Thyroid storm



Thyroid Storm

 

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Background

 

Thyroid storm is a rare yet mortality rates reported between 10-30%

It is often presents in patients (pts) with established hyperthyroid disease (Graves' disease, toxic multinodular goiter, solitary toxic adenoma)

 

Precipitating Factors: Trauma, infection, DKA, CVA, PE, MI, etc.

 

Presentation and Diagnosis

 

Thyroid storm is a clinical diagnosis of a severe and exaggerated form of thyrotoxicosis.  

Look for a triad:

Extreme Fever (often >104F)

Tachycardia (can be accompanied with AFib, widened pulse pressure)

Altered Mental Status



Other findings:

Tremor

Lid Lag

Proptosis/Periorbital Edema

Pretibial plaques/nodules/non-pitting edema

Goiter/Thyroid Nodules

 

 

Labs:

low TSH and high free T4 and/or T3 concentrations

mild hyperglycemia, mild hypercalcemia, abnormal liver function tests, leukocytosis, or leukopenia

 

 

Management

 

Supportive Care

Fever: Cooling measures and antipyretics. 

Agitation: Benzodiazepines 

Vascular instability: IV fluids

 

Beta Blockers:

β blockade is critical in the management of the peripheral actions of increased thyroid hormone.

Propranolol 0.5-1mg IV over 10 mins followed by redosing 1-3mg every few hours OR 60-80mg PO q4h

Alternative metoprolol, esmolol or atenolol 



Thionamides - Inhibit New Synthesis by blocking T4-to-T3 conversion

PTU for the acute treatment of life-threatening thyroid storm -

Propylthiouracil (PTU) 600-1000mg PO loading dose with 200-400mg PO q6-8h, Hepatotoxic

Methimazole for severe, but not life-threatening for a longer duration of action 

Methimazole 20-25mg PO q4-6h - longer half-life compared to PTU.



Iodines - blocks the release of pre-stored hormone, and decreases follicular transport and oxidation.

SSKI 5 drops PO q6h or Lugol’s Solution 4-8 drops PO q6-8h

Works through “Wolff-Chaikoff effect,” in which high levels of iodide will inhibit T3/T4 synthesis and release

Give AFTER antithyroid drugs, no sooner than 30-60 mins following PTU/Methimazole.

Lithium 300mg PO q6-8h - for iodine allergy or contraindication to iodine usage 

 

Other therapies to consider: 

Steroids (Inhibit Peripheral Conversion) Hydrocortisone 300mg IVx1 and then 100mg IV q8h or Dexamethasone 2-4mg IV q6h

Cholestyramine (4 g orally four times daily) - bile acid sequestrants to reduce enterohepatic circulation of thyroid hormone

Plasmapheresis: Offers temporary stabilization for a patient that has been unresponsive to antithyroid medications



References: EMDocs, UpToDate




POTD: Alcoholic Ketoacidosis

Today’s topic will be for the people who used this 3-day weekend for a bender:

Alcohol Ketoacidosis (AKA)

Clinical Scenario:

Someone who has been on a bender and shows up to your ED after two days of vomiting, has a low bicarb, elevated anion gap, elevated lactate, urine ketones, and an elevated BHB level...probably has AKA. 

Background

  • Alcoholic ketoacidosis (AKA) is a starvation state in an alcoholic or binge drinker

  • Alcohol + No Food + Dehydration = AKA

  • Most often associated with acute cessation of alcohol consumption after chronic alcohol abuse

  • Can also be associated with first-time alcohol binge

  • one of the causes of anion-gap metabolic acidosis 

Clinical Features

  • episode of heavy drinking followed by vomiting and an acute decrease in alcohol consumption

  • N/V, nonspecific abdominal pain

  • can have associated gastritis or pancreatitis

  • normal mental status, but if patient is altered, look for toxic alcohol ingestion, postictal states from withdrawal seizures, or occult head injury

  • exam with acetone odor on breath

  • tachypnea (Kussmaul respiration), tachycardia, and signs of dehydration

Pathophysiology

ethanol metabolism.png

Nicotinamide adenine dinucleotide (NAD, or “Needs Additional Dextrose”) is depleted by ethanol metabolism, leading to inhibition of the Kreb’s cycle (or aerobic metabolism) in favor of ketone formation, depletion of glycogen stores, and suppression of insulin secretion  

Diagnosis

  • low, normal, or slightly elevated glucose

  • binge-drinking that ends in N/V and decreased intake

  • wide AG metabolic acidosis, especially one without an alternative diagnosis

  • (+) serum ketones

  • can have associated hypophosphatemia, hyponatremia, and hypokalemia

Treatment

  • Sugar and water!

  • Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. 

  • Start with 5% dextrose in NS. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in 1/2 NS until oral intake is assured.

  • Give 100 mg thiamine (facilitates Krebs cycle)

  • Correct electrolytes

  • Repeat Chem7 to see if bicarb improving. If it’s not, consider ethylene glycol or methanol poisoning. This is the time for fomepizole and a call to your local toxicologist or poison center!

