose
given every 6–8h.
It is note-worthy that the US Food and Drug
Administration (FDA) has added a boxed warning, the strongest warning issued by the FDA, to
the prescribing information for PTU recommends
the following criteria be considered for prescribing PTU [37].
– Reserve PTU use for during rst trimester of
pregnancy or for patients who are allergic to
or intolerant of methimazole.
– Closely monitor patients undergoing PTU
therapy for signs and symptoms of liver injury,
particularly during the rst 6 months of
therapy.
– For suspected liver injury, promptly discon-
tinue PTU therapy and evaluate for evidence
of liver injury and provide supportive care.
– PTU should not be used in pediatric patients
unless the patient is allergic to or intolerant of
methimazole and no other treatment options
are available.
– Counsel patients to promptly contact their
health care provider for the following signs or
symptoms: fatigue, weakness, vague abdomi-
nal pain, loss of appetite, itching, easy bruis-
ing, or yellowing of the eyes or skin.
– If the patient is given PTU during treatment of
thyroid storm, this should be switched to
methimazole at the time of discharge unless
methimazole is contraindicated. If methima-
zole is contraindicated, alternative methods to
treat hyperthyroidism should be considered
after discharge, such as radioactive iodine or
surgery.
16.2.11.2 Inorganic Iodide (Iodine
Compounds)
Inorganic iodide is administered (PO/NGT) to
inhibit iodine pump, colloid proteolysis, and the
release of T4 and T3 from the thyroid gland. In
high dosage, iodine may reduce the synthesis of
thyroid hormone via the Wolff-Chaikoff effect
and its release via the Plummer effect [20]. Oral
dosages ranging between from 0.2–2 g/day are
recommended. It can be given as “Lugol’s solution” (eight drops/6–8h), or a saturated solution
of potassium iodide (SSKI) (ve drops/6 h). If
sodium iodide for intravenous (IV) use (sodium
ipodate or iopanoate) is available, it should be
infused slowly in a dosage of 0.5–1g/12h [38]. It
is particularly effective at preventing peripheral
conversion of T4–T3.
It is generally advised that iodine therapy not
be started until an effective blockade of new hormone synthesis has been established with ATDs
(approximately, 1h), because iodine alone will
lead to a further fortication of the thyrotoxic
state by enriching the thyroid hormone store [27].
It is also important that iodine should be administered for no longer than 4 or 5days, in order to
avoid further exaggeration of thyrotoxicosis [39].
Iodine preparations should be discontinued once
the acute phase resolves and the patient becomes
afebrile with normalization of cardiac and neurological status.
Dosing of SSKI (50mg iodide/drop) for thyrotoxic storm in neonates is 2 drops, PO/NGT,
every 6–8h, and in children, 2–5 drops, PO/NGT,
every 6 h. The dose of Lugol’s iodine (8 mg
iodine/drop) in children is 10 drops, PO/NGT,
every 8h.
16.2.11.3 Adrenergic Depletion
(Antiadrenergic Drugs)
Reserpine and guanethidine, either alone or in
combination with other modes of therapy, have
been successful in the treatment of thyrotoxic
storm to minimize sympathomimetic symptoms.
However, owing to hypotension and other untoward side effects, their use has been replaced by a
β-adrenergic receptor blocker such as propranolol, which also inhibits peripheral conversion of
T4–T3. The recommended dosage of propranolol
varies from 20 to 80mg orally (PO) or via NGT,
every 4–6h, and the dose adjusted based on heart
rate and blood pressure. For a more rapid effect,
propranolol may be given IV by slow push at an
initial dose of 0.5–1mg over 10min followed by
1–2mg over 10min every few hours and adjusted
based on vital signs along with continuous ECG
monitoring. In neonates, the recommended dose
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16 Thyroid andParathyroid Endocrine Emergencies
461
of propranolol is 2mg/kg/day (PO/NGT), divided
every 6–12h. In children, the recommended dose
is 0.5–4mg/kg/day (PO/NGT), divided every 6h
(not to exceed 60mg/day) or 0.01–0.02mg/kg IV
over 10min (may be repeated over 10min every
few hours to a maximum cumulative dose of
5mg).
Propranolol is, however, contraindicated in
patients with bronchial asthma, chronic
obstructive pulmonary disease (COPD),
peripheral vascular disease, or decompensated
heart failure. It should also be avoided in
patients with type-1 diabetes mellites (DM)
because it blocks the symptoms of hypoglycemia. On the other hand, severe bradycardia in
response to propranolol may be treated with
atropine, and bronchospasm or left ventricular
compromise may be treated with isoproterenol
[1]. Cardioselective β-blockers such as atenolol or metoprolol may be administered in
patients with reactive airway disease, and calcium channel blockers may be used when
β-blockers are contraindicated.
