2. Objectives
⢠Awareness of the 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.
4. Definitions
⢠Hyperthyroidism: Disorders resulting 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 a single âproblemâ but a
âconstellationâ 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
6.
7. Primary vs. Secondary Hypothyroidism
⢠Primary hyperthyroidism is caused by the excessive production of thyroid
hormones from the thyroid glands.
⢠Secondary hyperthyroidism is caused by the excessive production of
thyroidâreleasing hormones or thyroidâstimulating hormones (TSHs) in the
hypothalamus and pituitary, respectively.
⢠Other causes:
⢠Toxicological
⢠Ectopic thyroid tissue
⢠Cancerous
⢠metastatic thyroid carcinoma.
⢠Graves Disease
⢠In approximately 20â25% of cases, no acute precipitant is identified.
8. Toxicological Causes
⢠Amiodarone
⢠Amiodarone has iodineârich
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
10. Graves Disease
⢠Gravesâ 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 elevated metabolism and
sympathetic stress
⢠Metabolic/âConstitutionalâ
⢠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)
⢠âBulging eyesâ And âLid Lagâ
⢠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
13. Common Manifestations
⢠Eye Disorders
⢠Gravesâ ophthalmopathy or orbitopathy
⢠Bulging of the eyes
⢠Red or enflamed tissue around the eyes
⢠Visual distortions because of the swelling displacing
the yes
⢠âDouble Visionâ most common
⢠Skin Disorders
⢠âGraves Dermopathyâ
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, 325â650 mg PO/PR every 4â6 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
20. Epidemiology
⢠Rare condition that 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 Gravesâ disease
⢠Cancers are a leading cause
⢠Toxins
⢠Amiodarone
⢠Thyroid Hormones
⢠Iodine containing compounds
21. Triggers
⢠Untreated/undertreated thyroid disease (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 Gravesâ disease or multi
nodular goiter)
⢠Pseudoephedrine,
⢠salicylate use
⢠Ingestion of thyroid hormone
22. Thyroid Storm
⢠Treatment is largely symptomatic and etiology dependent
⢠Look back at the treatments in your hyperthyroid module
⢠Think also about the bodyâs functioning and the exaggerated
symptoms of hyperthyroidism that would be manifested during
thyroid storm
⢠The excess thyroxin causes a catecholamine toxicity
23. Classic Presentation
⢠Common Findings
⢠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?
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
⢠Symptomatic and 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 (Lugolâs
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 fluids and Dextrose
⢠Check BG, consider adding dextrose PRN
⢠Aggressive fluid resuscitation vs. concerns about CHF?
31. Inhibit / Block Thyroid 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 Hormone Release
⢠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
⢠Lugolâs solution: 4-8 gtt Q6 hours
⢠Lithium 300 mg Q6-8 hours (alternative if Lugolâs contraindicated)
33. Lugolâs solution
⢠Also known as Lugolâs iodine, this oral solution
is specifically indicated for patientâs 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 and symptoms in
thyroid storm mimics
sepsis and
distinguishing the two
can be difficult
Infection is a leading
precipitant for thyroid
storm
35. Comments about tachycardias and 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 â 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?
⢠Decreasing sympathetic 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 â 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
39. Treatment Summary
⢠Overall Goal: 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 (Lugolâs solution): High levels of iodide will initially
suppress release of thyroid hormone
⢠Treat cardiac symptoms, fever and hypertension
Hinweis der Redaktion
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.
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 saltThe 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.
Struma ovarii, an ectopic thyroid tissue, is a rare form of teratoma that produces thyroid hormones. Metastatic thyroid cancer and human chorionic gonadotropinâsecreting hydatidiform mole are other rare extrinsic causes of thyrotoxicosis.
Graves' disease is named for the doctorâRobert J. Gravesâwho first described it in a patient in 1835. The disease is also referred to as Basedow's diseaseânamed 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.
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 Gravesâ disease these antibodies (called the thyrotropin receptor antibodies (TRAb) or thyroid stimulating immunoglobulins (TSI) do the opposite â they cause the cells to work overtime. The antibodies in Gravesâ disease bind to receptors on the surface of thyroid cells and stimulate those cells to overproduce and release thyroid hormones.
HyperthyroidismThe majority of symptoms of Gravesâ 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 diseaseGravesâ 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 Gravesâ ophthalmopathy or orbitopathy). Overall, a third of patients with Gravesâ disease develop some signs and symptoms of Gravesâ 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 Gravesâ 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 Gravesâ disease who smoke cigarettes.
Skin diseaseRarely, patients with Gravesâ disease develop a lumpy reddish thickening of the skin in front of the shins known as pretibial myxedema (called Gravesâ dermopathy). This skin condition is usually painless and relatively mild, but it can be painful for some. Like the eye trouble of Gravesâ disease, the skin problem does not necessarily begin precisely when the hyperthyroidism starts. Its severity is not related to the level of thyroid hormone.
Supportive care
General:
oxygen, cardiac monitoring
Fever:
external cooling for febrile patients
acetaminophen, 325â650âmg PO/PR every 4â6âh
(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)
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.Â
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. Gravesâ disease, multi nodular goiter)
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.
ďŽ 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.
Burch and Wartofsky scaleThe 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.
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.Â
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)
Inhibit thyroid hormone synthesisPropylthiouracil (PTU)
Dose
Load: 600-1000 mg PO
300 mg PO Q6
Impairs conversion of T4Â to T3
Preferred in pregnancy
Methimazole: 20-30 mg Q6 hours
Both drugs can be given PO, NG or PR
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
Lugolâs solution: 4-8 gtt Q6 hours
Lithium 300 mg Q6-8 hours (alternative if SSKI/Lugolâs contraindicated)
Beta-blockade should be instigated immediately (unless contraindicated) so as to block the adrenergic consequences of thyroid hormone excess.Â
Propranolol most commonly used
Non-selectvie beta blockade effectively treated systemic effects
Additional benefit of blocking conversion of T4Â to T3
Dose: 0.5 â 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
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
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.