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2021 A Storm is Coming.pptx
This document discusses thyroid storm, a life-threatening condition caused by excess thyroid hormone levels. It begins by outlining the objectives of understanding the pathophysiology of hyperthyroidism, recognizing clinical presentations of thyroid storm, and providing optimal treatment guidelines. Key points include distinguishing primary from secondary hyperthyroidism, identifying potential triggers of thyroid storm like infection or trauma, and describing the classic presentation of fever, tachycardia, and altered mental status. Treatment involves supportive care as well as inhibiting thyroid hormone synthesis with drugs, blocking hormone release with iodine, treating symptoms like tachycardia, and using steroids or plasmapheresis in refractory cases. The goal is to reduce circulating thyroid hormone levels and control
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2021 A Storm is Coming.pptx
- 1. A Storm isComing…. PARRM 2223
- 2. Objectives • Awareness ofthe pathophysiology of Primary and Secondary hyperthyroidism • Recognition of the possible clinical presentation that the patient in Thyroid Storm. • Provide education on the optimal treatment for an apparent Hyperthyroidism and thyroid storms.
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- 4. Definitions • Hyperthyroidism: Disordersresulting from overproduction of thyroid hormone • Thyrotoxicosis: Disorders resulting from any cause of excess thyroid hormone • Thyroid Storm: A life-threatening, pathologic state in which the body manifests a myriad of symptoms ranging from high-output cardiac failure to severe alterations of mental status in response to excess circulating thyroid hormone • It can be life threatening but with quick response can be controlled and managed
- 5. Hyperthyroidism • Not asingle “problem” but a “constellation” of effects across multiple body systems stemming from a single organ. • Easy to misdiagnose • Treated, it can be manageable • Untreated/undertreated/neglected it can be life-threatening. • Incidence is far higher in the US compared to other countries due to our use of Iodized Salt
- 7. Primary vs. SecondaryHypothyroidism • Primary hyperthyroidism is caused by the excessive production of thyroid hormones from the thyroid glands. • Secondary hyperthyroidism is caused by the excessive production of thyroid‐releasing hormones or thyroid‐stimulating hormones (TSHs) in the hypothalamus and pituitary, respectively. • Other causes: • Toxicological • Ectopic thyroid tissue • Cancerous • metastatic thyroid carcinoma. • Graves Disease • In approximately 20–25% of cases, no acute precipitant is identified.
- 8. Toxicological Causes • Amiodarone •Amiodarone has iodine‐rich benzfuran content that increases the level of iodine upon intake, thus increasing the activity of the thyroid • Lithium • Thyroxin like drug overdoses • Synthroid, Levothyroxine • Radioactive Iodine s/p CT w/ Contrast (i.e. CT-A) • Withdrawal of antithyroid drugs
- 9. Graves Disease This Photo byUnknown Author is licensed under CC BY-SA
- 10. Graves Disease • Graves’disease is an autoimmune disease that leads to a generalized overactivity of the entire thyroid gland (hyperthyroidism). • It is the most common cause of hyperthyroidism in the United States. • Many severe cases of hyperthyroidism (Thyroid Storm) are related to Graves disease. • Symptoms are similar to hyperthyroidism as a whole
- 11. Think constant elevatedmetabolism and sympathetic stress • Metabolic/”Constitutional” • Unmitigated Weight loss • Increased appetite • Elevated Body temp, Sweating • Irregular or absent menstruation • Muscle Weakness and fatigue • Behavioral • Nervousness, anxiety and irritability • Insomnia • Psychosis, Tremors, • Transient Paralysis?? • Cardiovascular • Systolic Hypertension • Tachycardia, Palpitations • A-Fib • High Output Heart Failure • Physical • Brittle hair, Hair loss • Palpable thyroid gland (Goiter) • “Bulging eyes” And “Lid Lag” • Conjunctivitis • Pale Skin • Anemia • Lower elg edema with rash • Jaundice * Not all hyperthyroidism patients present with goiter • Other • Increased sensitivity to heat/cold • Rashes, particularly to lower extremities • Diarrhea, GI upset
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- 13. Common Manifestations • EyeDisorders • Graves’ ophthalmopathy or orbitopathy • Bulging of the eyes • Red or enflamed tissue around the eyes • Visual distortions because of the swelling displacing the yes • “Double Vision” most common • Skin Disorders • “Graves Dermopathy”
- 14. Marty Feldman(A comedic actor) usedhis bulging eyes, caused by Graves' disease, for comedic effect.
