Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.

1. Calming
THYROID STORM

2. Objectives
• to discuss the diagnostic criteria for thyroid storm
• to describe the therapeutic options available for
the management of this endocrine emergency
• to discuss updates on the management of thyroid
storm

3. Thyroid Storm
• A life threatening exacerbation of the hyperthyroid
state
• evidence of decompensation in one or more organ
systems
• Rare in literature
• Incidence of <10% among patients hospitalized
for thyroxicosis

4. Thyroid Storm
• Exacerbation of pre existing hyperthyroidism due
to any of the following:
• Graves’ disease
• Toxic multinodular goiter
• Toxic adenomas
• Hypersecretory thyroid carcinoma

5. Epidemiology
• Rare
• Japan (2012): estimated incidence of TS in
hospitalised patients of 0.20 per 100,000 per year
• Mortality rates: 11.0% in TS1 (definite) 9.5% in
TS2 (suspected)
Akamizu et. al Thyroid Volume 2, Number 7, 2012

6. Mortality Statistics: Local
• Untreated: FATAL
• PGH Series
• Odvina (1984): 8/27 = 31%
• Borlongan (1995) 5/37 = 14%
• Valera (2000); 8/71 = 11%
• Decreasing mortality rates

7. Pathogenesis - 1
• unclear
• are circulating thyroid hormones higher than
usual?
• No difference in thyroid hormone levels between
uncomplicated thyrotoxicosis and thyroid storm

8. Pathogenesis - 2
• Absolute levels not as important as the rapidity
with hormone levels rise
1. change in levels of binding proteins
2. production of thyroid hormone binding inhibitors
3. rapid release of hormones into the blood stream

9. Pathogenesis - 3
• Acute release of thyroid hormones and rapid
change in their concentrations explain many
cases of thyroid storm
• post RAI therapy
• post surgery
• sudden withdrawal of anti-thyroid drugs

10. Pathogenesis - 4
• Development of tissue intolerance of thyroid
hormones
• Activation of the adrenergic nervous system:
increased density of beta-adrenergic receptors

11. Clinical Presentation
• Generally have all the features of thyrotoxicosis
but exaggerated and severe
• Goiter is almost always present
• Usually with a history of thyroid disease that has
been partially treated
• Or history of symptoms of thyrotoxicosis for a
prolonged period

12. Common Essential Findings
• Altered mental status
• TIP#1: if mentation is normal, the diagnosis of thyroid
storm is not likely
• Defective thermoregulation
• TIP#2: this become apparent upon evaluation of
initial therapeutic measures
• A precipitating event or illness is essential to the
genesis of the thyroid storm

13. Precipitants of Thyroid Storm
• INFECTION
• Surgery
• RAI therapy
• Iodinated contrast dyes
• Withdrawal of ATD
• Amiodarone
• Kelp and thyroid
hormone ingestion
• Tooth extraction
• Thyroid Ca
• Diabetic ketoacidosis
• CHF
• Hypoglycemia
• Toxemia of pregnancy
• Parturition
• Severe emotional
stress
• Pulmonary embolism
• CVD
• Trauma
• Bowel obstruction

14. Precipitating Factors
• Acute illness, including infection, stroke, trauma,
surgery and treatment with RAI
• Emotional stress and vigorous palpation of the
thyroid gland have also been reported to
precipitate thyroid storm

15. Japan Survey (2012)
• Irregular use or
discontinuation of drugs - 122
• Infection - 89
• DKA - 12
• Nonthyroidal surgery - 8
• Radioactive iodine - 6
• Pregnancy/delivery - 5
• CVD - 3
• Intense exercise - 2
• Ischemic heart disease - 1
• Adrenocortical insufficiency -
1
• Administration of iodinated
contrast
• Tooth extraction 1
• Others - 1
Akamizu et. al Thyroid Volume 2, Number 7, 2012

16. Question?
• What clinical and laboratory findings are typically
associated with thyroid storm?
• How is it diagnosed?
Diagnosis is made clinically in the background
of thyrotoxicosis

