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Thyroid Storm Nursing Diagnosis and Nursing Care Plan

Last updated on August 16th, 2022 at 07:33 am

Thyroid Storm Nursing Care Plans Diagnosis and Interventions

Thyroid Storm NCLEX Review and Nursing Care Plans

Thyroid storm is a life-threatening medical emergency associated with exacerbated clinical manifestations of thyrotoxicosis. Thyroid storm is also called other names such as hyperthyroid crisis, thyroid crisis, and thyrotoxic crisis.

It is a rare condition that has become even less common due to improved treatments for hyperthyroidism. Thyroid storm may be difficult to diagnose due to its multi-system involvement.

However, early diagnosis and treatment are keys in reducing the mortality and morbidity associated with this serious condition.

The thyroid is a small gland found in the lower neck. It is mainly responsible for the production of two hormones that help regulate important body processes including the respiratory and heart rate.

Overactivity of this gland leads to a cascade of signs and symptoms which can further cause medical issues, including thyroid storm.

Signs and Symptoms of Thyroid Storm

Thyroid storm involves many organs in the body. It has similarities to the clinical manifestations of hyperactive thyroid, only more severe.

This is the reason why people experiencing thyroid storm may be too unwell to call for help on their own. The following are the signs and symptoms of thyroid storm:

• Severe tachycardia – heart rate may exceed 140 beats per minute
• Cardiac arrhythmias, particularly atrial fibrillation
• Profuse sweating
• Shaking or jittery behavior
• Restlessness
• Unconsciousness
• High blood pressure

Causes of Thyroid Storm

Thyroid storm stems out of thyrotoxicosis which is a condition that occurs due to high levels of circulating thyroid hormones. Of all forms of thyrotoxicosis, Grave’s disease is the lead cause of thyroid storm.

In general, thyroid storm is precipitated by three main reasons:

• Untreated hyperthyroidism
• Undertreated hyperthyroidism
• Acute illness
• Acute psychosis
• Post thyroidectomy
• Sudden discontinuation of antithyroid drugs
• Post administration of iodinated radiographic contrast
• Surgery (Thyroid and non-thyroid surgery)
• Diabetic ketoacidosis
• Pulmonary embolism
• Myocardial infarction
• Side effects from medications such as anesthetics and salicylates

Complications of Thyroid Storm

The mortality rate associated with thyroid storm is between 8 to 25 % of cases. Therefore, it is important that early diagnosis and treatment are made. Other complications are also known to be linked with thyroid storm and they are as follows:

• Arrhythmias
• High output cardiac failure
• Elevated liver enzymes
• Abdominal cramps, vomiting, and diarrhea
• Atrial fibrillation
• Thromboembolism

Diagnosis of Thyroid Storm

The diagnosis of thyroid storm is highly based on clinical assessment. It may also be more difficult to diagnose compared to other conditions due to its multisystem involvement. When thyroid storm is suspected, early treatment is necessary to reduce mortality and other serious complications.

• Physical assessment and medical history taking – these two processes are important in the diagnosis of thyroid storm. The basic parameters such as the vital signs and the presence of signs and symptoms will be evaluated and reviewed by the physician.
• Laboratory tests – blood tests including the measurement of thyroid stimulating hormone (TSH) will be taken. It may be expected to get a normal to below normal TSH level in people with thyroid storm. The levels of T3 and T4 will also be measured and will be expected to be higher than normal.
• Hyperthyroidism
• Grave’s Disease
• Atrial Fibrillation
• Hypoglycemic Attack
• Cardiovascular Accident
• Sympathomimetic toxicity

Treatment for Thyroid Storm

In the management of thyroid storm, treatment may begin prior to the arrival of test results. This is because of its associated mortality rate and serious complications. The main goals of the treatment for thyroid storm are the following:

• To block the production of thyroid hormones
• To block the sympathetic flow
• To block the conversion of T4 to T3

Several methods are found helpful in the management of thyroid storm:

• Thionamides – these are antithyroid medications commonly used in people with Grave’s disease. They facilitate the body to achieve a “euthyroid” state usually before undergoing a radioiodine therapy.
• Iodine compounds – iodine solutions may also be prescribed for people with thyroid storm. Iodine helps reduce the synthesis of thyroid hormones.
• Beta-blockers – these drugs are also used in the treatment of thyroid storm. Aside from their effect on the moderation of blood pressure, they also block the peripheral conversion of T4 to its active form.
• Steroids – similar to beta-blockers, steroids are also known to prevent the peripheral conversion of T4 to active form.
• Administration of muscle relaxants for muscular spasms
• Use of cooling blankets and medications for hyperthermia
• Administration of intravenous fluids and electrolytes for dehydration

Thyroid Storm Nursing Diagnosis

Thyroid storm nursing care plan 1.

Nursing Diagnosis: Hyperthermia related to thyroid storm secondary to post thyroidectomy as evidenced by body temperature of 40 degrees Celsius, rapid and shallow breathing, racing heart rate, flushed skin, and profuse sweating

        Desired Outcome: Within 4 hours of nursing interventions, the patient will have a stabilized temperature within the normal range.

Thyroid Storm Nursing Care Plan 2

Nursing Diagnosis: Hypertension related to increased cardiac output secondary to thyroid storm as evidenced by elevated blood pressure levels, persistent heart rate of >140 bpm, and cardiac arrythmias

Desired Outcome: The patient’s vital signs will be within normal range and the cardiac output will stabilize. 

Thyroid Storm Nursing Care Plan 3

Nursing Diagnosis: Deficient Knowledge related to new diagnosis of thyroid storm as evidenced by patient’s verbalization of “I want to know more about my new diagnosis and care”

Desired Outcome: At the end of the health teaching session, the patient will be able to demonstrate sufficient knowledge of thyroid storm and its management.

Thyroid Storm Nursing Care Plan 4

Nursing Diagnosis: Fatigue related to hypermetabolic state due to increased energy demand, as evidenced by overwhelming lack of energy, verbalization of tiredness, generalized weakness, irritability, and jittery behavior

Desired Outcome: The patient will demonstration active participation in necessary and desired activities and demonstrate increase in activity levels.

More Thyroid Storm Nursing Diagnosis

• Acute Confusion
• Risk for Disturbed Thought Processes

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020).  Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018).  Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020).  Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier.  Buy on Amazon

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This information is intended to be nursing education and should not be used as a substitute for professional diagnosis and treatment.

Anna Curran. RN, BSN, PHN

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Internet Book of Critical Care (IBCC)

Online Medical Education on Emergency Department (ED) Critical Care, Trauma, and Resuscitation

Thyroid Storm

April 4, 2023 by Josh Farkas

• Rapid Reference 🚀
• Approaching the diagnosis
• Diagnostic criteria
• Evaluation & treatment of any trigger
• Endocrine manipulations
• Cardiovascular stabilization
• Atrial fibrillation in thyroid storm
• Management of hyperthermia & agitation
• Refractory thyroid storm
• Questions & discussion

(back to contents)

evaluation 📖

• Glucose, electrolytes including Ca/Mg/Phos, complete blood count.
• TSH, free T4, free T3.
• Liver function tests.
• Creatinine kinase.
• Coagulation studies including DIC screen (INR, PTT, fibrinogen).
• If infection suspected: blood cultures, chest X-ray, possibly CT scan.

core initial therapies for thyroid storm

• Hydrocortisone 300 mg IV loading dose, then 100 mg IV q8.
• (If hydrocortisone unavailable: 125 mg IV methylprednisolone.)
• Thionamide : Methimazole 40 mg loading dose, then 20 mg q4hr.
• Lugol’s solution 8 drops (0.4 ml) PO q6.
• Saturated Solution of KI (SSKI) 5 drops (0.25 ml) PO q6.
• Cholestyramine 4 grams PO q6hr.
• Acetaminophen 650-1000 mg scheduled q6hr. 📖
• If infection suspected, start empiric antibiotic. 📖
• If >41 C, emergent temperature control. 📖

⚠️ exercise caution with beta-blockers 📖

• Some patients develop severe cardiomyopathy, with reduced ejection fraction. In this context, beta-blockade may cause hemodynamic collapse .
• Initial stabilization may involve fluid resuscitation and vasopressor support.
• Unless the heart rate is extremely rapid (>>150 b/m), slowing down the heart rate is unlikely to improve stability. Over-aggressive suppression of the heart rate may be dangerous initially, before the thyroid storm abates.

Thyroid storm is the most severe form of hyperthyroidism, wherein organ failure begins to occur. If left untreated, this may lead to multi-organ failure and death. Due to the rarity of this condition and its multitude of diverse presentations, diagnosis can be extremely challenging.

some cognitive triggers to consider thyroid storm

• Thyroid storm is very rare, so the main challenge is considering it. The possibility should be entertained in the following situations:
• (1) Patient with known hyperthyroidism plus any acute illness/deterioration.
• (2) New-onset atrial fibrillation and/or dilated cardiomyopathy.
• (3) New-onset delirium/psychosis plus abnormal vital signs (fever, tachycardia).
• (4) Hyperthermia (temperature above ~40C).
• (5) Septic-appearing patient without any focus of infection (i.e. distributive shock of unknown origin).

underlying etiology of hyperthyroidism in one series ( 31714398 )

• Amiodarone-induced thyroiditis (33%).
• Graves' disease (26%).
• Toxic solitary adenoma (6%).
• Toxic multinodular goiter (9%).
• Autoimmune thyroiditis (10%).

trigger of thyroid storm

• #1 = Infection.
• Surgery or trauma (especially trauma involving the neck, such as strangulation).
• Pulmonary embolism, myocardial infarction, stroke.
• Labor, preeclampsia.
• Diabetic ketoacidosis, hypoglycemia.
• Thyroid surgery.
• Radioiodine therapy.
• Noncompliance with anti-thyroid medications.
• Overdose of thyroid hormone.
• ☢️ Acute iodine load from contrast dye. ( 30299273 )
• Checkpoint inhibitors 📖 .
• Tyrosine kinase inhibitors (e.g., sorafenib).
• Aspirin intoxication (may increase free thyroid hormone levels). ( 31237256 )
• ~30% of patients have no identifiable precipitant. ( 23920160 )

signs & symptoms

• Tachycardia (including atrial fibrillation, ventricular fibrillation).
• High-output, distributive heart failure state.
• Systolic heart failure (e.g., with pulmonary edema).
• Systolic hypertension with wide pulse pressure can occur.
• Delirium, agitation, psychosis.
• Stupor, coma.
• May reach 40-41C (104-106F), classically with associated diaphoresis.
• Diarrhea, nausea, vomiting.
• Abdominal pain.
• Jaundice, hepatic failure.
• Weight loss.
• Tremor, restlessness.
• Goiter, scar from partial thyroidectomy.
• Exophthalmos.
• Thyroid labs aren't necessarily worse than uncomplicated hyperthyroidism . The differentiation between hyperthyroidism and thyroid storm is based on clinical findings – not how severe the lab abnormality is.
• The most invariable finding is TSH that is very low or undetectable .
• Elevated free T4.
• T3 levels are often elevated to a greater degree than T4 concentrations, due to preferential secretion of T3 by the hyperthyroid gland. (Vincent 2023)
• Hyperglycemia.
• Low or high white blood cell count.
• Abnormal liver function tests (if severe, consider the possibility of congestive hepatopathy as a result of heart failure).
• DIC. ( 32145820 )

Burch criteria for thyroid storm 🧮

• 37.2-37.7 (99-99.9) = 5 points.
• 37.8-38.2 (100-100.9) = 10 points.
• 38.3-38.8 (101-101.9) = 15 points.
• 38.9-39.4 (102-102.9) = 20 points.
• 39.5-39.9 (103-103.9) = 25 points.
• 40+ (104+) = 30 points.
• 99-109 = 5 points.
• 110-119 = 10 points.
• 120-129 = 15 points.
• 130-139 = 20 points.
• >140 = 25 points.
• Mild (e.g. agitation) = 10 points.
• Moderate (e.g. delirium, psychosis) = 20 points.
• Severe (e.g. seizure, coma) = 30 points.
• Diarrhea, n/v, abdominal pain = 10 points.
• Unexplained jaundice = 20 points.
• Mild (e.g. edema) = 5 points.
• Moderate (e.g. rales) = 10 points.
• Severe (e.g. pulmonary edema) = 15 points.
• Atrial fibrillation present = 10 points.
• Precipitant history present = 10 points.

interpretation of Burch criteria

• 45 or more: Highly suggestive of thyroid storm.
• 25-44: Supports diagnosis of thyroid storm or impending storm.
• <25: Thyroid storm unlikely.

not intended for rigid interpretation

• Thyroid storm is difficult to diagnose because there is a continuum of severity, ranging from severe hyperthyroidism to thyroid storm. Any specific binary cutoff is artificial.
• 1) The diagnosis of thyroid storm is a partially a diagnosis of exclusion . For example, sepsis with multi-organ failure could easily score >45 points on the above criteria. Therefore, a score >45 doesn't prove a diagnosis of thyroid storm.
• 2) Treatment for thyroid storm is reasonable in any patient with severe hyperthyroidism causing organ failure (especially heart failure) . Therefore, even if the patient doesn't have a score >45, it may be prudent to initiate therapy for thyroid storm. Patients with borderline storm may improve rapidly and then therapy can be de-escalated.

Evaluation includes securing a diagnosis of thyroid storm and simultaneously looking for any potential trigger of the episode. Consider the list of common precipitants above .

basic studies to order

• Glucose, electrolytes including Ca/Mg/Phos.
• Coagulation studies (thyroid storm can cause DIC).
• Creatinine kinase (thyroid storm can cause rhabdomyolysis).

if infection is suspected

• Blood cultures & infectious workup as indicated (e.g., chest X-ray, possibly CT scan).
• There should generally be a low threshold for initiation of antibiotics (e.g. if the patient has vasodilatory shock, or focal signs of infection). If antibiotics are being started, check procalcitonin.
• Steroid blocks release of T4 from the thyroid and also blocks peripheral activation of T4 into T3.
• The loading dose of hydrocortisone is 300 mg IV.
• The maintenance dose of hydrocortisone 100 mg IV Q8hr. This dose may be continued for several days until the thyroid storm improves, at which point it can be rapidly tapered off.
• If hydrocortisone isn't immediately available, may use methylprednisolone (125 mg initial dose, followed by 60 mg daily).

Thionamides block thyroid hormone synthesis. This is generally a cornerstone of therapy, although it may be ineffective in rare cases of thyroid storm due to thyroiditis. ( 25905165 )

methimazole 💊

• Methimazole is likely the safest thionamide (less hepatotoxic than propylthiouracil). However, methimazole can cause reversible agranulocytosis.
• Clinical evidence suggests that it may be equally effective as propylthiouracil.
• Methimazole may be the preferred agent, especially in patients with hepatitis or with unknown liver function tests.
• Methimazole dose: 40 mg loading dose, then 20 mg q4 hours. After 24 hours, the dose may be reduced to 20 mg q12 hours.

propylthiouracil 💊

• Propylthiouracil is theoretically more effective than methimazole, because it reduces peripheral conversion of T4 into T3.
• However, propylthiouracil is more hepatotoxic (with an FDA black box warning for causing hepatic failure). 🌊
• Propylthiouracil be preferred in more fulminant cases of thyroid storm, or in pregnancy.
• Loading dose of 600-1000 may be considered.
• Initial maintenance dose is 200 mg propylthiouracil q4.
• Transition to methimazole once patient is improving clinically.
• Iodine immediately suppresses thyroid hormone release via the Wolff-Chaikoff effect. 🌊
• Iodine must be given at least an hour after thionamide (to prevent increasing thyroid hormone synthesis).
• Lugol's Solution 8 drops (0.4 ml) PO q6hr (take with fluid/food to avoid gastritis).
• Saturated solution of KI (SSKI) , 5 drops (0.25 ml) PO q6hr.
• To convert between drops and ml: 1 drop = 0.05 mL.
• Iodine may be continued for up to ten days (eventually the suppressive effect will wear off).
• Some patients carry an “allergy” to iodine. However, iodine is an essential atom required for life, which lacks allergic properties. Consequently, such patients should be able to safely receive these therapies. ( 33547463 ) 

cholestyramine

• This binds thyroid hormone in the gut and prevents enterohepatic reabsorption. ( 18946743 )
• Cholestyramine is effective even in patients who haven't taken exogenous thyroid hormone (e.g. Graves disease).
• This is extremely safe (available over-the-counter, for treatment of diarrhea).
• Dose is 4 grams orally q6hrs.
• Continue until patient is fully improved.

thyroid storm may cause numerous hemodynamic derangements:

• 1) Hypovolemia (from diaphoresis, vomiting, diarrhea).
• 2) Systolic heart failure, including cardiogenic shock.
• 3) Distributive shock (increased tissue oxygenation causes systemic vasodilation).
• Moderate tachycardia may be a compensatory response to shock, which improves cardiac output.
• Severe tachycardia may be pathological , reducing ventricular filling and thereby exacerbating cardiovascular dysfunction.

initial stabilization

• Volume should be repleted based on echocardiography, lung sonography, and history (e.g. history of poor oral intake, fever, and diarrhea suggest volume depletion).
• Vasopressors may be needed to maintain an adequate blood pressure. If the patient is already very tachycardic, phenylephrine might be a reasonable consideration to avoid exacerbating tachycardia.
• Magnesium repletion is a good first step for patients with atrial fibrillation and rapid ventricular rate. Hyperthyroidism itself may cause hypomagnesemia.

be careful about beta-blockers

• Tachycardia is not the primary problem here . Aggressive beta-blockade may cause more harm than benefit.
• The literature contains numerous reports of patients who crash within 6 hours of initiation of therapy for thyroid storm. In many of these cases, beta-blockade may be the cause of deterioration. ( 30567262 )
• Don't blindly give beta-blockers without first performing a hemodynamic evaluation (echocardiogram plus lung ultrasonography to look for evidence of cardiogenic pulmonary edema). 📖
• Shock (especially cardiogenic shock with severely reduced ejection fraction).
• Cardiogenic pulmonary edema.
• Up-titrate to ensure that the patient can tolerate beta-blockade.
• Japanese guidelines recommend esmolol, due to increased mortality in patients with heart failure treated with propranolol. ( 27746415 )
• Theoretically desirable, since it blocks peripheral activation of T4 to T3. However, it is unclear whether this is clinically relevant.
• The starting dose is 20-40 mg PO q6hr. If tolerated, may up-titrate to a dose of 80 mg q6.

