o Thyroid Surgery
o Withdrawal to Therapy, Radioiodine Therapy o Iodinated Contrast Dye
o Condition associated with an Acute or Subacute Nonthyroidal Illness o Nonthyroidal Surgery
o Infection, CVA o Pulmonary Embolism o Parturition
o DKA
o Emotional Stress o Trauma
I. BURCH AND WARTOFSKY‟S DIAGNOSTIC CRITERIA FOR THYROID STORM
A. Thermoregulatory Dysfunction (Temperature)37.2 – 37.7 0C 5
37.8 – 38.2 0C 10
38.3 – 38.8 0C 15
38.9 – 39.3 0C 20
39.4 – 39.9 0C 25
> 40.0 0C 30
B. Central Nervous System Effects
Absent 0
Mild (Agitation) 10
Moderate (Delirium, Psychosis, Extreme Lethargy) 20
Severe (Seizure, Coma) 30
C. Gastrointestinal-Hepatic Dysfunction
Absent 0
Moderate (Diarrhea, Nausea/Vomiting, Abdominal Pain) 10
Severe (Unexplained Jaundice) 20
D. Cardiovascular Dysfunction
1. Tachycardia (Beats Per Minute)
99 – 109 5
110 – 119 10
120 – 129 15
130 – 139 20
> 140 25
2. Congestive Heart Failure
Absent 0
Mild (Pedal Edema) 5
Moderate (Bibasilar Rales) 10
Severe (Pulmonary Edema) 15
Atrial Fibrillation 10
3. Precipitant History
Negative 0
Positive 10
Scoring:
< 25 Unlikely Storm 25 – 44 Impending Storm
> 45 Highly Suggestive of Thyroid Storm
II. NOTES FROM LECTURE ON THYROID STORM A. Thyrotoxicosis VS Hyperthyroid
o Thyrotoxicosis: Clinical Syndrome resulting from Cellular Responses to Excessive Thyroid Hormone (may be EXOGENOUS or ENDOGENOUS)
o Hyperthyroid: Thyrotoxicosis that results from Increased Production of Thyroid Hormones from the Thyroid Gland itself (ENDOGENOUS)
B. Causes of Thyrotoxicosis:
PRIMARY THYROTOXICOSIS SECONDARY THYROTOXICOSIS THYROTOXICOSIS WITHOUT HYPERTHYROIDISM
TSH Secreting Pituitary Adenoma Thyroid Hormone Resistance Syndrome H-Mole
Leakage
Subacute Thyroiditis
Painless Thyroiditis
Suppurative Thyroiditis Thyrotoxicosis Factitia
Exogenous Thyroid Hormone
Diet Pills
Other Causes of Thyroid Gland Destruction:
Amiodarone
Radiation
Infarction of Adenoma Ectopic Thyroid Gland
Struma Ovarii (Thyroid Tissue in ovary) C. Thyroid Storm
o Extreme Accentuation of Hyperthyroidism, usually with Grave‟s Disease of Toxic Multinodular Goiter o < 10% of Hospital Admissions for Thyrotoxicosis
o Mortality Rate = 20-30%
o Point of which Thyrotoxicosis transforms to Storm is controversial 1. Precipitants of Thyroid Storm
Pre-Existing Thyrotoxicosis, Untreated or Partially Treated
Infection, Trauma, Surgery
Due to poorly prepared Thyroidectomy in Grave‟s Disease patient
Other conditions associated with a Rapid Rise in Hormone Levels:
Withdrawal of Antithyroid Drug Therapy
Radioiodine Therapy
Vigorous Thyroid Palpation
Iodinated Contrast Dyes
Salicylates (competes with Albumin Binding Increase in Free Thyroid Hormone Levels)
Conditions associated with an Acute or Subacute Non-Thyroidal Illness
Infection
CVA
Trauma
DKA 2. Pathophysiology
No evidence that there is an Increased Production of T3 or T4 causing the Storm
Magnitude of Increase in Thyroid Hormones does NOT appear to be Critical
Increased Catecholamine Receptors (Key Role)
Decreased Binding to TBG (Increased Free T3/T4) 3. Atypical Presentation
Suspect Hyperthyroid in patients with Fever and Atrial Fibrillation NOT controlled with appropriate Cardiac Management
Apathy and Coma RARE Manifestation of storm
Key to Management = EARLY Recognition 4. Some Laboratory Findings:
Increased FT4, Increased FT3
Decreased TSH
12 L ECG
Leukocytosis, shift to the Left if (+) Infection
Mild Hypercalcemia
Liver Function Test Abnormalities
Hyperglycemia (Mild to Moderate)
III. MANAGEMENT OF STORM
