Bedside Snapshot
- Normal (Adult)
- 0.4–4.0 mIU/L (typical; lab-specific)
- Critical Values
- No laboratory panic value. Act on suppressed (<0.1) or markedly high (>10 mIU/L) TSH only with free T4 and the clinical picture
- High Suggests
- Primary hypothyroidism (Hashimoto, post-ablation)
- Missed or low levothyroxine dose
- Recovery from non-thyroidal illness
- Low Suggests
- Graves disease or toxic nodules
- Levothyroxine excess
- Central hypothyroidism (low or inappropriately normal TSH with low free T4)
- Non-thyroidal illness
- Act Now If
- TSH above 10 with low free T4: overt hypothyroidism; arrange prompt follow-up. Myxedema signs (confusion, hypothermia, bradycardia, hypoventilation): emergency, transport. Storm signs (fever, tachycardia, agitation): ED or ICU
- Watch Out For
- Biotin supplements distort TSH and T4; stop at least 2 days before testing. TSH alone is unreliable in pituitary disease
Reference & Critical Ranges
Reference ranges
| Population | Conventional | SI | Notes |
|---|---|---|---|
| Adult (non-pregnant) | 0.4–4.0 mIU/L | 0.4–4.0 mU/L (µIU/mL) | Typical. Some labs use different limits (for example 0.5–5.0); use the range on the report. |
| Pregnancy | Trimester-specific | Same units | Prefer the lab's trimester-specific range over the non-pregnant range. If the lab has none, an upper limit of about 4.0 mIU/L is commonly used (2017 ATA pregnancy guideline). |
| Older adults | Upper limit often higher | Same units | TSH rises modestly with age. Interpret with free T4 and symptoms. |
| Children and adolescents | Age-specific (see lab report) | Same units | Use the lab's age-specific range. Newborn TSH rises shortly after birth; newborn screening uses its own cutoffs. |
Severity & critical values
| Level | Conventional | SI | What it means |
|---|---|---|---|
| Suppressed | <0.1 mIU/L | <0.1 mU/L | Overt hyperthyroidism, or over-replacement with levothyroxine. Confirm with free T4. |
| Low (subclinical range) | 0.1–0.4 mIU/L | 0.1–0.4 mU/L | Often subclinical hyperthyroidism when free T4 and T3 are normal. |
| Normal | 0.4–4.0 mIU/L | 0.4–4.0 mU/L | Euthyroid in most adults with normal free T4. |
| High (subclinical range) | Above 4.0 to 10 mIU/L | Above 4.0 to 10 mU/L | Often subclinical hypothyroidism when free T4 is normal. Repeat in 2–3 months before treating. |
| Treatment threshold (markedly high) | >10 mIU/L | >10 mU/L | Treatment threshold for hypothyroidism (not a laboratory panic value). Free T4 decides urgency. |
Conversion: mIU/L = mU/L = µIU/mL (1:1). Nothing to convert.