Thyroid storm is commonly accompanied by atrial fibrillation with rapid ventricular rate. 

basic management principles 📖

• Provide volume resuscitation for patients who are volume depleted.
• Support the systolic blood pressure with vasopressors if needed (phenylephrine may be useful here, to avoid accelerating the heart rate further).
• Treat hyperthermia with acetaminophen +/- physical cooling.
• Treat psychomotor agitation if present.
• Cardioversion is unlikely to work until the thyroid storm has resolved. ( 38033089 )
• Patients with systolic heart failure and thyroid storm may require permissive tachycardia to achieve adequate perfusion. For example, targeting a heart rate below ~130 b/m might be reasonable. Overly aggressive attempts to slow down the heart rate may precipitate cardiogenic shock.
• It may be impossible to achieve ideal heart rate control (e.g., heart rate <110 b/m) until the thyroid storm has subsided.

heart rate control: agents

• Propranolol 💊 may be a good choice for hemodynamically robust patients (e.g., preserved ejection fraction and hypertension). The starting dose is 20-40 mg PO q6hr. If tolerated, may up-titrate to a dose of 80 mg q6.
• Esmolol infusion 💉 may be useful if there is some concern that the patient will be unable to tolerate beta-blockade. If not tolerated, this can be rapidly discontinued.
• Amiodarone 💉 may be helpful in more unstable patients. This isn't a terrific long-term solution in these patients, but a few days of amiodarone may be required to stabilize the patient until their thyroid storm starts settling down. Amiodarone should be administered after methimazole, to reduce the risk of exacerbating the thyrotoxicosis (since amiodarone contains iodine).
• (1) Patients with thyrotoxicosis have increased renal clearance and an increased volume of distribution, which can make it difficult to achieve adequate digoxin levels.
• (2) The higher sympathetic tone of these patients may render digoxin relatively less effective . ( 28822529 )

hyperthermia management

• Hyperthermia is harmful because it increases cardiac workload and can also cause organ damage (e.g. rhabdomyolysis, delirium).
• However, induction of shivering is potentially dangerous, as this also increases myocardial workload. Fortunately, hyperthermia is due to increased heat generation by the tissues (rather than a change in hypothalamic set point), so shivering may not be a problem in these patients.
• Acetaminophen 650-1000 mg q6hr scheduled.
• Use of cooling blankets is recommended for high fever, if tolerated without shivering. ( 23920160 , 27746415 )
• Avoid salicylates or NSAIDs, since these may increase free thyroid hormone levels.

agitation management

• Agitation may worsen hyperthermia and impede ability to provide care.
• Case studies exist suggesting that haloperidol may precipitate thyroid storm. Although this is dubious, it might be a reason to prefer olanzapine over haloperidol. ( 27746415 )

refractory thyroid storm

• Clinical improvement should ideally be seen reasonably soon (e.g. ~24-48 hours).
• Some patients will fail to respond to optimal medical management.
• Treatment options for refractory thyroid storm include plasmapheresis or thyroidectomy.

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• Maintain a high index of suspicion for thyroid storm, as this will commonly mimic other conditions (e.g. psychosis, meningitis, hyperthermia, sepsis, cardiogenic shock).
• Avoid salicylates or NSAIDs, as these may bind to thyroid-binding globulin, causing increased levels of free thyroid hormone levels.
• Be cautious with beta-blockers , because some patients have thyrotoxicosis-induced cardiomyopathy and distributive shock. Aggressive beta-blockade may cause hemodynamic collapse in this situation, because the tachycardia is a compensatory response.
• Avoid administration of iodine (including iodinated contrast dye) until first giving methimazole.

Guide to emoji hyperlinks

• 18946743 Kaykhaei MA, Shams M, Sadegholvad A, Dabbaghmanesh MH, Omrani GR. Low doses of cholestyramine in the treatment of hyperthyroidism. Endocrine. 2008 Aug-Dec;34(1-3):52-5. doi: 10.1007/s12020-008-9107-5 [ PubMed ]
• 23920160 Chiha M, Samarasinghe S, Kabaker AS. Thyroid storm: an updated review. J Intensive Care Med. 2015 Mar;30(3):131-40. doi: 10.1177/0885066613498053 [ PubMed ]
• 25905165 De Groot LJ, Bartalena L, Feingold KR. Thyroid Storm. 2018 Dec 17. In: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dhatariya K, Dungan K, Grossman A, Hershman JM, Hofland J, Kalra S, Kaltsas G, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, McGee EA, McLachlan R, Morley JE, New M, Purnell J, Sahay R, Singer F, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000–. [ PubMed ]
• 27746415 Satoh T, Isozaki O, Suzuki A, Wakino S, Iburi T, Tsuboi K, Kanamoto N, Otani H, Furukawa Y, Teramukai S, Akamizu T. 2016 Guidelines for the management of thyroid storm from The Japan Thyroid Association and Japan Endocrine Society (First edition). Endocr J. 2016 Dec 30;63(12):1025-1064. doi: 10.1507/endocrj.EJ16-0336 [ PubMed ]
• 28822529 Reddy V, Taha W, Kundumadam S, Khan M. Atrial fibrillation and hyperthyroidism: A literature review. Indian Heart J. 2017 Jul-Aug;69(4):545-550. doi: 10.1016/j.ihj.2017.07.004 [ PubMed ]
• 30299273 Thumma S, Manchala V, Mattana J. Radiocontrast-Induced Thyroid Storm. Am J Ther. 2019 Sep/Oct;26(5):e644-e645. doi: 10.1097/MJT.0000000000000844 [ PubMed ]
• 30567262 Andrade Luz I, Pereira T, Catorze N. Thyroid storm: a case of haemodynamic failure promptly reversed by aggressive medical therapy with antithyroid agents and steroid pulse. BMJ Case Rep. 2018 Dec 14;11(1):e226669. doi: 10.1136/bcr-2018-226669 [ PubMed ]
• 30882392 Goodier CG. Endocrine Emergencies in Obstetrics. Clin Obstet Gynecol. 2019 Jun;62(2):339-346. doi: 10.1097/GRF.0000000000000433 [ PubMed ]
• 31237256 Ylli D, Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Pol Arch Intern Med. 2019 Aug 29;129(7-8):526-534. doi: 10.20452/pamw.14876 [ PubMed ]
• 31714398 Bourcier S, Coutrot M, Kimmoun A, Sonneville R, de Montmollin E, Persichini R, Schnell D, Charpentier J, Aubron C, Morawiec E, Bigé N, Nseir S, Terzi N, Razazi K, Azoulay E, Ferré A, Tandjaoui-Lambiotte Y, Ellrodt O, Hraiech S, Delmas C, Barbier F, Lautrette A, Aissaoui N, Repessé X, Pichereau C, Zerbib Y, Lascarrou JB, Carreira S, Reuter D, Frérou A, Peigne V, Fillatre P, Megarbane B, Voiriot G, Combes A, Schmidt M. Thyroid Storm in the ICU: A Retrospective Multicenter Study. Crit Care Med. 2020 Jan;48(1):83-90. doi: 10.1097/CCM.0000000000004078 [ PubMed ]
• 32145820 Park BD, Lyn-Kew K, Granchelli A, Mehta A. A 62-Year-Old Woman With Diffuse Myalgias, Fatigue, and Shortness of Breath. Chest. 2020 Mar;157(3):e75-e78. doi: 10.1016/j.chest.2019.09.041 [ PubMed ]
• 33547463 Wulf NR, Schmitz J, Choi A, Kapusnik-Uner J. Iodine allergy: Common misperceptions. Am J Health Syst Pharm. 2021 Apr 22;78(9):781-793. doi: 10.1093/ajhp/zxab033 [ PubMed ]
• 36118802 De Almeida R, McCalmon S, Cabandugama PK. Clinical Review and Update on the Management of Thyroid Storm. Mo Med. 2022 Jul-Aug;119(4):366-371. [ PubMed ]
• 38033089 Joglar JA, Chung MK, Armbruster AL, Benjamin EJ, Chyou JY, Cronin EM, Deswal A, Eckhardt LL, Goldberger ZD, Gopinathannair R, Gorenek B, Hess PL, Hlatky M, Hogan G, Ibeh C, Indik JH, Kido K, Kusumoto F, Link MS, Linta KT, Marcus GM, McCarthy PM, Patel N, Patton KK, Perez MV, Piccini JP, Russo AM, Sanders P, Streur MM, Thomas KL, Times S, Tisdale JE, Valente AM, Van Wagoner DR; Peer Review Committee Members. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024 Jan 2;149(1):e1-e156. doi: 10.1161/CIR.0000000000001193 [ PubMed ]

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Endocrinology

• Thyroid storm: A case from the endocrine teaching clinics

June 12, 2018

A 33-year-old woman presented to an outside facility with increasing shortness of breath, orthopnea, paroxysmal nocturnal dyspnea and increasing lower limb edema — findings suggestive of biventricular heart failure. Further questioning revealed a two- to three-month history of unintentional weight loss, heat intolerance, diarrhea, abdominal pain and palpitations.

The symptoms started about six months after her most recent delivery of a healthy child. Her past medical history was significant for obesity, mild asthma requiring occasional albuterol use and third trimester gestational hypertension during her recent pregnancy (managed without pharmacotherapy).

On presentation, the patient showed signs of tachycardia (118 beats per minute) and tachypnea (22 breaths per minute) and had lower extremity pitting edema. Laboratory testing was significant for hyperthyroidism:

• Thyroid-stimulating hormone (TSH) < 0.1 mIU/L (normal, 0.49 to 4.67 mIU/L)
• Free thyroxine (FT4) 2.6 ng/dL (normal, 0.7 to 1.8 ng/dL)

The serum brain natriuretic peptide was markedly increased at 2,819 pg/mL (normal < 100 pg/mL). Chest X-ray demonstrated cardiomegaly. The patient was diuresed and started on beta-adrenergic blockade and 10 mg of methimazole three times a day. An echocardiogram demonstrated a severely dilated left ventricle and an ejection fraction of 10 to 15 percent.

Cardiovascular surgery operating room at Mayo Clinic

This image from a cardiovascular surgery operating room is representative of the significant amount of equipment and coordinated care required during insertion, adjustment or both of ECMO or to support patients with ECMO who require an operation.

Despite treatment, shortness of breath and hypotension necessitated intra-aortic balloon pump placement and intubation, and she was transferred to Mayo Clinic in Rochester, Minnesota. On arrival, she was sedated, intubated and hypotensive on inotropic support. A repeat echocardiogram revealed an ejection fraction of 9 percent. Due to severe cardiogenic shock, venoarterial extracorporeal membrane oxygenation (VA ECMO) cannulation was initiated.

Endocrinology was consulted. Mild exophthalmos was noted without dermopathy or acropachy. The patient's presentation with decompensated heart failure, preceding gastrointestinal complaints, and tachycardia was highly suggestive of thyroid storm (Burch and Wartofsky Point Scale 40).

Aggressive therapy was started with 200 mg of propylthiouracil administered every four hours, 100 mg of hydrocortisone administered every eight hours and a saturated solution of potassium iodine administered two hours after propylthiouracil. Repeat biochemical testing revealed a TSH of < 0.01 mIU/L (normal, 0.4 to 4.0 mIU/L), FT4 of 3.4 ng/dL (normal, 0.9 to 1.7 ng/dL) and a total tri-iodothyronine of 308 ng/dL (normal, 80 to 200 ng/dL).

Right midthyroid lobe demonstrating increasing vascularity

Doppler ultrasound of right midthyroid lobe demonstrating increasing vascularity.

While thyroid receptor antibodies were pending, a bedside ultrasound revealed a hypervascular thyroid gland. The patient's clinical picture was most consistent with cardiogenic shock in the setting of thyroid storm of autoimmune origin, and possible postpartum cardiomyopathy.

Despite treatment, five days later the patient was still clinically and biochemically hyperthyroid with serum TSH of 0.02 mIU/L and FT4 of 5.4 ng/dL by equilibrium dialysis (employed because of her significantly altered protein status). Given the critical nature of the patient's condition and the need for rapid normalization of her thyroid status, total thyroidectomy was recommended.

Microscopic magnification of thyroid tissue

Low (A) and high (B) microscopic magnification of thyroid tissue demonstrating epithelial hypertrophy and invagination forming papillary projections and scalloping of colloid (red arrows) consistent with Graves' disease.

Plasmapheresis was initiated to optimize preoperative thyroid levels. Endocrine and cardiovascular surgeons collaborated to perform a total thyroidectomy during which anticoagulation, necessary for ECMO, was held. Pathology revealed diffuse follicular hyperplasia consistent with Graves' disease. As expected, the patient also had an elevated thyroid receptor antibody concentration of 20 IU/L (normal, 0 to 1.75 IU/L).

Postoperatively, anticoagulation was restarted without complication.

Following total thyroidectomy, the patient improved and was able to be weaned off vasopressor support and she was extubated. Thyroid replacement therapy was initiated. Unfortunately, her cardiac function remained suboptimal (ejection fraction of 15 percent), and therefore a left ventricular assist device was placed to bridge to cardiac transplantation.

As highlighted in an article in the journal Thyroid in 2012, thyroid storm is a life-threatening condition and early recognition is essential — mortality remains high (11 percent) despite improvements in management. The diagnosis should be considered in an individual with severe symptoms of multiorgan dysfunction and biochemical thyrotoxicosis. Several scoring systems have been devised to assist recognition and early implementation of aggressive treatment. The authors note that a high level of suspicion is important.

In this case, despite aggressive nonsurgical management of hyperthyroidism, additional cardiovascular support was required. ECMO can be used in such cases, and a growing body of literature supports its use in thyroid storm-induced cardiogenic shock refractory to usual treatment — as highlighted in an article in the journal Thyroid in 2011.

Total thyroidectomy for thyroid storm on ECMO, however, has not been reported, but occurred without complication in this case. Close collaboration between endocrinology, endocrine surgery and cardiovascular surgery is vital. Reports suggest that rapid cardiac function recovery with the normalization of thyroid hormone occur following thyroidectomy. In the current case, cardiac function improved, but left ventricular assist device (LVAD) therapy was eventually required to bridge to cardiac transplantation, suggesting an additional underlying cardiomyopathy. The patient was able to be discharged home with an LVAD, awaiting heart transplantation.

• Early recognition and appropriate treatment of thyroid storm — which may include thyroidectomy — is essential to improve outcome.
• Thyroidectomy should be pursued when medical therapy fails to control the thyrotoxicosis.
• ECMO should be considered as a means of cardiac support in patients who are unresponsive to conventional therapy until thyroid hormone normalization can be achieved.

For more information

Akamizu T, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid. 2012;22:661.

Hsu LM, et al. Extracorporeal membrane oxygenation rescues thyrotoxicosis-related circulatory collapse. Thyroid. 2011;21:439.

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Thyroid Storm

Author: Robert W. Wolford, M.D., M.M.M, University of Illinois College of Medicine at Peoria,

Editor: Doug Franzen, MD, M.Ed

Last Update: 2019

A 60-year-old female is brought to the Emergency Department by her family because of confusion, fever, and shortness of breath.  Her family notes a productive cough and fever that began two days ago. The family states she has been taking aspirin for her fever without improvement.  Over the last 24 hours, the patient has become increasingly confused with worsening shortness of breath and has had several episodes of watery, non-bloody diarrhea.  Past medical history is only significant for hypertension for which she takes hydrochlorothiazide. Reviewing her medical records finds that she had a routine appointment with her family physician two weeks earlier.  At that time, her examination was normal with the exception of a resting sinus tachycardia of 110 bpm. A thyroid stimulating hormone (TSH) level was obtained at that visit and was undetectable. She is scheduled for a follow-up visit with her doctor tomorrow.  The patient is only oriented to herself and is unable to provide any additional history or review of symptoms. Vital signs are: Temp 39.4°C, HR 135 bpm, RR 24 bpm, BP 140\45 mmHg, and pulse oximetry on room air of 89%. The cardiac monitor shows atrial fibrillation with rapid ventricular response at 135 bpm.  On physical examination she is tachycardic, tachypneic, has diminished breath sounds at the right lung base and diffuse, bilateral crackles, and 2+ pitting edema below the knees. A portable chest radiograph shows a large right lower lobe infiltrate with diffuse interstitial edema.

Upon finishing this module, the student will be able to:

• Describe the potential presenting symptoms and signs of thyroid storm.
• List common causes of thyroid storm.
• Discuss the diagnostic approach to thyroid storm.
• Describe the treatment of thyroid storm.

Introduction

Thyroid storm is an uncommon but potentially fatal endocrine emergency at the severe end of the spectrum of thyrotoxicosis. Thyrotoxicosis is thought to affect approximately 1.2% of the United States population and, of those, only 1 to 2% develop thyroid storm. Thyroid storm is more common in women and in the 3rd and 4th decades of life. Thyroid storm typically presents with the signs and symptoms of a hypermetabolic state; however co-existing illnesses, patient age, and the severity of the patient may result in deviations from the classic presentation and potentiate delays in diagnosis. To reduce the morbidity and mortality of thyroid storm, the clinician must consider the diagnosis and implement treatment in a timely fashion. Even with recognition and treatment, mortality is high, ranging from 10% to 75%, although more recent studies found a mortality of 3.6%.

A brief review of normal thyroid function follows. Iodide enters the thyroid cells through the sodium iodide symporter and specific thyroglobulin tyrosines are iodinated by thyroid peroxidase, creating mono and di-iodotyrosines. The iodotyrosines combine to form T3 and T4. In response to TSH, T4 and T3 are cleaved from the thyroglobulin and released into the circulation. T4 is the pro-hormone and T3 the active form of the hormone. Eighty percent of the circulating T3 is formed by the conversion of T4 to T3 in the peripheral tissues and the remaining 20% directly released from the thyroid gland. Approximately 99.97 % of T4 and 99.7% of T3 are bound to serum proteins (primarily thyroxine binding globulin) and it is only the free hormones that are metabolically active. Any factor which changes the amount of protein bound hormone (ex. salicylates, diphenylhydantoin, and heparin) may have an impact. Thyroid function is tightly controlled by a negative feedback loop. (Figure 1)

Hypothalamic-Pituitary-Thyroid Axis Wikimedia Commons –   Creative Commons Attribution-Share Alike 3.0 Unported no changes made

Initial Actions and Primary Survey

Thyroid storm is exceedingly uncommon in the ED but it should be considered in any patient presenting with a hypermetabolic state, and especially those with a history of thyroid disease. Determining where the symptoms of subacute or chronic thyrotoxicosis end and thyroid storm begins is difficult. The focus of the primary survey and the subsequent detailed history and physical examination is to identify those patients at risk for thyroid storm.

Prior to entering the room, review the vital signs. Fever and tachycardia are common findings in thyroid storm. Tachypnea may be seen, particularly in the setting of complicating heart failure. Hypertension and a widened pulse pressure may also be present. The patient may also be agitated and/or anxious.

Airway: The airway is typically not compromised by thyroid storm. However, these patients are often critically ill and the complications or inciting etiology of the patient’s thyroid storm may require active airway intervention.

Breathing: Tachypnea may occur for numerous reasons: increased basal metabolic rate; underlying heart failure as a complication of long standing thyrotoxicosis (high output heart failure, dilated cardiomyopathy, or cor pulmonale); or other diseases that precipitated thyroid storm (pneumonia).

Circulation: Tachycardia is common, either sinus tachycardia (most common rhythm) or atrial fibrillation (most common dysrhythmia). Supraventricular and ventricular dysrhythmias, including ventricular fibrillation, may occur. A widened pulse pressure and hypertension are frequently seen. However, hypotension and shock may be seen as a complication of the thyroid storm or as a result of the inciting event (e.g. septic shock).

