POTD: Tinea Pedis (Athlete's Foot)

This PODT is inspired by a recent case I had in while working in Peds and is something we may encounter often in the summer. This is a perfect example of a fast track compliant that we may have not seen a lot of during COVID.

The patient was a young male in his 20s who works in construction and wears heavy boots and socks for about 8 hours of the day in the heat. He presented with 1 days of sloughing of the skin of both of his feet with discharge.

 Lets discuss Tinea Pedis (Athlete’s Foot):

 Tines pedis is a dermatophyte infection of the skin on the foot.

 Etiology and Risk Factors:

• Usually occurs in adults and adolescents and is rare prior to puberty

• Infection is acquired by means of direct contact with the causative organism

• Commonly seen in patients who have a history of walking barefoot in locker rooms or swimming pool facilities

• Also commonly seen in patients who wear occlusive footwear

Predisposing factors to consider

• Diabetes Mellitus

• Immunodeficiency, Systemic corticosteroid use, or use of immune suppressive agents

• Poor peripheral circulation or lymphoedema

• Excessive sweating (hyperhidrosis)

 Who would have know that there are different types of tinea pedis?

•  Types of Tinea Pedis:

  • Interdigital tinea pedis: Manifests as pruritic erosions or scales between the toes, most commonly in the third and fourth digital interspaces

    • More severe form of this is known as Ulcerative tinea pedis. This is generally associated with secondary bacterial infection

  • Hyperkeratotic (Moccasin-Type): Characterized by diffuse hyperkeratotic eruption involving the soles and medial and lateral surfaces of the feet.    

  • Vesiculobullous (inflammatory-type): Pruritic, sometimes painful, vesicular or bullous eruption. Medial foot often affected 

Management:

• Topical antifungal therapy is treatment of choice for most patients.

  1. Example of topical antifungal: Azoles, Allylamines, Butenafine, Ciclopirox, Tolnaftate, and Amorolfine. Recommended to apply once or twice a day for four weeks. (Refer to references for dosages and frequency)

  2. Beneficial and more effective for patients to use the suspension formulation of these medications

• Systemic antifungal agents are primarily reserved for patients who fail topical therapy

  1.   Terbinafine 250mg per day for 2 weeks in adults

     1. Most check LFTs prior to administration and patients need to follow up and have LFTs checked while receiving treatment

     2. Peds dosing:

        • 10 to 20kg: 62.5mg/day

        • 20 to 40kg: 125mg/day

        • Above 40kg: standard adult dosing

  • Itraconazole 200mg per day for two weeks

    •   Peds dosing:

      • 3 to 5 mg/kg per day

  • Fluconazole 150mg once weekly for two to six weeks

    • Peds dosing:

      •   6mg/kg once weekly

• ·Ulcerative Tinea Pedis;

  •   Always treatment with systemic antifungal agents in addition to topical antifungals

  • Make sure to add in addition to your antifungal an antibiotic such as Keflex

  • Outpatient podiatry follow up should be given to patients

• Prevention

  • Use of sock with wick-away material

  • Use of desiccating foot powders

  • Tx of hyperhidrosis if there is history of moist feet

  •   Tx of shoes with antifungal powder

  •   Avoidance of occlusive foot wear

 We diagnosed our patient with ulcerative tinea pedis. We started the patient on Terbinafine, Ciclopriox, and Keflex and arranged for podiatry follow up. Our patients case was unique in the fact that the patient had bilateral involvement normally this occurs unilateral.

 References :

·      https://www.uptodate.com/contents/dermatophyte-tinea-infections?search=tinea%20pedis&source=search_result&selectedTitle=1~103&usage_type=default&display_rank=1#H2658711829

·      https://www.uptodate.com/contents/image?csi=18b425c8-5b1f-4694-a039-5bc8aa27c160&source=contentShare&imageKey=PC%2F76148

·      https://wikem.org/wiki/Tinea_pedis

·      https://www.aafp.org/afp/2014/1115/p702.html

·      https://accessemergencymedicine.mhmedical.com/content.aspx?sectionid=109447903&bookid=1658

·      https://dermnetnz.org/topics/tinea-pedis/

Stop Giving Amps of Bicarb!

Chapter 1: What dafuq is in an amp of bicarb?

Take a look!

• 50mL

• 8.4% NaHCO3 -> 50mEq

• The osmolarity of this solution is 2,000mOsm/L - twice that of 3% saline. < (click for emcrit)

Chapter 2: Sodium bicarbonate doesn't just magically raise pH...

Remember this thing?