Causes of Abnormal Results
High (TSH above 4.0 mIU/L)
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Primary hypothyroidism (gland failure) | Hashimoto thyroiditis; after radioactive iodine or thyroidectomy; neck radiation | Cold intolerance, fatigue, bradycardia, dry skin, goiter |
| Drug-induced thyroid failure | Lithium, amiodarone, interferon-alpha, tyrosine kinase inhibitors, immune checkpoint inhibitors | New medication; check TSH in patients on these drugs |
| Congenital hypothyroidism | Thyroid dysgenesis or dyshormonogenesis | Positive newborn screen; poor feeding, slow growth, prolonged jaundice |
| Iodine deficiency | Low dietary iodine; goiter | Goiter with hypothyroid labs; uncommon where iodine intake is adequate |
| Under-replacement | Missed or reduced levothyroxine; malabsorption; absorption interference (Section 8) | Known hypothyroidism with symptoms returning |
| Recovery phase | Recovery from non-thyroidal illness; resolving thyroiditis, including the hypothyroid phase of subacute or postpartum thyroiditis | Transient rise after critical illness; repeat after recovery |
| Thyroid hormone resistance | Genetic receptor defect | High TSH with normal or high free T4; family history |
| TSH-secreting pituitary adenoma | Pituitary tumor | High TSH with high free T4 (rare) |
Low (TSH below 0.4 mIU/L)
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Exogenous thyroid hormone | Levothyroxine excess; factitious thyrotoxicosis | Tachycardia, weight loss, tremor; check dose and adherence |
| Graves disease | TSH receptor-stimulating antibodies (TSI or TRAb) | Diffuse goiter, eye signs, heat intolerance |
| Toxic nodular goiter or toxic adenoma | Autonomous thyroid nodules | Nodular goiter; often older adults; atrial fibrillation |
| Thyroiditis (thyrotoxic phase) | Subacute, postpartum or painless (silent) thyroiditis | Painful neck (subacute); recent delivery (postpartum) |
| Iodine-induced thyrotoxicosis | Iodinated contrast or amiodarone in patients with nodular or iodine-deficient glands | Thyrotoxicosis after iodine exposure |
| hCG-mediated | Hyperemesis gravidarum; molar pregnancy | Early pregnancy with vomiting or very high hCG |
| Non-thyroidal illness | Acute or critical illness | Low TSH with low T3; do not treat with thyroid hormone |
| Central hypothyroidism | Pituitary or hypothalamic disease, including Sheehan syndrome and hypopituitarism | Low or inappropriately normal TSH with low free T4; other pituitary deficits |
Interpretation & Bedside Approach
Step-by-step approach
- Is it real? Ask about biotin and other supplements (Section 8). Check that the sample was not drawn after a recent levothyroxine change without the expected interval.
- How sick is the patient? Screen for myxedema coma and thyroid storm first. Treat the clinical picture before waiting for labs.
- Acute or chronic, and the trend. Pull up a prior TSH on the same assay if you can. One number can mislead during acute illness.
- Order free T4 with TSH. TSH alone won't do it. Add free T3 only if T3 toxicosis is suspected or the pattern is unclear.
- Classify using the pattern below. Confirm abnormal values on repeat when the patient is stable and not acutely ill.
- Escalate or dispose. Refer urgently for myxedema or storm. Refer routinely for subclinical disease, pregnancy or central hypothyroidism.
TSH and free T4 pattern
| TSH | Free T4 | Suggests |
|---|---|---|
| High | Low | Overt primary hypothyroidism |
| High | Normal | Subclinical hypothyroidism; repeat before treating |
| High | High | Thyroid hormone resistance or TSH-secreting adenoma (rare) |
| Low | High | Overt hyperthyroidism or exogenous excess |
| Low | Normal | Subclinical hyperthyroidism; early Graves; non-thyroidal illness |
| Low or normal | Low | Central hypothyroidism (pituitary or hypothalamic), or non-thyroidal illness |
| Normal | Normal | Euthyroid |
Subclinical disease: treatment thresholds
- Subclinical hypothyroidism, TSH above 10 mIU/L (confirmed on repeat): Levothyroxine is the common treatment.
- Subclinical hypothyroidism, TSH 4.0 to 10 mIU/L: Decide case by case. Consider treatment with positive TPO antibodies, symptoms, goiter, or pregnancy or planned pregnancy. Pregnancy-specific targets apply in that last group.
- Subclinical hyperthyroidism, TSH below 0.1 mIU/L: The risk of atrial fibrillation and bone loss is higher. Treatment is usually considered in higher-risk patients: age 65 or older, cardiac disease, osteoporosis, or symptoms.
- Subclinical hyperthyroidism, TSH 0.1 to 0.4 mIU/L: The risk is lower. Monitoring is usually enough unless the patient is symptomatic.
