Thyroid Emergencies

Another home-made infographic for today’s blog… this time a review of when and how to treat severe hypo & hyperthyroidism!

If there is one thing you take away from today's pearl, let it be this:

Both thyroid storm and myxedema coma are clinical diagnoses; they cannot be diagnosed definitively based on lab results. THERE IS NO CUT-OFF VALUE OF FREE T3 or FREE T4 to indicate when you should treat!! Decision to treat should be made based on severity of symptoms.

For thyrotoxicosis there is a scoring system, although not perfect, to help you make this distinction between early thyrotoxicosis and potentially life threatening thyroid storm. For myxedema coma, you may have to make this decision based on the pt's mental function & hemodynamic stability.

Other pearls:

- Thyroid storm and myxedema coma are the most severe manifestations of hyperthyroidism and hypothyroidism. Both typically present together with another medical emergency (a precipitant), most commonly sepsis.

- Hyperthyroidism is simply the state of elevated serum thyroid hormones. Thyrotoxicosis is the clinical syndrome of symptoms resulting from the effects of elevated thyroid hormones. one can be hyperthyroid but not thyrotoxic. Everyone who is thyrotoxic is hyperthyroid.

-Why do we give so many meds for thyroid storm?? Its actions, particularly on the heart, are immediately life threatening. So we attempt to stop the involved hormones in several diff ways:

1. Beta blockers are given to block the peripheral affects of T3

2. Thionamides inhibit thyroid hormone production by inhibition of thyroid peroxidase. PTU is traditionally preferred because it also has some action on peripherally preventing conversion of T4 to T3 by inhibiting 5'-deiodinase. **These meds MUST be given before Iodine so that iodine isn’t incorporated/more hormone isn’t synthesized

3. Iodine decreases the release of thyroid hormone from the thyroid gland

4. Steroids block peripheral conversion of T4 to active T3, and also helps in case of adrenal insufficiency

5. Last ditch: Apheresis can be used in critically ill pts to remove excess thyroid hormone from the serum

DKA & HHS

Today’s pearl is in the form of a home-made infographic!

Here are a few key take-home points:

-Start fluid resuscitation ASAP (20cc/kg. you do not have to have any labs back.) Hang whatever fluid is convenient & change it later. The main concern with NS is that it will worsen acidosis if you give a ton of it. This is just the first liter, dont worry about hunting down your fancy plasmalyte right now.

-Do NOT start insulin w/out getting a K level – severe hypoglycemia can initiate arrhythmia & cardiac arrest

-Do NOT give Sodium bicarb even for a really low pH (6.7? I dont care. Didnt you read Duncan's pearls last month?!). The Bicarb is turned into CO2 which then has to be breathed off, and your DKA pt is already ventilating at maximum rate to correct the metabolic acidosis - you will just make this worse and make them tire out faster. (one exception being the hemodynamically unstable pt requiring pressors. Epi will not work with pH of 6.7, so you may consider bicarb).

-Euglycemic DKA may have glucose <250. This is seen in pregnant pts, alcoholics, and people taking SGLT2-inhibitors (drugs that end with -flozin) which block the absorption of glucose back into the blood stream at the kidneys.

-AMS is what differentiates HHS from just regular hyperglycemia (which usually comes w/dehydration as well, but that pt shouldn’t be altered).

POTD: Myxedema Coma

POTD: Myxedema Coma

Clinical Features (Remember LOW and SLOW: low HR, BP, Temp, sugar, RR, Na, Mentation, reflexes):

• Decreased mental status

• Hypothermia (<95.9F)

• Hypotension  

• Hyponatremia

• Hypoglycemia  

• Bradycardia

• Bradypnea

Work-Up:

• CMP- looking for hyponatremia, elevated CPK, elevated creatinine, transaminasas

• CBC- looking for anemia, leukopenia

• TSH, FT4, FT3- In primary hypothyroidism, TSH will be elevated and T4 and T3 will be low. In secondary hypothyroidism (Pituitary dysfunction) the TSH can be low or normal and T4 and T3 will be low

• Blood cultures- looking for a secondary sepsis source

• Cortisol level

• Lipid panel-  Hyperlipidemia

• VBG-  looking for hypoglycemia, respiratory acidosis

• CXR- looking for pleural effusions

• ECG- looking for bradycardia and rhythm

• Cardiac POCUS- looking for pericardial effusion

Treatment:

• Levothyroxine(T4)  100 to 500 mcg IV (Potentially safer in patients with CAD) or

• Liothyronine (T3) 20mcg IV (Start with 10mcg if elderly or has CAD)

• Hydrocortisone 100mg IV q8hr

• Passive rewarming (Do not actively rewarm as rapid peripheral vasodilation may induce worsening hypotension)

• Mechanical ventilation early may prevent respiratory collapse and severe respiratory acidosis

• IVFs- dextrose containing fluids for hypoglycemia. If patient is hyponatremic, be cautious of too rapid fluid correction

• Broad spectrum Antibiotics

Prognosis:

• Mortality reaches as high as 60%  

Dispo:

• ICU admission 

Stay well,

TR Adam