A. Inhibit New Hormone Production 1. Propylthiouracil (PTU)
Inhibits Thyroid Peroxidase (which is involved in organification and coupling)
Drug of choice because it inhibits Peripheral Conversion of T4T3 (in HIGH doses)
Given in Large Doses: 600-1000mg Loading Dose and 200-300mg every 6 hours – given orally or by nasogastric tube or per rectum
2. Methimazole
20-25mg PO q6
Inhibit Hormone Synthesis Mechanism Of Action
Inhibit synthesis of thyroid hormones by inhibiting organification of iodine and coupling of the iodotyrosinases
Inhibit Peripheral Conversion of T4 to T3
Proposed to have direct effects on the immune system – producing a decrease in circulating thyroid-stimulating antibodies and restoration of normal suppressor cell activity
Goals in Management:
1) Stop Synthesis of New Hormones within the Thyroid
2) Halt release of stored Thyroid Hormone from Thyroid Gland
3) Prevent conversion of T4 to T3
4) Control Adrenergic Symptoms associated with Thyrotoxicosis
5) control systemic Decompensation with Treatment
6) Treat Underlying cause Key Notes:
Thyroid Hormone Levels will Normalize after 4-Weeks (TSH longer time to Normalize)
Some Tests done in the PGH Lab:
o Total T4/T3 o Free T4/T3 o Tsh
o Thyroglobulin Assay o Anti-TPO
o TgAb Liver Function Tests:
In Thyroid Storm, we give High Doses of PTU Monitor Liver Function Tests, Agranulocytosis
If Storm is resolving, Liver Function Tests should have a Decreasing Trend
If LFT‟s are still increasing, DECREASE the Dose of PTU
Grave’s Ophthalmopathy
90% will NOT go back to Normal
RAI can Worsen Ophthalmopathy if still in the Active Phase (wait until Ophthalmopathy is more stable before giving RAI)
B. Inhibit Hormone Release 1. Stable Iodide (SSKI)
Given 1 hour after PTU – it blocks the release of hormone from the gland (block the synthesis first before giving Iodine)
Wolff-Chaikoff Effect: One hour after the first dose of PTU, Stable Iodide is given to BLOCK Thyroid Hormone Synthesis via the Wolff-Chaikoff Effect (the DELAY allows the Antithyroid Drug to prevent the excess Iodine from being incorporated into new hormone)
Administration: A saturated solution of Potassium Iodide (5 drops SSKI every 6 hours), or Ipodate or Iopanoic Acid (0.5mg every 12h), may be given orally
**NOTE: Opposite of Wolff-Chaikoff = Jod Basedow (worsens) 2. Others:
To reduce tachycardia and other adrenergic manifestations
60-80mg PO q4 or 80-120mg q6
High doses or Propranolol decrease T4T3 conversion
CAUTION is needed to avoid Acute Negative Inotropic Effects, but controlling the heart rate is important, as some patients develop a form of High-Output Heart Failure
2. Cardioselective Agents (for patients with Pulmonary Diseases)
Atenolol 500-200mg PO QID
Metoprolol 100-200mg
Nadolol 3. Esmolol (IV)
50-100 ug/kg/min D. Supportive
o Acetaminophen 325-650mg PO/PRN q4-q6
o Hydrocortisone 100mg IV q8 (decreases T4 to T3 conversion; Vasomotor Stability) o Volume Depletion and Poor Nutrition:
IV Fluids / Electrolytes
Glucose 5-10%
Vitamins
Oxygen
Vasopressors
Treatment of CHF (Digoxin, Diuretics)
Glucocorticoids to correct Relative Adrenal Insufficiency E. Alternative Treatment
o Lithium Carbonate 300mg PO q8 (mimics iodine) o Potassium Perchlorate 1g PO QID
o Cholestyramine 4g PO QID F. Removal of T4 and T3 from the Serum:
Decreases Fractional Turnover of Thyroid Iodine and T4 Secretion Rate
Blocks Thyroid Hormone release
Lithium Carbonate:
Inhibits Coupling of Iodotyrosines
Inhibits release of Thyroid Hormones
Inhibit conversion of T4 to T3 by decreasing Type-1 Deiodinase Activity