Management Priorities
Emergency: Suspected myxedema coma
- Treat as an emergency: Get the airway secured and ventilation supported first. Rewarm passively, and avoid aggressive active rewarming, since it can drive vasodilation and hypotension. Treat hypoglycemia. Transport to ED or ICU.
- Use IV thyroid hormone: The FDA label advises against oral thyroid hormone for myxedema coma. Reach for an IV formulation per endocrinology or ICU protocol.
- Cover adrenal insufficiency: Adrenal insufficiency present, or not yet excluded? Give a glucocorticoid before thyroid hormone (FDA label, Section 5.4).
- Find the trigger and monitor: Find the precipitant (infection, drugs, cold exposure) and treat it. Check sodium and glucose. Go slow with fluids, and watch for hypotension and hyponatremia. Endocrinology has to be involved. Reassess mental status, temperature and rhythm.
Emergency: Suspected thyroid storm
- Treat in ED or ICU: Keep watch on rhythm, temperature and volume status. Cool the patient and give acetaminophen for fever. Avoid aspirin and other salicylates. They knock T4 off its binding proteins.
- Control adrenergic symptoms: Use beta-blockade per protocol (see the propranolol page). Go carefully in heart failure or bronchospasm.
- Sequence antithyroid therapy: The antithyroid drug goes in first, before any iodine. Give glucocorticoids per ICU or endocrine protocol (2016 ATA hyperthyroidism guideline).
- Escalate: Get endocrinology and the ICU involved. Do not hold transport for the TSH result.
Medications
| Indication | Adult | Pediatric | Onset / key notes |
|---|---|---|---|
| Levothyroxine (oral, hypothyroidism) | Full replacement 1.6 mcg/kg/day once daily; lower start if elderly or at risk of atrial fibrillation or cardiac disease. Titrate by 12.5–25 mcg every 4–6 weeks; every 6–8 weeks if at risk of atrial fibrillation, with cardiac disease, or geriatric. Check TSH 6–8 weeks after any change. Dosages above 200 mcg/day are seldom required | Starting doses by age, per kg/day: 0–3 mo 10–15; 3–6 mo 8–10; 6–12 mo 6–8; 1–5 y 5–6; 6–12 y 4–5; over 12 y with incomplete growth 2–3; growth complete 1.6. Newborns at risk of cardiac failure (birth to 3 mo): start lower and increase every 4–6 weeks. At risk of hyperactivity: start at one-quarter dose and increase weekly by one-quarter until full dose. Titrate to TSH or free T4 every 2 weeks | Empty stomach, 30–60 min before breakfast. Peak effect 4–6 weeks. Separate from calcium, iron, binders by at least 4 h. |
| Levothyroxine (IV, myxedema coma) | IV formulation only; dose per endocrinology or ICU protocol | Consult endocrinology | Oral product not recommended for myxedema coma (FDA label, Section 5.3). |
| Hydrocortisone (adjunct) | Per protocol; give before thyroid hormone when adrenal insufficiency is present or not excluded | Per protocol | Thyroid hormone increases glucocorticoid clearance. See the hydrocortisone page. |
| Propranolol (thyrotoxicosis) | Per protocol for adrenergic symptoms | Per protocol | Symptom control only; does not treat the thyroid. Check contraindications (asthma or bronchospasm, heart block, shock, decompensated heart failure). |
Doses are typical references. Follow local protocols, medical direction and institutional policy.
Definitive care & disposition
- Myxedema coma and thyroid storm: ICU-level care and endocrinology consultation.
- Central hypothyroidism: Evaluate the other pituitary axes and obtain pituitary imaging; monitor levothyroxine with free T4.
- Subclinical disease and pregnancy: Outpatient follow-up with trimester-specific TSH and free T4 per the 2017 ATA pregnancy guideline.
Field & Transport Considerations
Point-of-care testing
TSH is a laboratory immunoassay. Typical EMS field devices don't measure it, and it should never delay care. In the field, the patient is the test: mental status, temperature, heart rate and rhythm, and ventilation.
