Confronting the Storm: The Overactive Thyroid

by | Mar 16, 2023 | 0 comments

“When You Hear Hooves, Think Horse, Not Zebra” – Dr. Theodore Woodward

 

This above sentence is a dictum that every medical student has heard at some point during their training. It’s the reason, that when someone comes in febrile and agitated our first thoughts are to think of sympathomimetic toxidromes, serotonin syndrome, neuroleptic malignant syndrome, alcohol withdrawal, heat stroke, and even more common than that sepsis and intracranial infections such as meningitis and encephalitis.

The so-called “HOT AND CRAZY” differential is however home to a zebra that shouldn’t be forgotten – THYROID STORM.

In today’s blog post, we will aim to tackle this often forgotten but highly deadly complication of a hyperactive thyroid. From basic definitions, diagnosis and management, we hope this will be your one-stop-shop for everything thyroid storm related.

 

Back to Basics

 

“If you miss the beginning, the basics, then you are destined to go back and visit the basics” – Anonymous

 

Understanding the physiology of a functioning hypopituitary access, is the first step in understanding the overactive thyroid. So let’s take it step-by-step:

    • The hypothalamus releases thyrotropin releasing hormones [TRH].
    • TRH stimulates the anterior pituitary to produce thyroid stimulating hormone [TSH].
    • TSH stimulates the thyroid gland to produce thyroid hormones: a mixture of Triiodothyronine [T3] and Thyroxine [T4]. 
      • Important to remember: this above step requires the use of IODINE. 
    • T4 is converted peripherally into T3 via de-iodination. 
    • T3 raises the basal metabolic rate, by directly stimulating the Na-K-ATPase pump, causing an increased O2 demand and heat production. It also increases gluconeogenesis, and lyposis, while directly stimulating B1 cardiac receptors. 
      • Overactive Thyroid = Hyperadrenergic State

 

Under normal circumstances when there is an abundance of thyroid hormones, they operate on a negative feedback loop to decrease TRH and TSH release from the hypothalamus and anterior pituitary gland. However, when a disruption in this homeostatic environment occurs, the axis produces excess thyroid hormone [T3 and T4]. This typically occurs via one of three mechanisms: 

 Thyroid Hypopituitary Axis Disruption of the Hypopituitary Axis

 

Primary hyperthyroidism: Overproduction of thyroid hormones occurs directly at the level of the thyroid gland.

Example: Graves’ disease – Wherein antibodies chronically stimulate the third via TSH receptors.

 

Secondary hyperthyroidism: Disruption occurs above the level of the thyroid.

Example: pituitary adenomas which secrete TSH.

Exogenous Source

 

Additional T3 and T4 originating from outside the hypopituitary access.

Examples: Hydatidiform Moles or Synthroid Overdose
Thyroid Injury Endogenous Release

 

Direct injury to the thyroid, often from inflammation or infection, leads to a large release of T3 and T4.

 

This is Thyroiditis

 

Overactive Thyroid Entities

 

Hyperthyroidism is biochemically defined as an elevated T3 and T4. Often this is associated with a suppressed TSH; in the case of a functional hypopituitary axis. However, biochemical levels do not translate to the clinical environment. The hyperactive thyroid, therefore presents clinically along a spectrum:

 

    • Subclinical Hyperthyroidism:

State in which less TSH is produced despite normal biochemical levels of T3 and T4. Typically not associated with any clinical symptoms.

 

    • Hyperthyroidism and Thyrotoxicosis:
Hyperthyroidism Thyrotoxicosis Apathetic Thyrotoxicosis
Pathological state in which excess thyroid hormones are synthesized, from one of the three previously mentioned mechanisms. Hyperthyroidism is the term typically used to define the biochemical state of elevated T3/T4.  Clinical syndrome that occurs as a result of hyperthyroidism. Symptoms include tachycardia, pyrexia, hyperkinesis, weight loss, diarrhea, nausea, vomiting and more.

