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Badai Tiroid
Binod Pokhrel; Wajeeha Aiman; Kamal Bhusal.

Informasi dan Afiliasi Penulis

Pembaruan Terakhir: 6 Oktober 2022.

Kegiatan Pendidikan Berkelanjutan

Badai tiroid, juga dikenal sebagai krisis tirotoksik, adalah komplikasi akut yang mengancam jiwa
dari hipertiroidisme yang muncul dengan keterlibatan multi-sistem. Terlepas dari kemajuan
modern dalam pengobatan dan tindakan pendukungnya, kematian yang terkait dengan badai
tiroid diperkirakan 8 hingga 25%. Oleh karena itu, sangat penting untuk mengenalinya sejak dini
dan memulai pengobatan agresif untuk mengurangi kematian. Kegiatan ini meninjau alat yang
tersedia untuk membantu diagnosis dan pengelolaan badai tiroid dan menyoroti peran tim
interprofesional dalam merawat pasien yang terkena.

Tujuan:

Tentukan etiologi badai tiroid.

Menilai potensi komplikasi badai tiroid.

Evaluasi pilihan pengobatan yang tersedia untuk badai tiroid.

Komunikasikan pentingnya pendekatan tim interprofesional yang terkoordinasi dengan

baik saat mengelola pasien yang mengalami badai tiroid.

Akses pertanyaan pilihan ganda gratis tentang topik ini.

Perkenalan
Badai tiroid, juga dikenal sebagai krisis tirotoksik, adalah komplikasi hipertiroidisme yang akut
dan mengancam jiwa. Ini adalah presentasi tirotoksikosis yang berlebihan, dan disertai dengan
keterlibatan multisistem yang tiba-tiba. Kematian yang terkait dengan badai tiroid diperkirakan 8
hingga 25% meskipun ada kemajuan modern dalam pengobatan dan tindakan pendukungnya. [1]
Oleh karena itu, sangat penting untuk mengenalinya sejak dini dan memulai pengobatan agresif
untuk mengurangi kematian. Diagnosis badai tiroid bersifat klinis.

Etiologi
Faktor pemicu yang ditumpangkan menyebabkan badai tiroid pada pasien dengan
hipertiroidisme yang didiagnosis atau tidak terdiagnosis. Ini lebih sering terjadi dengan penyakit
Graves tetapi dapat terjadi dengan etiologi hipertiroidisme lainnya, seperti gondok multinodular
beracun dan adenoma tiroid beracun. [2] Faktor pemicunya adalah:

Penghentian obat antitiroid secara tiba-tiba

Operasi tiroid

Operasi non-tiroid
 Trauma

Penyakit akut seperti infeksi, termasuk COVID-19, ketoasidosis diabetik, infark miokard
akut, kecelakaan kardiovaskular, gagal jantung, dan reaksi obat[3]

Persalinan

Penggunaan media kontras beryodium baru-baru ini

Terapi radioiodium (jarang)

Luka bakar

Stroke atau cedera otak traumatis[4]

Efek samping obat, misalnya, amiodarone, anestesi, salisilat[5]

Hyperemesis gravidarum pada kehamilan[6]

Epidemiologi
Ini adalah presentasi hipertiroidisme yang langka. Badai tiroid menyumbang sekitar 1% hingga
2% dari penerimaan hipertiroidisme. Sesuai survei Amerika Serikat, insiden badai berkisar antara
0,57 hingga 0,76 kasus per 100.000 per tahun pada populasi normal dan 4,8 hingga 5,6 kasus per
100.000 per tahun pada pasien yang dirawat di rumah sakit. [7]

Per the Japanese National Survey, the incidence of thyroid storms was 0.2 per 100,000 people per
year, about 0.22% of all thyrotoxicosis patients and 5.4% of hospitalized thyrotoxicosis patients.
The average age of people with thyroid storm was 42 to 43 years, similar to those with
thyrotoxicosis without thyroid storm. The male-to-female ratio for the incidence of thyroid
storms was about 1:3, similar to that of thyrotoxicosis without storm groups.[8]