The ultrashort β-blocker “esmolol” has also
been reported to be successful in the perioperative management of thyrotoxic storm. A loading
dose of 250–500μg/kg over 1min, followed by a
continuous infusion of 50–100 μg/kg/min has
been recommended [40, 41]. Beta-blockers may
be discontinued once thyroid function
normalizes.
16.2.11.4 Bile Acid Sequestrants
Bile acid sequestrants prevent reabsorption of
free thyroid hormones in the gut (released from
conjugated thyroid hormone metabolites secreted
into bile through the entero-hepatic circulation).
A recommended dose is 4 g of cholestyramine
every 6h via a NGT.An alternative is 20–30g/
day of Colestipol-HCl [42].
16.2.11.5 Treatment ofSystemic
Decompensation—
Supporting Measures
In general, treatment of systemic decompensation includes reversal of hyperthermia, dehydration, congestive heart failure (CHF),
dysrhythmia, and prevention of adrenal crisis.
Hyperthermia should be aggressively treated
with antipyretics and peripheral cooling.
Acetaminophen (15 mg/kg orally or rectally
every 4h) is preferred to salicylates because the
latter increase free hormone levels by decreasing the binding to T4-binding globulin and
potentially could aggravate the thyroid storm
[27]. For peripheral cooling, alcohol sponges,
ice packs, and cooling blankets are frequently
used. It is important to prevent or decrease shivering during the rapid reduction in hyperthermia
with small doses of chlorpromazine and meperidine; the latter is used so as not to depress the
state of mentation [31].
To replace uid loss, a volume of 3–5L/day
may be required. A “CVP” catheter, pulmonary
wedge pressure monitoring, or both, is necessary to evaluate uid replacement carefully.
Dextrose solutions are the preferred intravenous
uids to cope with continuously high metabolic
demand.
Electrolytes, glucose, and vitamins, especially thiamine, are essential to replace possible deciency. Cardiovascular complications,
including atrial brillation and CHF, are treated
conventionally; however, larger doses of
digoxin may be required because of the more
rapid clearance in patients with marked hyperthyroidism. Serum digoxin levels should be
closely monitored, particularly with improvement of the thyroid storm and reduction of the
metabolic rate, to prevent digitalis intoxication
[1].
Hydrocortisone, given IV, 300 mg initially
followed by 100 mg/8 h, is administered to
decrease the extra-thyroidal conversion of T4–
T3, to prevent adrenal crisis because of relative
adrenal insufciency due to hyperthyroidism,
and to improve vasomotor symptoms.
Alternatively, dexamethasone can be given IV at
a dose of 1–2 mg every 6 h. In children, the
recommended dose of hydrocortisone for thyrotoxic storm is 5mg/kg (up to 100mg) IV every
6–8 h, while the dose of dexamethasone is
0.1–0.2 mg/kg/day, divided every 6–8 h.
Glucocorticoids should be weaned and stopped
and the dose of ATDs adjusted to maintain thyroid function in the normal range.
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M. Sakr
16.2.11.6 Treatment ofCo-existent
Illness
Because most patients in thyrotoxic storm have
fever and leukocytosis, an inammatory or infectious focus should be sought and bacterial cultures obtained. Nevertheless, prophylactic
antibiotics are not recommended [27]. Any coexistent hypoglycemia, hypercalcemia, or diabetic ketoacidosis (DKA) should be corrected,
and standard treatment for stroke or pulmonary
embolism should be instituted simultaneously
with the treatment of thyroid storm. It is reported
that 25–43% of patients with thyrotoxic storm
present with no known precipitating factor [22,
23, 27]. In the majority of patients, clinical
improvement is observed within 24h and complete recovery within a few days to a week. These
treatment modalities should be withdrawn gradually to prevent recurrent crisis, because the halflife of T4 is approximately 1week.
16.2.11.7 Plasmapheresis
Plasmapheresis is the removal, treatment, and
return or exchange of blood plasma or components thereof from and to the blood circulation. It
is thus an extra-corporeal therapy performed outside the body. Plasmapheresis removes cytokines,
antibodies, and thyroid hormones from [43]. It is
usually reserved for severe refractory cases of
thyroid storm as a bridge to surgery [44]. In 2004,
Petry etal. reported that, as a life-saving measure
in rare occasions, plasmapheresis can be used
effectively to treat thyrotoxic storm in adults [45].