Overactive Thyroid = Hyperadrenergic State

 Clinical syndrome where typical symptoms of hyperadrenergia are absent. Patients instead present with apathy, depression, and generalized weakness.

  • Over the age of 65, >1/3 of patients will present with apathetic thyrotoxicosis.
  • These patients often present in heart failure, due to higher proportions of uncontrolled atrial fibrillation causing tachy-mediated caridomyopathies.

 

    • Thyroid Storm:

Clinical syndrome defined by a triad of pyrexia, AMS and tachycardia, with evidence of end-organ damage.

Why do we Care?

Mortality Rate = 100% if untreated

Mortality Rate = 30-40% if treated

Thyroid Storm

 

Diagnosing Thyroid Storm

 

Thyroid Storm = CLINICAL Diagnosis

 

The above statement is an important one to remember. Although lab tests can help support your diagnosis, thyroid storm is ultimately a clinical diagnosis, based on the triad of symptoms discussed above. However, this triad of symptoms is non-specific for thyroid storm, as it can also be present in other entities that fit the “HOT AND CRAZY” differential. So what if their was a tool that could help you with your clinical acumen? 

In the literature, their are currently two clinical decision tools that have been developed to assist with the diagnosis of Thyroid Storm.  

    • Burch-Wartofsky Point Scale (BWPS)
      • Restrospectively developed in 1993, by Dr. Burch. The point scale aims to determine the likelihood that biochemical hyperthyroidism (i.e. elevated T3/T4) is representative of thyroid storm.
        • Score <25 = Unlikely 
        • Score 25-45 = Equivocal/Impending 
        • Score >45 = Likely 
      • It’s use is supported in the 2011 American Thyroid Association Guidelines. 
      • It relies on scoring of each one of the following clinical signs and symptoms along a spectrum: 
        • Temperature 
        • CNS Effects
        • GI/Hepatic Dysfunction 
        • HR
        • CHF 
        • Afib 
        • Precipitating Event 
      • Click HERE to be taken to MD Calc Scoring tool. 
    • Japanese Thyroid Association
      • Published in 2011 by the Japanese Thyroid Association. 
      • Derived from evaluation of thyroid storm patients in Japan from 2001 to 2011. 
      • Much like the BWPS it aims to determine the likelihood of thyroid storm, based on the symptoms listed in Table 3 below (click diagram to link to original paper). 
        • TSI | If CN Sx + 1 other Sx OR ≥ 3 symptoms (Not CNS manifestations) = Definitive Thyroid Storm
        • TS2 | If ≥2 Sx = Thyroid Storm Suspected

 

 

Should we use these tools?

As you can imagine based on the elements incorporated into each of these tools, these scoring systems have high sensitivity for thyroid storm, but have poor specificity. For example, sepsis with multi-organ failure could easily score >45 on the BWPS tool. A recent study of 125 patients hospitalized with a clinical diagnosis of compensated thyrotoxicosis with NO evidence of thyroid storm, as per the local endocrinology team, emphasized the over-diagnosis of thyroid storm with the use of these tools. In the study 21.6% of patients had a BWPS > 45, while 16.8% had a TS1 score, despite being stable hyperthyroid patients. Ultimately, the tools serve more as a guide to help with understanding the symptoms and signs of thyroid storm, and perhaps categorize the severity of cases. It really isn’t tools we foresee using in the ED. 

“Key message is that they’re not perfect and they don’t replace clinical judgement, e.g. can’t hang your hat on the score in many cases. But they can provide you a starting point to help assess severity of cases“

– Dr. Christopher Tran, FRCPC Endocrinologist

 

When should I consider the Dx of Thyroid Storm?

Here are a few clinical scenarios, that you should consider at minimum testing a TSH for the patient sitting in your emergency department: 

  • Patients with known hyperthyroidism and an acute illness/deterioration. 
  • New-onset atrial fibrillation and/or dilated cardiomyopathy. 
  • New-onset delirium/psychosis plus abnormal vital signs (fever, tachycardia). 
  • Hyperthermia (temperature 40C). 
  • Septic-appearing patient without any focus of infection (i.e. distributive shock of unknown origin). 
  • Classic “Hot and Crazy” presentation.
  • Hypo/Hyperactive delirium in the elderly; unless they have had a TSH in the last 3 months. 

