David Palacio Parra

cirujano ortopedista.

[Walter Suárez Carmona @a_fisiolog57853]

FRACTURA DE CADERA

¡¡¡A leer, zagales!!!

Link en mi bio

o

https://t.co/0gnKDL9oDi

[La Traumatóloga Geek @traumatogeek]

En la lesión de Koné se juntaron tres fuerzas a la vez:
peso cayendo desde arriba,
el pie clavado al césped
y un golpe lateral que convirtió la pierna en una palanca.

Y aquí viene lo importante:
el hueso no se rompe por donde recibe el golpe.
Se rompe por el lado contrario.

Ahora mismo hay un detalle de apenas un centímetro que puede decidirlo todo

#Kone #Mundial2026 #WorldCup2026 #Lesion #Traumatologia

[Afshine Emrani MD FACC @afshineemrani]

I'm a cardiologist. I prescribe cholesterol-lowering drugs every single day. They save lives. That science is settled and I will never tell you otherwise.
But I'm going to say something that will make a lot of my colleagues uncomfortable — because someone needs to say it, and your doctor probably won't.
Too many physicians make you feel crazy when you bring up statin side effects.
You walk into your appointment and say "my muscles ache constantly" — and you're told it's in your head. You say "I'm exhausted all the time" — and you're told it's your age. You say "my sex drive disappeared" — and you get an awkward silence followed by a subject change. You say "I don't feel like myself anymore" — and you're told the benefits outweigh the risks, take the pill, stop reading the internet.
I've watched it happen in my own field for twenty years. The conversation gets shut down. The patient gets dismissed. And then they do the one thing we should be most afraid of — they stop the medication entirely, without telling us, and lose the cardiovascular protection that's keeping them alive.
That is the real cost of not being honest. Not the side effects themselves — the silence that drives patients away from treatment.
In my practice, I see statin-related complications in at least 25% of my patients. Muscle pain. Fatigue that doesn't resolve with sleep. Reduced sexual drive. Brain fog. Cramping. Joint stiffness. Weakness that makes exercise — the very thing we tell them to do — feel impossible.
Some of these improve with CoQ10 supplementation and optimizing vitamin D. Many do not.
I wrote about the diabetes risk of statins in a New York Times op-ed in 2012. The backlash from the cardiology establishment was immediate. I was told I was undermining trust in a life-saving drug class. Fourteen years later, every major guideline acknowledges the risk I warned about. It's in the prescribing information. The physicians who attacked me for saying it now teach it to their residents.
The truth doesn't care about professional comfort. It never has.
Now a paper published this week in Science Advances has finally explained the mechanism behind statin myopathy — and the finding validates what millions of patients have been telling their doctors for years.
Researchers discovered that statins activate the NLRP3 inflammasome in muscle cells — triggering an inflammatory cascade that causes muscle cell death, activates atrophy pathways, and disrupts muscle metabolism. This is entirely independent of the drug's cholesterol-lowering effect.
The muscle damage isn't caused by lowering cholesterol. It's caused by a completely separate pharmacological action through a different pathway.
The critical implication: the side effect can potentially be separated from the benefit.
Blocking NLRP3 or restoring isoprenoids prevented muscle cell death without interfering with cholesterol reduction. Future therapies could preserve the cardiovascular protection while eliminating the muscle toxicity.
Even more striking — the researchers found that background systemic inflammation significantly lowered the statin dose needed to trigger muscle damage. Patients with chronic inflammation, gut dysbiosis, or metabolic syndrome may be experiencing myopathy at doses their doctors consider "too low to cause problems." They're not imagining it. Their inflammatory state is priming the pathway.
The muscle pain was never in their heads. It was in their NLRP3 inflammasome. And we finally have the molecular proof.
Here's what I actually do in my practice — because I refuse to choose between protecting the heart and respecting the patient.
Whenever possible, I avoid statins as my first-line approach for eligible patients by using alternatives that lower LDL through entirely different mechanisms with no muscle toxicity:
PCSK9 inhibitors — Repatha and Praluent. Injections every 2-4 weeks that dramatically lower LDL without touching muscle tissue. No myopathy. No fatigue. No brain fog. For patients who can access them, these are transformative.
Inclisiran — Leqvio. An siRNA injection I administer twice a year in my office. It silences the PCSK9 gene in the liver. Two shots a year. LDL drops roughly 50%. No muscle side effects. No daily pills. Now approved as first-line monotherapy. This is the future of lipid management and I use it aggressively.
When statins ARE clinically necessary — and sometimes they are, especially post-heart attack or in combination therapy — I choose hydrophilic statins like rosuvastatin or pravastatin. These do not easily cross the blood-brain barrier. The cognitive complaints — the fog, the memory issues, the feeling of "not being yourself" — are substantially less common with these formulations because the drug stays out of the central nervous system.
I never prescribe a statin without CoQ10. 100-300mg daily. Statins deplete the cellular energy molecule your muscles and heart depend on. Replenishing it reduces muscle symptoms in many patients. It should be standard practice. The fact that it isn't is a failure of our field.
I check vitamin D and optimize it aggressively. Low vitamin D — which is epidemic — worsens muscle symptoms independently and compounds whatever the statin is doing. Target 50-80 ng/mL, not the bare minimum of 30.
Bempedoic acid — Nexletol — for patients who can't tolerate any statin. Works upstream in the cholesterol pathway and is not active in muscle tissue. Specifically designed to avoid myopathy.
Ezetimibe added to a lower statin dose. Cut the statin intensity, add ezetimibe to maintain the LDL reduction, and halve the muscle exposure.
There is no excuse in 2026 for telling a patient "just deal with the muscle pain." The toolbox is deep. The alternatives exist. The only barrier is a physician's willingness to listen and adapt.
I want to speak directly to every patient who has been dismissed.
Your muscle pain is real. Your fatigue is real. Your cognitive changes are real. Your loss of drive — in every sense of the word — is real. A paper in Science Advances just proved the mechanism. You were never crazy. You were experiencing a documented inflammatory response in your muscle tissue that your doctor didn't have the science to explain — until this week.
And I want to speak directly to my colleagues.
We have to be honest. Not just about the benefits — which are enormous and undeniable — but about the side effects, the mechanism, and the alternatives. Patients who feel heard stay on treatment. Patients who feel dismissed stop their medications in silence — and die from the heart attacks we could have prevented if we'd simply been willing to have an honest conversation and switch the approach.
The cardiologist who tells you statins are flawless is not protecting you. The wellness influencer who tells you statins are poison is not protecting you either. The truth lives in the middle — where it always has.
Statins save lives. The side effects are real. The mechanism is now proven. The alternatives exist. And you deserve a doctor who holds all four of those truths at the same time.
Both things can be true. They always could.
Now we have the science to prove it.