- 15. Rodney Dangerfield- Graves can’t getno respect
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- 17. Chronic Treatment and Management •Radio-Iodine Therapy • Thyroid Blocker Medications • Beta-Blockers • Surgical Removal This Photo by Unknown Author is licensed under CC BY-NC
- 18. Prehospital treatment and management •Supportive care • General: • oxygen, cardiac monitoring • Fever: • external cooling for febrile patients • acetaminophen, 325–650 mg PO/PR every 4–6 h • (aspirin is contraindicated as it releases thyroxine from protein binding sites) • Dehydration: • i.v. isotonic saline • Hypoglycemia • Use dextrose containing isotonic saline if blood sugar low • Nutrition: • Thiamine can be considered (deficient secondary to hypermetabolism or alcoholism) This Photo by Unknown Author is licensed under CC BY-SA
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- 20. Epidemiology • Rare conditionthat is more common in women (80/100,000 per year) than in men (8/100,000 per year) • Extremely rare in children (0.9/100,000 per year) • Most cases are due to Graves’ disease • Cancers are a leading cause • Toxins • Amiodarone • Thyroid Hormones • Iodine containing compounds
- 21. Triggers • Untreated/undertreated thyroiddisease (i.e. medication non-compliance) • Trauma (direct trauma or as a result of stress to body) • Thyroid or non-thyroid surgery • Myocardial infarction/ischemia • Infection • Diabetic Ketoacidosis/Hyperosmolar Nonketotic Coma • Toxins: • Iodinated contrast (typically in susceptible patients with Graves’ disease or multi nodular goiter) • Pseudoephedrine, • salicylate use • Ingestion of thyroid hormone
- 22. Thyroid Storm • Treatmentis largely symptomatic and etiology dependent • Look back at the treatments in your hyperthyroid module • Think also about the body’s functioning and the exaggerated symptoms of hyperthyroidism that would be manifested during thyroid storm • The excess thyroxin causes a catecholamine toxicity
- 23. Classic Presentation • CommonFindings • Fever • Tachycardia • Altered Mental Status • Other Common Findings: • Atrial Fib / HO Heart Failure • Hepatic Failure • Seizures , Delirium, Coma • Ask your self, what are the mimics? • Methamphetamine Abuse • Sepsis • Stroke? Something Else?
- 24. Burch and Wartofsky'sdiagnostic parameters and scoring points for thyroid storm • 1. Thermoregulatory dysfunction • 37.2–37.7 (99–99.9) 5 • 37.7–38.3 (100–100.9) 10 • 38.3–38.8 (101–101.9) 15 • 38.9–39.4 (102–102.9) 20 • 39.4–39.9 (103–103.9) 25 • ≥40 (≥104.0) 30 • 2. Central nervous system effects • Absent 0 • Mild (agitation) 10 • Moderate 20 • (delirium, psychosis, extreme lethargy) • Severe (seizures, coma) 30 • 3. Gastrointestinal–hepatic dysfunction • Absent 0 • Moderate 10 • diarrhea, nausea/vomiting, • abdominal pain) • Severe (unexplained jaundice) 20 • 4. Cardiovascular dysfunction • Tachycardia, b.p.m. • 90–109 5 • 110–119 10 • 120–139 15 • ≥140 25 • 5. Congestive heart failure • Absent 0 • Mild (pedal edema) 5 • Moderate (bibasilar rales) 10 • Severe (pulmonary edema) 15 • 6. Atrial fibrillation • Absent 0 • Present 10 Scoring system: ≥45, highly suggestive of thyroid storm; 25–44, suggestive of impending storm; <25, unlikely to represent thyroid storm. Table reproduced from: Burch & Wartofsky (1993).5
- 27. Why is this important? •The mortality rate due to cardiac failure, arrhythmia, or hyperthermia is as high as 30%, even with treatment.
