POTD: Myxedema Coma

Adam Ranginwala · October 5, 2020 · Endocrine, Critical Care

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

POTD. Myxedema Coma.

Elliot Warman · February 17, 2020 · Endocrine, Critical Care

A nice week of spring fling came and went. in honor of the return of the cold. lets have a discu-shin about an uncommon, but deadly cause of hypothyroidism - myxedema coma.

Why do I care?
- because mortality rates in treated MC approach 60%
  - if missed and untreated, mortality approaches 100%.
How does it present?
- Severe hypothyroidism --> everything slows down. hypothermia and decreased mental status are hallmarks, other common signs are hypotension, bradycardia, hyponatremia, hypoventilation, and hypoglycemia.
  - interestingly, it is aka myxedema madness - as sometimes patients present with psychosis.
  - due to its rarity it can be a confusing Ddx - think of a patient with multiple failing organs whose lethargic, hypotensive, and hypothermic
  - ddx include sepsis, CHF, tox, adrenal crisis
  - to make things more complicated, myxedema coma usually occurs in a patient with hypothyroidism as a result of a precipitant
  - any systemic insult can push a patient in to myxedema (overdose, CHF, CVA, sepsis, trauma, etc.)
so youre saying the differential diagnosis can actually be the cause?
- YES I AM
So how will i recognize it????
- You'll send a thyroid panel to the lab
- and you'll realize that your standard treatments for whatever else may be present just are not working as well as you'd expect them to.
  - BP will not respond to pressors as well you'd expect.
How do I treat it?
- controversial. most agree to adminster both T3 and T4 (levothyroxine)
  - T4: 4mcg/kg IV
    - followed by 75-100 mcg daily IV until patient tolerates PO
  - T3: 10mcg IV
    - followed by 2.5-10 mcg IV daily
- concomitant adrenal insufficicnecy may be present
  - administer hydrocortisone 100 IV q8
where should i send this patient?
- to the MICU. and get your endocrinologists involved.

Pressors in cardiogenic shock

Aneri Sakhpara · October 17, 2019 · Critical Care, Cardiovascular

“Pressors” in Cardiogenic Shock in adults

Vasopressors- Pure vasoconstriction without any inotropy eg Phenylephrine and Vasopressin
Inotrope- Increase cardiac contractility à improving SV and cardiac output without any vasoconstriction eg Milrinone
Inopressors - a combination of vasopressors and inotropes, because they lead to both increased cardiac contractility and increased peripheral vasoconstriction eg Norepinephrine, Epinephrine and Dopamine

Norepinephrine- Inopressor

Considered the safest Inopressor
Less arrhythmogenic than Epinephrine and Dopamine

Mechanism of action

Stimulates alpha-1 and alpha-2 receptors
Small amount of beta-1 agonist- modest inotropic effect
Increased coronary blood flow and afterload
Increases venous tone and return with resultant increased preload

Adverse effects

Norepinephrine is considered safer than both epinephrine and dopamine.
Still carries risk of toxicity to cardiac myocytes, cardiac arrhythmias, and peripheral vasoconstriction leading to tissue ischemia

Indications

Norepinephrine is considered first-line in cardiogenic shock with profound hypotension (SBP < 70 mm Hg)
Should be used in conjunction with dobutamine in patients with cardiogenic shock and blood pressure higher than 70 mm Hg who fail to respond to dobutamine.

Dosing

Use weight-based dosing to avoid the adverse effects associated with norepinephrine use
Weight-based dosing is based on GFR
Norepinephrine has a rapid onset of action (minutes) and can be titrated every 2-5 minutes

Dobutamine- Inopressor

Mechanism of action

Stimulates beta-1 and beta-2 receptors at approximately a 3:1 ratio
At high doses (greater than 15 ug/kg/min), dobutamine also becomes a mild alpha-1 agonist.
Because it mainly stimulates beta-1 receptors, dobutamine is mostly an inotrope
Dobutamine’s stimulation of beta-2 receptors can result in peripheral vasodilation, though the magnitude of this effect is variable à blood pressure in some (but not all) patients.
Due to its vasodilatory effects, dobutamine has been shown to improve capillary perfusion independent of changes in blood pressure and cardiac index.

Adverse Effects

Studies have demonstrated increased myocardial oxygen demand and malignant arrhythmias typically occuring at doses higher than 15 ug/kg/min
Many patients experience hypotension associated with dobutamine use and should be used with caution in patients with systolic blood pressure less than 90 mmHg
Dobutamine should only be used in patients with adequate fluid resuscitation

Indications

Current ACC/AHA guidelines à first-line agent in management of hypotension associated with acute myocardial infarction
But because dobutamine can lower BP, it should only be used if SBP is between 70-100 mmHg, with norepinephrine ready (or already infusing) as well.
Dobutamine is typically recommended as the first line agent in cardiogenic shock , but this is not a strong recommendation because several studies have demonstrated benefits to norepinephrine in this setting.
If dobutamine is used as a first-line agent, then norepinephrine should be second-line or already infusing, followed by milrinone.

