POTD: 3 Common Anti-Vaxxer Beliefs

“It is better to light a candle than to curse the darkness” - Carl Sagan

In an era where “fake news” threatens the fabric of our society, we as physicians have a duty to educate our patients and fight the insidious creep of disinformation. We often think of anti-vaxxers as granola-eating, compost pile-making eccentrics living off the grid somewhere in Montana, when the truth is that even some amongst own hospital colleagues may espouse these beliefs.

Here, we discuss three common arguments made by anti-vaxxers in supporting their stance and counterarguments based on empirical evidence we may use to challenge them.   

FALSE: Vaccines cause undue harm due to antigenic overload

    ▪    A misconception propagated by Robert W. “Doctor Bob” Sears that holds infants are incapable of responding safely to the “large number” of vaccine antigens given and that antigenic overload results in a “cytokine storm” or “immune cascade” that triggers adverse health events.

    ▪    Not surprisingly, “Dr. Bob” failed to cite any data to support this claim.

Counterarguments:

    ▪    From the moment of their birth, infants encounter numerous microorganisms and their antigens at a level far exceeding the antigen exposure due to vaccines.

    ▪    Numerous studies show that vaccines are safe and efficacious at the routine vaccine schedule with no evidence of an “antigenic overload.”

    ▪    Infants and children today actually receive far less antigenic “exposure today” with routine vaccination than they did in the past. The smallpox vaccine given in the 1900s contained 200 proteins and the whole cell pertussis component of DTwP vaccine given in the US up until the 1990s contained approximately 3,000 proteins. Today, the entire schedule of 15 recommended vaccines from birth to age 5 contains no more than 150 proteins and polysaccharides.

FALSE: Vaccines can result in autoimmune diseases such as T1DM, MS, and GBS.

Counterarguments:

    ▪    A panel of experts of the Institute of Medicine recently reviewed more than 12,000 published reports and failed to find any evidence whatsoever for the development of any of these three autoimmune diseases as a result of vaccines.

    ▪    The diversity of antigens presented during “natural” infection support the counterclaim that infections are more likely than vaccines to result in autoimmune phenomena, such as influenza virus or Campylobacter infection causing GBS.

FALSE: Immunity produced by “natural infection” is safer than vaccine-induced immunity.

Counterarguments:


    ▪    Wild type influenza kills 1 in every 8,300 Americans.  No deaths have been attributed to the flu vaccine.

    ▪    The flu vaccine does not cause myocarditis, PNA, bronchitis, sinusitis, or significant amounts of lost work and school time — but “natural” influenza certainly does.

    ▪    While “natural” measles virus infection does provide lifelong immunity, it also causes death in about 1 out of every 3,000 cases, as well as other non-lethal and disabling complications. The measles vaccine has not been associated with death or disabling complications, despite billions of vaccine doses given.

Harms done by the anti-vaccine movement


    ▪    The anti-vaccine movement has successfully pressured numerous countries to discontinue use of the pertussis vaccine. These countries now have a documented 10- to 100-fold increased in morbidity and mortality from pertussis.

    ▪    Doctor Bob Sear’s alternative vaccination schedule has resulted in under-vaccination and measurable increased rates of measles and pertussis.

    ▪    Europe, Australia, New Zealand, and the Americas are now seeing major outbreaks of measles as a result of Wakefield’s fraudulent study claiming a link between the MMR vaccine and measles.

    ▪    In a Wisconsin survey, 31% of parents who refused vaccination cited “autism” as their reason.


Poland et al (2012) “The clinician’s guide to the anti-vaccinationists’ galaxy.” Human Immunology, Volume 73, Issue 859-866

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POTD: How to Treat Cellulitis...and Leishmaniasis

You diagnose a patient with cellulitis and you reach the old, familiar mental roadblock: which antibiotic do I use? Sure, you treated your last cellulitis patient with Keflex, but this patient has a small, mild abscess — do we use a different antibiotic?

UptoDate is tedious, and you’ve called the ED pharmacy 15 billion times today already for other med recommendations. Is there a better way?


B  E  H  O  L  D :  The IDSA Practice Guidelines

https://www.idsociety.org/practiceguidelines#/name_na_str/ASC/0/+/


From treating cellulitis to combat-related infections to leishmaniasis, the IDSA has the most current recommendations for you, the practitioner.

Back to our patient's skin infection. A quick search will yield this handy chart:

Screen Shot 2019-12-30 at 6.35.49 PM.png


Our patient is young, with no comorbidities, and he has a mild, superficial, purulent infection with no systemic symptoms. According to this chart, we could treat with I & D and NO ANTIBIOTICS AT ALL. However, the same patient with a more deep-seated infection, systemic symptoms, or any risk factors would warrant empiric treatment with doxy or bactrim.

IN SUM: The IDSA practice guidelines exist. Use them.