 

Managing Thyroid Storm

 

Step 1: Supportive Treatment

 

Supportive management should always be your first step in management. Remember your ABCs, and address each of these as you would in any other rescucitation. Treatment may include any of the following combinations:

    • Fluid Rescucitation +/- pressors for refractory hypotension and hypovolemia.
    • Antipyretics.
    • Passive and Active Cooling.
    • Benzodiazepines for management of extreme agitation. 
    • Investigations for Sepsis, including BCx, and early Abx. 

 

Step 2: Identify and Reverse Potential Triggers

 

Thyroid Storm often results from undiagnosed hyperthyroidism, that is pushed into overdrive due to an illness trigger. Common triggers are listed in the table below – consequently, most cases of possible thyroid storm should have a full septic work-up, and global metabolic panel including LFTs, VBG and lactate.  

Global Triggers Thyroid Specific
Surgery 

Trauma

ACS events

Strokes

DKA 

Sepsis/Major Infections 

Viral Illnesses

 Thyroid Surgery 

Radioiodine Therapy 

Cessation of Hyperthyroidism Therapy

Thyroid Hormon intentional or unintentional overdose (i.e. synthroid)

Aspirin Intoxication (How? It can increase free thyroid hormone levels by displacing thyroid hormone from its protein-binding sites)

 

Step 3: Thyroid Targeted Treatment

 

Remember the 5Bs

(Block Synthesis, Block Release, Block Conversion, Block Beta and Block Enterohepatic Circulation)

 

Block Synthesis: Thyroid Peroxidase Inhibitors

There are currently two thionamide drugs available on the market; Methimazole (MMI) and Propilthiouracil (PTU). These should be the first medication you reach for when you diagnose a thyroid storm, as they inhibit the formation of thyroid hormone, by competitive inhibition of thyroid peroxidase; the enzyme responsible for the conversion of iodide to iodine, and the formation of T4 and T3 from iodine and thyroglobulin. With two agents available on the market, which one should we be reaching for in the ED? 

PTU has long been recommended as the preferred agent over methimazole, due to it’s added quality of blocking peripheral conversion of T4 to T3. Early, research additionally demonstrated that PTU dropped T3 levels by 45% in the first 24hrs of treatment, compared to 15% after initiation of methimazole. As such, it is often recommended to use PTU in the cases of severe thyroid storm. However, their currently is no head-to-head trial that directly compares and demonstrates PTU’s superiority. Additionally, PTU does present the risk for liver failure (0.5% risk), and cannot be continued in the outpatient setting. Comparatively, MMI is the preferred agent upon discharge from hospital. Irregardless, use the thyroid perodidase inhibitor you have at your disposal, as per the recommended dosing regime below. 

REMEMBER: Although you may be starting these agents independently, you should reach out to your endocrinology colleagues as soon as possible. 

**Pregnancy Exception: Use PTU in the 1st trimester (due to rare MMI teratogenic effects). Use MMI in second and third trimesters. 

 

Block Release: Iodine 

To block the release of thyroid hormones, Iodine is typically administered. The excess iodine load leads to inhibiton of thyroid synthesis via the Wolff-Chaikoff Effect. In 2010, Takata et al., demonstrated higher efficacy at reaching a euthyroid state, when a thyroid peroxidase inhibitor was combined with iodine, compared to placebo. However, the use of iodine is a double-edged sword. In certain circumstances, the iodine load can actually induce an up-regulation of thyroid hormone release; this is called the Jod-Basedown Effect. It is this same principle that explains activation of hyperthyroidism when patients have underlying Grave’s and receive iodinated contrast. This effect is often seen in individuals with iodine deficiencies, or those who have toxic nodular goiter. This is why it is imperative, that iodine products be given 1 hour after the thyroid peroxidase inhibitors, so as to first limit the production of thyroid hormone, so that in the event that the Jod-Basedown Effect is inacted, their is less thyroid hormone release. 