Pathophysiology
The pathophysiological basis for the precipitation of thyroid storms in patients with
thyrotoxicosis is unclear. But, as mentioned above, a precipitating factor is always required to
cause a thyroid storm. Several hypotheses have been proposed. One theory suggests the
incidence of thyroid storm is due to the rapid increase in thyroid hormone levels rather than the
absolute hormone level that occurs during thyroid surgery, following radioactive iodine
treatment, after sudden discontinuation of the antithyroid drug, or after administration of the
large dose of iodine in contrast studies. The hyperactivity of the sympathetic nervous system with
increased response to catecholamine and an increased cellular response to thyroid hormone
during acute stress or infections, causing cytokines release and altered immunological
disturbances, are other possible mechanisms of thyroid storm. Most studies have failed to relate
higher thyroid hormone levels as a cause of thyroid storm, except for the study by Brooks and
others, which reported higher free thyroid hormone among the patients with thyroid storm.[9] In
other words, the degree of thyroid hormone level is not directly related to a higher incidence of
thyroid storm.[2]

The clinical features are due to the exaggerated effects of the thyroid hormone. There is an
intense metabolic activity that increases oxygen requirements. The resulting tachycardia to meet
the oxygen requirements can induce heart failure and predispose the patient to arrhythmias.
Similarly, CNS symptoms include irritability, seizures, delirium, and eventually coma.
Histopathology
Histopathology depends on the cause of the thyroid storm. The most common cause of Graves
disease is diffuse follicular hyperplasia, along with increased thyroid receptor antibodies and
increased vascularization of the tissue. If it is a tumor-originated storm, malignant cells infiltrate
and destroy the thyroid tissue and rupture the follicles.[10][11]

Toxicokinetics
Toxicokinetics includes the following precipitating factors:

Severe emotional distress

Stroke

Exercise

Pulmonary embolism

History and Physical

Presentation of thyroid storm is an exaggerated manifestation of hyperthyroidism, with the
presence of an acute precipitating factor. Fever, cardiovascular involvement (including
tachycardia, heart failure, arrhythmia), central nervous system (CNS) manifestations, and
gastrointestinal symptoms are common. Fever of 104° F to 106°F with diaphoresis is a key
presenting feature. Cardiovascular manifestations include tachycardia of more than 140
HR/minute, heart failure with pulmonary and peripheral edema, hypotension, arrhythmia, and
death from cardiac arrest. CNS involvement includes agitation, delirium, anxiety, psychosis, or
coma. Gastrointestinal (GI) symptoms include nausea, vomiting, diarrhea, abdominal pain,
intestinal obstruction, and acute hepatic failure.[12] A Japanese study found CNS involvement to
be a poor prognostic factor for increased mortality.[8] Physical examination findings may include
high temperature, tachycardia, orbitopathy, goiter, hand tremors, moist and warm skin,
hyperreflexia, systolic hypertension, and jaundice.

Evaluation
The diagnosis of thyroid storm needs clinical suspicion based on the presentation mentioned
above in a patient with hyperthyroidism or suspected hyperthyroidism. One should not wait for
lab results before starting treatment. Thyroid function tests can be obtained, which usually show
high FT4/FT3 and low TSH. It is not necessary to have a very high level of thyroid hormone to
cause a thyroid storm. Other lab abnormalities may include hypercalcemia, hyperglycemia (due
to inhibition of insulin release and increased glycogenolysis), abnormal LFTs, and high or low
white blood cell (WBC) count.

