see: [Dunn Thyroid storm](x-devonthink-item://466832EC-E181-4D5B-BAF5-AA46CBEA4649), [OSCE - Cabrini 2023 S6 - thyroid storm](x-devonthink-item://D90E1EF1-D379-482B-B0E3-4E77CFEC97FE) ==scroll to [[#Management|Management of thyroid storm]]== # causes of thyrotoxicosis - primary hyperthyroidism: - graves disease - toxic mulitinodular goitre - toxic adenoma - thyroiditis - de quervain syndrome - postpartum - radiation - central hyperthyroidism - pituitary adenoma - ectopic thyroid tissue - metastasis - drug-induced - [[​Lithium Toxicity|lithium]] - iodine - [[Amiodarone]] - excess thyroxine ingestion # Clinical features of thyrotoxicosis - nervousness, irritability - heat intollerance - tremor - weight loss - palpitations - goitre - pretibial myxoedema - sleep disturbances - sudden paralysis # mild hyperthyroidism - doesn't need ED treatment - can be referred to outpatient clinic ## initiation of treatment: - *carbimazole* 10-45mg od - OR - *propylthiouracil* 200-600mg od in 2-3 divided doses + propranolol 20mg TDS po # Lab tests ![[Pasted image 20241016002928.png]] ## TSH - hyperthyroidism results in lower TSH (except for excess TSH production form anterior pituitary) - normal is 0.4-5 mlU/L ## others - free T4 and T3 if it seems like hyperthyroidism but TSH is normal or high - # Thyroid storm > Rare and severe form of hyperthyroidism, usually precipitated by acute illness or surgery. Characterised by hyperpyrexia (body temperatures can exceed 40° C), severe agitation or delirium, and severe tachycardia with high output heart failure. Advanced cases a/w coma/obtundation, [[Seizures]], and haemodynamic instability. mortality can be ~25% even with treatment! ## Causes - undiagnosed hyperthyroidism (eg Grave's disease) - withdrawl of anti-thyroid drugs - infection, MI, DKA - surgery - iodine administration - thyroxine toxicity - vigorous palpation of thyroid gland ## findings - T4 and T3 levels only marginally greater in storm than prior - possible increased adrenergic sensitivity - possible altered peripheral response to T3 ## Assessment ==clinical diagnosis== - lab studies cannot differentiate thyroid storm from hyperthyroidism - fever - ALOC - abdo pain, nausea - **cardiac failure** - death is due to cardiovascular collpase and high output cardiac failure - may have crackles from congestive heart failure - wide [[pulse pressure]] - profusr sweating, dehydration ### Burch-Wartofsky Point Scale (BWPS) for Thyrotoxicosis (risks of thyroid storm) - temperature (0 if <99) - CNS effects (0 if absent) - gastrointestinal-hepatic dysfunction - HR (0 if <90) - congestive heart failure - AF present - precipitating event ## Diagnostic criteria - temp > 37.8 deg C - tachycardiac out of proportion to fever (can be up to 200 BPM AF) - high output cardiac failure) - CNS disturbance **DDx** - sepsis - heat stroke - malignant hyperthermia - neuroleptic malignant syndrome - pheychromocytoma - sympathomimetic ingestion ## Management - supportive - external cooling if T > 40 deg - *avoid aspirin and NSAIDS* (displaced T4 from thyroglobulin); (likely a FACTOR 6 if given) - DCCV (arrhythmias often resistant) > order of operations: beta blocker (propranolol), PTU or methimazole, and then iodine. **beta blockers** - block cardiac and peripheral adrenergic effects - ==propranolol== -- reduces conversion of T4 to T3 , but takes a week to occur. metoprolol likely just as effecive - *0.5-1mg/min IV to 10mg* - 1-2mg IV over 10 min; if tolerates then 1-2mg boluses q15 minutes until HR <100 - subsequent doses 20-120mg Q6 hourly po - if pre-existing heart disease or asthma, can use *esmolol* 250-500mcg/kg bolus then infusion 50-100mcg/kg/min titrated to effect > if the patient is shocked, likely withhold beta blockers until resuscitated and more stable; hydrocort will ALSO block peripheral conversion of T4→T3 **Propylthiouracil** - load orally or NGT 900-1200mg, starts working within one hour - 200-300mg Q6H **steroids** - [[hydrocortisone|hydrocort]] 100mg Q6h or dexamethasone 2mg Q6h / 4mg BD - inhibit peripheral conversion of T4 to T3 - help with any underlying [[Adrenal insufficiency]] **iodine**  - orally lugol's iodine 30-60 drops od or IV sodium iodine 1g q12 hourly - do not give until at least 1 hour after anti-thyroid rx has been given (otherwise provides substrate to produce more thyroid hormone) - lithium can be used in patients allergic to iodine **supportive measures**  - dehydration correciton - active cooling (no aspirin) **Arrhythmias/[[Atrial fibrillation]]** - treat [[hypokalemia|hypo-k]] and [[Hypomagnesemia|hypo-mg]] - can trial *digoxin*, but may be resistant - amiodarone causes changes to thyroid function tests that are not necessarily physiologically relevant so should not be used first line ## prognosis - 90% mortality if missed # subclinical hyperthyroidism Subclinical hyperthyroidism refers to a suppressed TSH with normal fT4 and fT3, often in the upper part of the normal range. Subclinical hyperthyroidism suggests a degree of autonomous thyroid hormone production. This is often due to the presence of nodular thyroid disease. Patients may not be symptomatic, but are at risk of the same long-term complications as frank hyperthyroidism (notably AF and osteoporosis), especially if the TSH is completely unmeasurable. Treatment is indicated to control symptoms, and can also be considered on a case-by-case basis in asymptomatic patients, dependent on comorbidities (e.g. AF) and extent of TSH suppression. Surveillance alone, until the development of frank hyperthyroidism, is an alternative. **ETG:** or a patient with subclinical or minimally overt thyrotoxicosis without symptoms, retest the serum TSH and T4 concentrations after 6 to 8 weeks to confirm that the disorder is persistent—transient disease can occur (eg subacute thyroiditis). For a symptomatic patient with overt thyrotoxicosis, start beta-blocker therapy straight away to relieve symptoms. For both groups of patients, further tests are required to differentiate the cause # hyperthyroidism and pregnancy > TSH has a similar molecular structure to β human chorionic gonadotrophin (β-HCG), therefore the hyperemesis of pregnancy (which is characterised by raised β-HCG) can be associated with mild biochemical hyperthyroidism. This usually resolves spontaneously in the second trimester of pregnancy. - Hyperemesis can cause hyperthyroidism (due to β-HCG) - Graves’ disease may improve during pregnancy - Growth retardation and fetal tachycardia if placental antibody transfer - Graves’ disease often worsens after delivery ## graves disease in pregnancy Patients with Graves’ disease require observation during pregnancy every 4–6 weeks, because of the increased risk of maternal complications as well as reduced fetal growth - PTU in first trimester (to reduce risk of teratogenesis) - Carbimazole in second and third trimesters (to reduce risk of PTU-induced hepatitis) - Use lowest dose of thionamide possible - Observe mother and baby every 4–6 weeks