While performing a primary survey, as with any seriously ill patient, the following should be obtained:

• Reliable vascular access, cardiac, SpO2, and BP monitoring. Supplemental oxygen if needed.
• Bedside point–of-care glucose.
• Electrocardiogram.

Presentation

Although the most common presentation is thyrotoxicosis, thyroid storm may be the initial manifestation of the patient’s thyroid disease. Patients classically present with evidence of multisystem decompensation, fever, tachycardia out of proportion to the temperature, and central nervous system dysfunction. Thyroid storm is part of the spectrum of thyrotoxicosis and can be difficult to distinguish from severe thyrotoxicosis. A scoring system has been proposed to identify the likelihood of thyroid storm. Thyroid storm should be near the top of the differential diagnoses for any patient with a history of thyrotoxicosis presenting with CNS dysfunction. Key items to look for on history and physical examination that suggest the presence of thyrotoxicosis and thyroid storm are:

• Is there a history of thyroid disease? If the patient was taking medication for thyroid disease, has the dosage changed recently (including missed doses)? 
• Did the patient have subacute or chronic symptoms of thyrotoxicosis that have acutely worsened? 
• Are symptoms of thyrotoxicosis found on review of systems? (Table 1)
• Are there new symptoms of depression, or apathy? Often seen in elderly – apathetic hyperthyroidism.
• Has the patient recently started any new medications, had radioiodine, or been given iodinated contrast? (Table 2)
• Any recent physiologic stressors? Infection is the most common trigger of thyroid storm, but also consider surgery, trauma, cardiac events, etc.

A list of common physical exam findings is shown in Table 1. 

Other findings include:

• Altered mental status (Spectrum from anxiety and agitation to coma).
• Fine tremor, especially on extension of arms
• Hyperreflexia
• Stare and lid lag are common
• Enlarged or tender thyroid; thyroid bruit

A thorough exam should target findings suggestive of precipitating causes for decompensation of thyroid disease into thyroid storm (sepsis, stroke, myocardial infarction, etc), as well as complications of thyroid storm such as stroke or congestive heart failure. Common triggers of thyroid storm are listed in Table 3.

Table 1. Symptoms & Signs of Thyrotoxicosis

Table 2. Medication associated thyrotoxicosis. (3)

Table 3. Thyroid storm triggers

To assist in the diagnosis of thyroid storm there are useful clinical calculators. One of these is the Burch-Wartofsky scale . Using the linked calculator can help to predict the likelihood that biochemical thyrotoxicosis is thyroid storm. 

Diagnostic Testing

Given the low incidence of thyroid storm, it is critical to maintain a broad differential and evaluate for other possible conditions that would explain the patient’s presentation. 

Although thyroid storm is primarily a clinical diagnosis, if thyroid storm is suspected thyroid specific laboratory studies should be obtained and usually include:

• Thyroid stimulating hormone (TSH) level.
• Free thyroxine (T4) level.
• Free triiodothyroxine (T3) level.

Most patients will demonstrate elevated free T4 and T3 levels and a low or undetectable TSH level. The TSH level may be normal in pituitary dependent thyrotoxicosis (pituitary not subject to negative feedback – very rare!). The free T4 may be normal with an elevated free T3 in cases of T3 thyrotoxicosis. The turnaround time for these labs can be hours to days; if thyroid storm is suspected treatment should be started without waiting for confirmatory tests.

Additional tests should be obtained to evaluate for possible precipitating causes (such as a chest radiograph and urinalysis to evaluate for infection) or concurrent conditions (such as electrolytes to evaluate other possible causes of a dysrhythmia, or a BNP to evaluate for heart failure). 

Patients with thyroid storm are usually critically ill and stabilization should be initiated immediately. These patients are frequently severely volume depleted and require aggressive fluid resuscitation, unless cardiac failure is suspected. Severe hyperthermia should be addressed with cooling and acetaminophen. Salicylates should be avoided as they will displace T4 and T3 from thyroxine binding globulin. Electrolyte abnormalities should be corrected, and dysrhythmias recognized and treated. The inciting etiologies and complications of thyroid storm must be identified and appropriately managed.

Specific treatment for thyroid storm utilizes 3 sequential steps: 1. Block the peripheral effect of the thyroid hormones, 2. Stop the production of hormone in the thyroid, and 3. Stop the release of T3 and T4 from the thyroid. Commonly used medications are listed in Table 5.

Table 5. Medications used in the treatment of thyroid storm. (Adult doses)

Table 5 by Doug Frazen

Peripheral symptom control (ex. tachycardia, chest pain, dyspnea, etc.) is done primarily through β blockade. Traditionally this has been achieved with either oral or intravenous propranolol. However, the serum half-life of propranolol is relatively long (3 to 6 hours) and may worsen symptoms of cardiac failure. Esmolol, with a markedly shorter half-life, may be a better choice in the setting where the patient’s cardiac status is unclear or if the patient has underlying reactive airway disease.

Inhibition of thyroid hormone synthesis is undertaken before inhibition of hormone release. Thioureas, either PTU or methimazole, are used to block additional hormone synthesis. PTU is preferred as it has the additional benefit of blocking peripheral conversion of T4 to T3. PTU is approved for use in pregnancy. However, it does have significant risks, including liver injury and failure and has received a black box warning from the US Food and Drug Administration.

Inhibition of hormone release is achieved with iodine therapy. Iodine therapy should not be started any sooner than one hour after the initiation of a thiourea. In the absence of a thiourea, iodine may actually stimulate release of preformed thyroid hormone. Iodine, in the presence of a thiourea, blocks the release of preformed hormone, decreases iodide transport into thyroid follicular cells, and prevents subsequent oxidation. This inhibition is short lived and ineffective after 48 hours of therapy.  Lithium carbonate may be considered in those patients who cannot receive iodine.

Glucocorticoids are also frequently given in thyroid storm as they may decrease the conversion of T4 to T3, although the significance of this effect is unknown. An unknown percentage of patients in thyroid storm also have adrenal insufficiency. Dexamethasone is typically preferred due to its lack of interference on an ACTH stimulation test. A random cortisol level should ideally be obtained prior to administration of a steroid.

All patients in thyroid storm should be admitted to an intensive care unit after stabilization and initiation of thyroid specific interventions. Even with aggressive care, a significant percentage of patients will die.

The patient is diagnosed with right lower lobe pneumonia, new onset atrial fibrillation, and congestive heart failure.  Antibiotics are administered to treat the pneumonia. Because of the history of the unexplained sinus tachycardia during her recent physician visit and the undetectable TSH, the patient is suspected to have undiagnosed thyrotoxicosis.  The Burch-Wartofsky score is calculated, yielding a value of 105 out of a possible 140. Thyroid storm is highly likely. Appropriate laboratory studies were ordered, treatment for thyroid storm initiated and the patient admitted to the ICU.  After a 6-day hospital stay, the patient is discharged home to her family.  

Pearls and Pitfalls

• Suspect thyroid storm in any patient with a history of thyroid disease (esp. thyrotoxicosis) and a hypermetabolic state.
• The diagnosis of thyroid storm is a clinical diagnosis.
• Always look for the trigger (ex. infection, myocardial infarction, etc.)
• Initiate thiourea treatment before starting iodine therapy.
• These patients are critically ill and have a significant mortality rate, even with appropriate therapy.
• Burch HB, Wartofsky L: Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin N Am 1993;22(2):263-77.
• Devereaux D, Tewelde SZ: Hyperthyroidism and Thyrotoxicosis. Emerg Med Clin N Am 2014;32:277-92.
• Galindo RJ, Hurtado CR, Pasquel FJ, et al:  National Trends in Incidence, Mortality, and Clinical Outcomes of Patients Hospitalized for Thyrotoxicosis With and Without Thyroid Storm in the United States, 2004-2013.  Thyroid 2018;10(10):1-8.
• Mills L, Lim S: Identifying and treating thyroid storm and myxedema coma in the Emergency Department. Emerg Med Pract 2009;11(8).
• Nayak B, Burman K: Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin N Am 2006;35:663-86.
• Ross DS, Burch HB, Cooper DS, et al.: 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid 2016;26(10):13431421.
• Wartofsky L, Kubo-Gwiezdzinska J.  2019. Thyroid Storm (Thyrotoxic Crisis).  In M Luster, LH Duntas, L Wartofsky (Eds), The Thyroid and Its Diseases:  A Comprehensive Guide for the Clinician. Pages 357-366. SpringerLINK ebook.  Accessed 3\20\2019.

MINI REVIEW article

Crash landing of thyroid storm: a case report and review of the role of extra-corporeal systems.

• 1 Department of Cardiology, National University Heart Center, Singapore, Singapore
• 2 Division of Endocrinology, Department of Medicine, National University Hospital, Singapore, Singapore
• 3 Department of Hematology-Oncology, National University Cancer Institute, Singapore, Singapore
• 4 Cardiothoracic Intensive Care Unit, National University Heart Center, Singapore, Singapore
• 5 Department of Surgery, Yong Loo Lin School of Medicine, Singapore, Singapore
• 6 Department of Medicine, Yong Loo Lin School of Medicine, Singapore, Singapore

Thyroid storm is a rare but life-threatening endocrinological emergency with significant mortality ranging from 10-30% with multi-organ involvement and failure. In view of the rarity of this condition and efficacy of established first line medical treatment, use of extra-corporeal treatments are uncommon, not well-studied, and its available evidence exists only from case reports and case series. We describe a 28-year-old man who presented with an out-of-hospital cardiac arrest secondary to thyroid storm. Despite conventional first-line pharmacotherapy, he developed cardiogenic shock and circulatory collapse with intravenous esmolol infusion, as well as multi-organ failure. He required therapeutic plasma exchange, concurrent renal replacement therapy, and veno-arterial extra-corporeal membrane oxygenation, one of the few reported cases in the literature. While there was clinical stabilization and improvement in tri-iodothyronine levels on three extra-corporeal systems, he suffered irreversible hypoxic-ischemic brain injury. We reviewed the use of early therapeutic plasma exchange and extra-corporeal membrane oxygenation, as well as the development of other novel extra-corporeal modalities when conventional pharmacotherapy is unsuccessful or contraindicated. This case also highlights the complexities in the management of thyroid storm, calling for caution with beta-blockade use in thyrocardiac disease, with close monitoring and prompt organ support.

Introduction

Thyroid storm (TS) is a life-threatening exacerbation of the hyperthyroid state characterized by multi-organ dysfunction of the cardiovascular, thermoregulatory, gastrointestinal-hepatic and central nervous systems. While the incidence among hospitalized patients is estimated to be low at 1-2% ( 1 ), the overall mortality is 10-30% ( 2 ), with a 12-fold increase in mortality compared to individuals with thyrotoxicosis ( 3 ). The diagnosis of TS is additionally challenging due to the absence of specific clinical or laboratory findings. Early recognition of this condition is key, as it allows for prompt and specific treatment, as well as early identification of organ dysfunction with initiation of supportive measures in the intensive care setting if required.

We present a case of TS in a young patient with undiagnosed Graves’ disease, presenting with an out-of-hospital cardiac arrest. Initially hemodynamically stable following return of spontaneous circulation, he developed circulatory collapse after intravenous esmolol infusion, initiated for control of tachycardia. There was consequent multi-organ failure which contraindicated the use of standard anti-thyroid drug therapy. He required three extra-corporeal systems of continuous renal replacement therapy (CRRT), veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) and therapeutic plasma exchange (TPE) for stabilization, one of the few reported cases in the literature.

Case Description

A 28-year-old male presented with an out-of-hospital ventricular fibrillation (VF) arrest, preceded by an acute respiratory illness. There was return of spontaneous circulation after 60 minutes of resuscitation with bystander cardiopulmonary resuscitation and external defibrillation by paramedics. In the Emergency Department, he was febrile at 40.5 degrees Celsius, hypertensive with a blood pressure of 146/83mmHg and tachycardic with a heart rate of 155 beats per minute. Physical examination was unremarkable, except for a Glasgow Coma Scale of 3. No goiter was seen on examination. Corroborative history from his family confirmed symptoms of heat intolerance, loss of weight, hand tremors and palpitations in the preceding two months, as well as a maternal history of Graves’ thyrotoxicosis.

Initial investigations showed elevated inflammatory markers, mixed respiratory and metabolic acidosis, raised troponin I, but with normal electrolyte levels. Electrocardiogram confirmed sinus tachycardia. Chest radiograph showed prominent pulmonary vasculature without evidence of pneumonia. Point-of-care echocardiogram showed impaired left ventricular systolic function without other obvious abnormalities; the marked sinus tachycardia precluded accurate estimation of the left ventricular ejection fraction (LVEF). Computed tomographic (CT) scan of the brain was normal, and urine drug screen was negative. A coronary angiogram performed was normal, and a provisional diagnosis of acute myocarditis was made. Thyroid function test, sent as part of investigations for myocarditis, showed thyrotoxicosis with an elevated serum free thyroxine (FT4) level of 42.1pmol/L (reference range: 8.0-16.0pmol/L) and a suppressed serum thyroid stimulating hormone (TSH) at <0.01mIU/L (reference range: 0.45-4.50mIU/L) ( Figure 1 ) – our patient had thyroid storm complicated by thyrocardiac disease, with a Burch-Wartofsky score of 105. His thyroid-stimulating hormone receptor antibody eventually returned elevated at >40IU/L (normal ≤2.0IU/L), confirming underlying Graves’ disease.

Figure 1 Timeline of key clinical events. T4, thyroxine; T3, tri-iodothyronine; TSH, thyroid-stimulating hormone; NG, nasogastric; IV, intravenous; PTU, propylthiouracil; NaI, sodium iodide; VA-ECMO, veno-arterial extra-corporeal membrane oxygenation; CRRT, continuous renal replacement therapy; TPE, therapeutic plasma exchange; MMZ, methimazole.

Treatment was promptly initiated with nasogastric propylthiouracil, intravenous sodium iodide and hydrocortisone ( Figure 1 ). Temperature was controlled with a cooling blanket. Judicious low dose esmolol infusion was commenced at 25mcg/kg/min to manage the tachycardia. This was followed shortly by a pulseless electrical activity arrest. Despite a short downtime of three minutes and prompt cessation of beta-blockade, he required high doses of noradrenaline and vasopressin thereafter. He remained persistently hypotensive with maximal dual vasopressor support, and was initiated on VA-ECMO support ( Figure 2 ).

Figure 2 Concurrent CRRT, VA-ECMO and TPE. O 2 , oxygen, CO 2 , carbon dioxide, others as per Figure 1 .

Further investigations revealed worsening transaminitis and anuric acute kidney injury, requiring CRRT. Transthoracic echocardiogram showed severe left ventricular systolic dysfunction with estimated LVEF of 10%. Pharmacological options were now limited to cholestyramine and hydrocortisone. We decided to institute TPE; with the first cycle performed on day 2 of admission, with 2.5L of albumin and 0.5L of saline ( Figure 1 ). After the first cycle, his vasopressor support reduced significantly (only requiring low dose noradrenaline infusion) and his tri-iodothyronine (T3) levels improved ( Figure 1 ). As his FT4 continued to worsen, nasogastric methimazole and Lugol’s iodine were cautiously started, along with second TPE cycle, on the third day.

His pupils were noted to be fixed and dilated with the second cycle of TPE ongoing. Urgent CT scan of the brain revealed diffuse cerebral edema with severe mass effect and tonsillar herniation. A decision was made in conjunction with his family for withdrawal of care, given the grave prognosis.

Evidence of Use of Extra-Corporeal Systems in TS

Our patient is one of the few reported cases where multiple extra-corporeal systems were used (TPE, CRRT, and VA-ECMO) in TS management. On review of the medical literature of articles in English, there has only been four case reports describing the concurrent use of TPE and ECMO in patients with thyrotoxicosis with circulatory collapse ( 4 – 7 ), with one of them reporting the use of three extra-corporeal systems ( 4 ).

Characterized by extreme multi-systemic manifestations of thyrotoxicosis, TS is uncommon but potentially fatal, with a mortality rate of 10-30% ( 2 ). Standard first-line pharmacotherapy in TS aims to block production and release of thyroid hormones with propylthiouracil or methimazole, inhibit release of pre-formed thyroid hormones with iodine, decrease peripheral conversion of T4 to T3 with propylthiouracil and steroids, and treat adrenergic symptoms with beta-blockade, prior to definitive treatment in the form of surgery or radioactive iodine (RAI) ablation. These methods are efficacious and rapid acting. However, certain patients are not able to tolerate, or fail pharmacotherapy, as seen in our patient with multi-organ failure precluding the use of conventional treatment. In such cases, alternative treatment including use of extra-corporeal systems must be considered, of which TPE is the most well established.

TPE is an extra-corporeal blood purification technique used for eliminating large molecular substances. Currently, TPE has a Class II indication for TS in the 2019 American Society for Apheresis (ASFA) guidelines, either as a standalone or adjunct therapy, although the grade 2C level of recommendation suggests the evidence arises mostly from case reports and case series, with an absence of prospective randomized controlled trials ( 8 ). TPE is postulated to work by several mechanisms including: 1) reducing protein-bound thyroid hormones of which 99.97% of total serum T4 and 99.7% of total serum T3 are bound to plasma proteins thyroxine binding globulin (TBG), transthyretin and albumin ( 9 ), 2) additionally reducing autoantibodies and cytokines of a predominantly Th1 pattern including interleukin-2, interferon-γ and tumor necrosis factor-α ( 10 – 12 ), and 3) removing 5’-monodeiodinase which converts T4 to T3 ( 12 ). TPE is shown to reduce all of free and total T4 and T3 ( 13 ), by an estimated 10-80% ( 12 ), and at a greater rate than standard medical therapy for patients with hyperthyroidism ( 14 ). However, these effects are transient and usually last for only 24-48 hours, with a potential risk for rebound thyrotoxicosis ( 12 ). This appears related to the fact that only thyroid hormones from the intravascular compartment is removed, with rapid re-equilibrium from the extravascular spaces. A study in 13 healthy individuals showed the intravascular component of thyroxine accounts for only 26% of the distribution ( 15 ), with the other sites of distribution found to be 14% in the liver, 34% in extrahepatic tissue and 26% in extracellular fluid pools. These transient effects suggest that multiple cycles of TPE may be required, and should be used only as a temporizing measure for definitive treatment ( 12 ). TPE can be performed with either plasma or albumin replacement, and the ASFA guideline does not preferentially recommend the use of plasma or albumin. It has been proposed that plasma has the theoretical advantage of containing binding proteins TBG and transthyretin, which has higher affinity to bind free T4 and T3, as well as avoid depleting coagulation factors thus avoiding complications of bleeding ( 13 ). However, there is similarly a theoretical risk of the presence of thyroid hormones from donor plasma, as well as higher risks of transfusions reactions and infections with use of plasma. Till date, there are no direct head-to-head trials between the use of plasma and albumin in TPE in patients with TS. TPE is generally well tolerated, with risks of minor side effects ranging from about 5% ( 9 ) to 36% ( 16 ), including nausea and vomiting, vagal or hypotensive response and transfusion reactions. The risk of death with TPE for any indication is exceedingly rare at 0.05% ( 17 ), and this is usually attributed to the severity of the underlying condition.