- 28. Storm Treatments • Symptomaticand supportive care • Treatments directed at thyroid gland and hormones • Inhibition of new hormone synthesis with Thioamide drugs such as PTU and methimazole • Inhibition of hormone release with Iodine & potassium iodide (Lugol’s solution) & Lithium carbonate
- 29. Treatment- Common Strategies •VOMIT + Cooling + Dextrose + Antibiotics + B- Blockers • V: Vital Signs • O: Oxygen • M:EKG Monitoring • I: Intravenous access and fluids • T: Transport to ICU capable facility + • COOLING (Severe cases) • Dextrose (for hypoglycemia from increased metabolic rate) • Antibiotics • B- Blockers and rate control • Steroids
- 30. Comments about fluidsand Dextrose • Check BG, consider adding dextrose PRN • Aggressive fluid resuscitation vs. concerns about CHF?
- 31. Inhibit / BlockThyroid Hormone synthesis • Propylthiouracil (PTU) • Dose: 600-1000 mg PO, then 300 mg PO Q6 • Impairs conversion of T4 to T3 • Preferred in pregnancy • Methimazole: 20-30 mg Q6 hours • Both drugs can be given PO, NG or PR
- 32. Block Thyroid HormoneRelease • Blocking synthesis does not stop release of preformed thyroid hormone • Blocks release of stored thyroid hormone • Can increase synthesis of thyroid hormone so should be held for at least 1 hour after initiation of PTU • Medication options: • Potassium Iodide (SSKI): 5 gtt Q6 hours • Lugol’s solution: 4-8 gtt Q6 hours • Lithium 300 mg Q6-8 hours (alternative if Lugol’s contraindicated)
- 33. Lugol’s solution • Alsoknown as Lugol’s iodine, this oral solution is specifically indicated for patient’s with thyroid storm or preoperatively for a patient with hyperthyroidism • It is a mix of iodine, potassium iodide and distilled water • Administered Orally • It is also used to enhance color and growth for coral in home aquariums!
- 34. Why Antibiotics? Signs andsymptoms in thyroid storm mimics sepsis and distinguishing the two can be difficult Infection is a leading precipitant for thyroid storm
- 35. Comments about tachycardiasand High Output Heart Failure • Oxygen • Hemodynamic Support • Fluids: High Output Heart Failure is Pre-load dependent. Fluids support Pre-load. • Vasopressors- Nor-epi but not epi or any that will raise HR • Rate Control • Betablockers – best supported in evidence • Ca Channel Blockers only if Refractory to Beta Blockers • Cardioversion for refractory and unstable severe tachycardias • Respiratory Support • Oxygen for anemia • CPAP for Pulmonary edema • Intubation as needed
- 36. Why Betablockers? • Decreasingsympathetic surge • Propranolol most commonly used • Non-selective beta blockade effectively treated systemic effects • Additional benefit of blocking conversion of T4 to T3 • Dose: 0.5 – 1 mg IV over 3-5 minutes, repeate Q 5-10 • Titrate to HR < 100 • Keep a close eye on blood pressure • Esmolol • Can be substituted if concern for hemodynamic collapse. Very short acting • Dose • Load: 250-500 mcg/kg Q 5-10 Minutes • Infusion: 50-100 mcg/kg/min • Role of beta blocker with signs of heart failure • Heart failure typically high-output and beta blockade will still be beneficial • Start slow with test dose and follow response prior to additional doses
- 37. Steroids (again) • Function:Block conversion of T4 to T3 • Block release of hormone from the thyroid gland • Concomitant adrenal insufficiency is common • Same doses as discussed for Adrenal Crisis
- 38. Plasmapheresis Plasmapheresis can significantly lowerthyroid hormone levels in refractory patients. This Photo by Unknown Author is licensed under CC BY-SA