16.2.12 Surgical Care—Denitive
Treatment
Patients with Graves’ disease who need urgent
treatment of hyperthyroidism but have absolute
contraindications to thionamides may be treated
acutely with β-blockers, I2 preparations, glucocorticoids, and bile acid sequestrants.
Plasmapheresis is sometimes used as a last resort
if other measures are not effective. Subsequently,
thyroidectomy may be performed after about
7 days of iodine administration. Iodine reduces
the vascularity of the gland and the risk for thy-
roid storm. Surgery provides a denitive treatment of thyrotoxicosis. Unless contraindicated,
β-blockade should be continued during the postoperative period.
In rare patients with hyperthyroidism, thyroid
artery embolization has been used as adjunctive
therapy [46–48]. In the case series reported by
Brzozowski etal. (2012), this method resulted in an
increase in thyroid hormone levels over the rst
3days following embolization followed by a subsequent reduction in levels, with normalization in
75% of patients (9/12) by 12weeks, but the majority did not achieve permanent remission [48]. More
recently, in 2016, Rohr et al. reported that in a
64-year-old gentleman in whom thyroid hormone
levels remained elevated and the patient remained
unstable despite steroids, ATD, β-blockers, and
plasmapheresis, thyroid artery embolization was
performed as the patient had contraindications to
RAI and surgery [47]. Thyroid hormone levels
increased over the rst 2–3 days, but decreased
from baseline after a week of the procedure. The
goal of embolization in this patient was to cause
atrophy, but not acute necrosis of the gland given
the risk of thyroid storm with the latter. Subsequently,
the patient’s clinical condition improved and underwent a successful thyroidectomy.
16.2.13 Summary ofGuidelines
In 2016, the Japan Thyroid Association (JTA)
and Japan Endocrine Society (JES) released
guidelines for the management of thyrotoxic
storm as follows [36]:
– A multimodality approach with ATDs, inor-
ganic iodide, corticosteroids, β-adrenergic
receptor antagonists, and antipyretic agents
should be used to ameliorate thyrotoxicosis
and its adverse effects on multiple organ
systems.
– ATDs, either methimazole or PTU, should be
administered for the treatment of hyperthy-
roidism in thyroid storm.
– Methimazole IV is recommended in severely
ill patients with consciousness disturbances or
impaired gastrointestinal tract function.
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16 Thyroid andParathyroid Endocrine Emergencies
463
– Inorganic iodide should be administered
simultaneously with ATDs to patients with
thyroid storm caused by thyrotoxic diseases
associated with hyperthyroidism.
– Corticosteroids (100mg/8h hydrocortisone or
8mg/day dexamethasone) should be administered to patients with thyroid storm regardless
of its origin.
– Aggressive cooling with acetaminophen and
mechanical cooling with cooling blankets or
ice packs should be performed for thyroid
storm patients with high fever.
– The focus of infection should be investigated
in patients with high fever and accompanying
infection should be treated.
– In addition to prompt treatment of thyrotoxi-
cosis, differential diagnosis and treatment of
acute disturbances of consciousness, psychosis, and convulsion in thyroid storm should be
done based on established psychiatric or neurological guidelines.
– Since thyrotoxicosis and dysfunction of mul-
tiple organs such as the liver and kidney can
affect pharmacokinetics in thyroid storm
patients, the condition of each patient should
be considered individually when selecting and
adjusting doses of psychotropic medications.
– β1-selective adrenergic receptor antagonists
should be the rst choice of treatment for
tachycardia in thyroid storm; other β1-selective
oral drugs are also recommended; although
the nonselective β-adrenergic receptor antagonist propranolol is not contraindicated, it is
not recommended for the treatment of tachycardia in thyroid storm.
– When atrial brillation occurs, digitalis is
used in patients without severe renal dysfunction (IV, at an initial dose of 0.125–0.25mg,
followed by an appropriate maintenance dose
with careful monitoring for signs and symptoms of digitalis toxicity); when hemodynamics are impaired rapidly because of atrial
brillation, cardio-version is recommended
when left atrial thrombus has been ruled out;
class Ia and Ic anti-arrythmics are recommended to maintain sinus rhythm after cardioversion (amiodarone may be considered for
patients with impaired left ventricular systolic
function).
– Anti-coagulation should be used for persistent
atrial brillation based on the CHADS2 (CHF,
hypertension, age ≥ 75, DM, stroke) score,
which has been used to evaluate the risk of
stroke onset.