ECMO is an established life-saving treatment option for patients who develop acute cardiopulmonary failure ( 18 ), although its use in endocrinological emergencies is still under research ( 19 ). Use of ECMO in patients with thyrotoxicosis have largely been reported in the form of case reports or case series within the literature. In 2011, Hsu et al. ( 20 ) first reported a series with the use of supportive ECMO ranging from 19-114 hours in four cases of thyrotoxicosis-induced cardiovascular collapse. Three patients survived, with normalization of thyroid function and improved cardiovascular function. A subsequent review by White et al. ( 21 ) published in 2018 reported the successful use of ECMO with survival in 11 out of 14 patients ( 22 – 24 ) between 1970 to 2017 with thyrotoxicosis-induced cardiomyopathy, with near complete recovery of left ventricular function. A review of the cases with the use of ECMO and other extra-corporeal systems in patients with severe thyrotoxicosis or thyroid storm has been summarized in Table 1 , including additional new cases reported from 2018 to 2021 ( 25 – 28 ) and conference poster reports ( 29 – 32 ). These 27 cases (inclusive of our case) showed survival in 85.2% (23 of the 27 cases), with survival in all four of the reported cases requiring additional extra-corporeal support of TPE or CRRT ( 4 – 7 ). ECMO was initiated for either cardiovascular collapse or circulatory shock, and lasted between 19 hours to 18 days. Within the reports of successful outcomes, all cases reported clinical and biochemical improvement in thyrotoxicosis, as well as improvement in cardiac function, although numerical data were not available in some of the reports. The details of these cases are reported in Table 1 . The use of ECMO however, must be weighed against the contraindications and complications of ECMO use, including bleeding, thromboembolism, strokes and access injuries such as hemorrhage, arterial dissection, and distal limb ischemia ( 18 ).

Table 1 Summary of cases with use of ECMO and other extra-corporeal systems in patients with severe thyrotoxicosis or thyroid storm.

Novel therapies are also increasingly considered for TS, using principles similar to TPE by removing protein bound thyroid hormones. Case reports with the use of dialysis has been proposed in management of thyroid storm, most notably with CRRT, which is preferred due to its better tolerability in hemodynamically unstable patients due to its slower rate of exchange of fluids and solutes. Parikh et al. ( 33 ) and Koball et al. ( 34 ) illustrated the sequential use of single pass continuous veno-venous albumin dialysis after limited response to TPE, demonstrating a more sustained improvement in thyroid hormones with less rebound thyrotoxicosis, as well as greater removal of thyroid hormones overall. Other studies have shown the additive effects of TPE and CRRT in removal of thyroid hormones ( 35 ), while another study reported a correlation of improvement of total T3 and free T4 levels of up to 80% with concomitant CRRT and standard medical therapy (without TPE), although the exact mechanisms are unclear ( 36 ). The Molecular Adsorption Recirculation Systems (MARS) has also been used, with one case report with TS and severe liver dysfunction showing rapid resolution of thyroid hormones and improvement of bilirubin ( 37 ). A retrospective case series also demonstrated significant improvement in thyroid hormone levels in patients with hyperthyroidism with severe liver dysfunction (although this study was primarily powered to show improvement and safety of use of RAI with combined with MARS in patients with severe hyperthyroidism and liver disease) ( 38 ). These reports provide early evidence of the utility of novel extra-corporeal systems in correcting thyroid hormone levels especially in patients with either kidney or liver dysfunction, although more research into the underlying mechanism and validation of results are required before recommendations can be made for its supportive use.

These cases provide some evidence of the use and benefits of extra-corporeal systems in the management of TS, after conventional pharmacotherapy is unsuccessful or contraindicated. Owing to the efficacy of pharmacotherapy and risks of extra-corporeal systems, conventional pharmacotherapy should be always be instituted as initial therapy. Comparison trials between pharmacotherapy and extra-corporeal systems or randomized controlled trials are unavailable due to the rarity of TS, and are unlikely to be performed now given the established efficacy of first line pharmacological agents. Retrospective analysis from the National Inpatient Database in Japan has shown that use of extra-corporeal systems is associated with higher mortality. It reported increased mortality in patients requiring hemodialysis and TPE with adjusted odds ratio for mortality at 4.81. The mortality was 61.9% in 13 out of 21 patients, compared to a mortality of 43.3% requiring either hemodialysis or TPE, and 7.8% requiring neither support. The use of ECMO had a trend towards increased mortality (2.86, CI 0.69-11.92), with a mortality of 72.2% among 13 of 18 patients, as compared to 9.3% in patients not requiring ECMO ( 39 ). These numbers, albeit small, suggest a significantly higher mortality in patients requiring use of extra-corporeal systems, and this differs from the established mortality rate of 10-30%, and vary significantly from the numbers in our review and White et al.’s review in patients requiring ECMO ( 21 ). Similarly Muller et al. ( 12 ) showed the use of TPE showed significant clinical and biochemical improvement. As patients requiring extra-corporeal systems are typically patients who are more critically ill and have multi-organ failure, as well as the possibility of publication bias, it is likely that the true survival rate of these patients in thyroid storm treated with extra-corporeal systems is likely lower than the published literature. Further research, possibly in the form of prospective multinational studies, may be required in view of the small numbers and limited data currently.

Beta-Blockade – A Double-Edged Sword in TS

While our patient received guideline-directed TS pharmacological therapy in a timely fashion, the development of circulatory collapse with consequent multi-organ failure following intravenous esmolol infusion, an ultra-short acting beta-blocker, deserves further discussion.

The cardiovascular effects in TS are driven largely by T3, leading to increased chronotropy and inotropy, improved diastolic relaxation and decreased peripheral resistance, eventually resulting in high cardiac output (CO) heart failure (HF), estimated to be seen in 6% of patients with thyrotoxicosis. This is thought to be reversible with treatment with thyrotoxicosis, with a small study showing improving in LVEF from 28% to 55% ( 40 ). Cardiomyopathy and LV dysfunction, on the other hand, are only seen in 1% ( 20 , 41 ). HF with low CO has been reported with prolonged severe hyperthyroidism, consequent to persistent tachycardia, and pathologic increase in cardiac workload with demand-supply mismatch ( 42 ). Aside from cardiomyopathy, there is an increased risk of arrhythmias with thyrotoxicosis, typically supraventricular, with rare reported cases of thyrotoxicosis-related VF related to congenital coronary anomalies, hypokalemia, coronary vasospasm and early repolarization ( 43 ), none of which were present in our patient. It is plausible that our patient had low CO thyrocardiac disease with an additional component of myocardial stunning post-cardiac arrest, but his stormy course precluded detailed cardiac imaging.

Tachycardia is almost always present in TS, and patients with tachycardia exceeding 150 beats per minute are associated with a higher mortality rate in a retrospective Japanese cohort ( 44 ). Accordingly, the Japanese Thyroid Association and Japanese Endocrine Society 2016 guidelines ( 45 ) recommend aggressive control of tachycardia including the use of ultra-short acting beta-blockers including esmolol or landiolol. New data are emerging which support the use of esmolol over propranolol, due to its shorter half-life elimination (nine minutes, versus 2.3 hours respectively) and duration of action, as well as its relatively higher beta 1-selectivity ( 46 ). The comparative use of esmolol and propranolol has been studied in other populations such as patients with supraventricular tachycardia, which showed similar response rate but more adverse effect of hypotension seen in the esmolol group (45%, as compared to 18%), although these were mostly asymptomatic and resolved quickly with no complications ( 47 ). Regardless of choice of beta-blockers, its use must be considered with caution in patients with decompensated HF or other features of low CO, where the thyroid-induced hyperadrenergic state plays an important compensatory role in maintaining CO. This is related to either direct catecholamine action or an interaction between the adrenergic system and excessive circulating thyroid hormone ( 48 ). The abolishment of that sympathetic drive through the use of beta-blockers is postulated to lead to the circulatory collapse, as seen in our case. Though initially hypertensive, the temporal association of esmolol infusion and PEA arrest led us to conclude it caused or at least triggered the hemodynamic decompensation in our patient. Abubaker et al. ( 49 ) reviewed a total of 11 cases of circulatory collapse with the use of beta-blockade, mostly with long acting agents including bisoprolol, metoprolol, propranolol, with all but one patient showing evidence of underlying heart failure or cardiomyopathy. The author also highlighted the challenges in managing uncontrolled tachycardia in these patients, with two cases eventually requiring esmolol and landiolol use. To date, there has been no head-to-head trials between the longer acting propranolol as compared to the ultra-short acting esmolol or landiolol. There has no reports of circulatory collapse with use of intravenous esmolol, and only one case report with landiolol ( 50 ). Despite the use of ultra-short acting esmolol, circulatory collapse in our case underscores its class effect, and is strongly associated with fatal outcomes in TS. Close cardiac monitoring and prompt institution of VA ECMO support, as what was done in this case, are recommended. Other forms of supportive therapy including CRRT may be considered until effective and definitive therapies can be instituted to treat TS.

We highlight a case of TS presenting with out-of-hospital cardiac arrest, with further hemodynamic decompensation following beta-blockade and multi-organ failure which limited therapeutic options. Despite prompt initiation of CRRT, VA-ECMO and TPE, he sustained hypoxic-ischemic brain injury. Underscoring the complexities in TS, this case calls for caution with beta-blockade in thyrocardiac disease, close monitoring and prompt organ support, and consideration of early TPE when conventional options fail. A review of the use of TPE and other extra-corporeal systems shows that TPE may be an underutilized rescue treatment for severe thyroid storm not amenable to conventional pharmacotherapy or contraindicated due to side effects or multi-organ involvement. Further study of novel extra-corporeal therapies for TS is needed to uncover its therapeutic potential, especially in the Intensive Care setting.

Author Contributions

All authors were involved in the management of the patient. SL, KW, and SY wrote the first draft of the manuscript. PL and KR reviewed and edited the manuscript. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Keywords: thyroid storm, multi-organ failure, extra-corporeal membrane oxygenation, therapeutic plasma exchange, continuous renal replacement therapy, out-of-hospital cardiac arrest

Citation: Lim SL, Wang K, Lui PL, Ramanathan K and Yang SP (2021) Crash Landing of Thyroid Storm: A Case Report and Review of the Role of Extra-Corporeal Systems. Front. Endocrinol. 12:725559. doi: 10.3389/fendo.2021.725559

Received: 15 June 2021; Accepted: 06 August 2021; Published: 20 August 2021.

Reviewed by:

Copyright © 2021 Lim, Wang, Lui, Ramanathan and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Shir Lynn Lim, [email protected]

† These authors have contributed equally to this work and share first authorship

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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Thyroid Storm NCLEX Review

Thyroid storm NCLEX review notes for students who are prepping to take the NCLEX exam. The endocrine system is made-up of many disorders, such as thyroid storm which is a complication of untreated hyperthyroidism . This NCLEX review is part of an endocrine series of thyroid disorders.

As a student prepping for NCLEX, it is very important you know the details of thyroid storm and how to care for a patient experiencing this condition.

As the nurse taking care of the patient in thyroid storm it is important you understand the signs and symptoms, pathophysiology, causes, nursing interventions, and medical treatments.

Don’t forget to take the quiz on thyroid storm .

In this NCLEX review, you will learn the following:

-Pathophysiology of the thyroid storm -Signs and symptoms of thyroid storm -Causes of thyroid storm -Nursing Interventions -Medications for thyroid storm -Treatments

Lecture on Thyroid Storm

Thyroid Storm

Definition: Life-threatening complication that develops in someone who has hyperthyroidism which is an excessive secretion of thyroid hormones (T3 and T4).

It is usually because hyperthyroidism is not being treated properly, the patient is undiagnosed, or the patient experienced an illness.

In addition, thyroid storm can develop after a thyroidectomy due to the thyroid being manipulated during removal which can cause high amounts of T3 and T4 to enter into the blood stream. However, it is rare because today patients are placed on medications to help combat this.

Causes of Thyroid Storm

Patients will already have hyperthyroidism along with any of the following:

• got an illness or experienced trauma/stress (septic, DKA, surgery, trauma to the gland)
• suffers from Grave’s Disease that is under treated or they became sick
• not taking antithyroid medications properly
• taking medications that increase thyroid hormones (Salicylates: ASA)
• radioactive iodine therapy (CT scan or as treatment) remember the thyroid loves iodine and uses it to make thyroid hormone

Signs & Symptoms of Thyroid Storm

The patient will have typical hyperthyroidism symptoms but they will be S EVERE to the point of death…remember the function of T3 and T4 is to increase body’s metabolism and temperature and to stimulate the sympathetic nervous system (this will be happening at an accelerated rate).

Remember this condition as: A violent storm on the body at an accelerated rate.

• Fever (not just heat intolerance)
• Hypertension—going to exhaust the heart to the point of failure (CHF or MI)
• Tachycardia— going to exhaust the heart to the point of failure (CHF or MI)
• Increase respirations—due to the body working so hard and it needs more oxygen and nutrients…will get respiratory failure if not treated fast
• Very restless, irritable, confused …this will progress to seizures, delirium, coma

Nursing Interventions for Thyroid Storm

• Monitor HR, BP, RR (respiratory failure…may need mechanical ventilation), EKG, Temperature
• Keep environment quiet and patient cool (cooling blankets and sedatives as prescribed)
• No foods containing iodine (seafood…seaweed, dairy, eggs)

Pharmacological Management of Thyroid Storm

• Need to decrease the thyroid hormone:
• Tapazole “Methimazole” : has fewer side effects than PTU…not for first trimester of pregnancy
• P TU “Propylthiouracil” : can be used during 1st trimester…watch for liver failure

Side Effects with these medications: Agranulocytosis and thrombocytopenia and watch for toxicity which will present as signs and symptoms of HYPOTHYROIDISM : slow heart rate, intolerance to cold, drowsy

• Lugol’s solution : Side effects: taste changes metal taste in mouth

2. Decrease fever:

Tylenol NO Salicylates or cooling blankets

3. Decrease effects of thyroid hormones on the body by blocking peripheral conversion of T3 and T4:

•   Beta Blockers: Inderal (not for people with asthma or history of bronchospasm…watch in diabetics can mask hypoglycemia)

4. Prevent further secretion and conversion of thyroid hormones by suppressing immune system with:

• Glucocorticoids (Dexamethasone )

You may be interested in: Diabetes NCLEX Reviews

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Copyright Notice

Recognizing thyroid storm in the neurologically impaired patient

Affiliation.

• 1 Jefferson Hospital for Neuroscience, Philadelphia, PA, USA.
• PMID: 17396537
• DOI: 10.1097/01376517-200702000-00008

Thyroid storm is a life-threatening complication of thyroid dysfunction that is manifested by signs of cardiac arrhythmias, fever, and neurological impairment. These symptoms can easily be attributed to a multitude of factors commonly seen in neurological intensive care units, making the recognition and diagnosis of this event difficult. In this case study, a patient presents with a complicated course of hospitalization exacerbated by thyroid storm. Early nursing care and medical collaboration offset a potentially fatal condition.

Publication types

• Case Reports
• Consciousness Disorders / etiology
• Consciousness Disorders / nursing*
• Critical Care / methods*
• Intracranial Aneurysm / complications
• Intracranial Aneurysm / nursing*
• Nursing Assessment / methods*
• Thyroid Crisis / complications
• Thyroid Crisis / diagnosis
• Thyroid Crisis / nursing*

8 Hyperthyroidism Nursing Care Plans

Use this nursing care plan and management guide to provide care for patients with hyperthyroidism. Enhance your understanding of nursing assessment , interventions, goals, and nursing diagnosis , all specifically tailored to address the unique needs of individuals with hyperthyroidism.

Table of Contents

What is hyperthyroidism, nursing problem priorities, nursing assessment, nursing diagnosis, nursing goals, 1. managing cardiac symptoms, 2. preventing fatigue and enhancing energy balance, 3. maintaining adequate nutrition balance, 4. reducing anxiety and providing emotional support, 5. maintaining tissue integrity, 6. improving thought processes, 7. initiating patient education and health teachings, 8. administer medications and provide pharmacologic support, 9. monitoring results of diagnostic and laboratory procedures, recommended resources.

Hyperthyroidism , also known as Grave’s disease, Basedow’s disease , or thyrotoxicosis  is a metabolic imbalance that results from the overproduction of thyroid hormones triiodothyronine (T3) and thyroxine (T4). The most common form is Graves’ disease, but other forms of hyperthyroidism include toxic adenoma, TSH-secreting pituitary tumor , subacute or silent thyroiditis, and some forms of thyroid cancer .

A thyroid storm  is a rarely encountered manifestation of hyperthyroidism that can be precipitated by such events as thyroid ablation ( surgical or radioiodine), medication overdosage, and trauma . This condition constitutes a medical emergency.

Nursing Care Plans and Management

The nursing care plan and management for patients with hyperthyroidism are focused on promoting optimal thyroid hormone balance, symptom management, and patient education . These goals include ensuring adherence to medication regimen, monitoring vital signs, and assessing for signs of thyroid storm.

The following are the nursing priorities for patients with hyperthyroidism:

• Monitor thyroid function and hormone levels regularly.
• Administer appropriate medications, such as antithyroid drugs or beta blockers.
• Monitor and manage symptoms associated with hyperthyroidism, such as rapid heart rate or weight loss .

Assess for the following subjective and objective data :

• Rapid heartbeat (tachycardia)
• Increased appetite and unintentional weight loss
• Excessive sweating and heat intolerance
• Nervousness, irritability, and anxiety
• Tremors or shaking of the hands
• Fatigue or muscle weakness
• Difficulty sleeping ( insomnia )
• Changes in menstrual patterns
• Frequent bowel movements or diarrhea
• Enlarged thyroid gland (goiter)
• Fine, brittle hair and thinning of the skin
• Bulging eyes (exophthalmos) in Graves’ disease, a specific form of hyperthyroidism.

Following a thorough assessment , a nursing diagnosis is formulated to specifically address the challenges associated with hyperthyroidism based on the nurse ’s clinical judgement and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities.

Goals and expected outcomes may include:

• The client will maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.
• The client will verbalize an increase in the level of energy.
• The client will display an improved ability to participate in desired activities.
• The client will maintain the usual reality orientation.
• The client will recognize changes in thinking/behavior and causative factors.
• The client will demonstrate stable weight with  normal laboratory values  and be free of signs of malnutrition .
• The client will report reduced anxiety to a manageable level.
• The client will maintain moist eye membranes, free of ulcerations.
• The client will identify measures to provide protection for the eyes and prevent complications.
• The client will verbalize understanding of the disease process, therapeutic needs, and potential complications.
• The client will identify the relationship of signs/symptoms to the disease process and correlate symptoms with causative factors.
• The client will initiate necessary lifestyle changes and participate in the treatment regimen.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with hyperthyroidism may include:

Hyperthyroidism can cause a hypermetabolic state which leads to an increased demand for oxygen and nutrients by the body, including the heart. This increased demand can lead to an increase in cardiac load and a decrease in cardiac output, which can be further exacerbated by alterations in heart rate , rhythm, and conduction, as well as changes in venous return and vascular resistance. If left uncontrolled, these factors can contribute to a higher risk of reduced cardiac output and potentially even heart failure in patients with hyperthyroidism.

Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse, poor capillary refill, decreased urinary output, and hypotension . Rapid dehydration can occur, which reduces the circulating volume and compromises cardiac output.

Note history of asthma and bronchoconstrictive disease, sinus bradycardia and heart blocks , advanced HF, or current pregnancy. The presence or potential recurrence of these conditions affects the choice of therapy. For example, use of [beta]-adrenergic blocking agents are contraindicated.

Observe for adverse side effects of adrenergic antagonists: severe decrease in pulse, BP; signs of vascular congestion /HF; cardiac arrest. Indicates the need for reduction or discontinuation of therapy.

Investigate reports of chest pain or angina. This may reflect increased myocardial oxygen demands or ischemia .

Assess pulse and heart rate while the patient is sleeping. Provides a more accurate assessment of tachycardia.

Auscultate heart sounds, note extra heart sounds, development of gallops, and systolic murmurs. Prominent S 1 and murmurs are associated with a forceful cardiac output of a hypermetabolic state; the development of S 3 may warn of impending cardiac failure.

Auscultate breath sounds. Note adventitious sounds. An early sign of pulmonary congestion , reflecting developing cardiac failure.

Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure. General or orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects a compensatory increase in stroke volume and decreased systemic vascular resistance (SVR).

Monitor temperature; provide a cool environment, limit bed linens or clothes, and administer tepid sponge baths. Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis and/or dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.

Record I&O. Note urine specific gravity. Significant fluid losses through vomiting , diarrhea , diuresis, and diaphoresis can lead to profound dehydration , concentrated urine, and weight loss.

Weigh daily. Encourage chair rest or bed rest . Limit unnecessary activities. Activity increases metabolic and circulatory demands, which may potentiate cardiac failure.

Monitor ECG , noting rate and rhythm. Document dysrhythmias. Tachycardia (greater than normally expected with fever and/or increased circulatory demand) may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac output.

Monitor central venous pressure (CVP), if available. Provides a more direct measure of circulating volume and cardiac function.

Monitor laboratory and diagnostic studies . See Laboratory and Diagnostic Procedures

Provide supplemental O 2 as indicated. May be necessary to support increased metabolic demands and/or O 2 consumption.

Provide a hypothermia blanket as indicated. Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O 2   consumption and cardiac workload.

Administer IV fluids as indicated. Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure and the need for inotropic support.

Administer medications as indicated. See Pharmacologic Management

Administer transfusions; assist with plasmapheresis, hemoperfusion, and dialysis. May be done to achieve rapid depletion of the extrathyroidal hormone pool in a desperately ill or comatose patient.

Prepare for possible surgery . Subtotal thyroidectomy (removal of five-sixths of the gland) may be the treatment of choice for hyperthyroidism once a euthyroid state is achieved.

Fatigue is a common symptom of hyperthyroidism, which can be related to the hypermetabolic state that increases the demand for energy in the body, leading to exhaustion . The hyperactivity of the central nervous system and alterations in body chemistry, including changes in hormone levels and electrolyte imbalances, can contribute to feelings of fatigue and weakness in individuals with hyperthyroidism.

Monitor vital signs, noting pulse rate at rest and when active. Pulse is typically elevated and, even at rest, tachycardia (up to 160 beats/min) may be noted.

Note the development of tachypnea , dyspnea , pallor, and cyanosis . O 2 demand and consumption are increased in the hypermetabolic state, potentiating the risk of hypoxia with activity.

Provide a quiet environment; cool room, decreased sensory stimuli, soothing colors, and quiet music. Reduces stimuli that may aggravate agitation, hyperactivity, and insomnia .

Encourage the patient to restrict activity and rest in bed as much as possible. Helps counteract the effects of increased metabolism.

Provide comfort measures: touch therapy or massage , cool showers. Patients with dyspnea will be most comfortable sitting in a high Fowler’s position. May decrease nervous energy, promoting relaxation .

Provide diversional activities that are calming, e.g., reading, radio, and television. Allows for use of nervous energy in a constructive manner and may reduce anxiety.

Avoid topics that irritate or upset patients. Discuss ways to respond to these feelings. Increased irritability of the CNS may cause the patient to be easily excited, agitated, and prone to emotional outbursts.

Discuss with SO reasons for fatigue and emotional lability. Understanding that the behavior is physically based may enhance coping with the current situation and encourage SO to respond positively and provide support for the patient.

Administer medications as indicated: Sedatives such as phenobarbital (Luminal); antianxiety agents; chlordiazepoxide (Librium) See Pharmacologic Management

Patients with hyperthyroidism often experience weight loss due to increased metabolic rate, decreased appetite, and increased nutrient utilization. The excess production of thyroid hormones speeds up the body’s metabolism, causing a higher rate of calorie burning and subsequent weight loss. Moreover, the increased metabolic activity may lead to increased nutrient requirements and nutrient depletion, necessitating a focus on adequate nutrition and nutrient supplementation to address potential deficiencies.

Monitor daily food intake. Weigh daily and report losses. Continued weight loss in the face of adequate caloric intake may indicate failure of antithyroid therapy.

Encourage the patient to eat and increase the number of meals and snacks. Give or suggest high-calorie foods that are easily digested. Aids in keeping caloric intake high enough to keep up with the rapid expenditure of calories caused by the hypermetabolic state.

Provide a balanced diet, with six meals per day. To promote weight gain . Note: If the patient has edema , suggest a low- sodium diet.

Avoid foods that increase peristalsis and fluids that cause diarrhea . Increased motility of the GI tract may result in diarrhea and impair the absorption of needed nutrients.

Consult with a dietitian to provide a diet high in calories, protein, carbohydrates, and vitamins. May need assistance to ensure adequate intake of nutrients, and identify appropriate supplements.

Administer medications as indicated: glucose , vitamin B complex, and insulin (small doses). Given to meet energy requirements and prevent or correct hypoglycemia . Insulin aids in controlling serum glucose if elevated.

Anxiety is a common symptom of hyperthyroidism, which can be related to the hypermetabolic state that increases the body’s production of stress hormones, such as cortisol, and the pseudo-catecholamine effect of thyroid hormones. This can lead to an overstimulation of the sympathetic nervous system, causing symptoms of anxiety, nervousness, and irritability in individuals with hyperthyroidism.

Observe behavior indicative of the level of anxiety. Mild anxiety may be displayed by irritability and insomnia . Severe anxiety progressing to the panic state may produce feelings of impending doom, terror, inability to speak or move, shouting, or swearing.

Monitor physical responses, noting palpitations, repetitive movements, hyperventilation, and insomnia . Increased number of [beta]-adrenergic receptor sites, coupled with effects of excess thyroid hormones, produce clinical manifestations of catecholamine excess even when normal levels of norepinephrine or epinephrine exist.

Stay with the patient, maintaining a calm manner. Acknowledge fear and allow the patient’s behavior to belong to the patient. Affirms to the patient or SO that although the patient feels out of control, the environment is safe. Avoiding personal responses to inappropriate remarks or actions prevents conflicts or overreactions to a stressful situation.

Describe and explain procedures, the surrounding environment, or sounds that may be heard by the patient. Provides accurate information, which reduces distortions and confusion that can contribute to anxiety and/or fear reactions.

Speak in brief statements. Use simple words. Attention span may be shortened, and concentration reduced, limiting the ability to assimilate information.

Reduce external stimuli: Place in a quiet room; provide soft, soothing music; reduce bright lights; reduce the number of persons having contact with the patient. Creates a therapeutic environment; shows recognition that unit activity or personnel may increase patient’s anxiety.

Discuss with the patient and/or SO reasons for emotional lability and/or psychotic reaction. Understanding that behavior is physically based enhances acceptance of the situation and encourages different responses and approaches.

Reinforce the expectation that emotional control should return as drug therapy progresses. Provides information and reassures the patient that the situation is temporary and will improve with treatment.

Administer antianxiety agents or sedatives and monitor their effects. May be used in conjunction with a medical regimen to reduce the effects of hyperthyroid secretion.

Refer to support systems as needed: counseling, social services, pastoral care. Ongoing therapy support may be desired or required by the patient/SO if the crisis precipitates lifestyle alterations

Due to alterations in the protective mechanisms of the eye, including impaired closure of the eyelid and the development of exophthalmos (protrusion of the eyeball). These changes can lead to an increased risk of eye infections, corneal ulcers, and other complications that can impair tissue integrity and compromise visual function in individuals with hyperthyroidism.

Encourage the use of dark glasses when awake and taping the eyelids shut during sleep as needed. Suggest the use of sunglasses or eyepatch. Moisten conjunctiva often with isotonic eye drops . Protects exposed cornea if the patient is unable to close eyelids completely because of edema or fibrosis of fat pads and/or exophthalmos.

Elevate the head of the bed and restrict salt intake if indicated. Decreases tissue edema when appropriate: HF, which can aggravate existing exophthalmos.

Instruct patient in extraocular muscle exercises if appropriate. Improves circulation and maintains the mobility of the eyelids.

Provide an opportunity for the patient to discuss feelings about altered appearance and measures to enhance self-image. Protruding eyes may be viewed as unattractive. Appearance can be enhanced with the proper use of makeup, overall grooming , and the use of shaded glasses.

Administer medications as indicated . See Pharmacologic Management

Prepare for possible surgery as indicated. Eyelids may need to be sutured shut temporarily to protect the corneas until edema resolves (rare) or increasing space within the sinus cavity and adjusting musculature may return the eye to a more normal position.

Patients with hyperthyroidism may experience changes in their thought processes due to the effects of excess thyroid hormone on the brain and nervous system. These changes can include increased irritability, anxiety, restlessness, difficulty concentrating, and rapid or racing thoughts.

Assess the thinking process. Determine attention span, and orientation to place, person, or time. Determines the extent of interference with sensory processing

Note changes in behavior. May be hypervigilant, restless, extremely sensitive, or crying or may develop frank psychosis.

Assess the level of anxiety. Anxiety may alter thought processes.

Provide a quiet environment; decreased stimuli, cool room, dim lights. Limit procedures and/or personnel. Reduction of external stimuli may decrease hyperactivity or reflexes, CNS irritability, and auditory and/or visual hallucinations .

Reorient to person, place, or time as indicated. Helps establish and maintain awareness of reality and the environment.

Present reality concisely and briefly without challenging illogical thinking. Limits defensive reaction.

Provide a clock, calendar, and room with an outside window; alter the level of lighting to simulate day or night. Promotes continual orientation cues to assist the patient in maintaining a sense of normalcy.

Encourage visits by family and/or SO. Provide support as needed. Aids in maintaining socialization and orientation. Note: The patient’s agitation and/or psychotic behavior may precipitate family conflicts.

Provide safety measures. Pad side rails , close supervision, and applying soft restraints as last resort as necessary. Prevents injury to the patient who may be hallucinating or disoriented.

Administer medication as indicated: sedatives, antianxiety agents, and/or antipsychotic drugs. Promotes relaxation , and reduces CNS hyperactivity and agitation to enhance thinking ability.

Patient education and health teachings for patients with hyperthyroidism include providing information about the condition, its causes, symptoms, and potential complications. Patients should be educated about the importance of medication adherence, regular follow-up appointments, and lifestyle modifications such as stress management, adequate rest, and a balanced diet to support the patient’s well-being and thyroid health.

Identify signs and symptoms requiring medical evaluation : fever, sore throat , and skin eruptions. Early identification of toxic reactions (thiourea therapy) and prompt intervention are important in preventing the development of agranulocytosis.

Monitor CBC periodically. To detect leukopenia, thrombocytopenia, and agranulocytosis if the patient is taking propylthiouracil and methimazole . Instruct to take medications with meals to minimize GI distress and to avoid OTC cough preparations because many contain iodine.

Identify stressors and discuss precipitators to thyroid crises: personal or social and job concerns, infection , pregnancy. Psychogenic factors are often of prime importance in the occurrence and/or exacerbation of this disease.

Review the disease process and future expectations. Provides a knowledge base from which patients can make informed choices.

Provide information appropriate to the individual situation. This information includes the severity of the condition, cause, age, and concurrent complications to determine the course of treatment.

Provide information about the signs and symptoms of hypothyroidism and the need for continuous follow-up care. A patient who has been treated for hyperthyroidism needs to be aware of the possible development of hypothyroidism , which can occur immediately after treatment or as long as 5 yr later.

After Radioactive Iodine (I-131) therapy, tell the patient not to expectorate or cough freely. Stress the need for repeated measurement of serum T4 levels. Saliva will be radioactive for 24 hours.

Discuss drug therapy, including the need for adhering to the regimen, and expected therapeutic and side effects. Antithyroid medication (either as primary therapy or in preparation for thyroidectomy) requires adherence to a medical regimen over an extended period to inhibit hormone production. Agranulocytosis is the most serious side effect that can occur, and alternative drugs may be given if problems arise.

Explain the need to check with a physician and/or pharmacist before taking other prescribed or OTC drugs. Antithyroid medications can affect or be affected by numerous other medications, requiring monitoring of medication levels, side effects, and interactions.

Emphasize the importance of planned rest periods. Prevents undue fatigue ; reduces metabolic demands. As the euthyroid state is achieved, stamina and activity levels will increase.

Review the need for a nutritious diet and periodic review of nutrient needs. Tell the patient to avoid caffeine, red/yellow food dyes, and artificial preservatives. Provides adequate nutrients to support the hypermetabolic state. A hormonal imbalance is corrected, and the diet will need to be readjusted to prevent excessive weight gain. Irritants and stimulants should be limited to avoid cumulative systemic effects.

Stress the necessity of continued medical follow-up. Necessary for monitoring the effectiveness of therapy and prevention of potentially fatal complications.

Medications used for the management of hyperthyroidism may include antithyroid drugs such as methimazole or propylthiouracil, which work to reduce the production of thyroid hormones. Beta-blockers like propranolol may be prescribed to alleviate symptoms such as rapid heart rate, tremors, and anxiety. These medications help to regulate thyroid hormone levels and alleviate the associated symptoms and promote thyroid function.

Thyroid hormone antagonists: propylthiouracil (PTU), methimazole ( Tapazole ) May be a definitive treatment or used to prepare the patient for surgery , but the effect is slow and so may not relieve thyroid storm. Once PTU therapy is begun, abrupt withdrawal may precipitate a thyroid crisis. Acts to prevent the release of thyroid hormone into circulation by increasing the amount of thyroid hormone stored within the gland. May interfere with RAI treatment and may exacerbate the disease in some people.

Beta-blockers: propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol (Visken) Given to control the thyrotoxic effects of tachycardia, tremors, and nervousness, and is the first drug of choice for an acute storm. Decreases heart rate or cardiac work by blocking [beta]-adrenergic receptor sites and blocking the conversion of T4 to T3. If severe bradycardia develops, atropine may be required. Blocks thyroid hormone synthesis and inhibits the peripheral conversion of T4 to T3.

Strong iodine solution (Lugol’s solution) or supersaturated potassium iodide (SSKI) PO May be used as surgical preparation to decrease the size and vascularity of the gland or to treat thyroid storm. Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine. If iodide is part of the treatment, mix it with milk juice, or water to prevent GI distress and administer it through a straw to prevent tooth discoloration.

RAI (Na131I or Na125I) following NRC regulations for radiopharmaceutical Radioactive iodine therapy is the treatment of choice for almost all patients with Graves’ disease because it destroys abnormally functioning gland tissue. Peak results take 6–12 wk (several treatments may be necessary); however, a single dose controls hyperthyroidism in about 90% of patients. This therapy is contraindicated during pregnancy. Also, people preparing or administering the dose must have their own thyroid burden measured, and contaminated supplies and equipment must be monitored and stored until decayed.

Corticosteroids: dexamethasone (Decadron) Provides glucocorticoid support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces the peripheral conversion of T3 from T4. May be given before thyroidectomy and discontinued after surgery .

Digoxin (Lanoxin) Digitalization may be required in patients with HF before [beta]-adrenergic blocking therapy can be considered or safely initiated.

Potassium (KCl, K-Lyte) Increased losses of K+ through intestinal and/or renal routes may result in dysrhythmias if not corrected.

Acetaminophen (Tylenol) Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases the level of circulating thyroid hormones by blocking the binding of T3 and T4 with thyroid-binding proteins.

Sedative, barbiturates Promotes rest, thereby reducing metabolic demands and cardiac workload.

Furosemide ( Lasix ) Diuresis may be necessary if HF occurs. It also may be effective in reducing calcium level if the neuromuscular function is impaired.

Muscle relaxants Reduces shivering associated with hyperthermia, which can further increase metabolic demands.

Sedatives such as phenobarbital (Luminal); antianxiety agents; chlordiazepoxide (Librium) Combats nervousness, hyperactivity, and insomnia.

Methylcellulose drops Lubricates the eyes, reducing the risk of lesion formation.

Adrenocorticotropic hormone (ACTH), prednisone Given to decrease rapidly progressive and marked inflammation.

Antithyroid drugs May decrease signs and symptoms or prevent the worsening of the condition.

Laboratory and diagnostic procedures for patients with hyperthyroidism commonly include thyroid function tests such as measurement of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and total or free triiodothyronine (T3). These tests help evaluate the levels of thyroid hormones in the blood and determine the functioning of the thyroid gland. While potassium and calcium tests are done to assess the electrolyte balance and detect any abnormalities that may occur due to the thyroid hormone imbalance.

Serum potassium Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. In the presence of thyrotoxic paralysis (primarily occurring in Asian men), close monitoring and cautious replacement are indicated because rebound hyperkalemia can occur as the condition abates releasing potassium from the cells.

Serum calcium Elevation may alter cardiac contractility.

Sputum culture Pulmonary infection is the most frequent precipitating factor of crisis.

Serial ECGs May demonstrate the effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in the presence of increased metabolic demands.

Chest X-ray s Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy .

Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.

Nursing Care Plans – Nursing Diagnosis & Intervention (10th Edition) Includes over two hundred care plans that reflect the most recent evidence-based guidelines. New to this edition are ICNP diagnoses, care plans on LGBTQ health issues, and on electrolytes and acid-base balance.

Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales Quick-reference tool includes all you need to identify the correct diagnoses for efficient patient care planning. The sixteenth edition includes the most recent nursing diagnoses and interventions and an alphabetized listing of nursing diagnoses covering more than 400 disorders.

Nursing Diagnosis Manual: Planning, Individualizing, and Documenting Client Care  Identify interventions to plan, individualize, and document care for more than 800 diseases and disorders. Only in the Nursing Diagnosis Manual will you find for each diagnosis subjectively and objectively – sample clinical applications, prioritized action/interventions with rationales – a documentation section, and much more!

