PNBschool

03/01/2026

Stop stacking opioids. (I am not anti opioid)
Start targeting mechanisms.

Pain is not one pathway — it’s peripheral inflammation, central sensitization, NMDA activation, and afferent transmission. If you treat it with one drug, you’re leaving physiology untouched.

Multimodal analgesia works because the mechanisms differ — not because drugs accumulate.

• NSAIDs ↓ prostaglandins
• Acetaminophen modulates central pathways
• Ketamine / magnesium blunt NMDA wind-up
• Regional anesthesia blocks transmission at the source
• Opioids are powerful — but side-effect limited

The goal isn’t “more medication.”
It’s smarter mechanism coverage.

Start before incision. Combine non-redundant agents. Use regional when appropriate.

What’s your go-to multimodal stack for major ortho or abdominal cases?

02/28/2026

Methadone - not “just another opioid.”

It’s a full μ-agonist + NMDA antagonist with serotonin/norepinephrine reuptake inhibition — which means:
• Potent, long-acting analgesia
• Reduced central sensitization
• Less postoperative opioid requirement
• Potential attenuation of opioid-induced hyperalgesia

A single dose after induction (commonly 10–20 mg IV in appropriate patients) can meaningfully shape the entire postoperative pain trajectory.

But this is not a casual drug:
• Long and variable half-life (24–36+ hrs)
• Delayed respiratory depression risk
• QTc prolongation — know your baseline
• Caution in hepatic dysfunction and severe OSA

Used intentionally, methadone can be a powerful ERAS tool — especially in spine, thoracic, and opioid-tolerant patients.

Do you use intraoperative methadone routinely, selectively, or not at all?

02/28/2026

How many times have you battled a patient on Lisinopril?

Essential hypertension is the most common coexisting disease we manage in the OR.

Most of the time, it’s “controlled”… until induction.

What matters intraoperatively isn’t the diagnosis — it’s the variability.

Chronic hypertension shifts autoregulation curves rightward. That means:
• These patients tolerate hypotension poorly
• Cerebral and myocardial perfusion may fall at “normal” pressures
• Repeated MAP drops below their baseline matter

Positioning also changes the equation:
• Beach chair → reduced cerebral perfusion pressure
• Prone → venous congestion + ocular perfusion concerns
• Reverse Trendelenburg → preload reduction

Prolonged hypotension has been associated with:
• Myocardial injury
• Acute kidney injury
• Postoperative stroke
• And yes — perioperative visual loss in high-risk settings

The goal isn’t perfection.
It’s preventing large, repeated swings.

Maintain MAP within ~20% of baseline when feasible.
Treat trends, not isolated numbers.

Educational content for anesthesia professionals. Practice varies.

Ref: ACC/AHA Hypertension Guideline 2017; Walsh et al. Anesthesiology 2013.

02/28/2026

The PENG block is targeted analgesia for the anterior hip capsule — not a complete hip block, not perfect.

Alone, it does not reliably cover the femoral nerve, vastus musculature, or the full anterior thigh. Expect partial anterior hip analgesia — not comprehensive surgical anesthesia.

Where it shines: combine it.

PENG + LFCN + multimodal analgesia (acetaminophen, NSAIDs if appropriate, regional optimization) can significantly reduce perioperative opioid requirements while preserving motor function. That layered approach changes outcomes more than PENG alone.

The question is DO YOU ADD THE LFCN to your PENG Blocks for total hips? Need a little help? Stay tuned….

Source: Short AJ et al. Reg Anesth Pain Med. 2021;46(3):376-382. Nilsson K et al. Reg Anesth Pain Med. 2022;47(1):61-68.

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02/27/2026

Nitrous oxide is one of the oldest agents we still use — and it remains very clinically relevant.

Key reminders for practice:

• MAC ~105% → weak anesthetic, but useful adjunct
• Provides mild analgesia and sedation
• Minimal myocardial depression compared to volatile agents

But physiology matters.

Diffusion hypoxia is real — wash out with 100% O₂ at emergence.
Avoid in pneumothorax or air-filled spaces (middle ear, bowel obstruction, intracranial air).
Be mindful of B₁₂ inactivation and bone marrow suppression with prolonged or repeated exposure.

I have an admission…I love nitrous. I use it as much as I possible can. I think of it this way. If we don’t use nitrous we will use more Sevo or Fentanyl or Propofol. I always use it at 50%. My patients don’t get sick. I really don’t see the downside.

How often are you still using N₂O in your practice — routinely, rarely, or never?

02/26/2026

The Pericapsular Nerve Group (PENG) block targets the articular branches of the femoral nerve, obturator nerve, and accessory obturator nerve along the superior p***c ramus — providing focused anterior hip capsule analgesia.