– Gastrointestinal (GI) symptoms, including
diarrhea, nausea, and vomiting, are associated
with thyrotoxicosis, heart failure, neurologic
disorders, and GI infection; treatment for GI
infection should be performed in parallel with
that for thyrotoxicosis to improve GI
symptoms.
– Administration of large doses of corticoste-
roids, coagulopathy associated with thyroid
storm, and ICU stay with prolonged mechani-
cal ventilation may be risk factors for GI hem-
orrhage and mortality; acid-suppressive drugs
such as proton pump inhibitors or histamine-2
receptor antagonists are recommended for
patients in these instances.
– Hepatotoxicity with or without jaundice in
thyroid storm can be caused by hepatocyte
damage due to thyrotoxicosis, heart failure,
precipitating hepatic-biliary infection, or
drug-induced liver damage; patient prognosis
is worse when total bilirubin levels are
≥3.0mg/dL; differential diagnosis for the ori-
gin of hepatic dysfunction and appropriate
treatment based on its origin should be
performed, including therapeutic plasmapher-
esis for acute hepatic failure.
– ICU admission should be recommended for
all thyroid storm patients; patients with poten-
tially fatal conditions such as shock, dissemi-
nated intravascular coagulation (DIC), and
multiple organ failure (MOF) should immedi-
ately be admitted to the ICU.
– It is strongly recommended that patients with
APACHE II (Acute Physiologic Assessment
and Chronic Health Evaluation II) scores
above 9 be admitted to the ICU.
– DIC, which is often complicated with thyroid
storm, should be intensively treated because it
was shown to be associated with high mortal-
ity in the JTA nationwide surveys.
– The APACHE II score or Sequential Organ
Failure Assessment (SOFA) score can be
used for the prognostic prediction of thyroid
storm.
t.me/Dr_Mouayyad_AlbtousH
464
M. Sakr
– Care should be taken to prevent thyroid storm
in patients with poor adherence who are
undergoing antithyroid drug treatment.
– Denitive treatment of Graves’ disease, either
by RAI or thyroidectomy, should be considered to prevent recurrent thyroid storm in
patients successfully managed during the
acute stage of thyroid storm.
– When patients with high fever (≥38 °C),
marked tachycardia (≥130 bpm), and symptoms originating from multiple organ systems
such as the CNS, cardiovascular system, and
gastrointestinal tract present, it is important to
consider the possibility of thyroid storm.
16.2.14 Prognosis
Currently, the mortality rate of thyrotoxic storm
has currently fallen from 90 to 100% to about
20% due to early diagnosis of the condition and
better understanding and institution of appropriate management [22, 24]. Without early clinical
recognition and initiation of therapy, thyroid
storm carries 10–75% mortality in hospitalized
populations [27]. Death from thyrotoxic storm
may result from cardiac arrhythmia, CHF, hyperthermia, MOF, or other factors [42], though the
precipitating factor is often the cause of death.
With adequate thyroid-suppressive therapy
and sympathetic blockade, clinical improvement
should occur within 24 h. Adequate therapy
should resolve the thyrotoxic crisis within a
week. Treatment for adults has reduced mortality
to <20%. In one retrospective study from Japan
of 1324 patients who were diagnosed with thyroid storm, the overall mortality was 10% [49]. In
the same study, the following factors were associated with increased mortality risk in thyroid
storm, (1) age 60 years or older, (2) CNS dysfunction on admission, (3) lack of ATD and
β-blockade use, and (4) the need for mechanical
ventilation and plasma exchange along with
hemodialysis [49]. In addition, a study by Swee
et al. (2015) of 28 patients with thyroid storm
reported that CNS dysfunction of greater than
mild severity appeared to be a risk factor for mortality [50].
Using the National (Nationwide) Inpatient
Sample database, a recent study by Waqar etal.
(2021) indicated that in hospitalized patients with
thyroid storm, the in-hospital mortality rate is
higher in those with cardiovascular events than in
individuals without (3.5% vs. 0.2%, respectively). The cardiovascular events that were most
frequently associated with thyroid storm in hospitalized patients were arrhythmia (96.8%), acute
heart failure (14.2%), and ischemic events
(3.9%). Of patients with an ischemic event,
16.7% suffered in-hospital mortality, compared
with 3.6% and 3.2% of those with acute heart
failure or arrhythmia, respectively [51].
In 2020, a retrospective study by Bourcier
et al. of 31 French ICUs found that in ICU
patients with thyroid storm, MOF (as evaluated
using the SOFA score, absent the cardiovascular
component), and the occurrence, within 48h following ICU admission, of cardiogenic shock are
independent risk factors for mortality in the ICU
[52].
