Transcript Thyrotoxic storm

Thyroid Storm
Dr RAMA NARAYANA
Thyrotoxic storm
 Exaggerated or florid state of thyrotoxicosis"
 Rare but "Life threatening, sudden onset of
thyroid hyperactivity“
 May represent end stage of a continuum :
– Thyroid hyperactivity to thyrotoxicosis to
thyrotoxic crisis
 "Probably reflects the addition of adrenergic
hyperactivity, induced by a nonspecific stress, into
the setting of untreated or undertreated
hyperthyroidism"
Thyrotoxic storm
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Prevalence: 1-2% - admissions for
thyrotoxicosis
Mortality: 30 - 50%
Decompensation of one or more organ
system
No specific Thyroid hormone levels
Precipitating factor
When does thyrotoxicosis become a
storm?
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Subjective
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Controversial
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Consider severe toxicosis as impending
storm and Rx aggressively
CAUSES
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Graves disease usually - Rarely MNG or
solitary adenoma; TSH secreting pituitary
adenoma
Post Sx
RAI therapy / amiodarone
Trauma
Others: Single case reports
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Strangulation (South Med J 97(6):608-610, 2004.)
Thyroiditis (Thyroid. January 1, 2007, 17(1): 73-76.)
Partial Hydatidiform mole (Thyroid. 2008 Apr; 18(4):47981)
Precipitating factors
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A precipitating factor is always present – onset
is acute
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infectious disease (usually MCC)
Trauma
iodine intake – I131 Rx, amiodarone
thyroid surgery
Others: delivery, toxemia of pregnancy, CVA,
Pulmonary embolism
DKA
Degree of increase in TH decides rather than
the actual levels
Pathogenesis
Illness
Binding inhibitors
High free T3 and T4
Catecholamine release
Increased adrenergic load
S T O R M
Clinical features
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Severe hyper metabolism with features of multisystem decompensation
Fever
ST or SVT,AF associated with cardiac failure
CNS Symptoms: restlessness, tremulousness,
agitation, confusion, delirium and rarely coma
GI: vomiting, diarrhea, unexplained jaundice (poor
prognosis), dehydration & electrolyte imbalancepre renal failure
Diagnosis
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No arbitrary serum T4 or T3 that discriminates
severe toxicosis vs storm
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Scoring system evolved by Burch & Wartofsky to
differentiate storm from impending storm & severe
toxicosis
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Both should be treated similarly
Scoring system
Management
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Admission to ICU
3 Main targets
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Block effects of TH- beta blockers
Inhibition of TH synthesis - ATD, Steroids
Inhibit TH release- iodides
Management of precipitating factor
These measures should give clinical improvement in 12-24
hrs
Beta blockers
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Primary role to ameliorate effects of catecholamine
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Propronalol: (or atenelol or metaprolol)
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Rapid reduction of heart rate (diltiazem if contraindicated)
Improvement in cardiac output
Dose: 80 -120 mg orally 6hrly
1-3 mg IV over 10 min & 2-3 mg 3 hrly till oral drug action
Esmolol:
200 - 500 g/kg/min IV stat & then continuous
infusion of 50-100 g/kg/min
Short acting esmolol and labetolol- may be safer
than propronolol in this situation
AF in toxicosis
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Are they at risk for embolic phenomenon?