17. Diagnostic Criteria
• Burch and Wartofsky (1993)
• diagnostic point scale (BWS)
• distinguish uncomplicated thyrotoxicosis from
impending and established thyroid storm
• for triage at the ER

18. Diagnostic Criteria for
Thyroid Storm
• Thermoregulatory
dysfunction
• Central nervous
system effects
• Gastrointestinal
hepatic
dysfunction
• Cardiovascular
dysfunction
A. Tachycardia
B. CHF
C. AF
• Precipitant History
Burch HB, Wartofsky L. Endocrinol. Metab Clin 22:23-277

19. Burch HB, Wartofsky L. Endocrinol. Metab Clin 22:23-277

20. Burch and Wartofsky Scoring
System
• Assign points to the highest weighted description
applicable in each category
• Points are given so as to bias the diagnosis of
thyroid storm e.g. when not possible to distinguish
between effects of intercurrent illness and thyroid
storm per se
• Tip#3 When in doubt, treat

21. P.E. at the ER
• BP: 140/70mmHg
• CR: 136 irreg, irreg
• RR: 28 br/min
• Temp: 39.2
• Stuporous
• Icteric sclerae, diffuse goiter 2x enlarged (-) bruit, (+)stare
• (+) Fine crackles at LLLF
• Irregularly irregular rhythm, tachycardic, (-) murmur, AB displaced 6th ICS LAAL
• Scaphoid abdomen, liver edge not palpable
• Grade 2 bipedal edema, +++ DTR’s

22. BW Score for the Case pt
Temp 39.2 20
CNS decrease sensorium 20
GIT jaundice 20
Heart rate 136 20
CHF pedal edema 20
AF (+) RVR 10
Ppt Hx Pneumonia 10
105

23. Japanese Criteria
Grade of TS
Combination of
features
Requirements for diagnosis
TS1 First combination
Thyrotoxicosis and at least one CNS manifestation and
on of the ff: fever, tachycardia, CHF or GI/hepatic
manifestations
TS1
Alternate
combinations
Thyrotoxicosis and at least 3 combinations of fever
tachycardia, CHF or GI/hepatic manifestations
TS2 First combination
Thyrotoxicosis and at least 2 of the ff: fever,
tachycardia, CHF or GI/hepatic manifestations
TS2
Alternate
combination
Patients who meet the diagnostic criteria for TS1 except
that serum FT3 and FT4 values are not available but
whose data before or after the episode suggest that they
are thyrotoxic at the time of TS
Akamizu et. al Thyroid Volume 2, Number 7, 2012

24. Japanese Criteria:
Definitions
• Thyrotoxicosis: Elevated to FT3 and FT4
• CNS manifestations: restlessness, delirium, mental
aberation/psychosis, somnolence/lethargy,
convulsion, coma including a score of 14 or lower
on the Glasgow Coma Scale
• Fever: 38c or higher
• Tachycardia: 130 beats per minute (arrhythmia
such as AF are evaluated my measuring the heart
rate)
Akamizu et. al Thyroid Volume 2, Number 7, 2012

25. Laboratory Findings
• Hyperglycemia, marked leukocytosis, mild
hypercalcemia due to hemoconcentration and
the effect of thyroid hormone on bone
resorption
• Hepatic dysfunction: elevated ALT, LDH and
bilirubins
• Elevated total and free thyroid hormones with
suppressed TSH

26. Treatment Principles
• Correct hyperthyroidism
• Block synthesis of additional hormones
• Block release of preformed hormones
• Inhibit peripheral conversion to T4 to T3
• Measures to decrease circulating hormone levels
• Definitive treatment
• Normal homeostatic decompensation
• Treat precipitating events

27. Drugs Affecting T3-T4
Synthesis
• Block Synthesis:
• Thioamides (PTU, Methimazole, Carbimazole)
• thioamides inhibit peroxidase to block
organification and coupling
• BLOCK RELEASE OF PREFORMED
HORMONES: High dose inorganic iodides reduce
T3-T4 release by inhibiting thyroglobulin
proteolysis