Burmeister (2019) reported a mortality rate of
38% in patients with thyroid storm–related coma,
including 70% between 1935 and 1977, and 11%
between 1978 and 2019. The investigator found
that there was a greater tendency for patients to
awaken from their coma when total and free T4
values, and possibly, the total T3 value, was
reduced. Moreover, the employment of ATDs,
corticosteroids, β-blockers, and intubation correlated positively with lower death rates. Although
plasmapheresis-related awakenings occurred in
67% of patients in which plasmapheresis was
used, the procedure was not linked to a reduction
in the death rate [53].
16.3 Myxedema Coma
16.3.1 Introduction
Myxedema coma is another endocrine (thyroid)
emergency that was described for the rst time at
the beginning of 1900, as the result of severe and
long-term untreated hypothyroidism. The term
“myxedema coma” refers to a state that represents the extreme degree of severe hypothyroid-
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16 Thyroid andParathyroid Endocrine Emergencies
465
ism. It is rare and is usually, but not exclusively,
encountered in elderly women during the winter
months. An approximate incidence of 0.22 cases/
million individuals/year is estimated [54, 55].
Most patients have long-standing untreated hypothyroidism or have discontinued thyroid hormone
replacement. Currently, clinical parameters and
thyroid prole have been developed for diagnosis
[56, 57]. Although the prognosis for myxedema
coma is markedly improved by adequate medical
treatment, it is still associated with a mortality
rate of about 20% [58].
16.3.2 Etiology
The pathogenesis of myxedema coma is not completely understood. Up to 95% of myxedema
coma cases occur in patients with primary hypothyroidism [59]. In the majority of cases, myxedema coma occurs in patients with
hypothyroidism after abandonment of treatment,
as well as in those under regular treatment in
whom some physiological stress situation would
trigger the event. Several precipitating factors
have been reported (Table 16.4) and include
infection/sepsis, trauma, withdrawal of thyroid
hormone, trauma (e.g., fractures) cerebrovascular
accident/stroke, myocardial infarction, heart failure, exposure to cold, gastrointestinal bleeding,
electrolyte imbalance, consumption of considerable amounts of “brassica” vegetable (a member
of a family that includes cabbage, cauliower,
broccoli, turnips, kale, rapeseed, and eld mustard), drugs especially amiodarone [60] and others such as diuretics, lithium carbonate, sedatives,
tranquilizers, narcotics, and anesthetics) [31,
59–64]. Decompensation of DM such as DKA
and hyperglycemic hyperosmolar state are less
frequent triggering factors. Other factors include
surgery [65] and labor [66].
16.3.3 Clinical Presentation
The main clinical features of myxedema coma
are hypothermia, progressive deterioration of the
level of consciousness, hypoventilation, hyponatremia, bradycardia, hypotension, and seizures.
Because patients often present in coma, it may be
difcult to know whether the patient has had a
stroke, has myxedema coma, or both.
16.3.3.1 Hypothermia
Hypothermia, with a temperature as low as
24–34 °C, is commonly encountered in myxedema coma and may precede its development. It
results from severe hypo-metabolism, adaptive
peripheral vasoconstriction, and relatively unopposed α-adrenergic stimulation by thyroid hormone [60]. Underlying hypoglycemia contributes
to, and concurrent infection may impede, the
development of hypothermia. It has been considered as a prognostic marker since a body temperature equal to or <32 °C is associated with
higher mortality.
Table 16.4 Triggering factors of myxedema coma
– Hypothyroidism
– Exposure to cold
– Congestive heart failure (CHF)
– Acute myocardial infarction
– Burns
– Trauma
– Stroke
– Sepsis or infections
– Metabolic disorders (acidosis, hypoglycemia,
hyponatremia, and hypercapnia)
– Medications
– Gastro-intestinal bleeding
– Anesthesia-/Surgery
– Labor
– Ingestion of brassica vegetable
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16.3.3.2 Neurological Alterations
Decreased CNS function is an important feature
of myxedema coma. Lethargy, stupor, confusion,
psychiatric symptoms, seizures, and status epilepticus may precede the coma. The causes of the
altered mental status and CNS decompensation in
patients with severe hypothyroidism include
hyponatremia, carbon dioxide (CO2) narcosis,
hypoxemia due to low cerebral perfusion [67],
hypoglycemia, postictal psychosis (PIP—an episode of psychosis occurring after a cluster of seizures), and co-existent sepsis or hypoadrenalism.
Administration of sedatives and tranquilizers may
further suppress the CNS because the clearance of
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