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“Pressors” in Distributive Shock in Adults

“Pressors” in Distributive Shock in Adults

Thank you, Dr Dastmalchi, for requesting this POTD. I will review “pressors” for cardiogenic shock separately

  • 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

  • First line vasopressor in septic shock per Surviving Sepsis Guidelines

  • 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.

  • ARR of 11% compared to dopamine with NNT 9

  • NE superior in improving CVP, urinary output, and arterial lactate levels compared to Epinephrine, Phenylephrine, and Vasopressin.

Indications

  • First-line pressor choice in distributive shock, including both neurogenic and septic shock

  • Norepinephrine as the only first-line pressor per SSC guidelines

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

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

  • SSC guidelines recommend epinephrine as a second-line agent, after norepinephrine

  • “push-dose pressor”

  • Due to beta-2 receptors agonism causing bronchodilation, epinephrine is first-line agent for anaphylactic shock

Dosing

  • Guidelines for anaphylactic shock recommend an initial bolus of 0.1 mg (1:10,000) over 5 minutes, followed by an infusion of 2-15 mcg/min however associated with adverse cardiovascular events

  • For septic shock start epinephrine at 0.05 mcg/kg/min (generally 3-5 mcg/min) and titrate by 0.05 to 0.2 mcg/kg/min every 10 minutes. maximum drip rate is 2 mcg/kg/min

Dopamine- Inopressor

  • Fallen out of favor

  • Associated with higher arrhythmogenic events

Mechanism of action

  • Effects are dose-dependent

  • Low doses à dopaminergic receptors à leads to renal vasodilation à increased renal blood flow and GFR although studies failed to demonstrate improved renal function with dopamine use clinically

  • Moderate doses à beta-1 agonism à increased cardiac contractility and heart rate

  • High doses à alpha-1 adrenergic effects à arterial vasoconstriction and increased blood pressure

Adverse Effects

  • Several large, multi-center studies that demonstrate increased morbidity associated with its use

  • Significantly higher rates of dysrhythmias à NNH 9

Indications

  • Rescue medication when shock is refractory to other medications

Dosing

  • Start at 2 mcg/kg/min and titrate to a maximum dose of 20 mcg/kg/min.

  • Less than < 5 mcg/kg/min à vasodilation in the renal vasculature

  • 5-10mcg/kg/min à beta-1 agonism

  • 10 mcg/kg/min à alpha-1 adrenergic

Vasopressin- Vasopressor

  • Add vasopressin (doses up to 0.04 units/min) to norepinephrine to help achieve MAP target or decrease norepinephrine dosage

  • Restore catecholamine receptor responsiveness, particularly in cases of severe metabolic acidosis.

  • pH independent

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

Mechanism of action

  • At low doses (< 0.04 units/min) à increases vascular resistance (V1)

  • No effect on heart rate and cardiac contractility

Adverse Effects

  • Vasopressin has been shown to be as safe as norepinephrine at lower doses

  • Increases SVR and afterload and decreases cardiac output although unclear if effect significant at lower doses

Indications

  • Second line vasopressors per SSC guidelines for septic shock

  • pH independent- Vasopressin in combination with epinephrine demonstrated improved ROSC in cardiac arrest patients with initial arterial pH <7.2 compared with epinephrine alone

Dosing

  • Steady dose at 0.03-0.04 units/min

  • Vasopressin is not titrated to clinical effect as are other vasopressors

  • Think about it more as a replacement therapy and treatment of relative vasopressin deficiency

Phenylephrine- Vasopressor

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

  • SSC guidelines does not make rated recommendations on Phenylephrine

  • Limited clinical trial data

Mechanism of action

α1 agonism with peripheral vasoconstriction

Adverse Effects

  • Bradycardia - decrease in heart rate mediated by the carotid baroreceptor reflex 2/2 increase in SVR

  • Increases SVR and afterload and decreases cardiac output

Indications

  • Patients that are susceptible to beta-adrenergic generated arrhythmia

  • Push dose formulation

  • Refractory shock

Dosing

0.1-2mcg/kg/min (onset: minutes, duration: up to ~20 minutes)

References:

Emdocs

LITFL

Pollard, Sacha, Stephanie B. Edwin, and Cesar Alaniz. "Vasopressor and inotropic management of patients with septic shock." Pharmacy and Therapeutics 40.7 (2015): 438.

Amlal, Hassane, Sulaiman Sheriff, and Manoocher Soleimani. "Upregulation of collecting duct aquaporin-2 by metabolic acidosis: role of vasopressin." American Journal of Physiology-Cell Physiology 286.5 (2004): C1019-C1030.

Khanna, Ashish, and Nicholas A. Peters. "The Vasopressor Toolbox for Defending Blood Pressure."

Turner, DeAnna W., Rebecca L. Attridge, and Darrel W. Hughes. "Vasopressin associated with an increase in return of spontaneous circulation in acidotic cardiopulmonary arrest patients." Annals of Pharmacotherapy 48.8 (2014): 986-991.

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