THYROID STORM

PRESENTED BY : AYA QATTOUSH

 Definition
 Epidemiology
 Etiology
 Pathophysiology
 Clinical Manifestations
 Diagnosis
 Medical Management
 Pharmacologic Management
 Nursing Management
 Case Report
 References
DEFINITION

 Thyroid storm always occurs as a complication of preexisting hyperthyroidism.

 Hyperthyroidism, also called thyrotoxicosis, occurs when the thyroid gland produces thyroid hormone in
excess of the body’s need

 The primary cause of hyperthyroidism is Graves disease, an autoimmune condition that affects 3% of
women and 0.5% of men in the United States.

 Thyroid storm, also called thyroid crisis, is a rare and life threatening exacerbation of hyperthyroidism.
 Stopping antithyroid medications and major stressors such as infection, surgery, trauma, pregnancy, or
critical illness can precipitate thyroid storm in any patient with preexisting hyperthyroidism. Mortality from
thyroid storm is reported at 10%
EPIDEMIOLOGY
Incidence

 Incidence of thyroid storm is not precisely known. Incidence in general population was reported as 0.57-0.76
per case per year in USA and 0.20 per lac per year in Japan, whereas incidence in hospitalized patients was
4.8-5.6 per case per year(Akamizu, 2018) .
 Hospital data suggest that it occurs in 1–2% of patients admitted for thyrotoxicosis . It occurs more commonly
in women and patients with Graves’ disease

Mortality

 Seventy-five percent of patients hospitalized with thyroid storm die ,Overall mortality rate has been reported to
be 10–20%.Multiple system dysfunction is the commonest cause of death, followed by heart failure ,
respiratory failure , and sepsis (Nai et al., 2018).
ETIOLOGY

 Although thyroid storm can develop in patients with longstanding untreated hyperthyroidism (Graves'
disease, toxic multinodular goiter, solitary toxic adenoma), it is often precipitated by an acute event such
as thyroid or nonthyroidal surgery, trauma, infection, an acute iodine load (including amiodarone use), or
parturition. In addition, irregular use or discontinuation of antithyroid drugs and poor access to health
care are commonly reported precipitants of thyroid storm
PATHOPHYSIOLOGY

 Thyroid hormone increases cellular oxygen consumption in almost all metabolically active cells. Excess
metabolism generates heat and critically high fever. Cellular oxygen demands are dramatically
increased with increased cardiac output to meet tissue demands. The oxygen demands in the
hypermetabolic state are so great that the cardiac system cannot compensate adequately. Hypertension
and tachycardia follow.

 Gastrointestinal peristalsis increases, resulting in diarrhea, nausea, and vomiting. These symptoms all
lead to dehydration and compound the problem of malnutrition and weight loss. Muscular weakness
occurs and is compounded by the excessive protein breakdown. Metabolic acidosis is a potential
problem.
CONT.’

 Hypersensitivity to the increased adrenergic-binding sites potentiates the cardiovascular and nervous
system responses to the hypermetabolic state. Atrial fibrillation is a common dysrhythmia in patients
with hyperthyroidism, and tachydysrhythmias should be anticipated in thyroid storm, especially in
patients with underlying heart disease.

 Pulmonary edema and acute heart failure also can occur. Increased beta-adrenergic activity manifests
as emotional lability, fine muscular tremors, agitation, and delirium
CLINICAL MANIFESTATIONS
DIAGNOSIS

 The diagnosis of thyroid storm is based upon the presence of severe and life-threatening symptoms
(hyperpyrexia, cardiovascular dysfunction, altered mentation) in a patient with biochemical evidence of
hyperthyroidism (elevation of free T4 and/or T3 and suppression of TSH).

 There are no universally accepted criteria or validated clinical tools for diagnosing thyroid storm. In
1993, Burch and Wartofsky introduced a scoring system using precise clinical criteria for the
identification of thyroid storm.

 A score of 45 or more is highly suggestive of thyroid storm, whereas a score below 25 makes thyroid
storm unlikely. A score of 25 to 44 is suggestive of impending storm. While this scoring system is likely
sensitive, it is not very specific. For example, a mildly hyperthyroid patient with influenza, a fever, and
nausea could score high enough to meet the criteria for storm.
CONT.
CONT.’

