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Weathering the Thyroid Storm

CASE

History:

  • 50 yo female with PMH notable for an asymptomatic thyroid nodule presented to the ED due to a month of worsening abdominal pain and distention

  • Seen at outside hospital 6 weeks prior where CT abdomen/pelvis showed ascites

  • Endorsed dyspnea on exertion, orthopnea and increased bilateral lower extremity swelling. Also endorsed poor PO intake, nausea and vomiting

  • Denied fevers, chills, chest pain, palpitations, personal or family history of heart disease

Physical Exam:

  • Vitals: BP 108/73 HR 177 RR 26 O2 Sat 96% RA

  • Exam was notable for goiter of neck, diminished breath sounds at lung bases, tachycardic regular heart rhythm, distended abdomen with tenderness to palpation diffusely and 2+ pitting edema of lower extremities bilaterally

ED Course:

  • Patient’s EKG revealed SVT. Vagal maneuvers successfully reverted to sinus tachycardia

Fig 1: EKG showing supraventricular tachycardia
  • Bedside echocardiogram showed severely reduced EF ~ 10 to 15%, dilated LV and biatrial enlargement, but no pericardial effusion

  • CTA C/A/P showed large right pleural effusion, large volume ascites and cardiomegaly

Fig. 2: CTA showing abdominopelvice ascites

Fig. 3: CTA showing pleural effusion and cardiomegaly

  • Labs were notable for TSH < 0.02, free T4 6.5, pro-BNP 11,087, lactate 4.2, abnormal LFTs

  • Patient was treated with Lasix, hydrocortisone and PTU, and admitted to the CCU

Clinical Question: What is thyroid storm, how is it diagnosed and how is it best managed in the ED? What considerations must be given for patients who present with heart failure?


SUMMARY OF EVIDENCE

Diagnosis:

  • Thyroid storm (TS) is a life-threatening endocrine emergency at the end of the thyrotoxicosis spectrum. Patients present in a hypermetabolic state with signs and symptoms such as fever, hypertension, tachycardia, palpitations, diaphoresis, agitation, altered mental status etc, Patients may also present with various degrees of organ failure[1]

  • TS is a clinical diagnosis but the Burch-Wartofsky Point Scale (BWPS) and the diagnostic criteria from the Japan Thyroid Association (JTA) can assist with diagnosis

Table 1: Burch Wartofsky Point Scale*
Table 2: Japan Thyroid Association diagnostic criteria**

o Data suggests that the JTA categories are more likely to underdiagnose thyroid storm when compared to the BWPS. In a retrospective cohort study of 25 hospitalized patients in TS, BWPS was ≥ 45 (thyroid storm) in 20 patients and 25 – 44 (impending storm) in five. JTA categories identified the 20 patients, but the other five did not meet criteria[4]

o There is, however, limited data on the use of these scoring systems in the ED


Management:

  • A multimodal approach using beta blockers, corticosteroids, antithyroid drugs, iodine and supportive treatment is used for thyroid storm management.

  • Beta-blockers are used to inhibit the peripheral effects of thyroid hormone and reduce symptoms resulting from increased adrenergic tone. Corticosteroids and high doses of beta blockers inhibit the conversion of T4 to T3 (more potent hormone)[1]

  • Anti-thyroid drugs (ATD), propylthiouracil (PTU) and methimazole (MMI), are used to decrease production of new thyroid hormone by inhibiting thyroid peroxidase action[1]

    • The American Thyroid Association (ATA) recommends PTU over MMI because of its added effect on T4 to T3 conversion. A study of 19 patients hospitalized with hyperthyroidism who were treated with either PTU or MMI combined with iodide found about a 45% decrease in T3 levels in patients on PTU at 24hrs compared to 10-15% decrease in patients on MMI (p < 0.001)[5]

    • The JTA recommends MMI over PTU. A nationwide epidemiologic survey in Japan found no significant difference in mortality between patients in TS treated with PTU vs. MMI (p = 0.5058). They also found that increasing doses of MMI, but not PTU were significantly correlated with disease severity[6]

    • There are no observational or trial studies of patients in TS treated with PTU or MMI which demonstrate superiority of one ATD over the other.

