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MANAGEMENT OF THYROID
STORM
BY DR GEETHA SUBRAHAMANIAM
CME OF NUCLEAR MEDICINE
29TH SEPTEMBER 2021
DEFINITION
Mortality 11-25%
(especially if you miss it)
Characterized by a multisystem disorder by
triggering event in conjunction with underlying
hyperthyroid conditions.
WHO DOES IT HAPPEN TO ?
Underlying thyroid disorders
• Grave’s disease
• Multinodular Goitre
• Hashimoto
• Thyroid adenoma
• Administration of iodinated contrast/radioactive iodine
• Diabetic ketoacidosis
• Severe Infection/sepsis
• Cardiac event
• Thyroidal or non-thyroidal surgery
• Trauma
• Pregnancy/post natal
• Adrenal insufficiency
Untreated / Undiagnosed/ Non-
compliant/discontinuation ATH
PATHOPHYSIOLOGY
DIAGNOSIS OF THYROID STORM
• MADE CLINICALLY IN A THYROTOXIC PATIENT WITH EVIDENCE OF
DECOMPENSTATION, ITS OFTEN OVERLAP WITH CLINICAL FEATURES OF OTHER
CRITICAL MEDICAL CONDITIONS
• AID DIAGNOSTIC METHODS
• BURCH–WARTOFSKY POINT SCALE (RECOMMENDED TOOL, MORE SENSITIVE)
• THE NEWER JAPAN THYROID ASSOCIATION
BURCH–WARTOFSKY POINT SCALE
Score
• more/equal 45
thyroid storm
• 25-44 : Impending
thyroid storm
• <25 : Thyroid
storm unlikely
Score of 25-44,
requires clinical
judgement to look
for decompensation
THE NEWER JAPAN THYROID ASSOCIATION
*Grade TS2 :
requires clinical
judgement to
look for
decompensatio
n
MANAGEMENT
AIM OF MANAGEMENT OF THYROID STORM ;
• INHIBITING SYNTHESIS AND RELEASE OF THYROID HORMONE
• INHIBITING PERIPHERAL ACTION OF THYROID HORMONE
• REVERSING SYSTEMIC DECOMPENSATION
• TREATING PRECIPITATING EVENT
• ADDRESSING DEFINITIVE THERAPHY
ANTI-THYROID DRUG: MMI/PTU
• HIGH DOSE OF PROPYLTHIOURACIL(PTU) RECOMMENDED, WITH LOADING DOSE 500-1000MG THEN
250MG 4H
• IN THE PRESENCE OF CONTRAINDICATIONS, HIGH DOSE OF METHIMAZOLE (MMI) 60-80MG/DAY,
SINGLE DOSE OR DIVIDED INTO TWO EQUAL DOSES.
• PTU IS PREFERRABLY USED FOR COMPARED TO MMI IN THYROID STORM, AS LATTER HAS THE ADDED
BENEFITS OF INHIBITING TYPE 1 DEIODINASE ACTIVITY IN THE THYROID GLAND AND OTHER
PERIPHERAL ORGANS( REDUCE THE CONVERSION OF T4 TO T3), T3 LEVELS DROP BY 45% WITHIN
ONE HOUR OF PTU ADMINISTRATION BUT ONLY ABOUT 10-15% AFTER STARTING MMI.
• NO OUTCOME DIFFERENCES BETWEEN MMI AND PTU
ADJUVANT TREATMENT FOR THYROID STORM
LITHIUM CAN BE USED ALTERNATIVE FOR PATIENT WHO CANNOT TOLERATE MMI/PTU.
• WORKS BY INHIBITING RELEASE OF THYROID HORMONE BY THYROID GLAND THROUGH UNKOWN
MECHANISM
• DOSE: 300MG TDS, MONITORED LITHIUM TOXICITY
BETA ADRENERGIC RECEPTOR ANTAGONISTS.
• KEY TO CONTROL HEART RATE AND INHIBIT OTHER PERIPHERAL ACTIONS OF
THYROID HORMONES IN THYROID STORM.
• ABILITY INHIBITS TYPE 1 DEIODINASE SUCH AS PROPRANOLOL, 60-80MG/4H
• BETA BLOCKERS WITH SELECTIVE B-1 BLOCKADE SUCH AS BISOPROLOL,
LANDIOLOL AND ESMOLOL INFUSION HAVE MORE FAVORABLE CVS BENEFITS IN
THYROID STORM WITH CARDIAC COMPROMISE.
• IV ESMOLOL LOADING DOSE 250-500MCG , MAINTAINANCE 50-1OOMCG/KG/MIN
• CONTRAINDICATIONS TO BETA BLOCKERS SUCH AS PATIENT WITH BRONCHIAL
ASTHMA OR COPD, DILTIAZEM CAN BE USED IN INTENSIVE CARE SETTING TO
CONTROL HR.