Burch-Wartofsky Point Scale (BWPS) [2]

In 1993, the following scoring system for the diagnosis of thyroid storm was introduced:

Temperature: 5 points per 1 F above 99 F (maximum 30 points)

CNS dysfunction: 10 points for mild (agitation), 20 for moderate (delirium, psychosis, or
extreme lethargy), and 30 for severe (seizure or coma)
 Tachycardia: 5 (99-109), 10 (110 -119), 15 (120 -129), 20 (130 -139) and 25 (greater than
140)

Presence of atrial fibrillation:10

Heart failure: 5 for mild (pedal edema), 10 for moderate (bi-basilar rales), 15 for severe
(pulmonary edema)

GI dysfunction: 10 for moderate (diarrhea, nausea/vomiting, or abdominal pain) and 20 for

severe (unexplained jaundice)

Presence of Precipitating factor: 10 points

Diagnosis: A score of more than 45 highly suggests thyroid storm, 25 to 44 supports the
diagnosis, and less than 25 makes the diagnosis unlikely.

The Japanese Thyroid Association (JTA)

This is a different scoring system based on similar clinical findings.[8] Thyrotoxicosis (elevated
FT3 and/or FT4) is a prerequisite, and it requires various combinations of the following
symptoms:

CNS manifestation (restlessness, delirium, psychosis/mental aberration,

lethargy/somnolence, coma)

Fever (38 C/100.4 F or greater)

Tachycardia (130/min or higher)

CHF (pulmonary edema, rales, cardiogenic shock, or NYHA class IV)

GI/Hepatic Manifestation (Nausea, vomiting, diarrhea, total Bilirubin 3 mg/dl or more

Diagnosis

Definite Thyroid Storm (TS1): Thyrotoxicosis (elevated FT3 and/or FT4) plus

At least 1 CNS manifestation plus 1 or more other symptoms (fever, tachycardia, CHF,
GI/Hepatic) ‘OR’ A combination of at least 3 features among fever, GI/Hepatic, CHF, or
tachycardia

Suspected Thyroid Storm (TS2): Thyrotoxicosis (elevated FT3 and/or FT4) plus

A combination of at least 2 features among tachycardia, CHF, GI/Hepatic, Fever ‘OR’ A

patient with h/o thyroid disease, presence of goiter and exophthalmos who meets criteria
for TS1 but TFTs not available

These scoring systems are just guidelines. The actual diagnosis is based on clinical judgment.
Based on the BWPS scoring system, a score of 45 or more is more sensitive but less specific than
JTA scoring systems TS1 or TS2 to detect thyroid storm cases. A BWPS score of 25 to 45 may
suggest an impending storm. A chest X-ray may help assess heart failure, and a head CT may
help exclude a neurological cause in some patients. An ECG is often done to monitor for
arrhythmias.

Treatment / Management
Treatment of thyroid storm consists of supportive measures like intravenous (IV) fluids, oxygen,
cooling blankets, acetaminophen, and specific measures to treat hyperthyroidism. If any
precipitating factors, for example, infection, are present, that needs to be addressed. Patients with
thyroid storm must be admitted to the intensive care unit with close cardiac monitoring and
ventilatory support if needed.[1][13]