  • Iodine blocks new hormone synthesis and inhibits the release of preformed hormones[1]

    • ATA guidelines recommend waiting an hour after giving ATDs to prevent an increase in thyroid hormone synthesis with exogenous iodine.

  • In refractory cases of TS, plasma exchange or thyroidectomy may be used[1]

Heart Failure Considerations:

  • Heart failure in hyperthyroid states is often high-output heart failure, however, some patients in TS develop decompensated heart failure with marked volume overload or cardiogenic shock, for which beta-blockers may be detrimental.[7]

    • There are multiple case study reports of patients in TS deteriorating rapidly following the initiation of beta-blockers[8-10]

RECOMMENDATIONS

  • Maintain a high index of suspicion for TS in patients who present in a hypermetabolic state with known or unknown thyroid disease, or goiter on exam

  • TS is a clinical diagnosis, but the BWPS can be used as a diagnostic aid. For high BWPS scores, begin aggressive treatment early. For those who lie in the impending TS category, TS treatment should be initiated and de-escalated as needed

  • Multimodal treatment including beta-blockers, steroids, ATDs and iodine should be used.

  • Given the lack of significant evidence demonstrating superiority of PTU over MMI or vice versa in TS, side effect profiles and existing comorbidities should be weighed when selecting an ATD

  • Avoid beta-blockers in patients in TS with decompensated heart failure

  • Consider plasmapheresis or thyroidectomy for patients without improvement after ~ 48h

REFERENCES

1. M C, S S, AS K. Thyroid storm: an updated review. Journal of intensive care medicine. 2015 Mar 2015;30(3)doi:10.1177/0885066613498053

2. HB B, L W. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinology and metabolism clinics of North America. 1993 Jun 1993;22(2)

3. T S, O I, A S, et al. 2016 Guidelines for the management of thyroid storm from The Japan Thyroid Association and Japan Endocrine Society (First edition). Endocrine journal. 12/30/2016 2016;63(12)doi:10.1507/endocrj.EJ16-0336

4. Angell TE, Division of Endocrinology and Diabetes (T.E.A. MGL, C.T.N., V.L.S., J.T.N., J.S.L.), USC Keck Medical Center, Los Angeles, California 90033, Division of Endocrinology D, and Hypertension (T.E.A., M.G.L.), Brigham and Women's Hospital, Boston, Massachusetts 02215, et al. Clinical Features and Hospital Outcomes in Thyroid Storm: A Retrospective Cohort Study. The Journal of Clinical Endocrinology & Metabolism. 2022;100(2):451-459. doi:10.1210/jc.2014-2850

5. J A, PR L. Triiodothyronine and thyroxine in hyperthyroidism. Comparison of the acute changes during therapy with antithyroid agents. The Journal of clinical investigation. 1974 Jul 1974;54(1)doi:10.1172/JCI107744

6. O I, T S, S W, et al. Treatment and management of thyroid storm: analysis of the nationwide surveys: The taskforce committee of the Japan Thyroid Association and Japan Endocrine Society for the establishment of diagnostic criteria and nationwide surveys for thyroid storm. Clinical endocrinology. 2016 Jun 2016;84(6)doi:10.1111/cen.12949

7. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. review-article. 2022-05-03 2022;doi:10.1161/CIR.0000000000001063

8. K M, S K, F N, S K, T S, J K. Cardiac arrest caused by landiolol in a patient in thyroid crisis. Journal of cardiology cases. 06/01/2016 2016;14(2)doi:10.1016/j.jccase.2016.04.002

9. AS N, DC LT. Thyrotoxic heart disease. Resuscitation. 2006 Aug 2006;70(2)doi:10.1016/j.resuscitation.2006.01.009

10. R D, MK L. Cardiovascular collapse associated with beta blockade in thyroid storm. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2007 Jun 2007;115(6)doi:10.1055/s-2007-971065



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