• AF PATIENT, CARDIOVERSION CONSIDERED AFTER R/OUT CARDIAC THROMBOSIS
IF HEMODYNAMICS ARE IMPAIRED.
CORTICOSTEROIDS
• TO INHIBIT BOTH THYROID HORMONE SYNTHESIS AND PERIPHERAL CONVERSION
OF T4-T3
• GIVEN AS PROPHYLAXIS FOR RELATIVE ADRENAL INSUFFICIENCY CAUSED BY
HYPERMETABOLIC STATE IN THYROID STORM.
• IV IS PREFERRED WHEN RAPID REACTION IS PREFFERED , WITH THE
IMPROVEMENT IN CLINICAL CONDITION DOSES SHOULD BE REDUCED AND
TAPERED OFF TO PREVENT ADVERSE EFFECT.
• DEXAMETHASONE (MEDIAN DOSE 6MG/DAY)
• HYDROCORTISONE (300MG/DAY)
• PREDNISALONE (25MG/DAY)
INORGANIC IODIDE(LUGOL’S IODINE/SATURATED SOLUTIONS OF POTASSIUM
IODIDE,SSKI)
• USED TO DECREASE T4 LEVELS BY INHIBITION OF IODIDE OXIDATION AND
ORGANIFICATION AND INHIBITS RELEASE OF THYROID HORMONE.
• RECOMMENDED DOSE 5DROPS OF LUGOL’S IODIDE 6H(6.25MG IODINE/DROP) OR
10DROPS OF LUGOL’S IODINE 8H
• THIS SOLUTION SHOULD BE DILUTED IN WATER OR TAKEN WITH BREAD TO AVOID
MUCUSAL IRRITATION.
• THIS AGENTS CAN BE USED IN COMBINATION WITH ATT.
• THESE AGENTS SHOULD ONLY BE GIVEN AT LEAST AFTER ONE HOUR OF ATT
DRUGS ADMINISTRATION, TO PREVENT USE OF IODINE AS SUBTRATE FOR
THYROID HORMONE SYNTHESIS.
• AFTER CLINICAL IMPROVEMENT, THE LUGOL’S SHOULD BE TAPERED AND
STOPPED BEFORE THE ANTITHYROID.
• LUGOL’S IODINE SHOULD NOT GIVEN BEYOND 10DAYS OR ELSE THIS WOULD
LEAD TO ESCAPE FROM WOLFF-CHAIKOFF PHENOMENON.
• CONTRAINDICATED: KNOWN TO BE ALLERGIC TO INORGANIC IODIDE
SUPPORTIVE TREATMENT
• INTRAVENOUS FLUIDS
• RESPIRATORY SUPPORT INCLUDES INVASSIVE/NON-INVASSIVE
• NUTRITIONAL SUPPORT
• ACUTE INFECTIONS- SHOULD BE TREATED WITH BROAD SPECTRUM ABX
DEFINITIVE THERAPHY
URGENT/ EARLY THYROIDECTOMY
• IS AN OPTION IN PATIENTS WHO HAVE CONTRAINDICATIONS TO ATT, LARGE GOITRE
• PATIENTS SHOULD RENDERED TO EUTHYROID STATE PRIOR TO SURGERY TO MINIMISE RISK OF
THYROID STORM
• RAI IODINE IS CONSIDERED AND LUGOL’S IODINE HAS BEEN ADMINISTERED DURING THYROID STORM ,
THE RAI SHOULD BE DEFERRED UNTIL ABOUT 3-4 MONTHS AFTER.
PRECIPATING FACTORS: NON-COMPLIANCE
• PATIENT SHOULD BE EDUCATED ON THIS ASPECT
Thyroid storm
Thyroid storm
Thyroid storm

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Thyroid storm

  • 1. MANAGEMENT OF THYROID STORM BY DR GEETHA SUBRAHAMANIAM CME OF NUCLEAR MEDICINE 29TH SEPTEMBER 2021
  • 2. DEFINITION Mortality 11-25% (especially if you miss it) Characterized by a multisystem disorder by triggering event in conjunction with underlying hyperthyroid conditions.
