POTD: TPA in PE

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POTD: TPA in PE

  • Massive PE can lead to hemodynamic instability and death

  • Smaller but clinically significant PEs can lead to pulmonary hypertension, RV dysfunction and subsequently poor quality of life (decreased exercise tolerance and even dyspnea at rest)

  • TPA in PE is surrounded by controversy with various opinions on the matter

AHA:

  • Massive: hemodynamic instability defined as SBP<90 (or 40 point drop from baseline) for >15 minutes=

  • Thrombolysis indicated unless there are contraindications

  • Sub-massive: hemodynamically stable but with signs of RV strain (elevated troponin/BNP, echo findings of RV dysfunction) = Thrombolysis may be considered (level IIb/C)

ACEP:

  • Hemodynamically unstable patients: Thrombolysis indicated if benefits outweigh risks of bleeding

  • Level B recommendation

  • Hemodynamically stable patients: insufficient evidence to do thrombolysis

MOPETT (Moderate Pulmonary Embolism Treated with Thrombolysis):

If

  • Symptomatic moderate defined as ≥2 signs/symptoms (7 total in inclusion criteria) in addition to CTPA involvement of >70% involvement of thrombus in ≥2 lobar, or left or right main pulmonary arteries

  • Ventilation/perfusion scan showing mismatch in ≥2 lobes

  • SBP<95 excluded

Then

  • enoxaparin/heparin only vs enoxaparin/heparin + half dose tPA (10mg bolus then 40mg over 2 hours)

  • primary end point: pulmonary HTN at 28 months

  • rates in treatment group=16%, control group=57%

  • combined end point: pulmonary HTN at 28 months + recurrent PE

  • treatment group=16%, control group=63%

  • no patients in either group bled

Conclusion:

  • Studies suggest that half-dose thrombolysis is safe/effective in the treatment of moderate PE, with a significant immediate reduction in pulmonary artery pressure that was maintained at 28 months

  • ”Thrombolytics have demonstrated faster improvements in RV function and pulmonary perfusion, but these benefits have not translated to improvements in mortality.”

  • So the measured outcome is of questionable significance as opposed to actual measurements of quality-of-life

  • Perhaps consider in your young patient in whom potential improvement in exercise tolerance in remaining lifetime may be more relevant than in older, immobile patients

Stay well,

TR Adam

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POTD: Myxedema Coma

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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

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POTD. Myxedema Coma.

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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. 

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