Specific Strategic Steps for Treatment

1. Therapy to control increased adrenergic tone: Beta-blocker

2. Therapy to reduce thyroid hormone synthesis: Thionamide

3. Therapy to reduce the release of thyroid hormone: Iodine solution

4. Therapy to block peripheral conversion of T4 to T3: Iodinated radiocontrast agent,

glucocorticoid, PTU, propranolol

5. Therapy to reduce enterohepatic recycling of thyroid hormone: Bile acid sequestrant

After initial supportive measures, a beta-blocker should be started for any case of a suspected
thyroid storm. Typically, propranolol 40 mg to 80 mg is given every 4 to 6 hours. Then, a loading
dose of propylthiouracil (PTU) 500 mg to 1000 mg followed by 250 mg every 4 hours or
Methimazole (MMI) 20 mg every 4 to 6 hours should be given. Propylthiouracil is favored
because it has a small additional effect blocking the peripheral conversion of T4 to T3. An hour
after administering propylthiouracil or methimazole, give 5 drops of SSKI (supersaturated
potassium iodide) by mouth every 6 hours. Always administer thionamide before starting iodine
solution (SSKI) therapy.[14][15][16] This prevents the imminent increase in thyroid hormone
synthesis due to increased iodine load from super saturated potassium iodide. Hydrocortisone
100 mg IV every 8 hours (or dexamethasone 2 mg every 6 hours) should also be started. Oral
cholestyramine 4 grams 4 times daily can be started for severe cases if available. One should
look for precipitating factors and treat them accordingly. Aspirin should be avoided due to its
potential risk of increasing free thyroid hormone levels by interfering with thyroid-binding
protein.

In the first 24 hours of treatment, propylthiouracil decreases the T3 level by 45%, but
methimazole drops the T3 level by only 10 % to 15%. Methimazole causes more rapid
normalization of serum T3 levels after a few weeks of treatment, and it has less hepatotoxicity
compared to propylthiouracil. Therefore, after initial stabilization, we should treat
with methimazole, and if propylthiouracil was started at the beginning, it should be changed
to methimazole later. For patients who cannot take oral antithyroid medicine, liquid preparation
(pharmacist may have to compound) can be given as enemas. Sometimes, pharmacists can
prepare an IV form of antithyroid medicine by dissolving the tablet.[17][18][19]

Esmolol, a short-acting beta-blocker, can be given in an ICU setting at a loading dose of 250
mcg/kg to 500 mcg/kg followed by 50 mcg/kg to -100 mcg/kg/minute. Cardiovascular beta-
blockers like atenolol or metoprolol should be chosen for patients with reactive airway disease. If
there is a contraindication for using beta-blockers, diltiazem is an alternative. If thionamide
therapy is contraindicated because of an allergic reaction, thyroidectomy is needed after
treatment with a beta-blocker, hydrocortisone, cholestyramine, and iodine solution.
Plasmapheresis is the last resort if all other measures fail.
Once patients’ clinical conditions improve, the iodine solution should be stopped, glucocorticoids
can be tapered and stopped, and beta-blockers should be adjusted. Thionamide therapy should be
titrated, and if propylthiouracil is used initially, it should be switched to methimazole. Patients
should be recommended for definitive treatment with radioiodine (RAI) therapy or
thyroidectomy. Surgery may be required in patients with Graves disease to treat hyperthyroidism.
These patients must be pretreated with beta-blockers, glucocorticoids, and iodine formulas.
Surgery is usually done after 5 to 7 days. As recently reported, therapeutic plasma exchange is
potentially helpful in resistant cases that do not respond to conventional treatments.[20][17]

Differential Diagnosis
Thyroid storm should be differentiated from other diseases with similar symptoms and signs.
[21] Fever is the most common presentation of multiple conditions; therefore, it can be
misdiagnosed. The differential diagnoses include:

Sepsis

Infection

Psychosis

Cocaine use

Pheochromocytoma

Neuroleptic malignant syndrome

Hyperthermia

Surgical Oncology
If toxic adenoma or multinodular goiter is causing this disease, then surgical resection and
radioactive iodine ablation are the mainstays of treatment. Thyroidectomy is preferred if a patient
has compressive symptoms. Patients who refuse ablation or have contraindications to surgery can
be treated with long-term antithyroid medicines.[22] Grave's disease with intrathoracic mass
causes severe compressive symptoms, and thyroidectomy is preferred in these cases.
Thyroidectomy has other adverse effects, like recurrent laryngeal nerve damage and
hypoparathyroidism.[23][24]

Radiation Oncology
Radioiodine-131 (I) therapy is helpful in hyperfunctioning nodules, but the risk of
hypothyroidism is 60% after a 20-year follow-up in a retrospective study.[25] Other factors
increasing the risk of hypothyroidism in these patients are:

Methimazole therapy

Age

Pertinent Studies and Ongoing Trials

Randomized trials are still being processed to determine the efficacy and safety of more
medicines.[24]
Toxicity and Adverse Effect Management
Complete surgical resection of the thyroid and radioiodine ablation can cause hypothyroidism.
So, these patients need lifetime exogenous thyroxine therapy and should be monitored for
hyperthyroidism. Dose adjustments by endocrinologists are crucial as the patient is at risk of both
hypothyroidism and hyperthyroidism.[26] Antithyroid drugs, MMI, and PTU cause
agranulocytosis. Patients on these drugs should be monitored with CBC, especially white cell
count. If the white cell count starts decreasing, these drugs should be discontinued due to the
increased risk of infection.[27] Other toxicities can cause hepatic failure, cholestasis, rash,
gastrointestinal toxicity, and musculoskeletal pains.[28][29]

Prognosis
A thyroid storm is a true medical emergency that is fatal if left untreated. The cause of death may
be heart failure, arrhythmias, or multiple organ failure. However, with treatment, most patients
see an improvement within 24 hours. Risk factors for poor prognosis include:

Advanced age

Neurological deficits on admission[12]

Failure to use beta-blockers and antithyroid medications

Need for dialysis and/or mechanical ventilation

Complications
If left untreated, thyroid storm can lead to the following complications:

Arrhythmias

High-output cardiac failure

Seizures, delirium, coma

Elevated liver enzymes, jaundice

Abdominal cramps, vomiting, diarrhea

Atrial fibrillation and thromboembolism[30]

Deterrence and Patient Education

Patients with hyperthyroidism should be educated about the warning symptoms of thyroid storm,
a serious but rare emergency. It is a dangerous disease, but early diagnosis and prompt treatment
can improve the condition. Hyperthyroid patients should not delay visiting the emergency
department after experiencing any symptoms. After the first crisis, non-compliant behaviors
should be addressed, and treatment benefits and complications should be described.[31]

Pearls and Other Issues

There are multiple factors responsible for delayed diagnosis and treatment of this emergency
condition:

Unavailability of skilled thyroid surgeons

 Lack of suitable nuclear medicine units

Lack of patient education

Lack of internal physician communication

Enhancing Healthcare Team Outcomes

A thyroid storm is a rare, life-threatening medical emergency that is difficult to diagnose. Thus,
an interprofessional healthcare team that includes an intensivist, cardiologist, endocrinologist,
internist, emergency department physician, and infectious disease expert is recommended. These
patients are best managed in the ICU and monitored by ICU nurses. Nurses must be fully aware
of the potential complications and notify the physician if there is any change in the hemodynamic
status. Pharmacists can also weigh in to see if the patient takes thyrotoxic medications. The
situation requires open communication channels between all professionals to bring about the best
possible outcome.

Treating thyroid storms involves supportive measures like intravenous (IV) fluids, oxygen,
cooling blankets, acetaminophen, and specific measures to treat hyperthyroidism. If any
precipitating factors, for example, an infection, are present, they must be taken care of first.
Patients with thyroid storm must be admitted to the intensive care unit with close cardiac
monitoring and ventilatory support as needed.[1][13]

The pharmacist may need to prepare a special formula of iodine that can be administered
intravenously. Radiocontrast dyes may help some patients. In some cases, plasmapheresis may be
life-saving. The nephrologist/hematologist must be involved early in caring for these patients and
anticipate plasmapheresis needs. The team must communicate to avoid the high mortality of
thyroid storms. The outlook for patients with thyroid storm is guarded. It depends on the patient's
age, the number of organs involved, comorbidities, need for mechanical ventilation, renal failure,
and response to treatment.[32][33]

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Disclosure: Binod Pokhrel declares no relevant financial relationships with ineligible companies.

Disclosure: Wajeeha Aiman declares no relevant financial relationships with ineligible companies.

Disclosure: Kamal Bhusal declares no relevant financial relationships with ineligible companies.

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