All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health   Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.

Other recommended site resources for this nursing care plan:

• Nursing Care Plans (NCP): Ultimate Guide and Database MUST READ! Over 150+ nursing care plans for different diseases and conditions. Includes our easy-to-follow guide on how to create nursing care plans from scratch.
• Nursing Diagnosis Guide and List: All You Need to Know to Master Diagnosing Our comprehensive guide on how to create and write diagnostic labels. Includes detailed nursing care plan guides for common nursing diagnostic labels.

Other nursing care plans related to endocrine system and metabolism disorders:

• Respiratory Acidosis  Nursing Care Plan
• Respiratory Alkalosis Nursing Care Plan
• Metabolic Acidosis Nursing Care Plan
• Metabolic Alkalosis Nursing Care Plan
• Addison’s Disease  | 3 Care Plans
• Cushing’s Disease  | 6 Care Plans
• Diabetes Mellitus Type 1 (Juvenile Diabetes) | 4 Care Plans
• Diabetes Mellitus Type 2  | 20 Care Plans UPDATED!
• Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)  | 4 Care Plans
• Eating Disorders: Anorexia & Bulimia Nervosa  | 7 Care Plans
• Fluid Balance: Hypervolemia & Hypovolemia
• Potassium (K) Imbalances: Hyperkalemia and Hypokalemia
• Sodium (Na) Imbalances: Hypernatremia and Hyponatremia
• Magnesium (Mg) Imbalances: Hypermagnesemia and Hypomagnesemia
• Calcium (Ca) Imbalances: Hypercalcemia and Hypocalcemia
• Gestational Diabetes Mellitus | 4 Care Plans
• Hyperthyroidism  | 7 Care Plans
• Hypothyroidism  | 3 Care Plans
• Obesity  | 5 Care Plans
• Thyroidectomy  | 5 Care Plans

5 thoughts on “8 Hyperthyroidism Nursing Care Plans”

Super post. Do you have any other ones you can give? I like super stuff. :)

This content has really improved my knowledge about hyperthyroidism. Thank you so much

Wow, this information just made my nursing carrier much easier.

Hi Arom, Awesome to know the hyperthyroidism care plans are making your nursing life easier! If you need more tips or info on anything else, feel free to reach out. Here to help!

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Thyrotoxicosis (Thyroid Storm) Nursing Care Plan & Management

Description.

Thyroid storm is a life-threatening condition in which  patients with underling thyroid dysfunction inhibit exaggerated signs and symptoms of hyperthyroidism. Thyroid storm is precipitated by stressors such as infection, trauma, DKA, surgery, heart failure, or stroke. The condition can result from discontinuation of antithyroid medication or as a result of untreated or inadequate treatment of hyperthyroidism. The excess thyroid hormones increase metabolism and affect the sympathetic nervous system, thus increasing oxygen consumption and heat production and altering fluid and electrolyte levels.

image by: http://hyperthyroidismsymptomsx.com/

Signs And Symptoms

• Sudden onset of fever
• Profuse palm sweating
• Tachydysrhythmias
• Extreme restlessness
• Weight loss
• Muscle weakness

Physical Examination

Vital signs.

• Systolic hypertension or hypotension
• HR: tachycardia disproportionate to the degree  of fever
• RR: >20 breaths/ min
• Temperature >102.2 °F can be higher
• Delirious coma

Cardiovascular

• Bounding pulses
• Systolic murmur
• Widening pulse
• Weak thready pulses
• Tachycardia
• Crackles may be present

Gastrointestinal

• Increased bowel sounds
• Thyroid may be enlarged or nodular

Acute Care Patient Management

Nursing Diagnosis: Decreased cardiac output related to increased cardiac work secondary to increased adrenergic activity; Deficient fluid volume secondary to increased metabolism and diaphoresis.

Outcome Criteria

• Patient alert and oriented
• Peripheral pulses palpable
• Lung clear to auscultation
• Urine output 30 ml/hr
• Absence of life-threatening dysrhythmias

Patient Monitoring

• Continuously monitor ECG for dysrhythmias or HR ? 140 beats/min that can adversely affect cardiac output and monitor for ST segment changes indicative of myocardial ischemia.
• Continuously monitor oxygen saturation with pulse oximetry.
• Continuously monitor pulmonary artery pressure.
• Monitor fluid volume status; measure urine output hourly and determine fluid balance every 8 hours.

Patient Assessment

• Assess cardiovascular status; extra heart sounds, complaints of orthopnea or dyspnea on exertion.
• Assess hydration status because dehydration can further decrease circulating volume and compromise cardiac output.
• Assess for pressure ulcer development secondary to hypoperfusion.

Diagnostic Assessment

• REVIEW THYROID STUDIES AS AVAILABLE.
• Review serial serum electrolytes, serum glucose, and serum calcium levels to evaluate the patient’s response to therapy.
• Review serial ABGs for hypoxemia and acid-base imbalance, which can adversely affect cardiac function.
• Review serial chest radiographs for cardiac enlargement and pulmonary congestion.

Patient Management

• Administer dextrose-containing intravenous fluids as ordered to correct fluid and glucose deficits.
• Carefully assess the patient for heart failure or pulmonary edema.
• Dopamine may be used to support blood pressure.
• Provide supplemental oxygen as ordered to help meet increased metabolic demands.
• Once the patient is hemodynamically stable, provide pulmonary hygiene to reduce pulmonary complications.
• If the patient is in heart failure, typical pharmacologic agents for treatment of heart failure may also be indicated.
• Reduce oxygen demands by decreasing anxiety, reduce fever, decrease pain, and limit visitors if necessary.
• Anticipate aggressive treatment of precipitating factor.
• Institute pressure ulcer strategies.

[mtouchquiz 476]

Nursing Care Plan

Hyperthyroidism nursing care plan, nursing diagnosis.

• Risk for Decreased Cardiac Output

Risk factors may include

• Uncontrolled hyperthyroidism, hypermetabolic state
• Increasing cardiac workload
• Changes in venous return and systemic vascular resistance
• Alterations in rate, rhythm, conduction

Possibly evidenced by

• Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred and nursing interventions are directed at prevention.

Desired Outcomes

• Maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.

Nursing Interventions

• Rationale: General or orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects compensatory increase in stroke volume and decreased systemic vascular resistance (SVR).
• Rationale: Provides more direct measure of circulating volume and cardiac function.
• Rationale: May reflect increased myocardial oxygen demands or ischemia.
• Rationale: Provides a more accurate assessment of tachycardia.
• Rationale: Prominent S 1  and murmurs are associated with forceful cardiac output of hypermetabolic state; development of S 3  may warn of impending cardiac failure.
• Rationale: Tachycardia (greater than normally expected with fever and/or increased circulatory demand) may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac output.
• Rationale: Early sign of pulmonary congestion, reflecting developing cardiac failure.
• Rationale: Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis and/or dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.
• Rationale: Rapid dehydration can occur, which reduces circulating volume and compromises cardiac output.
• Rationale: Significant fluid losses through vomiting, diarrhea, diuresis, and diaphoresis can lead to profound dehydration, concentrated urine, and weight loss.
• Rationale: Activity increases metabolic and circulatory demands, which may potentiate cardiac failure.
• Rationale: Presence or potential recurrence of these conditions affects choice of therapy. For example: use of [beta]-adrenergic blocking agents is contraindicated.
• Rationale: Indicates need for reduction or discontinuation of therapy.
• Rationale: Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure and need for inotropic support.

Administer medications as indicated:

• Rationale: May be definitive treatment or used to prepare patient for surgery; but effect is slow and so may not relieve thyroid storm. Once PTU therapy is begun, abrupt withdrawal may precipitate thyroid crisis. Acts to prevent release of thyroid hormone into circulation by increasing the amount of thyroid hormone stored within the gland. May interfere with RAI treatment and may exacerbate the disease in some people.
• Rationale: Given to control thyrotoxic effects of tachycardia, tremors, and nervousness and is first drug of choice for acute storm. Decreases heart rate or cardiac work by blocking [beta]-adrenergic receptor sites and blocking conversion of T 4  to T 3 . If severe bradycardia develops, atropine may be required. Blocks thyroid hormone synthesis and inhibits peripheral conversion of T 4  to T 3 .
• Rationale: May be used as surgical preparation to decrease size and vascularity of the gland or to treat thyroid storm. Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine. If iodide is part of treatment, mix with milk juice, or water to prevent GI distress and administer through a straw to prevent tooth discoloration.
• Rationale: Radioactive iodine therapy is the treatment of choice for almost all patients with Graves’ disease because it destroys abnormally functioning gland tissue. Peak results take 6–12 wk (several treatments may be necessary); however, a single dose controls hyperthyroidism in about 90% of patients. This therapy is contraindicated during pregnancy. Also people preparing or administering the dose must have their own thyroid burden measured, and contaminated supplies and equipment must be monitored and stored until decayed.
• Rationale: Provides glucocorticoid support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces peripheral conversion of T 3  from T 4 . May be given before thyroidectomy and discontinued after surgery.
• Rationale: Digitalization may be required in patients with HF before [beta]-adrenergic blocking therapy can be considered or safely initiated.
• Rationale: Increased losses of K +  through intestinal and/or renal routes may result in dysrhythmias if not corrected.
• Rationale: Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases level of circulating thyroid hormones by blocking binding of T 3  and T 4  with thyroid-binding proteins.
• Rationale: Promotes rest, thereby reducing metabolic demands and cardiac workload.
• Rationale: Diuresis may be necessary if HF occurs. It also may be effective in reducing calcium level if neuromuscular function is impaired.
• Rationale: Reduces shivering associated with hyperthermia, which can further increase metabolic demands.
• Rationale: May be necessary to support increased metabolic demands and/or O 2  consumption.
• Rationale: Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O 2   consumption and cardiac workload.

Monitor laboratory and diagnostic studies:

• Rationale: Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. In the presence of thyrotoxic paralysis (primarily occurring in Asian men), close monitoring and cautious replacement are indicated because rebound hyperkalemia can occur as condition abates releasing potassium from the cells.
• Rationale: Elevation may alter cardiac contractility.
• Rationale: Pulmonary infection is most frequent precipitating factor of crisis.
• Rationale: May demonstrate effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in presence of increased metabolic demands.
• Rationale: Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.
• Rationale: May be done to achieve rapid depletion of extrathyroidal hormone pool in desperately ill or comatose patient.
• Rationale: Subtotal thyroidectomy (removal of five-sixths of the gland) may be treatment of choice for hyperthyroidism once euthyroid state is achieved.

May be related to

• Hypermetabolic state with increased energy requirements
• Irritability of central nervous system (CNS); altered body chemistry
• Verbalization of overwhelming lack of energy to maintain usual routine, decreased performance
• Emotional lability/irritability; nervousness, tension
• Jittery behavior
• Impaired ability to concentrate
• Verbalize increase in level of energy.
• Display improved ability to participate in desired activities.
• Rationale: Pulse is typically elevated and, even at rest, tachycardia (up to 160 beats/min) may be noted.
• Rationale: O 2  demand and consumption are increased in hypermetabolic state, potentiating risk of hypoxia with activity.
• Rationale: Reduces stimuli that may aggravate agitation, hyperactivity, and insomnia.
• Rationale: Helps counteract effects of increased metabolism.
• Rationale: May decrease nervous energy, promoting relaxation.
• Rationale: Allows for use of nervous energy in a constructive manner and may reduce anxiety.
• Rationale: Increased irritability of the CNS may cause patient to be easily excited, agitated, and prone to emotional outbursts.
• Rationale: Understanding that the behavior is physically based may enhance coping with current situation and encourage SO to respond positively and provide support for patient.
• Rationale: Combats nervousness, hyperactivity, and insomnia.
• Risk for Disturbed Thought Processes
• Physiological changes: increased CNS stimulation/accelerated mental activity
• Altered sleep patterns
• Maintain usual reality orientation.
• Recognize changes in thinking/behavior and causative factors.
• Rationale: Determines extent of interference with sensory processing
• Rationale: May be hypervigilant, restless, extremely sensitive, or crying or may develop frank psychosis.
• Rationale: Anxiety may alter thought processes.
• Rationale: Reduction of external stimuli may decrease hyperactivity or reflexia, CNS irritability, auditory and/or visual hallucinations.
• Rationale: Helps establish and maintain awareness of reality and environment.
• Rationale: Limits defensive reaction.
• Rationale: Promotes continual orientation cues to assist patient in maintaining sense of normalcy.
• Rationale: Aids in maintaining socialization and orientation. Note: Patient’s agitation and/or psychotic behavior may precipitate family conflicts.
• Rationale: Prevents injury to patient who may be hallucinating or disoriented.
• Rationale: Promotes relaxation, reduces CNS hyperactivity and agitation to enhance thinking ability.

Nursing Diagnosis

• Risk for Imbalanced Nutrition: Less Than Body Requirements
• Increased metabolism (increased appetite/intake with loss of weight)
• Nausea/vomiting, diarrhea
• Relative insulin insufficiency; hyperglycemia
• Demonstrate stable weight with normal laboratory values and be free of signs of malnutrition.
• Rationale: Continued weight loss in face of adequate caloric intake may indicate failure of antithyroid therapy.
• Rationale: Aids in keeping caloric intake high enough to keep up with rapid expenditure of calories caused by hypermetabolic state.
• Rationale: To promote weight gain. Note: If patient has edema, suggest a low-sodium diet.
• Rationale: Increased motility of GI tract may result in diarrhea and impair absorption of needed nutrients.
• Rationale: May need assistance to ensure adequate intake of nutrients, identify appropriate supplements.
• Rationale: Given to meet energy requirements and prevent or correct hypoglycemia. Insulin aids in controlling serum glucose if elevated.
• Anxiety [specify level]
• Physiological factors: hypermetabolic state (CNS stimulation), pseudo catecholamine effect of thyroid hormones
• Increased feelings of apprehension, shakiness, loss of control, panic
• Changes in cognition, distortion of environmental stimuli
• Extraneous movements, restlessness, tremors
• Appear relaxed.
• Report anxiety reduced to a manageable level.
• Identify healthy ways to deal with feelings.
• Rationale: Mild anxiety may be displayed by irritability and insomnia. Severe anxiety progressing to panic state may produce feelings of impending doom, terror, inability to speak or move, shouting or swearing.
• Rationale: Increased number of [beta]-adrenergic receptor sites, coupled with effects of excess thyroid hormones, produces clinical manifestations of catecholamine excess even when normal levels of norepinephrine or epinephrine exist.
• Rationale: Affirms to patient or SO that although patient feels out of control, environment is safe. Avoiding personal responses to inappropriate remarks or actions prevents conflicts or overreaction to stressful situation.
• Rationale: Provides accurate information, which reduces distortions and confusion that can contribute to anxiety and/or fear reactions.
• Rationale: Attention span may be shortened, concentration reduced, limiting ability to assimilate information.
• Rationale: Creates a therapeutic environment; shows recognition that unit activity or personnel may increase patient’s anxiety.
• Rationale: Understanding that behavior is physically based enhances acceptance of situation and encourages different responses and approaches.
• Rationale: Provides information and reassures patient that the situation is temporary and will improve with treatment.
• Rationale: May be used in conjunction with medical regimen to reduce effects of hyperthyroid secretion.
• Rationale: Ongoing therapy support may be desired or required by patient/SO if crisis precipitates lifestyle alterations
• Risk for Impaired Tissue Integrity
• Alterations of protective mechanisms of eye: impaired closure of eyelid/exophthalmos
• Maintain moist eye membranes, free of ulcerations.
• Identify measures to provide protection for eyes and prevent complications.
• Rationale: Protects exposed cornea if patient is unable to close eyelids completely because of edema or fibrosis of fat pads and/or exophthalmos.
• Rationale: Decreases tissue edema when appropriate: HF, which can aggravate existing exophthalmos.
• Rationale: Improves circulation and maintains mobility of the eyelids.
• Rationale: Protruding eyes may be viewed as unattractive. Appearance can be enhanced with proper use of makeup, overall grooming, and use of shaded glasses.
• Rationale: Lubricates the eyes, reducing risk of lesion formation.
• Rationale: Given to decrease rapidly progressive and marked inflammation.
• Rationale: May decrease signs and symptoms or prevent worsening of the condition.
• Rationale: Can decrease edema in mild involvement.
• Rationale: Eyelids may need to be sutured shut temporarily to protect the corneas until edema resolves (rare) or increasing space within sinus cavity and adjusting musculature may return eye to a more normal position.
• Knowledge, deficient [Learning Need] regarding condition, prognosis, treatment, self-care, and discharge needs
• Lack of exposure/recall
• Information misinterpretation
• Unfamiliarity with information resources
• Questions, request for information, statement of misconception
• Inaccurate follow-through of instructions/development of preventable complications
• Verbalize understanding of disease process and potential complications.
• Identify relationship of signs/symptoms to the disease process and correlate symptoms with causative factors.
• Verbalize understanding of therapeutic needs.
• Initiate necessary lifestyle changes and participate in treatment regimen.
• Rationale: Provides knowledge base from which patient can make informed choices.
• Rationale: Severity of condition, cause, age, and concurrent complications determine course of treatment.
• Rationale: Psychogenic factors are often of prime importance in the occurrence and/or exacerbation of this disease.
• Rationale: Patient who has been treated for hyperthyroidism needs to be aware of possible development of hypothyroidism, which can occur immediately after treatment or as long as 5 yr later.
• Rationale: Saliva will be radioactive for 24 hours.
• Rationale: To detect leukopenia, thrombocytopenia, and agranulocytosis if the patient is taking propylthiouracil and methimazole. Instruct to take medications with meals to minimize GI distress and to avoid OTC cough preparations because many contain iodine.
• Rationale: Antithyroid medication (either as primary therapy or in preparation for thyroidectomy) requires adherence to a medical regimen over an extended period to inhibit hormone production. Agranulocytosis is the most serious side effect that can occur, and alternative drugs may be given if problems arise.
• Rationale: Early identification of toxic reactions (thiourea therapy) and prompt intervention are important in preventing development of agranulocytosis.
• Rationale: Antithyroid medications can affect or be affected by numerous other medications, requiring monitoring of medication levels, side effects, and interactions.
• Rationale: Prevents undue fatigue; reduces metabolic demands. As euthyroid state is achieved, stamina and activity level will increase.
• Rationale: Provides adequate nutrients to support hypermetabolic state. A hormonal imbalance is corrected, diet will need to be readjusted to prevent excessive weight gain. Irritants and stimulants should be limited to avoid cumulative systemic effects.
• Rationale: Necessary for monitoring effectiveness of therapy and prevention of potentially fatal complications.

