![[Pasted image 20241016002928.png]] > Serum thyroid hormone concentrations are often abnormal during critical illness; *do not start treatment for a thyroid disorder based on thyroid function tests alone.* > > During critical illness, a common finding is a low serum TSH concentration with a low serum T4concentration, which otherwise suggests hypothyroidism secondary to hypopituitarism; however, a persistent pituitary abnormality is rare. These changes are usually caused by transient central inhibition of TSH secretion (either spontaneous or caused by drugs), altered deiodination, and accelerated clearance of thyroid hormones related to critical illness. > > High serum TSH concentration with normal or low serum T4 concentration, which usually indicates primary hypothyroidism, can occur transiently during recovery from critical illness. # causes usually long-standing untreated hypothyroidism precipitated by a secondary insult: - medication non-compliance - **iodine deficiency** most common cause worldwide - autoimmune disease more common in Australia - [[hypothermia]] - increased incidence in winter months - infection (pneumonia > UTI > cellulitis) - CVA - AMI - trauma - medications -- amiodarone, lithium, anaesthetics, diuretics # myxoedema coma > **myxoedema coma:** altered mental state, features of hypothyroidism, and ==hypothermia== usually a precipitating event eg infection, stroke, trauma, MI mortality ~50% ## clinical features - altered mental state/coma from cerebral oedema, hypoxia, hypercarbia - seizures sometimes - hypothermia temps usually < 32.2 deg C ==without shiver== - hypotension - bradycardia - pericardial effusion, rare tamponade - [[hypoglycaemia]] - [[hyponatremia|hyponatraemia]] → may be just an [association](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470237/) - paralytic ileus, megacolon - Urinary retention - Dry coarse skin - Peripheral oedema ## Treatment 1. replace thyroid hormones (T4 and T3) 1. levothyroxine (T4) 200-400 mcg IV loading then 50mcg IV daily (oral load 500 mcg if no IV available) 2. triiodothyrone (liothyronine -T3) bolus 50mcg then 5-20 mcg IV TDS 2. [[hydrocortisone]] 50-100mg QID (for co-existent [[Adrenal insufficiency]] 3. supportive care 1. IVF 2. vasopressors noradrenaline target MAP 65 4. electrolyte rmanagement 1. [[Calcium Gluconate]] 5. Gentle re-warming (but avoid vasodilation hypotension) **pathophysiology challenges unique to this condition and relevant modifications in resus and treatment** | pathophys challenge | modificaiton to mgmt | | --------------------------------------------------------------- | ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- | | upper airway obstruction from glottic oedema, vocal cord oedema | - difficult intubation set up<br>- smaller sized ETT<br>- video laryngoscopy | | hypothermia | passive re-warming preferred (active results in vasodilaiton and worse hypotension) | | cardiac impairment | - bradycardia, ↓ myocardial contractility, low cardiac output state and hypotension<br>- +/- pericardial effusion<br>- vasopressors inefficient without thyroid hormone replacement | <u>James Hayes answer from 2013:</u> - immediately tx any ABC issues - treat any hypoglycaemia  - judicious IVF; beware hyponatremia and fluid overload (saline with oral free H2O restriction) - warming measures and monitor core body temperature ; rewarm with caution (rebound vasodilation and hypotension) - hydrocortisone 100mg IV Q6H - +/- abx - IV liothyronine (synthetic T3) better than oral thyroxine (faster onset) eg 20 mcg by slow IV injection once or twice daily ; otherwise 500mcg thyroxine oral loading dose followed by 100 mcg orally daily .  IV thyroxine 300mcg followed by 75 mcg od # subclinical hypothyroidism Subclinical hypothyroidism refers to a normal fT4 with elevated TSH. If patients are asymptomatic, treatment may not be needed; thyroid function spontaneously reverts to normal during repeat testing in 10–15% of patients. Guidelines recommend *starting thyroxine if TSH is >10 mIU/L* even if patients are asymptomatic, because of the high likelihood of progression to frank hypothyroidism. Treatment should also be considered at lower levels of TSH elevation (TSH 5–10 mIU/L) in women planning pregnancy, on a trial basis in symptomatic patients and in patients with significant dyslipidaemia. **ETG:** *Subclinical asymptomatic hypothyroidism with mildly elevated serum TSH concentration* (in the range 4 to 10 milliunits/L) may not require treatment. - Retest the serum TSH concentration after 4 to 8 weeks to confirm the hypothyroidism is persistent, and also test for thyroid peroxidase antibody. - Patients with a positive thyroid peroxidase antibody are more likely to progress to overt hypothyroidism—repeat thyroid function tests after 3 months, then 6- to 12-monthly thereafter. - Start treatment if the patient has a progressive rise in TSH or if symptoms occur. Patients with a negative thyroid peroxidase antibody can be assessed less frequently (eg every 12 months).