- 39. Treatment Summary • OverallGoal: Reduce circulation thyroid levels and control symptoms • Beta blockers; decreases adrenergic hyperactivity (sympathetic outflow) • PTU (large amounts): prevents synthesis of the hormone • Glucocorticoids: inhibit hormone production and decrease peripheral conversion from T4 to T3. • Sodium iodide solution (Lugol’s solution): High levels of iodide will initially suppress release of thyroid hormone • Treat cardiac symptoms, fever and hypertension
Editor's Notes
- #4 Hyperthyroidism presents as a constellation of symptoms due to elevated levels of circulating thyroid hormones. Because of the many actions of thyroid hormone on various organ systems in the body, the spectrum of clinical signs produced by the condition is broad. The presenting symptoms can be subtle and nonspecific, making hyperthyroidism difficult to diagnose in its early stages without the aid of laboratory data. The term hyperthyroidism refers to inappropriately elevated thyroid function. Though often used interchangeably, the term thyrotoxicosis, which refers to an excessive amount of circulating thyroid hormone, is not synonymous with hyperthyroidism. Increased levels of hormone can occur despite otherwise normal thyroid function, such as in instances of inappropriate exogenous thyroid hormone or excessive release of stored hormone from an inflamed thyroid gland.
- #6 Hyperthyroidism presents as a constellation of symptoms due to elevated levels of circulating thyroid hormones. Because of the many actions of thyroid hormone on various organ systems in the body, the spectrum of clinical signs produced by the condition is broad. The presenting symptoms can be subtle and nonspecific, making hyperthyroidism difficult to diagnose in its early stages without the aid of laboratory data. The term hyperthyroidism refers to inappropriately elevated thyroid function. Though often used interchangeably, the term thyrotoxicosis, which refers to an excessive amount of circulating thyroid hormone, is not synonymous with hyperthyroidism. Increased levels of hormone can occur despite otherwise normal thyroid function, such as in instances of inappropriate exogenous thyroid hormone or excessive release of stored hormone from an inflamed thyroid gland. Too much iodine can make hyperthyroidism worse by leading the thyroid gland to produce too much thyroid hormone. A person with hyperthyroidism should avoid eating excessive amounts of iodine-rich foods, such as: iodized salt The incidence of thyroid storm in hospitalized patients in Japan is estimated to be 0.20 per 100,000 per year with more than 10% mortality.1 In the USA, the overall incidence of hyperthyroidism is estimated to be between 0.05% and 1.3%, with the majority of cases being subclinical in terms of presentation.
- #8 Struma ovarii, an ectopic thyroid tissue, is a rare form of teratoma that produces thyroid hormones. Metastatic thyroid cancer and human chorionic gonadotropin‐secreting hydatidiform mole are other rare extrinsic causes of thyrotoxicosis.
- #10 Graves' disease is named for the doctor—Robert J. Graves—who first described it in a patient in 1835. The disease is also referred to as Basedow's disease—named after a German, Karl Adolph van Basedow, who described the disease in 1840. He didn't know that Graves had described the same disease just a few years earlier. Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism). Although a number of disorders may result in hyperthyroidism, Graves' disease is a common cause. Thyroid hormones affect many body systems, so signs and symptoms of Graves' disease can be wide ranging. Although Graves' disease may affect anyone, it's more common among women and in people younger than age 40. The primary treatment goals are to reduce the amount of thyroid hormones that the body produces and lessen the severity of symptoms.