Other Possible Nursing Care Plans

• Imbalanced Nutrition: Less Than Body Requirements —may be related intake less than metabolic needs secondary to excessive metabolic rate.
• Risk for Injury —related to tremors.
• Risk for Hyperthermia —may be related to lack of metabolic compensatory mechanisms secondary to hyperthyroidism.
• Activity Intolerance —may be related to fatigue, exhaustion secondary to excessive metabolic rate.
• Diarrhea —may be related to increased peristalsis secondary to excessive metabolic rate.
• Impaired Comfort —may be related to heat intolerance and profuse diaphoresis.
• Risk for Impaired Tissue Integrity: Corneal—may be related to inability to close eyelids secondary to exophthalmos.
• Risk for Ineffective Therapeutic Regimen Management —may be related to insufficient knowledge of condition, treatment regimen, pharmacologic therapy, eye care, dietary management, and signs and symptoms of complication.

Related Posts

Billroth surgery, increased intracranial pressure nursing care plan & management.

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Article Contents

Primary specialties involved other than cardiology, introduction, case presentation, lead author biography, supplementary material.

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Case report: a patient with thyroid storm, refractory cardiogenic shock, and cardiac arrest treated with Lugol's iodine solution and veno-arterial extra corporal membrane oxygenation support

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Marianne Voll, Kristin Astrid Øystese, Erik Høiskar, Odd Johansen, Cecilie Nyvold, Ingrid Norheim, Thomas G von Lueder, Geir Øystein Andersen, Case report: a patient with thyroid storm, refractory cardiogenic shock, and cardiac arrest treated with Lugol's iodine solution and veno-arterial extra corporal membrane oxygenation support, European Heart Journal - Case Reports , Volume 5, Issue 2, February 2021, ytab017, https://doi.org/10.1093/ehjcr/ytab017

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Thyroid storm is a life-threatening condition. Refractory cardiogenic shock and cardiac arrest are rare complications of thyroid storm and the treatment options are limited.

A 35-year- old woman treated for Grave’s disease was admitted with thyrotoxicosis complicated by infection and neutropenia caused by thionamide treatment. After treatment including beta-blockers, steroids, and Lugol’s iodine solution, she went into cardiac arrest. Echocardiography after resuscitation demonstrated severe biventricular heart failure. The patient was in refractory cardiogenic shock with recurrent cardiac arrest and mechanical circulatory support with a veno-arterial extra corporal membrane oxygenation (V-A ECMO) circuit was established. After 2 days on V-A ECMO and supportive treatment with iodine solution, glucocorticosteroids, and levosimendan, her myocardial function recovered and thyroid hormone levels were normalized. Veno-arterial extra corporal membrane oxygenation was discontinued, and the patient was treated with early total thyroidectomy. The patient made a full recovery with no neurological/cognitive impairment, as assessed after 4 weeks.

Adverse reactions to standard treatment of hyperthyroidism contributed to this patient’s development of thyroid storm and the following refractory cardiogenic shock. When she was critically unstable, levosimendan improved myocardial function while inotropic support with dobutamine was ineffective, likely due to prolonged beta-antagonist administration. Temporary support with V-A ECMO, until effective lowering of thyroid hormone levels and improvement in myocardial function were obtained, was life-saving in this young patient and may be considered in refractory cardiogenic shock caused by thyroid storm.

Refractory cardiogenic shock with cardiac arrest is a rare complication of thyroid storm

Extracorporeal life support in combination with iodine treatment may be a treatment option in severe cases

Anesthesiology, Intensive care medicine, Endocrine surgery.

Hyperthyroidism affects the heart and the peripheral vasculature by increasing blood volume, heart rate, contractility, cardiac output, and decreasing systemic vascular resistance. 1 Pulmonary hypertension may also be associated with hyperthyroidism and is a contributing cause of right-sided heart failure in these patients. 2 Thyroid storm is an extreme form of hyperthyroidism with heart failure as the leading cause of mortality 3 and a mortality rate as high as 30% in patients developing cardiogenic shock. 4

The patient, a 35-year-old woman without prior heart disease or other comorbidities, was diagnosed with autoimmune hyperthyroidism (Grave’s disease) 2 years before the current event. She received standard treatment with thionamides (carbimazole) for 2 months after being diagnosed with Grave’s. Carbimazole was the discontinued due to development of neutropenia. The patient had untreated Grave’s disease for 2 years. Increased thyrotoxic symptoms forced her to see a doctor. Grave’s disease was again diagnosed (Free T4: 79 pmol/L, free T3: 47 pmol/L, and TRAB-thyroid receptor antibody were high). Treatment was started with carbimazole 10 mg twice daily and a non-selective beta-blocker (propranolol 20 mg 1–2 tablets daily).

One month later, 2 days after discontinuation of carbimazole due to recurring severe neutropenia, she was admitted to her local hospital. At the time of admission, she had high fever, sinus tachycardia (heart rate 110 beats per minute), and general fatigue. Physical examination revealed normal auscultation of the heart and lungs. A diagnosis was made of thyroid storm and a suspected neutropenic sepsis [leucocytes 0.8 × 10 9 /L (ref. 3.5–10.0 × 10 9 /L) and neutrophils 0.0 × 10 9 /L (ref. 1.5–7.3 × 10 9 /L)] related to clinical signs of tonsillitis. Treatment with broad-spectrum antibiotics (penicillin 3 g four times daily and gentamicin 240 mg once daily, both intravenous), high dosage of glucocorticosteroids (hydrocortisone 100 mg four times daily intravenously), and increased dosage of the non-selective beta-blocker propranolol (20 mg four times daily) was initiated. Lugol’s iodine solution (4.5 mg three times daily) was added to the treatment on Day 3. High fever and tachycardia were still present. On the fourth day after admission, acute dyspnoea developed together with circulatory collapse and subsequent cardiac arrest with pulseless electrical activity (PEA). Cardiopulmonary resuscitation (CPR) was started, and a return of spontaneous circulation (ROSC) was obtained after 4 min. After ROSC, she remained severely hypotensive (blood pressure 60/40 mmHg) with sinus tachycardia. She was transferred to the university hospital in a critical unstable state.

On arrival at the university hospital’s emergency department the initial clinical examination revealed a conscious, but cognitively impaired patient, respiratory rate of 30–50 per minute, blood pressure 60/40 mmHg, heart rate 120 beats per minute, temperature 37.8°C, normal respiratory sounds, Graves' ophthalmopathy, and arterial blood gas showed severe lactic acidosis [lactate 17 mmol/L (ref. 0.4–0.8 mmol/L), pH 7.2 (ref. 7.35–7.45) pCO 2 2.9 kPa (ref. 4.7–6.0 kPa), and pO 2 19 kPa (ref 10.0–14. kPa).

Acute pulmonary embolism was suspected as the cause of the cardiac arrest. Bedside echocardiography demonstrated severe biventricular cardiac failure (left ventricular ejection fraction <20%) with the paradoxical movement of the septum ( Figure 1A and B ) and tricuspid regurgitation. Pulmonary embolism could not be excluded based on these findings and computed tomography (CT) pulmonary angiography was indicated but was not performed immediately due to the prohibitive requirement for iodine-containing contrast agents in this setting. Due to the patient’s clinical instability, thrombolysis was given to cover for the possibility of pulmonary embolism. Eventually, a CT scan was performed in the emergency department and pulmonary embolism was excluded.

Echocardiography at admission to the University hospitals’ emergency department demonstrating severe biventricular cardiac failure with dilated right and left ventricle with large tricuspid regurgitation ( A ) and paradoxical movement of the interventricular septum in systole and moderate mitral regurgitation ( B ).

The patient was transferred to the intensive care unit (ICU) in cardiogenic shock with ongoing circulatory support with high doses of norepinephrine, dobutamine, and phenylephrine. Immediately after arriving to the ICU, the patient experienced recurrent episodes of cardiac arrest with PEA with the only temporary effect of CPR.

As the patient was severely haemodynamically unstable due to refractory cardiogenic shock and recurrent cardiac arrest caused by the thyroid storm, the decision was made for a mechanical circulatory support by a veno-arterial extra corporal membrane oxygenation (V-A ECMO) circuit. Support on V-A ECMO was established without complications. Coronary angiography demonstrated normal coronary arteries and an intra-aortic balloon pump (IABP) was inserted. The thyroid storm was treated pharmacologically with escalating doses of iodine solution (Lugol’s iodine solution 22 mg three times daily) and glucocorticoids (hydrocortisone 100 mg four times daily intravenously). Rapid normalization of thyroid hormone levels was obtained ( Figures 2A and 3B ). Beta-blockers were discontinued and levosimendan was commenced on the theoretical consideration of an enhanced inotropic effect 10 compared to conventional β-adrenergic agonists. Myocardial function recovered rapidly ( Figure 3A and B ). After 3 days, V-A ECMO was discontinued, and the patient was extubated the next day. Uneventful total thyroidectomy was performed 5 days later. The patient was discharged after 4 weeks of hospitalization without cognitive sequelae, without any symptoms of heart failure, with normalized myocardial function as judged by echocardiography, and with scheduled close follow-up by endocrinologist.

Temporal profile of free T3 ( A ) and free T4 ( B ) in pmol/L (ref.values: free T3 2.8–7 pmol/L and free T4 8–21 pmol/L).

Stroke volume at the first day ( A ) and second day ( B ) on extra corporal membrane oxygenation treatment. Additional treatment with levosimendan and iodine solution was given.

We herein report on a patient in cardiogenic shock with cardiac arrest due to thyroid storm who was successfully treated with temporary support on V-A ECMO, Lugol’s iodine solution, and surgical thyroidectomy. Cardiogenic shock and cardiac arrest are extremely rare complications of thyrotoxicosis and associated with high mortality, 4 but as demonstrated here, with a potential for complete recovery of myocardial function with excellent prognosis if the patient survives the critical phase. Standard treatment of thyrotoxicosis with non-selective beta-blockers may be detrimental in patients developing heart failure with severely reduced stroke volume due to their negative inotropic and chronotropic effect in a situation where heart rate is critical to maintain cardiac output.

Beyond beta-blockers, standard treatment for autoimmune hyperthyroidism includes thionamides. 1 , 8 Our patient developed agranulocytosis, a rare (0.2–0.5%) adverse effect. 5 Occurrence of agranulocytosis mandates immediate discontinuation of the drug and administration of broad-spectrum antibiotics. 5 The patient was in need of rapid reduction of the markedly elevated thyroid hormones. Glucocorticoids inhibit the conversion of T4 to T3 and are indicated in severe disease. 6 Lugols’s iodine solution rapidly decreases thyroid hormone levels and reduces glandular blood flow. 7

The role of iodine here is worthy of further comment: when our patient acutely deteriorated a CT scan was warranted to exclude pulmonary embolism. Administration of iodine-containing contrast is usually contraindicated in thyrotoxicosis due to the risk of worsening hyperthyroidism. 9 Iodine administration to patients with latent or manifest thyroid disease may have a two-fold effect: early on and within hours, high-dose iodine administration blocks the release of thyroid hormones and inhibits the iodination of thyroglobulin. 9 Since this rapid effect of iodine on lowering thyroid levels usually is transient, only short-term use is recommended. 8 As iodine also is a substrate for new thyroid hormone formation, iodine given over time may lead to hypersecretion of thyroid hormones, usually developing over 2–12 weeks. 9 Since Lugols’s solution also reduces blood flow within the gland, it is used preoperatively before thyroidectomy.

When our patient became critically unstable with cardiogenic shock, she was non-responsive to inotropic support with dobutamine. Dobutamine is an inotropic with an affinity for β1-adrenergic receptors 10 and was probably ineffective due to concomitant use of high dosages of propranolol. The α 1 -adrenergic receptor agonists norepinephrine and phenylephrine had minimal effects on blood pressure in this case. 10 The binding affinities of individual catecholamine’s may be diminished under extreme situations with hypoxia and/or acidosis 10 and our patient had severe lactic acidosis [lactate 17 mmol/L (ref. 0.4–0.8 mmol/L)]. Hyperthyroidism may directly reduce systemic vascular resistance through arterial smooth muscle relaxation. 11 In addition, preclinical data suggest that thyroxine may attenuate the α 1 -receptor-mediated vasoconstrictory effect of adrenaline on the vasculature. 12

The mechanisms underlying the rapid development of severe myocardial dysfunction and cardiogenic shock in our patient are complex and not fully understood. A combination of myocardial dysfunction and reduced diastolic filling time secondary to sustained tachycardia resulting in a hyperdynamic cardiocirculatory state, a negative inotropic effect of beta-blocker administration in a setting with severely reduced stroke volume, and finally, a direct vasoplegic effect of thyroxine 11 resulting in low systemic resistance may have contributed to the clinical scenario.

Here, treatment with Lugol’s iodine solution resulted in rapid decrease in free T3 levels. While hemodynamic support was maintained by V-A ECMO and IABP, stroke volume improved gradually ( Figure 3A and B ). Levosimendan infusion was added in an attempt to further augment contractility. Levosimendan is believed to mediate an inotropic effect through calcium sensitization in addition to phosphodiesterase-3 inhibition, 13 is not affected by beta-blockade and may facilitate weaning from V-A ECMO. Fortunately, our patient responded rapidly to the above treatment, and was only supported by V-A ECMO for 3 days. The definitive treatment of her hyperthyroidism was a total thyroidectomy which was performed without complications. Levothyroxine substitution was started, cardiac function recovered completely, and the patient was discharged without cognitive sequelae or symptoms of heart failure. The potential for complete normalization of myocardial function is a crucial factor in determining whether one should initiate V-A ECMO treatment as a bridge to recovery in similar severe cases of thyroid storm and cardiogenic shock.

Marianne Voll, MD, graduated from Semmelweis University, Budapest, in 2012. Since then she has worked in her home country Norway as a resident in internal medicine and cardiology at Notodden Hospital, then as a resident in internal medicine at Bærum Hospital and now she is a resident in cardiology at Oslo University Hospital, Ullevål. Her field of interest is acute cardiovascular care, including cardiogenic shock, cardiac arrest, and acute heart failure.

Supplementary material is available at European Heart Journal - Case Reports online.

Slide sets: A fully edited slide set detailing these cases and suitable for local presentation is available online as Supplementary data .

Consent: The author/s confirm that written consent for submission and publication of this case report including image(s) and associated text has been obtained from the patient in line with COPE guidance.

Conflict of interest : None declared.

Funding : None declared.

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• cardiac arrest
• beta-blockers
• hyperthyroidism
• extracorporeal membrane oxygenation
• thyrotoxicosis
• levosimendan
• thyroid hormones
• alveolar ventilation function
• cardiogenic shock
• tissue membrane
• thyroid crisis
• thyroidectomy
• cell respiration

Supplementary data

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Crash Landing of Thyroid Storm: A Case Report and Review of the Role of Extra-Corporeal Systems

Shir lynn lim.

1 Department of Cardiology, National University Heart Center, Singapore, Singapore

Kangjie Wang

2 Division of Endocrinology, Department of Medicine, National University Hospital, Singapore, Singapore

Pak Ling Lui

3 Department of Hematology-Oncology, National University Cancer Institute, Singapore, Singapore

Kollengode Ramanathan

4 Cardiothoracic Intensive Care Unit, National University Heart Center, Singapore, Singapore

5 Department of Surgery, Yong Loo Lin School of Medicine, Singapore, Singapore

Samantha Peiling Yang

6 Department of Medicine, Yong Loo Lin School of Medicine, Singapore, Singapore

Thyroid storm is a rare but life-threatening endocrinological emergency with significant mortality ranging from 10-30% with multi-organ involvement and failure. In view of the rarity of this condition and efficacy of established first line medical treatment, use of extra-corporeal treatments are uncommon, not well-studied, and its available evidence exists only from case reports and case series. We describe a 28-year-old man who presented with an out-of-hospital cardiac arrest secondary to thyroid storm. Despite conventional first-line pharmacotherapy, he developed cardiogenic shock and circulatory collapse with intravenous esmolol infusion, as well as multi-organ failure. He required therapeutic plasma exchange, concurrent renal replacement therapy, and veno-arterial extra-corporeal membrane oxygenation, one of the few reported cases in the literature. While there was clinical stabilization and improvement in tri-iodothyronine levels on three extra-corporeal systems, he suffered irreversible hypoxic-ischemic brain injury. We reviewed the use of early therapeutic plasma exchange and extra-corporeal membrane oxygenation, as well as the development of other novel extra-corporeal modalities when conventional pharmacotherapy is unsuccessful or contraindicated. This case also highlights the complexities in the management of thyroid storm, calling for caution with beta-blockade use in thyrocardiac disease, with close monitoring and prompt organ support.

Introduction

Thyroid storm (TS) is a life-threatening exacerbation of the hyperthyroid state characterized by multi-organ dysfunction of the cardiovascular, thermoregulatory, gastrointestinal-hepatic and central nervous systems. While the incidence among hospitalized patients is estimated to be low at 1-2% ( 1 ), the overall mortality is 10-30% ( 2 ), with a 12-fold increase in mortality compared to individuals with thyrotoxicosis ( 3 ). The diagnosis of TS is additionally challenging due to the absence of specific clinical or laboratory findings. Early recognition of this condition is key, as it allows for prompt and specific treatment, as well as early identification of organ dysfunction with initiation of supportive measures in the intensive care setting if required.

We present a case of TS in a young patient with undiagnosed Graves’ disease, presenting with an out-of-hospital cardiac arrest. Initially hemodynamically stable following return of spontaneous circulation, he developed circulatory collapse after intravenous esmolol infusion, initiated for control of tachycardia. There was consequent multi-organ failure which contraindicated the use of standard anti-thyroid drug therapy. He required three extra-corporeal systems of continuous renal replacement therapy (CRRT), veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) and therapeutic plasma exchange (TPE) for stabilization, one of the few reported cases in the literature.

Case Description

A 28-year-old male presented with an out-of-hospital ventricular fibrillation (VF) arrest, preceded by an acute respiratory illness. There was return of spontaneous circulation after 60 minutes of resuscitation with bystander cardiopulmonary resuscitation and external defibrillation by paramedics. In the Emergency Department, he was febrile at 40.5 degrees Celsius, hypertensive with a blood pressure of 146/83mmHg and tachycardic with a heart rate of 155 beats per minute. Physical examination was unremarkable, except for a Glasgow Coma Scale of 3. No goiter was seen on examination. Corroborative history from his family confirmed symptoms of heat intolerance, loss of weight, hand tremors and palpitations in the preceding two months, as well as a maternal history of Graves’ thyrotoxicosis.

Initial investigations showed elevated inflammatory markers, mixed respiratory and metabolic acidosis, raised troponin I, but with normal electrolyte levels. Electrocardiogram confirmed sinus tachycardia. Chest radiograph showed prominent pulmonary vasculature without evidence of pneumonia. Point-of-care echocardiogram showed impaired left ventricular systolic function without other obvious abnormalities; the marked sinus tachycardia precluded accurate estimation of the left ventricular ejection fraction (LVEF). Computed tomographic (CT) scan of the brain was normal, and urine drug screen was negative. A coronary angiogram performed was normal, and a provisional diagnosis of acute myocarditis was made. Thyroid function test, sent as part of investigations for myocarditis, showed thyrotoxicosis with an elevated serum free thyroxine (FT4) level of 42.1pmol/L (reference range: 8.0-16.0pmol/L) and a suppressed serum thyroid stimulating hormone (TSH) at <0.01mIU/L (reference range: 0.45-4.50mIU/L) ( Figure 1 ) – our patient had thyroid storm complicated by thyrocardiac disease, with a Burch-Wartofsky score of 105. His thyroid-stimulating hormone receptor antibody eventually returned elevated at >40IU/L (normal ≤2.0IU/L), confirming underlying Graves’ disease.