Dosing

Dobutamine can be started at 2 mcg/kg/min and titrated to effect, with a maximum dose of 20 mcg/kg/min.
Onset of action is 1-2 minutes and the half-life is also approximately 2 minutes à rapidly reversible.

Milrinone- Inodilator

Mechanism of action

Milrinone is a phosphodiesterase-3 (PDE3) inhibitor à leads to cardiac smooth muscle relaxation and peripheral vasoconstriction
Potent inotropy + diastolic relaxation and vasodilation à to reduced preload, afterload, and systemic vascular resistance (SVR)
Milrinone has no beta-adrenergic activity à minimal chronotropic effects.

Adverse Effects

Because milrinone decreases preload (and therefore often leads to hypotension), it should only be used in patients who have undergone appropriate fluid resuscitation
Use of milrinone often necessitates concurrent vasopressor administration.
Because milrinone is metabolized in the kidneys, it should be avoided in patients with renal disease

Indications

Recommended for use in patients with daily beta-blocker use and in patients with long-standing heart failure who have developed resistance to catecholamine derivatives
Due to PDE’s vasodilatory effect on pulmonary vasculature à theoretical benefit in patients with pulmonary hypertension

Dosing

The starting dose of milrinone should ideally be chosen based on that patient’s renal function. The general range is 0.25-0.75 mcg/kg/min.
Avoid its use in patients with creatinine clearance less than 50 mL/min.
Because of its long onset of action and half-life, milrinone should be titrated every 2 hours (or slower, in the presence of renal disease).

Vasopressin- Pressor

Mechanism of action

Vasopressin is an endogenously released hormone (also known as anti-diuretic hormone) à vasopressin receptors in the kidneys à improve GFR
Vasopressin receptors on the peripheral vasculature à vasoconstriction.
Also causes coronary and cerebral vasodilation

Adverse Effects

Vasopressin increases the risk of digital ischemia more significantly than the catecholamine derivatives.
No evidence to support the use of vasopressin through a peripheral intravenous line
Vasopressin does not have an antidote if extravasation does occur.

Indications

Due to its increased risk for digital ischemia à avoid vasopressin in patients with known PVD
It has been proposed that because vasopressin leads to coronary vasodilation, it may be a preferable agent in cardiogenic shock but few RCTs investigating vasopressin use in cardiogenic shock.
Vasopressin may not lead to pulmonary vasoconstriction à ideal pressor choice in hypotension secondary to pulmonary hypertension à but not enough literature to support routine use in this setting

Dosing

Vasopressin is an endogenous à no utility to titrating vasopressin à used at a set dose of 0.04 U/min, regardless of weight.

Epinephrine- Inopressor

Mechanism of action

Beta-1 and beta-2 receptors agonism à more inotropic effects than norepinephrine
Epinephrine greatly increases chronotropy (heart rate) and thus stroke volume
Some stimulatory effect on alpha-1 receptors
Lower doses (1-10 mcg/min) à a beta-1 agonist
Higher doses (greater than 10 mcg/min) à an alpha-1 agonist

Adverse effects

Associated with an increased risk of tachycardia and lactic acidosis
Hyperglycemia
Increased incidence of arrhythmogenic events associated with epinephrine
More difficult use lactate as a marker of the patient’s response to treatment

Indications

Should be used with extreme caution in cases of cardiogenic shock:

RCT of 219 patients with cardiogenic shock found epinephrine to be independently associated with increased 90-day mortality and worsened renal function compared to dobutamine and norepinephrine (not validated).
Known increased incidence of arrhythmogenic events associated with epinephrine

Dosing

doses of 1-10 mcg/min predominantly activate beta-1 receptors, while doses greater than 10 mcg/min begin to primarily affect alpha-1-mediated vasoconstriction.

Phenylephrine: Not recommended in Cardiogenic shock

Resource: Awesome chart summarizing plessors

http://www.emdocs.net/wp-content/uploads/2018/02/Inopressor-Summary_chart.pdf

References:

http://www.emdocs.net/evidence-based-approach-pressors-shock-part/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part I - emDOCs.net - Emergency Medicine Education

www.emdocs.net

http://www.emdocs.net/evidence-based-approach-pressors-shock-part-ii/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part II - emDOCs.net - Emergency Medicine Education

www.emdocs.net

Tarvasmäki T, Lassus J, Varpula M, Sionis A, Sund R, Køber L, et al. Current real-life use of vasopressors and inotropes in cardiogenic shock-adrenaline use is associated with excess organ injury and mortality. Critical Care. 2016;20(1):208.