Disposition

Discharge if tolerating PO!

References

https://emcrit.org/toxhound/aka-aka/

https://lifeinthefastlane.com/ccc/alcoholic-ketoacidosis/

Tintanelli’s

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Sepsis minus a source? ADDrenal?

Adrenal Crisis Loss of mineralocorticoid and/or glucocorticoid production. Dysfunction is at level of pituitary (secondary or tertiary cause) or the adrenals (primary) with multiple causes:

  • autoimmune

  • suppression from exogenous hormone use

  • hemorrhage

  • tumor

  • infection

Clinical picture:

  • abdominal pain

  • vomiting

  • diarrhea

  • hypotension

  • refractory shock

  • fever

  • confusion

Chronic insufficiency will also give: weight loss, fatigue, arthralgia, myalgia, anorexia, mood change, syncope history, salt cravings, hyper pigmentation, vitiligo

Fever, shock, and confusion sounds like septic shock can labs help?

**for adrenal crisis a random cortisol level below 3 μg/dl (80 mmol/L) is diagnostic but will not be low in all cases

other labs you can expect to find, hypoglycemia, hyponatremia, hyperkalemia, elevated BUN creatinine, hypo-osmolarity

Treatment:

  • supportive measures

  • stress dose steroid hydrocortisone 100mg IV Q6

Bottom line -in your patients with refractory shock send cortisol level and give stress dose steroid

-consider this diagnosis in patients with autoimmune history, recently postpartum, chronic steroids, Sepsis with no source,

Disposition:

ICU

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Cause You're Hot Then You're Cold

Today we will start a miniseries on endocrine emergencies. Myxedema coma -severe hypothyroidism Clinical Features: -Hypothermia -Hypoglycemia -Hypoventilation--> hypoxia, hypercapnia, -Hyponatremia in 50% of patients -Hypotension & bradycardia -Hypomentation, obtunded can conversely have psychosis -Myxedema, nonpitting edema due to deposition mucin & albumin --> can complicate airway -Seizure

Work up: -Work up other pathology -TSH (high) -T4 (low) -T3 (low) -Cortisol (to check for adrenal insufficiency)

Specific treatment: -Initial dose 200-400mcg T4(levothyroxine) IV then daily 50-100mcg IV -Plus initial dose 5-20mcg T3(liothyronine) then 2.5-10mcg every 8 hours,  continue T3 until patient stable -Optimal dose may be moderate dose, use lower doses in older frailer patients -Stress dose steroid hydrocortisone 100 mg every 8 hours

Disposition: ICU

 

Thyroid storm -too much thyroid, think elevated metabolism and stress response Clinical Features: -Tachycardia--> 60% patients have tachycardia or atrial fibrillation -CHF -Arrhythmia -Cardiac arrest -Hyperpyrexia often 104-106 -Agitation -Psychosis -May be obtunded or comatose -Hand tremor -Diaphoretic -Nausea, diarrhea, and vomiting

Work up: -TSH (low) -T3 (high) -T4 (high) may also have hyperglycemia, mild hypercalcemia, leukocytosis,

Specific treatment: (it is important to give betablocker before inhibiting thyroid hormone synthesis) 1. Propanolol 0.5-1mg IV over 3-5 minutes repeat every 5-10 minutes till heart rate <100 -OR use esmolol, load 250-500mcg/kg, infusion 50-100mcg/kg/min -CHF is high output still give test doses betablocker 2. PTU (propylthiouracil) load 600-1000mg then 300mg every 6 hours give PO, NG, PR (preffered in pregnancy) -OR use methimazole20-30 mg every 6 hours 3. corticosteroid, hydrocortisone 100mg IV every 8 hours -OR use Dexamethazone 2-4mg IV every 6 hours (dexamethazone does not scew cortisol tests) 4. inhibit thyroid production with inorganic iodine -Potassium Iodide: 5 oral drops -OR Lugol's solution 10 oral drops

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Thyroid Storm-POD

THYROID STORM PRESENTATION

  • Fever

  • Altered mental status

  • Tachycardia

CAUSES

  • Infection

  • MI

  • DKA

  • Pregnancy

  • Trauma

  • Untreated thyroid disease

  • Ingestion of thyroid hormone

TREATMENT

  • Control body temperature

    • Cool IV fluids, external cooling

  • IV Fluids

    • High output cardiac failure- preload dependent

    • Add glucose as they have low glycogen stores

  • Beta Blocker

    • Propranolol 0.5- 1mg IV over 3-5 minutes

      • Prevents conversion of T4àT3

      • Non selective beta blocker

      • Titrate to HR<100

    • Stop Thyroid hormone synthesis

      • Propylthiouracil 1000mg PO/NG or PR

        • Preferred in pregnancy

        • Prevents conversion of T4àT3

      • Hydrocortisone 100mg IV q 8

        • Blocks T4àT3

        • Thyroid storm causes depression of hypothalamic- pituitary axis

      • Iodine

        • Inhibits thyroid hormone release

        • Do not give for at least 1 hour after starting PTU

      • Antibiotics

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