Timeline of key clinical events. T4, thyroxine; T3, tri-iodothyronine; TSH, thyroid-stimulating hormone; NG, nasogastric; IV, intravenous; PTU, propylthiouracil; NaI, sodium iodide; VA-ECMO, veno-arterial extra-corporeal membrane oxygenation; CRRT, continuous renal replacement therapy; TPE, therapeutic plasma exchange; MMZ, methimazole.

Treatment was promptly initiated with nasogastric propylthiouracil, intravenous sodium iodide and hydrocortisone ( Figure 1 ). Temperature was controlled with a cooling blanket. Judicious low dose esmolol infusion was commenced at 25mcg/kg/min to manage the tachycardia. This was followed shortly by a pulseless electrical activity arrest. Despite a short downtime of three minutes and prompt cessation of beta-blockade, he required high doses of noradrenaline and vasopressin thereafter. He remained persistently hypotensive with maximal dual vasopressor support, and was initiated on VA-ECMO support ( Figure 2 ).

Concurrent CRRT, VA-ECMO and TPE. O 2 , oxygen, CO 2 , carbon dioxide, others as per Figure 1 .

Further investigations revealed worsening transaminitis and anuric acute kidney injury, requiring CRRT. Transthoracic echocardiogram showed severe left ventricular systolic dysfunction with estimated LVEF of 10%. Pharmacological options were now limited to cholestyramine and hydrocortisone. We decided to institute TPE; with the first cycle performed on day 2 of admission, with 2.5L of albumin and 0.5L of saline ( Figure 1 ). After the first cycle, his vasopressor support reduced significantly (only requiring low dose noradrenaline infusion) and his tri-iodothyronine (T3) levels improved ( Figure 1 ). As his FT4 continued to worsen, nasogastric methimazole and Lugol’s iodine were cautiously started, along with second TPE cycle, on the third day.

His pupils were noted to be fixed and dilated with the second cycle of TPE ongoing. Urgent CT scan of the brain revealed diffuse cerebral edema with severe mass effect and tonsillar herniation. A decision was made in conjunction with his family for withdrawal of care, given the grave prognosis.

Evidence of Use of Extra-Corporeal Systems in TS

Our patient is one of the few reported cases where multiple extra-corporeal systems were used (TPE, CRRT, and VA-ECMO) in TS management. On review of the medical literature of articles in English, there has only been four case reports describing the concurrent use of TPE and ECMO in patients with thyrotoxicosis with circulatory collapse ( 4 – 7 ), with one of them reporting the use of three extra-corporeal systems ( 4 ).

Characterized by extreme multi-systemic manifestations of thyrotoxicosis, TS is uncommon but potentially fatal, with a mortality rate of 10-30% ( 2 ). Standard first-line pharmacotherapy in TS aims to block production and release of thyroid hormones with propylthiouracil or methimazole, inhibit release of pre-formed thyroid hormones with iodine, decrease peripheral conversion of T4 to T3 with propylthiouracil and steroids, and treat adrenergic symptoms with beta-blockade, prior to definitive treatment in the form of surgery or radioactive iodine (RAI) ablation. These methods are efficacious and rapid acting. However, certain patients are not able to tolerate, or fail pharmacotherapy, as seen in our patient with multi-organ failure precluding the use of conventional treatment. In such cases, alternative treatment including use of extra-corporeal systems must be considered, of which TPE is the most well established.

TPE is an extra-corporeal blood purification technique used for eliminating large molecular substances. Currently, TPE has a Class II indication for TS in the 2019 American Society for Apheresis (ASFA) guidelines, either as a standalone or adjunct therapy, although the grade 2C level of recommendation suggests the evidence arises mostly from case reports and case series, with an absence of prospective randomized controlled trials ( 8 ). TPE is postulated to work by several mechanisms including: 1) reducing protein-bound thyroid hormones of which 99.97% of total serum T4 and 99.7% of total serum T3 are bound to plasma proteins thyroxine binding globulin (TBG), transthyretin and albumin ( 9 ), 2) additionally reducing autoantibodies and cytokines of a predominantly Th1 pattern including interleukin-2, interferon-γ and tumor necrosis factor-α ( 10 – 12 ), and 3) removing 5’-monodeiodinase which converts T4 to T3 ( 12 ). TPE is shown to reduce all of free and total T4 and T3 ( 13 ), by an estimated 10-80% ( 12 ), and at a greater rate than standard medical therapy for patients with hyperthyroidism ( 14 ). However, these effects are transient and usually last for only 24-48 hours, with a potential risk for rebound thyrotoxicosis ( 12 ). This appears related to the fact that only thyroid hormones from the intravascular compartment is removed, with rapid re-equilibrium from the extravascular spaces. A study in 13 healthy individuals showed the intravascular component of thyroxine accounts for only 26% of the distribution ( 15 ), with the other sites of distribution found to be 14% in the liver, 34% in extrahepatic tissue and 26% in extracellular fluid pools. These transient effects suggest that multiple cycles of TPE may be required, and should be used only as a temporizing measure for definitive treatment ( 12 ). TPE can be performed with either plasma or albumin replacement, and the ASFA guideline does not preferentially recommend the use of plasma or albumin. It has been proposed that plasma has the theoretical advantage of containing binding proteins TBG and transthyretin, which has higher affinity to bind free T4 and T3, as well as avoid depleting coagulation factors thus avoiding complications of bleeding ( 13 ). However, there is similarly a theoretical risk of the presence of thyroid hormones from donor plasma, as well as higher risks of transfusions reactions and infections with use of plasma. Till date, there are no direct head-to-head trials between the use of plasma and albumin in TPE in patients with TS. TPE is generally well tolerated, with risks of minor side effects ranging from about 5% ( 9 ) to 36% ( 16 ), including nausea and vomiting, vagal or hypotensive response and transfusion reactions. The risk of death with TPE for any indication is exceedingly rare at 0.05% ( 17 ), and this is usually attributed to the severity of the underlying condition.

ECMO is an established life-saving treatment option for patients who develop acute cardiopulmonary failure ( 18 ), although its use in endocrinological emergencies is still under research ( 19 ). Use of ECMO in patients with thyrotoxicosis have largely been reported in the form of case reports or case series within the literature. In 2011, Hsu et al. ( 20 ) first reported a series with the use of supportive ECMO ranging from 19-114 hours in four cases of thyrotoxicosis-induced cardiovascular collapse. Three patients survived, with normalization of thyroid function and improved cardiovascular function. A subsequent review by White et al. ( 21 ) published in 2018 reported the successful use of ECMO with survival in 11 out of 14 patients ( 22 – 24 ) between 1970 to 2017 with thyrotoxicosis-induced cardiomyopathy, with near complete recovery of left ventricular function. A review of the cases with the use of ECMO and other extra-corporeal systems in patients with severe thyrotoxicosis or thyroid storm has been summarized in Table 1 , including additional new cases reported from 2018 to 2021 ( 25 – 28 ) and conference poster reports ( 29 – 32 ). These 27 cases (inclusive of our case) showed survival in 85.2% (23 of the 27 cases), with survival in all four of the reported cases requiring additional extra-corporeal support of TPE or CRRT ( 4 – 7 ). ECMO was initiated for either cardiovascular collapse or circulatory shock, and lasted between 19 hours to 18 days. Within the reports of successful outcomes, all cases reported clinical and biochemical improvement in thyrotoxicosis, as well as improvement in cardiac function, although numerical data were not available in some of the reports. The details of these cases are reported in Table 1 . The use of ECMO however, must be weighed against the contraindications and complications of ECMO use, including bleeding, thromboembolism, strokes and access injuries such as hemorrhage, arterial dissection, and distal limb ischemia ( 18 ).

Table 1

Summary of cases with use of ECMO and other extra-corporeal systems in patients with severe thyrotoxicosis or thyroid storm.

‘*’ denotes incomplete data from articles, while ‘-’ denotes absence of reported data.

Novel therapies are also increasingly considered for TS, using principles similar to TPE by removing protein bound thyroid hormones. Case reports with the use of dialysis has been proposed in management of thyroid storm, most notably with CRRT, which is preferred due to its better tolerability in hemodynamically unstable patients due to its slower rate of exchange of fluids and solutes. Parikh et al. ( 33 ) and Koball et al. ( 34 ) illustrated the sequential use of single pass continuous veno-venous albumin dialysis after limited response to TPE, demonstrating a more sustained improvement in thyroid hormones with less rebound thyrotoxicosis, as well as greater removal of thyroid hormones overall. Other studies have shown the additive effects of TPE and CRRT in removal of thyroid hormones ( 35 ), while another study reported a correlation of improvement of total T3 and free T4 levels of up to 80% with concomitant CRRT and standard medical therapy (without TPE), although the exact mechanisms are unclear ( 36 ). The Molecular Adsorption Recirculation Systems (MARS) has also been used, with one case report with TS and severe liver dysfunction showing rapid resolution of thyroid hormones and improvement of bilirubin ( 37 ). A retrospective case series also demonstrated significant improvement in thyroid hormone levels in patients with hyperthyroidism with severe liver dysfunction (although this study was primarily powered to show improvement and safety of use of RAI with combined with MARS in patients with severe hyperthyroidism and liver disease) ( 38 ). These reports provide early evidence of the utility of novel extra-corporeal systems in correcting thyroid hormone levels especially in patients with either kidney or liver dysfunction, although more research into the underlying mechanism and validation of results are required before recommendations can be made for its supportive use.

These cases provide some evidence of the use and benefits of extra-corporeal systems in the management of TS, after conventional pharmacotherapy is unsuccessful or contraindicated. Owing to the efficacy of pharmacotherapy and risks of extra-corporeal systems, conventional pharmacotherapy should be always be instituted as initial therapy. Comparison trials between pharmacotherapy and extra-corporeal systems or randomized controlled trials are unavailable due to the rarity of TS, and are unlikely to be performed now given the established efficacy of first line pharmacological agents. Retrospective analysis from the National Inpatient Database in Japan has shown that use of extra-corporeal systems is associated with higher mortality. It reported increased mortality in patients requiring hemodialysis and TPE with adjusted odds ratio for mortality at 4.81. The mortality was 61.9% in 13 out of 21 patients, compared to a mortality of 43.3% requiring either hemodialysis or TPE, and 7.8% requiring neither support. The use of ECMO had a trend towards increased mortality (2.86, CI 0.69-11.92), with a mortality of 72.2% among 13 of 18 patients, as compared to 9.3% in patients not requiring ECMO ( 39 ). These numbers, albeit small, suggest a significantly higher mortality in patients requiring use of extra-corporeal systems, and this differs from the established mortality rate of 10-30%, and vary significantly from the numbers in our review and White et al.’s review in patients requiring ECMO ( 21 ). Similarly Muller et al. ( 12 ) showed the use of TPE showed significant clinical and biochemical improvement. As patients requiring extra-corporeal systems are typically patients who are more critically ill and have multi-organ failure, as well as the possibility of publication bias, it is likely that the true survival rate of these patients in thyroid storm treated with extra-corporeal systems is likely lower than the published literature. Further research, possibly in the form of prospective multinational studies, may be required in view of the small numbers and limited data currently.

Beta-Blockade – A Double-Edged Sword in TS

While our patient received guideline-directed TS pharmacological therapy in a timely fashion, the development of circulatory collapse with consequent multi-organ failure following intravenous esmolol infusion, an ultra-short acting beta-blocker, deserves further discussion.

The cardiovascular effects in TS are driven largely by T3, leading to increased chronotropy and inotropy, improved diastolic relaxation and decreased peripheral resistance, eventually resulting in high cardiac output (CO) heart failure (HF), estimated to be seen in 6% of patients with thyrotoxicosis. This is thought to be reversible with treatment with thyrotoxicosis, with a small study showing improving in LVEF from 28% to 55% ( 40 ). Cardiomyopathy and LV dysfunction, on the other hand, are only seen in 1% ( 20 , 41 ). HF with low CO has been reported with prolonged severe hyperthyroidism, consequent to persistent tachycardia, and pathologic increase in cardiac workload with demand-supply mismatch ( 42 ). Aside from cardiomyopathy, there is an increased risk of arrhythmias with thyrotoxicosis, typically supraventricular, with rare reported cases of thyrotoxicosis-related VF related to congenital coronary anomalies, hypokalemia, coronary vasospasm and early repolarization ( 43 ), none of which were present in our patient. It is plausible that our patient had low CO thyrocardiac disease with an additional component of myocardial stunning post-cardiac arrest, but his stormy course precluded detailed cardiac imaging.

Tachycardia is almost always present in TS, and patients with tachycardia exceeding 150 beats per minute are associated with a higher mortality rate in a retrospective Japanese cohort ( 44 ). Accordingly, the Japanese Thyroid Association and Japanese Endocrine Society 2016 guidelines ( 45 ) recommend aggressive control of tachycardia including the use of ultra-short acting beta-blockers including esmolol or landiolol. New data are emerging which support the use of esmolol over propranolol, due to its shorter half-life elimination (nine minutes, versus 2.3 hours respectively) and duration of action, as well as its relatively higher beta 1-selectivity ( 46 ). The comparative use of esmolol and propranolol has been studied in other populations such as patients with supraventricular tachycardia, which showed similar response rate but more adverse effect of hypotension seen in the esmolol group (45%, as compared to 18%), although these were mostly asymptomatic and resolved quickly with no complications ( 47 ). Regardless of choice of beta-blockers, its use must be considered with caution in patients with decompensated HF or other features of low CO, where the thyroid-induced hyperadrenergic state plays an important compensatory role in maintaining CO. This is related to either direct catecholamine action or an interaction between the adrenergic system and excessive circulating thyroid hormone ( 48 ). The abolishment of that sympathetic drive through the use of beta-blockers is postulated to lead to the circulatory collapse, as seen in our case. Though initially hypertensive, the temporal association of esmolol infusion and PEA arrest led us to conclude it caused or at least triggered the hemodynamic decompensation in our patient. Abubaker et al. ( 49 ) reviewed a total of 11 cases of circulatory collapse with the use of beta-blockade, mostly with long acting agents including bisoprolol, metoprolol, propranolol, with all but one patient showing evidence of underlying heart failure or cardiomyopathy. The author also highlighted the challenges in managing uncontrolled tachycardia in these patients, with two cases eventually requiring esmolol and landiolol use. To date, there has been no head-to-head trials between the longer acting propranolol as compared to the ultra-short acting esmolol or landiolol. There has no reports of circulatory collapse with use of intravenous esmolol, and only one case report with landiolol ( 50 ). Despite the use of ultra-short acting esmolol, circulatory collapse in our case underscores its class effect, and is strongly associated with fatal outcomes in TS. Close cardiac monitoring and prompt institution of VA ECMO support, as what was done in this case, are recommended. Other forms of supportive therapy including CRRT may be considered until effective and definitive therapies can be instituted to treat TS.

We highlight a case of TS presenting with out-of-hospital cardiac arrest, with further hemodynamic decompensation following beta-blockade and multi-organ failure which limited therapeutic options. Despite prompt initiation of CRRT, VA-ECMO and TPE, he sustained hypoxic-ischemic brain injury. Underscoring the complexities in TS, this case calls for caution with beta-blockade in thyrocardiac disease, close monitoring and prompt organ support, and consideration of early TPE when conventional options fail. A review of the use of TPE and other extra-corporeal systems shows that TPE may be an underutilized rescue treatment for severe thyroid storm not amenable to conventional pharmacotherapy or contraindicated due to side effects or multi-organ involvement. Further study of novel extra-corporeal therapies for TS is needed to uncover its therapeutic potential, especially in the Intensive Care setting.

Author Contributions

All authors were involved in the management of the patient. SL, KW, and SY wrote the first draft of the manuscript. PL and KR reviewed and edited the manuscript. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Nursing Care and Pathophysiology for Hyperthyroidism

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Hyperthyroidism: There is an excess thyroid hormone secreted by the thyroid gland.

• Excess secretion of thyroid hormone (TH) from thyroid gland
• Results in Increased Metabolic Rate

Nursing Points

• Graves’ Disease (autoimmune)
• Excess secretion of TSH from Pituitary
• Thyroid, Pituitary, or Hypothalamic Tumor
• Medication Reaction
• Acute Exacerbation due to infection, stress, trauma
• ↑ T3, T4, Free T4 hormones
• Positive radioactive iodine uptake scan
• Tachycardia, HTN, palpitations
• Hyperactive reflexes, hand tremor
• Emotional instability, agitation
• Exophthalmos (bulging eyes)
• Blurred vision
• Fine, thin hair
• Some patients experience increased libido, while others report decreased libido
• Hypermetabolic
• ↑ Temperature
• Heat intolerance
• Weight Loss
• Due to excess Calcitonin
• Febrile state
• Tachycardia, HTN

Therapeutic Management

• Provide rest in a cool, quiet environment
• Cardiac Monitoring
• Maintain Patent Airway
• Regular eye exams
• Eye drops for moisture
• Antithyroid medications → propylthiouracil or methimazole
• Destroys some thyroid cells over 6-8 weeks
• Avoid in pregnancy
• Monitor for hypothyroidism
• Assess for obstruction, stridor, dysphagia
• Have tracheotomy equipment available
• Maintain in upright position
• Assess for bleeding
• Due to removal of parathyroid glands
• **Note: incorrectly stated in video**
• Have calcium gluconate available PRN
• Minimal talking after surgery

Nursing Concepts

• Administer medications (PTU or methimazole)
• Monitor hormone levels (T3, T4, Free T4, TSH)
• Monitor for s/s Thyroid Storm
• Keep in a cool environment
• Monitor temperature for fever
• Ensure adequate nutritional intake
• Increased caloric needs

Patient Education

• Avoid caffeine and reduce stress
• Smoking Cessation
• S/s to report to provider (Thyroid Storm)
• Medication Instructions

Nursing Care Plan (NCP) for Hyperthyroidism

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Med-surg | metabolic / endocrine.

The Metabolic and Endocrine Course reviews the major organs and glands involved in secreting hormones in our bodies. Hormones are responsible for regulating nearly every basic function of our body, like our heart rate and processing blood sugar. This course breaks down what happens when each gland is overactive or underactive. We will also walk you through the sometimes confusing condition known as Diabetes Mellitus.

0 – Metabolic / Endocrine Introduction

1 – endocrine disorders.

• 11 Questions
• 10 Questions
• 5 Questions
• 16 Questions
• 20 Questions
• 7 Questions
• 6 Questions

2 – Diabetes Mellitus

• 17 Questions
• 1 Questions
• 9 Questions

3 – Metabolic Conditions

• 3 Questions