- #11 In the case of thyroid storm, the most common underlying cause of hyperthyroidism is Graves' disease. It is caused by the thyrotropin receptor antibodies that stimulate excessive and uncontrolled thyroidal synthesis and secretion of thyroid hormones. It occurs most frequently in young women (10 times more common in women compared to men) at any age group In Graves’ disease these antibodies (called the thyrotropin receptor antibodies (TRAb) or thyroid stimulating immunoglobulins (TSI) do the opposite – they cause the cells to work overtime. The antibodies in Graves’ disease bind to receptors on the surface of thyroid cells and stimulate those cells to overproduce and release thyroid hormones.
- #14 Hyperthyroidism The majority of symptoms of Graves’ disease are caused by the excessive production of thyroid hormones by the thyroid gland (see Hyperthyroidism brochure). These may include, but are not limited to, racing heartbeat, hand tremors, trouble sleeping, weight loss, muscle weakness, neuropsychiatric symptoms and heat intolerance. Eye disease Graves’ disease is the only kind of hyperthyroidism that can be associated with inflammation of the eyes, swelling of the tissues around the eyes and bulging of the eyes (called Graves’ ophthalmopathy or orbitopathy). Overall, a third of patients with Graves’ disease develop some signs and symptoms of Graves’ eye disease but only 5% have moderate-to-severe inflammation of the eye tissues to cause serious or permanent vision trouble. Patients who have any suggestion of eye symptoms should seek an evaluation with an eye doctor (an ophthalmologist) as well as their endocrinologist. Eye symptoms most often begin about six months before or after the diagnosis of Graves’ disease has been made. Seldom do eye problems occur long after the disease has been treated. In some patients with eye symptoms, hyperthyroidism never develops and, rarely, patients may be hypothyroid. The severity of the eye symptoms is not related to the severity of the hyperthyroidism. Early signs of trouble might be red or inflamed eyes, a bulging of the eyes due to inflammation of the tissues behind the eyeball or double vision. Diminished vision or double vision are rare problems that usually occur later, if at all. We do not know why, but problems with the eyes occur much more often and are more severe in people with Graves’ disease who smoke cigarettes. Skin disease Rarely, patients with Graves’ disease develop a lumpy reddish thickening of the skin in front of the shins known as pretibial myxedema (called Graves’ dermopathy). This skin condition is usually painless and relatively mild, but it can be painful for some. Like the eye trouble of Graves’ disease, the skin problem does not necessarily begin precisely when the hyperthyroidism starts. Its severity is not related to the level of thyroid hormone.
- #19 Supportive care General: oxygen, cardiac monitoring Fever: external cooling for febrile patients acetaminophen, 325–650 mg PO/PR every 4–6 h (aspirin is contraindicated as it releases thyroxine from protein binding sites) Dehydration: i.v. isotonic saline Hypoglycemia Use dextrose containing isotonic saline if blood sugar low Nutrition: Thiamine can be considered (deficient secondary to hypermetabolism or alcoholism)
- #20 Thyroid storm is a rare and potentially fatal complication of hyperthyroidism. [1] It typically occurs in patients with untreated or partially treated thyrotoxicosis who experience a precipitating event such as surgery, infection, or trauma. Thyroid storm must be recognized and treated on clinical grounds alone, as laboratory confirmation often cannot be obtained in a timely manner. Patients typically appear markedly hypermetabolic with high fevers, tachycardia, nausea and vomiting, tremulousness, agitation, and psychosis. Late in the progression of disease, patients may become stuporous or comatose with hypotension. TS is a dangerous expression of thyrotoxicosis precipitated by several events. The presence of heart collapse, coagulation abnormalities and organ failure determines a poor outcome and all the therapeutic strategies are involved to reduce hormonal activity, to prevent organ damage and to sustain vital capacity.