28. Treatment Modalities
1. Block synthesis of hormones
A. Propylthiouracil (PTU) -
• preferred: + inhibits peripheral conversion of T4 to
T3
• LD: 600 to 1000mg -> 200-250mg q4 hrs (1200 -
1500 mg daily dose)
2. Methimazole: LD of 600mg then 20mg q4 hrs (120
mg total daily dose)

29. Agents to block release of
hormones: Inorganic iodides
• Administered only after the inhibition of further
thyroid hormone synthesis has been achieved
with PTU or MMI
• Also inhibit hormone synthesis by blocking iodine
organification (Wolff-Chaikoff effect)
• Iodines + thioamides: T4 may normalize in 4-
5days

30. Agent to block release of
hormones: Inorganic iodides
• Orally by NGT
• Saturated solution of potassium iodide (SSKI), 5
drops q6 hrs
• Lugol’s solution 30 drops in 3-4 doses
• Radiographic contrast dyes e.g. ipodate
(Orografin) and iopanoate (Telepaque)
• Ipodate: 617mg iodine/g - 0.5-3g/day

31. Agent to inhibit peripheral
conversion of T4 to T3
• T4 is a prohormone
• T3 is 3x more potent than T4
• PTU (but not MMI)
• High dose iodides
• Beta-blockers (Propanolol)
• Corticosteroids (dexa 2mg q6 hrs)

32. Measures to decrease
circulating hormone levels
• Plasmapheresis
• Plasma exchange
• Peritoneal dialysis
• Exchange transfusion
• Charcoal plasmaperfusion
Reserved for those patients who fail to respond to the conventional
medical therapy

33. Plasmapheresis
• The half-life of thyroid hormones is so long that
quick improvement is not always achieved even
by sufficient doses of anti-thyroid drugs.
• Thus, plasma exchange in combination with
conventional therapy appears to be effective in
relieving the life threatening thyroid crisis.

34. Homeostatic
Decompensation
• Dehydration, hypoglycemia and electrolyte
imbalance
• Correct volume depletion, pressor support
• CHF; invasive monitoring
• Multivitamins to replete stores

35. Homeostatic
Decompensation
• Antiadrenergic agents
• Reserpine and guanethidine
• Propranolol: 20 to 40 mg q6 hours up to 240-
480mg/day
• Esmolol, a short acting B1 selective agent for
thyroid storm, peri-op

36. Homeostatic
Decompensation
• Aggressive treatment of hyperthermia
• Aimed at central thermoregulation centers, as well
as peripheral heat dissipation
• Do not use aspirin
• Peripheral measures: ice packs, cooling blankets,
paracetamol BUT avoid shivering

37. Homeostatic
Decompensation
• Glucocorticoids: given for potential relative adrenal
insufficiency
• Thyrotoxicosis: accelerated production and degradation
of cortisol
• Patient in storm have inappropriately normal cortisol
levels
• Dexamethasone 2mg q6
• Hydrocortisone 100 mg q8

38. Treatment Principles
• Correct hyperthyroidism
• Block synthesis of additional hormones
• Block release of preformed hormones
• Inhibit peripheral conversion of T4 to T3
• Measures to decrease circulating hormone levels
• Definitive treatment
• Normalize homeostatic decompensation
• Treat precipitating events i.e broad spectrum antibiotics

39. Summary
• High dose thioamides: PTU or MMI
• High dose iodides i.e SSKI 2 drops every 6 hrs
• Propranolol (or esmolol): watch the BP
• Control the temperature
• Address the precipitants i.e infection
• Prevent another episode

40. Prognosis
• if appropriate therapeutic measures are
implemented and these measures are successful,
these patient usually improve in 1 to 2 days and
recover within a week
• Mortality rate remains high (10%) even with
prompt and aggressive treatment typically due to
arrhythmia, heart failure or refractory hyperthermia

41. Poor prognostic indicators
• Coma
• Jaundice
• Shock
• Young patients (<40 years): more labile and
variable course and tend to have hyperadrenergic
state

42. Thank You