Before and during interfacility transport
- Obtain: Known thyroid diagnosis, levothyroxine dose and adherence, recent medication changes (amiodarone, lithium, contrast), and supplements including biotin.
- Treat en route: Hypothermia, hypoglycemia and hypoventilation in a patient with suspected myxedema; tachyarrhythmia and fever in suspected storm (per protocol).
- Re-check: Mental status, temperature, heart rate and rhythm, and respiratory effort at each reassessment.
- Do not delay transport for a TSH result in a patient with suspected myxedema coma or thyroid storm.
| Setting | Consideration |
|---|---|
| EMS | Recognize myxedema and storm patterns; document history and medications; transport |
| ED / ICU | Draw TSH with free T4 before or alongside treatment; do not wait for results to start protocol treatment |
| Transport | Watch for rhythm change and hypothermia; the thyroid medication plan is set by the receiving team |
Timing & Kinetics
| Parameter | Value | Clinical implication |
|---|---|---|
| Levothyroxine peak effect | May take 4–6 weeks after a dose change (FDA label, Section 2.2) | Do not judge a new dose before this time. |
| Titration interval (adults) | Steps of 12.5–25 mcg every 4–6 weeks; every 6–8 weeks if at risk of atrial fibrillation, with cardiac disease, or geriatric (FDA label, Table 1) | Do not step faster than the interval; cardiac and older patients are titrated more slowly. |
| TSH recheck after a dose change | 6–8 weeks after any change in adults (FDA label, Section 2.4) | Recheck once the new steady state is reached. Frequent changes cause oscillating TSH. |
| Pregnancy monitoring | TSH every 4 weeks until a stable dose (FDA label) | Return to the pre-pregnancy dose immediately after delivery; recheck TSH 4–8 weeks postpartum. |
| Biotin washout | Stop at least 2 days (48 h) before testing (FDA label) | Supplements left on the day of draw can falsely change TSH and T4 results. |
| Diurnal variation | TSH varies through the day | Draw at the same time of day for serial comparison. |
Special Populations
| Population | What changes | Clinical implication |
|---|---|---|
| Neonates and infants | Congenital hypothyroidism is detected on newborn screening; neonatal TSH rises shortly after birth | Use age-specific ranges; treat early in weight-based doses (FDA label, Table 2). |
| Children and adolescents | Requirements are weight-based and change with age | Titrate every 2 weeks to TSH or free T4 until euthyroid; undertreatment harms development. |
| Pregnancy | Requirements can rise; TSH targets are trimester-specific | Measure TSH and free T4 at confirmation and each trimester. Pre-existing hypothyroidism with TSH above the trimester range: increase by 12.5–25 mcg/day, with TSH every 4 weeks until stable. New-onset hypothyroidism: 1.6 mcg/kg/day if TSH is 10 or higher, or 1 mcg/kg/day if TSH is below 10, with TSH every 4 weeks (FDA label, Table 3). |
| Older adults | Higher cardiac sensitivity; TSH upper limit may be higher | Start below 1.6 mcg/kg/day; titrate slowly; avoid over-suppression (atrial fibrillation risk). |
| Central hypothyroidism | TSH is not a reliable marker of replacement | Titrate to free T4 in the upper half of normal (FDA label, Section 2.2). |
Interfering Factors & Pitfalls
Medications and supplements
| Factor | Effect | Why | Avoid or fix |
|---|---|---|---|
| High-dose biotin | False − TSH; false + free T4 and T3 | Biotin-streptavidin immunoassays | Stop at least 2 days before testing (FDA label) |
| Calcium, iron, binders | ↑ TSH (under-replacement) | Reduced levothyroxine absorption | Separate by at least 4 h (FDA label, Table 5) |
| Proton pump inhibitors, sucralfate, antacids | ↑ TSH | Reduced gastric acidity lowers absorption | Monitor TSH after starting or stopping (FDA label) |
| Oral estrogen | Total T4 ↑; free T4 normal. May raise levothyroxine requirement in treated hypothyroidism | Raises TBG | Use free T4 for dosing decisions; recheck TSH after starting or stopping estrogen (FDA label, Table 6) |