High-yield uses:
• Hip fractures
• Total hip arthroplasty
• Hip dislocation reduction
• Severe preop hip pain limiting positioning

Why it matters:
• Opioid-sparing
• Preserves quadriceps strength (when done correctly)
• Improves positioning for spinal
• Clean ultrasound landmarks

Key technical point:
Needle to the iliop***c eminence. Confirm spread deep to psoas tendon along the p***c ramus — not intramuscular.

Pro tip: combine with the LFCN Block for total hip arthroplasty.

Save this. Share with someone who still defaults to femoral for every hip.

02/25/2026

OSA

Watch, follow, and discover more trending content.

02/25/2026

Ketamine isn’t just an induction drug — at subanesthetic doses, it’s one of the most useful tools in your multimodal toolbox.

Small doses matter.

• 0.15–0.3 mg/kg at induction can blunt early nociceptive input
• 0.1–0.25 mg/kg bolus provides meaningful analgesia
• 2–5 mcg/kg/min intraop can reduce opioid requirements
• 1–2 mcg/kg/min postop may extend benefit without excessive psychomimetic effects

The goal isn’t dissociation — it’s NMDA modulation and prevention of central sensitization.

When used thoughtfully, lower-dose ketamine can:
✔ Reduce opioid consumption
✔ Improve pain control in opioid-tolerant patients
✔ Support ERAS pathways
✔ Provide analgesia without respiratory depression

The mistake? Confusing analgesic dosing with induction dosing.

Used correctly, small doses are often where the real value is.

How are you incorporating low-dose ketamine into your multimodal strategy?

02/24/2026

12 seconds. One image. Real anatomy.

Use rapid self-testing like this to train pattern recognition —

Repeat daily.
Builds anatomy recognition.
Recognition builds confidence.

This is how you get more consistent — not just smarter on paper. After each block ask, why didn’t I see “that”. Improve a little each time.

02/24/2026

Ever have a case where the vitals are all over the place — tachycardia, hypertension, hyperthermia, diaphoresis — and you can’t quite explain why?

Before you chase… think serotonin syndrome.

In anesthesia, we often trigger it unintentionally when a patient is already loaded with serotonergic medications.

🔎 Most common outpatient culprits:
• SSRIs (sertraline, fluoxetine, escitalopram)
• SNRIs (venlafaxine, duloxetine)
• MAOIs
• Bupropion (less serotonergic but often co-prescribed)
• Trazodone
• Linezolid
• Triptans
• St. John’s Wort

💉 Intraoperative triggers we add:
• Meperidine
• Tramadol
• Fentanyl (rare but reported, especially in polypharmacy)
• Methylene blue

The pattern that should make you pause:
👉 Rapid onset
👉 Hyperreflexia + clonus
👉 Autonomic instability
👉 No clear anesthetic explanation

This is a clinical diagnosis. Dantrolene is not standard therapy. Benzodiazepines and supportive care are first-line.

Polypharmacy is common. We probabaly experience some form of serotonin syndrome more often than we realize.

Have you ever had a labile intraop case that, in hindsight, may have been serotonergic toxicity? Let’s talk about it.

02/23/2026

Haters are gonna hate. We all get to pick our path. Just because we make our job look really easy doesn’t mean we should be judged.

They can “Hey anesthesia” me all they want as long as I have my comfy chair.

Just now this, if I’m on my feet everyone better be on high alert. Something is going down. Either that or I’m about to get relieved and I only know that because I’ve been studying the schedule…..while sitting in my chair.

Bring the comments.

02/23/2026

Tranexamic acid (TXA) has become a cornerstone of modern perioperative blood management.

As an antifibrinolytic, TXA competitively inhibits plasminogen activation, stabilizing clot formation and reducing surgical blood loss. Robust data across trauma, cardiac, orthopedic, and obstetric populations demonstrate reductions in transfusion requirements when administered appropriately and early.

Key considerations:
• Timing matters — ideally prior to incision or at the earliest sign of bleeding
• Typical dosing: 10–20 mg/kg IV loading dose ± infusion (procedure-dependent)
• Re-dose in prolonged cases when clinically indicated
• Use caution in patients with recent thromboembolic events, seizure history, or significant renal impairment

In total joint arthroplasty, it’s almost become part of the “unofficial ortho ACLS protocol” — TXA, Ancef, and bone cement.😂😂😂😂

TXA’s benefit is timing and patient selection, not routine reflex. Evidence supports its safety profile when used appropriately, but as always, practice should align with institutional protocols and current guidelines.

How are you dosing TXA in your joint cases — bolus only or bolus + infusion or topical only?