IMPORTANT: Wait 1h post Thyroid Peroxidase Inhibitor administration before giving iodine.

 

Block Conversion: Steroids

Administration of steroids, decreases peripheral conversion of T4 to T3. They are also favoured in refractory hypotension in the context of thyroid storm, as they may also address relative adrenal insufficiency resulting from the hypermetabolic state. 

 

Block Beta : A Word of Caution with the use of Beta-Blockers

The use of beta-blockers is purely to assist with the symptoms that ensue from the adrenergic response triggered by thyroid storm. They provide symptomatic relief from tremors and palpitaitons, while also controlling tachycardia and increasing diastolic filling times (Tagami et al., 2012). It has NO effect on thyroid hormone levels. 

However, the blind use of beta-blockers in thyroid storm should be met with caution by the emergency medicine physician. In reviewing the literature, their are enumerable case reports of precipitous decline and death following treatment of thyroid storm with beta-blockers. And this precipitous decline can be equated to the same principles that justify us to avoid use of beta-blockers in decompensated HFrEF – the negative inotropy conveyed by beta-blockers can easily precipitate cardiogenic shock in a patient with severe AS and/or severe HFrEF. Furthermore, up to 1% of hyperthyroidism may have undiagnosed cardiomyopathies with reduced LV function. 

Rate control should be reserved for the patients with atrial fibrillation and RVR who have a preserved ejection fraction, or for those patients who are no longer in frank shock. 

As the ED physician, it is therefore our role to evaluate the patient in shock in front of us, do a POCUS to assess LV function, and ascertain if it is safe to introduce the beta-blockers or not. Our local ICU/EM expert Dr. Ariel Hendin, also had the following to say:

“If a patient is hypotensive and tachy with thyroid storm, I would be most worried about cardiogenic shock. I would treat them as any other cardiogenic shock patient, and I would think carefully about antibiotics and steroids.I would not purse rate control, including propranolol, if in sinu. This is a patient who is potentially teetering on the edge of completely decompensating, and negative inotropy may precipitate that“

– Dr. Ariel Hendin, FRCPC Intensivist & FRCPC EM

When safe to do so, the following agents can be introduced for symptom management, and should be continued upon patient discharge, as they have a large positive impact on a patient’s overall quality of life.  

IMPORTANT: Assess safety of beta-blockade in patients with “profound” shock

 

Block Enterohepatic Circulation

This is NOT a medication that would be expected to be started in the ED. Use of cholestyramine to reduce enterohepatic circulation and endogenous re-uptake, was shown in a study from 2005 by Tsai et al., to decrease serum T3/T4 measurement at 2 and 4 weeks more than use of PTU and propanolol alone. It is not required in the acute phase. 

 

Conclusion

 

    • Consider THYROID STORM as a potential Zebra in any of your “Hot and Crazy” presentations, especially when no alternative cause can be found.

 

    • Recognition of Thyroid Storm is the most important. 

 

    • Thyroid storm is a CLINICAL DIAGNOSIS. Composed of a triad of pyrexia, AMS and tachycardia, with end-organ damage evidence on biochemical assays.

 

    • In the ED, treatment should focus on early administration of MMI or PTU (Thyroid Peroxidase Inhibitors), to inhibit the synthesis of additional thyroid hormone. In addition to acute rescucitation of your ABCs.  

 

    • Be cautious of the use of beta-blockers in the severe thyroid storm with shock. Assess LV function and risk of cardiogenic shock before preceding with their administration.  

 

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Author

  • Josee Malette

    Dr. Josée Malette is an Emergency Medicine Resident in the Department of Emergency Medicine, University of Ottawa. She is a Senior Editor with the Digital Scholarship and Knowledge Dissemination team for the EMOttawaBlog. Her interests involve critical care in low resource settings, medical education, rural medicine and prehospital medicine.

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