- #21 Graves’ disease Toxic adenoma (single responsible nodule) Toxic multinodular goiter Thyrotoxicosis with thyroiditis Hashimoto’s thyroiditis Subacute thyroiditis Postpartum thyroiditis Exogenous thyroid hormone abuse Iatrogenic (i.e.) Amiodarone induced thyroiditis Oncologic TSH-producing pituitary tumor Metastatic follicular thyroid carcinoma hCG-mediated thyrotoxicosis Hydatidiform mole Metastatic choriocarcinoma
- #22 T4 produced by the thyroid is deiodinated to the more active T3 form Most (> 99%) of thyroid hormone is protein bound and, thus inactive. Only free thyroid hormone is metabolically active Thyroid hormone affects metabolism in all tissues in the body via a variety of mechanisms Thyroid hormone increases the expression and sensitivity of beta-adrenergic receptors resulting in an increased response to endogenous catecholamines (this accounts for many of the symptoms seen in thyroid storm) Wolff-Chaikoff Effect: Excess iodide transiently inhibits thyroglobulin iodination and release of thyroid hormone Jod-Basedown Effect: Iodide load induces hyperthyroidism in susceptible subgroups (i.e. Graves’ disease, multi nodular goiter)
- #23 Patients with thyroid storm have relatively higher levels of free thyroid hormones(THs) than patients with uncomplicated thyrotoxicosis, even though total TH levels may not be increased. Adrenergic receptor activation is a hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of betaadrenergic receptors, thereby enhancing the effect of catecholamines.
- #26 Burch and Wartofsky scale The Burch-Wartofsky Point Scale (BWPS) is a quantitative diagnostic tool based on 3 major observations in patients with thyroid storm: Continuum of end organ dysfunction. High variability of symptoms and signs between patients. High mortality associated with missed diagnosis.
- #30 Why antibiotics? Thyroid storm may be precipitated by a number of factors including intercurrent illness, especially infections (Table 1). Pneumonia, upper respiratory tract infection, enteric infections, or any other infection can precipitate thyroid storm.
- #31 Insensible fluid losses from fever can be high in these patients High output cardiac failure is common and preload should be maintained in these patients Add dextrose to fluids (patients often have depleted glycogen stores)
- #32 Inhibit thyroid hormone synthesisPropylthiouracil (PTU) Dose Load: 600-1000 mg PO 300 mg PO Q6 Impairs conversion of T4 to T3 Preferred in pregnancy Methimazole: 20-30 mg Q6 hours Both drugs can be given PO, NG or PR
- #33 Inhibit thyroid hormone release with inorganic iodineMechanism of action Blocking synthesis does not stop release of preformed thyroid hormone Blocks release of stored thyroid hormone Can increase synthesis of thyroid hormone so should be held for at least 1 hour after initiation of PTU Medication options Potassium Iodide (SSKI): 5 gtt Q6 hours Lugol’s solution: 4-8 gtt Q6 hours Lithium 300 mg Q6-8 hours (alternative if SSKI/Lugol’s contraindicated)
- #37 Beta-blockade should be instigated immediately (unless contraindicated) so as to block the adrenergic consequences of thyroid hormone excess. Propranolol most commonly used Non-selectvie beta blockade effectively treated systemic effects Additional benefit of blocking conversion of T4 to T3 Dose: 0.5 – 1 mg IV over 3-5 minutes Can repeat dose q5-10 minutes Titrate to HR < 100 Keep a close eye on blood pressure Esmolol Can be substituted if concern for hemodynamic collapse Dose Load: 250-500 mcg/kg Infusion: 50-100 mcg/kg/min Role of beta blocker with signs of heart failure Heart failure typically high-output and beta blockade will still be beneficial Start slow with test dose and follow response prior to additional doses
- #38 The immediate goals when treating thyroid storm are to decrease thyroid hormone synthesis, prevent thyroid hormone release, decrease peripheral action of circulating thyroid hormone to reduce heart rate and support the circulation, and to treat the precipitating condition
- #39 Plasmapheresis is a process in which the liquid part of the blood, or plasma, is separated from the blood cells. Typically, the plasma is replaced with another solution such as saline or albumin, or the plasma is treated and then returned to your body.