  • 3. WHO DOES IT HAPPEN TO ? Underlying thyroid disorders • Grave’s disease • Multinodular Goitre • Hashimoto • Thyroid adenoma • Administration of iodinated contrast/radioactive iodine • Diabetic ketoacidosis • Severe Infection/sepsis • Cardiac event • Thyroidal or non-thyroidal surgery • Trauma • Pregnancy/post natal • Adrenal insufficiency Untreated / Undiagnosed/ Non- compliant/discontinuation ATH
  • 5. DIAGNOSIS OF THYROID STORM • MADE CLINICALLY IN A THYROTOXIC PATIENT WITH EVIDENCE OF DECOMPENSTATION, ITS OFTEN OVERLAP WITH CLINICAL FEATURES OF OTHER CRITICAL MEDICAL CONDITIONS • AID DIAGNOSTIC METHODS • BURCH–WARTOFSKY POINT SCALE (RECOMMENDED TOOL, MORE SENSITIVE) • THE NEWER JAPAN THYROID ASSOCIATION
  • 6. BURCH–WARTOFSKY POINT SCALE Score • more/equal 45 thyroid storm • 25-44 : Impending thyroid storm • <25 : Thyroid storm unlikely Score of 25-44, requires clinical judgement to look for decompensation
  • 7. THE NEWER JAPAN THYROID ASSOCIATION *Grade TS2 : requires clinical judgement to look for decompensatio n
  • 8. MANAGEMENT AIM OF MANAGEMENT OF THYROID STORM ; • INHIBITING SYNTHESIS AND RELEASE OF THYROID HORMONE • INHIBITING PERIPHERAL ACTION OF THYROID HORMONE • REVERSING SYSTEMIC DECOMPENSATION • TREATING PRECIPITATING EVENT • ADDRESSING DEFINITIVE THERAPHY
  • 9. ANTI-THYROID DRUG: MMI/PTU • HIGH DOSE OF PROPYLTHIOURACIL(PTU) RECOMMENDED, WITH LOADING DOSE 500-1000MG THEN 250MG 4H • IN THE PRESENCE OF CONTRAINDICATIONS, HIGH DOSE OF METHIMAZOLE (MMI) 60-80MG/DAY, SINGLE DOSE OR DIVIDED INTO TWO EQUAL DOSES. • PTU IS PREFERRABLY USED FOR COMPARED TO MMI IN THYROID STORM, AS LATTER HAS THE ADDED BENEFITS OF INHIBITING TYPE 1 DEIODINASE ACTIVITY IN THE THYROID GLAND AND OTHER PERIPHERAL ORGANS( REDUCE THE CONVERSION OF T4 TO T3), T3 LEVELS DROP BY 45% WITHIN ONE HOUR OF PTU ADMINISTRATION BUT ONLY ABOUT 10-15% AFTER STARTING MMI. • NO OUTCOME DIFFERENCES BETWEEN MMI AND PTU ADJUVANT TREATMENT FOR THYROID STORM LITHIUM CAN BE USED ALTERNATIVE FOR PATIENT WHO CANNOT TOLERATE MMI/PTU. • WORKS BY INHIBITING RELEASE OF THYROID HORMONE BY THYROID GLAND THROUGH UNKOWN MECHANISM • DOSE: 300MG TDS, MONITORED LITHIUM TOXICITY
  • 10.
  • 11. BETA ADRENERGIC RECEPTOR ANTAGONISTS. • KEY TO CONTROL HEART RATE AND INHIBIT OTHER PERIPHERAL ACTIONS OF THYROID HORMONES IN THYROID STORM. • ABILITY INHIBITS TYPE 1 DEIODINASE SUCH AS PROPRANOLOL, 60-80MG/4H • BETA BLOCKERS WITH SELECTIVE B-1 BLOCKADE SUCH AS BISOPROLOL, LANDIOLOL AND ESMOLOL INFUSION HAVE MORE FAVORABLE CVS BENEFITS IN THYROID STORM WITH CARDIAC COMPROMISE. • IV ESMOLOL LOADING DOSE 250-500MCG , MAINTAINANCE 50-1OOMCG/KG/MIN • CONTRAINDICATIONS TO BETA BLOCKERS SUCH AS PATIENT WITH BRONCHIAL ASTHMA OR COPD, DILTIAZEM CAN BE USED IN INTENSIVE CARE SETTING TO CONTROL HR. • AF PATIENT, CARDIOVERSION CONSIDERED AFTER R/OUT CARDIAC THROMBOSIS IF HEMODYNAMICS ARE IMPAIRED.