CO2 + H20 <=> H2CO3 <=> HCO3 + H

It's complicated. Bicarb binds to acid. Then it turns to CO2 and water, so you can breathe it out.

Basically if you're giving bicarb, you can only raise your pH as long as you can breathe off your CO2, increasing your RATE or VOLUME.

**This is particularly a problem in patients who are not in control of their breathing (vented), aren't breathing (arrest), or who have maximized the efficiency of their breathing (Kussmal breathing in DKA).**

That's right - you need to increase your minute ventilation to have a change in pH.

Here's Weingart's take.

Chapter 3: Sodium bicarb amps can cause harm!

FIRST:

One amp of bicarb is like giving 100cc of 3% hypertonic saline!! But as Josh Farkas points out, we typically have no hesitation giving "a couple of amps of bicarb."
This is a huge osmotic load which can lead to huge fluid shifts - prepare for that amp to increase intravascular fluid by 1/4 liter with every push. (Is this what you want to give to your renal failure pt? Your heart failure pt?)

SECOND:

You are worsening acidosis.
What? Huh? But I thought...
No. Stop. Shush. You're worsening acidosis.

Remember, you're increasing CO2 - whether you can breathe it off or not, this CO2 rises in but blood BUT ALSO rises in the tissues and may worsen acidosis in these tissues. < (click for litfl.com article)

THIRD:

Be ready to cause hypernatremia - expect a rise of 1mEq Na per amp of bicarb.

FOURTH:

Extravasation can cause tissue necrosis.

FIFTH:

CSF acidosis, hypocalcemia. Increased lactate. (Some may argue that's not a bad thing.)

If you do manage to fix the acidosis, you can overshoot and create an alkalosis and even screw up the oxygen dissociation curve (in a bad way).

Chapter 4: It just doesn't f&$%ing work
Cardiac arrest: it doesn't do anything. No increased survival. and AHA says it should not be given routinely.

Lactic acidosis: There's a whole section on UpToDate - there's minimal research for pH < 7.1 so you can consider it at that point... but otherwise, nah.

DKA: Take it from a nephrologist: In ketoacidosis, it is almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired. Therapy with fluids and electrolytes restores extracellular volume and renal blood flow, thus enhancing the renal excretion of acid and regenerating bicarbonate.

Hyperkalemia: Amps of bicarb, even in hyperK emergencies, have not been shown to lower potassium. Click that UpToDate link or listen to Scott Weingart talk about it on EMRAP.
Patients with hyperK should be started on isotonic bicarbonate drips for 4-6hours, a treatment that works better in acidotic patients.

CHAPTER 5: Soooo who gets bicarb?
AMPS:

• Bicarb ampules in sodium channel blockade (like TCAs) are, as Dr. Bogoch said yesterday, the cornerstone of therapy

• Bicarb ampules may be appropriate to alkalinize urine in certain toxicities

• Seizing hyponatremic patients

DRIPS:

• Appropriate in hyperK patients who can handle fluid

• Appropriate in patients with AKI and pH < 7.2 (BICAR-ICU Trial)

• May be appropriate for pH < 7.0 or 7.1, depending on who you talk to...

**If the pH is < 7.1 and you wanna give an amp of bicarb, there isn't enough data to say you're wrong. If it's a last-ditch effort, you might as well.

https://www.uptodate.com/contents/bicarbonate-therapy-in-lactic-acidosis?search=sodium%20bicarbonate&source=search_result&selectedTitle=3~148&usage_type=default&display_rank=2

Other references embedded in text.

Benzodiazepines

Benzo dosing and pharmacology has always been confusing to me. Here are some tidbits and pearls that stick with me:

Our very own fabulous Dr. Reuben Strayer’s IV to IM conversion of commonly utilized benzodiazepines. As he notes as well, conversions are more of an art than a science.

PO conversion: 1 mg lorazepam = 10 mg diazepam = 25mg chlordiazepoxide (librium)

Short acting: midazolam, alprazolam/xanax

Medium acting: lorazepam, clonazepam/klonopin

Long acting: diazepam, librium  

IM midazolam, not IM lorazepam. Lorazepam’s intramuscular absorption is erratic/slower and it is longer acting than versed.  

Lorazepam is not a code white medication.  

10mg IM midazolam -> this patient goes to resus at least initially. This is an increasingly common dose for someone to receive by pre-hospital.  

Be wary of ETOH + benzos, these are extremely high risk patients.

The treatment of severe ETOH withdrawl/DT's requires probably an uncomfortable amount of benzos.