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Controversial
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Standard risk for thrombo-embolism - of age,
underlying myocardial disease – apply to toxicosis
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Thrombolytic treatment: warfarin
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Standard antiarrhythmic drugs can be used including
digoxin (usually in higher than normal dose) after
correction of hypokalemia
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Commonest cause of death-arrhythmia and cardiac
failure
Antithyroid drugs
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Decrease Thyroid Hormone production:
Large doses of ATDs ( PTU 600mg or 60mg
of carbimazole stat and half this dose q6h)
- orally, by naso-gastric tube or rectally (ECNA 2006)
– PTU is preferred –inhibits extra-thyroidal conversion of
T4 – T3
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Start 1 or 2 hrs before iodine – to inhibit the
synthesis of additional TH from the
administered iodide (jod basedows
phenomenon)
Iodine
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Inorganic iodine blocks release of TH
(Wolff-Chaikof effect) after 3-4 hrs of PTU/MMI
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Lugol’s iodine 10 drops (8mg/drop) 12 hrly or SSKI 3
drops (38mg/drop) 12hrly
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Iopanic acid 2 gm IV – then 1gm daily -not available
Lithium: if allergic to iodine – 300mg 6hrly
– Directly decreases thyroid hormone secretion
Steroids
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Glucocorticoids:
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Relative or associated adrenal insufficiency
Inhibits the release of hormone – like iodide
Inhibits T4 - T3 peripherally- like PTU
Hydrocortisone 100 mg 8 hrly
or
Dexamethasone 2mg 6 hrly
Discontinue when patient improves clinically
Combination of iodide, BB and steroids restore
T3 con within 24-48hrs.
Others
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Mx of precipitating events
Fluid & Electrolyte balance
Dextrose fluids to replenish glycogen stores
Thiamine given to prevent Wernicke encephalopathy
Pyrexia
– Acetaminophen – avoid salicylates – increases Free
hormone conc.
– Cooling (alcohol sponging, ice pack, cooling bankets
– Chlorpromazine(50-100mg IM) – inhibitory central
thermoregulation
Colestyramine (3gm tds) – reduces enterohepatic
circulation of TH
Potassium perchlorate
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Competitive inhibitor of I transport
Regime- 1 gram daily + MMI 30-50 mg
/d– normalize thyroid hormone levels in 4
week
Aplastic anemia and nephrotic syndrome
did not occur in this short duration
Not in use presently
Anti adrenergic agents
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Reserpine
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Guanethidine
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An alkaloid that depletes catecholamine stores in
sympathetic nerve terminals and in CNS
CNS depressant action
Dose 2.5-5 mg IM every 4th hourly
Inhibit release of catecholamines
30-40 mg PO 6th hourly
Side effects- hypotension ,diarrhea
Rarely used now a days
Plasmapheresis, charcoal,
resin hemoperfusion
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Indication- progressive clinical
deterioration despite aggressive medical
mx
? Possibly remove TBG bound TH &
stimulating autoantibody
Effect last only for 24-48 hrs
Definitive therapy
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Once life threatening aspects treatedconsider definitive therapy
Thionamides and PPL continued
RAI ablation cannot be used for weeks to
months if iodine is used for treatment of
storm
Thyroidectomy can be advised after
several weeks of euthyroid status
Thyroid arterial embolization
Thyroid arterial embolization for the treatment of
hyperthyroidism in a patient with thyrotoxic crisis.
Zhao W, Gao BL, Yi GF, Yang HY, Li H. Medical Imaging Center, First
Affiliated Hospital, Kunming Medical College, Yunnan Province, China.
PURPOSE: a case of hyperthyroidism in a young woman caused by
Graves' disease that was successfully treated with thyroid arterial
embolization.
CLINICAL DETAILS: A 35 year-old woman with a history of thyrotoxic
crises was admitted after the last thyroid crisis. Thyroid arterial
embolization was used to treat the hyperthyroidism after it had been
controlled. Immediately after embolization, the enlarged thyroid gland
shrank and vascular murmurs disappeared. Serum thyroid hormones
increased on day 3 following embolization but decreased gradually.
Thyroid hormone returned to normal 2 months after embolization and
remained normal at three years.
CONCLUSION: Thyroid arterial embolization is an effective means to treat
refractory hyperthyroidism.
Thyroid Storm
Prognosis
Old references quote almost 100 %
mortality untreated, and 20 % treated
(but these reports were before use of
beta blockers)
Current mortality ? should be < 5%
(although not well studied or reported
due to rarity of cases)
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