| Amiodarone | Variable; hypo- or hyperthyroidism | Iodine load and thyroiditis | Baseline and periodic TSH and free T4 during therapy |
| High-dose glucocorticoids | ↓ TSH | Suppress pituitary TSH | Interpret with free T4 and clinical picture |
| Dopamine infusion | ↓ TSH | Dopamine suppresses pituitary TSH release | Interpret TSH with free T4 in ICU and transport patients on dopamine |
Physiologic and assay factors
| Factor | Effect | Why | Avoid or fix |
|---|---|---|---|
| Non-thyroidal illness | ↓ or normal TSH; transient ↑ during recovery | Altered hypothalamic-pituitary drive | Do not treat with thyroid hormone; recheck after recovery |
| Early pregnancy (hCG) | ↓ TSH | hCG has weak TSH-like activity | Use trimester-specific range |
| Heterophile antibodies or macro-TSH | False + or − TSH (assay-dependent) | Assay interference | Repeat with a different method if values conflict with the clinical picture |
| Assay and lab differences | Different limits between labs | Immunoassay methods differ | Compare with prior results from the same lab |
Common misinterpretations
- A normal TSH rules out thyroid disease? Not in central hypothyroidism or early disease. Check free T4.
- An abnormal TSH during acute illness does not make a diagnosis on its own.
- A TSH drawn soon after a dose change still reflects the old dose.
- Giving thyroid hormone for a low TSH in a critically ill patient is not indicated.
Physiology & Test Basics
What it measures
This page is about thyroid-stimulating hormone (TSH), which the pituitary makes. The thyroid hormones it controls (T4, T3) have their own pages. TSH is the most sensitive test for primary thyroid disease, so it is the first screen when thyroid function is in question. Free T4 is the required partner test.
Physiology & regulation
- Axis: The hypothalamus releases TRH. TRH tells the pituitary thyrotrophs to release TSH.
- Effect: TSH drives iodine uptake, thyroglobulin synthesis and release of T4 and T3. It also keeps the thyroid growing.
- Feedback: Thyroid hormones turn down TRH and TSH. A small shift in free T4 causes a large, opposite shift in TSH.
- Central disease: When the pituitary or hypothalamus fails, TSH stays low or inappropriately normal even though free T4 is low.
How it is measured
The lab runs TSH on serum with a sensitive (third-generation) immunoassay. Use the serum tube your lab specifies. Draw at the same time of day if you plan to compare results. Results come back in mIU/L, the same unit as µIU/mL and mU/L.
Why it matters
In emergency care, the pair sorts the picture. Low TSH with high free T4 means thyrotoxicosis. High TSH with low free T4 means hypothyroidism. Myxedema coma and thyroid storm are clinical diagnoses. You can't wait for a TSH result to act on them.
Clinical Pearls
References
- U.S. Food and Drug Administration. LEVO-T (levothyroxine sodium) tablets, prescribing information. Revised 2026 (Reference ID 5792104). https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/021342s028lbl.pdf
- Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315–389. https://doi.org/10.1089/thy.2016.0457
- Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343–1421. https://doi.org/10.1089/thy.2016.0229
- Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association task force on thyroid hormone replacement. Thyroid. 2014;24(12):1670–1751. https://doi.org/10.1089/thy.2014.0028
Medical Disclaimer
- For Educational Purposes Only: This content is intended for educational reference and should not be used for clinical decision-making.
- Not a Substitute for Professional Judgment: Always consult your local protocols, institutional guidelines, and supervising physicians.
- Verify Before Acting: Users are responsible for verifying information through authoritative sources before any clinical application.