 Thyroid function tests – Thyroid function tests (TSH) should be assessed in all patients in whom there is
a clinical suspicion of thyroid storm (hyperpyrexia with temperature >103°F [39.4°C], goiter,
cardiovascular dysfunction, altered mentation, atrial fibrillation, history of antithyroid drug therapy for
hyperthyroidism, recent thyroid or nonthyroidal surgery, recent exposure to iodine-containing contrast). If
the TSH is below normal, free T4 and T3 should be measured. The degree of hyperthyroidism (elevation
of T4 and/or T3 and suppression of TSH) in patients with thyroid storm is, in general, comparable with
that in patients with uncomplicated overt hyperthyroidism. Thus, the degree of hyperthyroidism is not a
criterion for diagnosing thyroid storm.
CONT.

 Determining the etiology – Determining the etiology of thyrotoxicosis in patients with thyroid storm
should not delay prompt treatment of patients with clinical manifestations of thyroid storm.

 Most patients with thyroid storm have Graves' disease, and some have toxic adenoma or toxic
multinodular goiter. In a multicenter study from France, amiodarone use was the most common
precipitating factor (Bourcier et al., 2020).
 No laboratory test is available to differentiate thyroid storm from its predecessor, thyrotoxicosis, for
which the laboratory values may be similar. Thyroid storm is identified by a combination of the patient’s
medical history and exacerbation of clinical manifestations
MEDICAL MANAGEMENT

 The goal of acute medical management of thyroid storm is to reduce the clinical effects of thyroid
hormone as rapidly as possible. This includes preventing cardiac decompensation, reducing
hyperthermia, and fluid administration to reverse dehydration caused by fever or gastrointestinal losses.
In severe cases, surgical partial thyroidectomy, or therapeutic plasmapheresis (plasma exchange) is
used to rapidly reduce circulating thyroid hormone levels.
CONT.

Prevent Cardiovascular Collapse

 The body’s heightened sensitivity to the increased adrenergic and catecholamine receptors must be
suppressed. Atrial dysrhythmias need to be controlled, and progression of heart failure must be halted.
Beta-blockers are the mainstay of therapy for cardiac protection
CONT.

Reduce Hyperthermia

 Reduction in body temperature is achieved by use of a cooling blanket and the antipyretic agent
acetaminophen. Salicylates (aspirin) are contraindicated, because they inhibit protein binding of T3 to
T4, increasing the level of free, metabolically active thyroid hormone.
CONT.

Fluid Replacement

 Vigorous fluid replacement must be instituted to treat or prevent dehydration. Antibiotic therapy may be
warranted in the presence of systemic infection. Dehydration is treated with large volumes of glucose
and isotonic sodium solutions to replace circulating fluid and sodium losses from hypermetabolism
 CONT.

Plasmapheresis

 Plasmapheresis has been tried when traditional therapy has not been successful [37,51-55]. It is an
option for patients who cannot tolerate thionamides and in patients who are being prepared for urgent
thyroidectomy. Plasmapheresis removes cytokines, antibodies, and thyroid hormones from plasma. The
effects of plasmapheresis are transient, lasting 24 to 48 hours.
PHARMACOLOGICAL MANAGEMENT

 Pharmacologic treatment is essential in treatment of thyroid storm. A multimodal medication approach is

Medications That Block Catecholamine Effect

 Beta-adrenergic blocking agents are used to decrease the catecholamine effects of excessive thyroid
hormone .Beta-blockers have no effect on thyroid hormone but reduce the exaggerated myocardial
stimulation and slow the atrioventricular conduction rate. Therapeutic doses vary from patient to patient,
but higher doses are typically required for effective control of symptoms. Options include propranolol
(oral) or esmolol, a short acting IV beta-blocker. Nondihydropyridine calcium channel blockers
(verapamil, diltiazem) may be used to lower HR in patients who cannot take beta-blockers. However,
beta blockers always represent first-line emergency treatment.
CONT.

Medications That Block Thyroid Synthesis

 The synthesis of new thyroid hormone is blocked by the administration of antithyroid medications. Two
agents are frequently used: propylthiouracil (PTU) and methimazole. These medications are
administered by mouth or via a feeding tube. PTU is especially therapeutic, because it blocks thyroid
synthesis and blocks conversion of T4 to T3. Methimazole has a slower rate of action but is more potent
than PTU. Both medications act within 1 to 2 hours after absorption from the gastrointestinal tract.
These medications have no effect on previously released thyroid hormone
CONT.