  • 12. CORTICOSTEROIDS • TO INHIBIT BOTH THYROID HORMONE SYNTHESIS AND PERIPHERAL CONVERSION OF T4-T3 • GIVEN AS PROPHYLAXIS FOR RELATIVE ADRENAL INSUFFICIENCY CAUSED BY HYPERMETABOLIC STATE IN THYROID STORM. • IV IS PREFERRED WHEN RAPID REACTION IS PREFFERED , WITH THE IMPROVEMENT IN CLINICAL CONDITION DOSES SHOULD BE REDUCED AND TAPERED OFF TO PREVENT ADVERSE EFFECT. • DEXAMETHASONE (MEDIAN DOSE 6MG/DAY) • HYDROCORTISONE (300MG/DAY) • PREDNISALONE (25MG/DAY)
  • 13. INORGANIC IODIDE(LUGOL’S IODINE/SATURATED SOLUTIONS OF POTASSIUM IODIDE,SSKI) • USED TO DECREASE T4 LEVELS BY INHIBITION OF IODIDE OXIDATION AND ORGANIFICATION AND INHIBITS RELEASE OF THYROID HORMONE. • RECOMMENDED DOSE 5DROPS OF LUGOL’S IODIDE 6H(6.25MG IODINE/DROP) OR 10DROPS OF LUGOL’S IODINE 8H • THIS SOLUTION SHOULD BE DILUTED IN WATER OR TAKEN WITH BREAD TO AVOID MUCUSAL IRRITATION. • THIS AGENTS CAN BE USED IN COMBINATION WITH ATT. • THESE AGENTS SHOULD ONLY BE GIVEN AT LEAST AFTER ONE HOUR OF ATT DRUGS ADMINISTRATION, TO PREVENT USE OF IODINE AS SUBTRATE FOR THYROID HORMONE SYNTHESIS. • AFTER CLINICAL IMPROVEMENT, THE LUGOL’S SHOULD BE TAPERED AND STOPPED BEFORE THE ANTITHYROID. • LUGOL’S IODINE SHOULD NOT GIVEN BEYOND 10DAYS OR ELSE THIS WOULD LEAD TO ESCAPE FROM WOLFF-CHAIKOFF PHENOMENON. • CONTRAINDICATED: KNOWN TO BE ALLERGIC TO INORGANIC IODIDE
  • 14.
  • 15. SUPPORTIVE TREATMENT • INTRAVENOUS FLUIDS • RESPIRATORY SUPPORT INCLUDES INVASSIVE/NON-INVASSIVE • NUTRITIONAL SUPPORT • ACUTE INFECTIONS- SHOULD BE TREATED WITH BROAD SPECTRUM ABX DEFINITIVE THERAPHY URGENT/ EARLY THYROIDECTOMY • IS AN OPTION IN PATIENTS WHO HAVE CONTRAINDICATIONS TO ATT, LARGE GOITRE • PATIENTS SHOULD RENDERED TO EUTHYROID STATE PRIOR TO SURGERY TO MINIMISE RISK OF THYROID STORM • RAI IODINE IS CONSIDERED AND LUGOL’S IODINE HAS BEEN ADMINISTERED DURING THYROID STORM , THE RAI SHOULD BE DEFERRED UNTIL ABOUT 3-4 MONTHS AFTER. PRECIPATING FACTORS: NON-COMPLIANCE • PATIENT SHOULD BE EDUCATED ON THIS ASPECT

Editor's Notes

  1. thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) to be transported. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of thyroid storm may be triggered by conditions (as explained earlier, the causes) that lead to the following: Individuals with thyroid storm tend to have increased levels of free thyroid hormone, although total thyroid hormone levels may not be much higher than in uncomplicated hyperthyroidism.[9] The rise in the availability of free thyroid hormone may be the result of manipulating the thyroid gland. In the setting of an individual receiving radioactive iodine therapy, free thyroid hormone levels may acutely increase due to the release of hormone from ablated thyroid tissue increases in thyroid hormone availability, it is also suggested that thyroid storm is characterized by the body's heightened sensitivity to thyroid hormone, which may be related to sympathetic activation Sympathetic nervous system activation during times of stress may also play a significant role in thyroid storm.[3] Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in thyroid storm.
  2. As with hyperthyroidism, TSH is suppressed. Both free and serum (or total) T3 and T4 are elevated.[5] An elevation in thyroid hormone levels is suggestive of thyroid storm when accompanied by signs of severe hyperthyroidism but is not diagnostic as it may also correlate with uncomplicated hyperthyroidism. The diagnosis of thyroid storm is based on the presence of signs and symptoms consistent with severe hyperthyroidism.[9] Multiple approaches have been proposed to calculate the probability of thyroid storm based on clinical criteria, however, none have been universally adopted by clinicians.
  3. Burch-wartofsky assigning a numerical value based on the presence of specific signs and symptoms organized within the following categories: temperature, cardiovascular dysfunction (including heart rate and presence of atrial fibrillation or congestive heart failure), central nervous system (CNS) dysfunction, gastrointestinal or liver dysfunction and presence of a precipitating event
  4. Japanese Thyroid Association (JTA) criteria, derived from a large cohort of patients with thyroid storm in Japan and published in 2012, provide a qualitative method to determine the probability of thyroid storm. The JTA criteria separate the diagnosis of thyroid storm into definite versus suspected based on the specific combination of signs and symptoms a patient exhibits and require elevated free triiodothyronine (T3) or free thyroxine (T4) for definite thyroid storm.[14]