Medications That Block Release of Thyroid Hormone

 Administration of inorganic iodine blocks the release of any preformed thyroxine that is already in the
thyroid gland but not yet released. It is essential that iodine therapy not be administered until adequate
inhibition of new hormone synthesis has occurred. The iodide preparations are rapid acting and have a
short duration. They are given approximately 1 hour after administration of the antithyroid medications to
prevent the iodide from being used for thyroid hormone production and possible worsening of the clinical
state.

 Some patients with thyroid storm have concomitant adrenal insufficiency and may be prescribed
hydrocortisone or dexamethasone during the initial stages of thyroid storm management.
CONT.
SUBSEQUENT MANAGEMENT

After there is evidence of clinical improvement (defervescence, resolution of central nervous system and
cardiovascular manifestations), some medications can be discontinued and others reduced.

 Iodine therapy can be discontinued (unless a thyroidectomy is planned in the next 10 to 14 days).

 Beta blockers can be withdrawn, but only after thyroid function tests have returned to normal.

 Glucocorticoids are tapered and discontinued. The pace of the glucocorticoid taper depends upon the clinical
course of the patient; a slower taper is necessary in patients who had a prolonged intensive care unit (ICU)
stay with longer duration of glucocorticoid treatment. Some patients may need testing of adrenal function prior
to discontinuing glucocorticoids.
CONT.

 Propylthiouracil (PTU), if given, should be switched to methimazole once the T3 is declining and hospital
discharge is anticipated. Methimazole is preferred because of its better safety profile and better
compliance rates. When switching to methimazole, the initial dose is generally high, 30 to 40 mg daily in
divided doses, depending on the patient's clinical status. The dose is then titrated down to maintain
euthyroidism. Monitoring, dosing, and duration of thionamide therapy are reviewed in detail separately.
NURSING MANAGEMENT

 Nursing management is directed toward safe administration and monitoring of the effects of prescribed
medications, normalizing body temperature, rehydration with correction of other metabolic
derangements, and patient education.
CONT.
Medication Administration

 The timely and ordered sequence of medication administration is essential in the management of thyroid
storm (see previous sections on pharmacologic management). The patient in thyroid storm is agitated,
anxious, and unable to rest and benefits from a calm environment. The effects of the antithyroid
medications, iodides, and beta-adrenergic blocking agents gradually decrease the neurologic symptoms
related to catecholamine sensitivity. HR should decrease with beta-blockade.

 The patient and family need to be reassured that this extreme agitation is the result of the disease
process and that the medications will help control the nonstop fidgeting and tremors. Frequent
reassurance and clear, simple explanations of the patient’s condition help decrease the fear brought on
by the onset of thyroid storm.
CONT.

Normalize Body Temperature

 In thyroid storm, the patient has hyperthermia related to a hypermetabolic state, as evidenced by a
critically high body temperature; diaphoresis; hot, flushed skin; intolerance to heat; tachycardia; and
tachypnea. Temperature is assessed frequently until normal body temperature is attained. Nursing
measures to provide comfort while the patient is intolerant to heat include a room with a cool
environment and a fan to circulate air and comfortable, nonrestrictive bedclothes. A tepid sponge bath
helps to reduce heat by evaporation, and cold-pack applications to the groin and axilla increase heat
loss at major blood vessels. If antipyretic medications are required, acetaminophen is the agent of
choice and salicylates are avoided.
CONT.

Rehydration and Correction of Metabolic Derangements

 Hyperthermia, tachypnea, diaphoresis, vomiting, and diarrhea predispose the patient to a fluid volume
deficit. Fluids and electrolytes are as vigorously replaced as the decompensated cardiovascular system
can tolerate. Glucose solutions are given to replace glycogen stores, which are depleted. Insulin is
administered to treat the hyperglycemia that results from mobilization of nutrients and glucocorticoids.
Hyponatremia from active loss (e.g., vomiting) is monitored by means of laboratory serum values.
Hyponatremia can be prevented or treated with isotonic IV fluid replacement. Additional nursing
measures focus on frequent hydration assessments
CONT.
CONT.
Patient and Family Education

 During the critical events surrounding the thyroid storm, the patient and family are given information according
to their emotional state and cognitive level of understanding. The cause of the high fever, anxiety, and cardiac
dysrhythmias is explained in understandable terms.

 The patient and family often are relieved to know that the agitation and nervousness result from circulating
hormones that may be decreased by taking daily medications

 Side effects of the specific medication therapy are taught before discharge. Patients treated with beta-
blockers are taught to report signs of bradycardia, unexplained fatigue, and orthostatic hypotension, among
other untoward effects. Patients discharged with antithyroid medications are alerted to the potential side effect
of agranulocytosis

 Symptoms of agranulocytosis include sudden cough, fever, rash, and inflammation. For management of
elevated temperature, patients are instructed to use acetaminophen rather than salicylates, because
salicylates increase the amount of free thyroid hormone in circulation.
CASE REPORT

 A 57-year-old male with a past medical history of generalized anxiety disorder presented to the ED with
a complaint of dyspnea and palpitations. Initial examination showed a heart rate of 193 bpm and a
temperature of 37.80 C. ECG revealed atrial fibrillation.

 Initially, he was administered Cardizem (diltiazem), but no change in heart rate was observed.
Laboratory examination revealed significantly low thyroid stimulating hormone (TSH) of 0.005 and free
T4 of 3.87, indicating thyrotoxicosis. Furthermore, increased free T3 levels were also observed (>20).

 Diltiazem drip was immediately stopped, and the case was discussed with the consultants of the
endocrinology department. Burch-Wartofsky Point Scale (BWPS) for thyrotoxicosis score was
calculated, which turned out to be greater than 45, indicating a TS. The patient was started on
methimazole and propranolol. Atrial fibrillation was persistent but was rate controlled. Warfarin was
started for anticoagulation.
CONT.

 Within six hours after the administration of methimazole and propranolol, the patient became
hypotensive, severely bradycardic, and went into cardiac arrest. After achieving a return of spontaneous
circulation via cardiopulmonary resuscitation (CPR) and defibrillation, a glucagon drip was administered
to reverse the effect of propranolol. Following an attempt with external transcutaneous pacing, a
transvenous pacer was inserted per electrophysiologist recommendations.

 The patient was started on vasopressors and was admitted to the ICU. X-ray of the chest revealed
severe cardiomegaly (Figure 1). CT scan of the chest showed bilateral pleural effusions and dilated
pulmonary artery, indicating pulmonary artery hypertension. A very low ejection fraction of 10% was
found on an echocardiogram. An intra-aortic balloon pump was placed, which was successfully removed
a few days later.
CONT.
CONT.

 The patient also tested positive for COVID-19 infection; however, neither remdesivir nor a monoclonal
antibody was given since COVID-19 was not thought to be the likely cause of his respiratory symptoms.
After that, a second echocardiography revealed an ejection fraction of 30%. The patient was
downgraded to the telemetry unit since his hemodynamics improved, and his T3 and T4 levels trended
down to 3.90 and 0.98, respectively.

 The patient again developed atrial fibrillation in the telemetry unit, and IV digoxin pushes were
administered. Warfarin was continued, and amiodarone was also started on a scheduled basis for
anticoagulation and rhythm control. He then subsequently shifted to a sinus rhythm followed by sinus
bradycardia. Additionally, he experienced encephalopathy while in the hospital. MRI and CT scans of the
brain did not identify any apparent abnormalities.
CONT.

 Cultures of blood and urine revealed no bacterial growth. Severe pharyngeal dysphagia diagnosed
during the videofluoroscopic swallow study (VFSS) was documented by speech therapy. The patient
received antibiotic treatment for potential aspiration pneumonia. The patient's mentation eventually
returned to baseline during the hospital stay. Due to occasional bradycardia throughout his hospital stay,
beta-blockers were not prescribed. He was discharged on losartan and aspirin for his cardiomyopathy
and methimazole for thyrotoxicosis. Moreover, he was deemed not a candidate for a life vest on
discharge because of his significant deconditioning, and rather close cardiology follow-up on out-patient
was advised.
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