[DiarioTES - Javier G. Rendo @DiarioTES]

Buenas tardes emergencistas!

Vamos a hablar de una entidad conocida, pero quizás poco entendida para algunos a nivel fisiopatológico.

Hablamos de la fractura de pélvis.

Al lío!

[Physio Meets Science @PhysioMeScience]

Neuroimmune interactions in arthritis: linking pain sensitisation and inflammation

https://t.co/9RW3AX01la

[Dr. Javier Flores @farmacotips]

SCIHUB ya NO FUNCIONA

Aquí tienes 7 alternativas para tener

ARTÍCULOS CIENTÍFICOS GRATIS.

[The Bone & Joint Journal @BoneJointJ]

Compared with conventional bone transport, the shortening and in situ relengthening technique may offer distinct advantages when addressing defects in the metaphyseal region.

#IlizarovTechnique #Bone #Surgery #BJJ

https://t.co/AMgkDQOIi2

[Dr.Marlon Villanueva™ 🩺 𝕏 @MarlonVFZR]

✅𝗣𝗿𝗼𝘁𝗼𝗰𝗼𝗹𝗼 𝗱𝗲 𝗮𝗻𝘁𝗶𝗯𝗶𝗼𝘁𝗶𝗰𝗼𝘁𝗲𝗿𝗮𝗽𝗶𝗮 𝗲𝗻 𝗹𝗮 𝗮𝗴𝘂𝗱𝗶𝘇𝗮𝗰𝗶𝗼́𝗻 𝗱𝗲 𝗹𝗮 𝗘𝗣𝗢𝗖 (𝗔𝗘𝗣𝗢𝗖)🫁
⬇️⬇️⬇️⬇️

🔹 𝗣𝗔𝗦𝗢 𝟭. ¿𝗘𝘀𝘁𝗮́ 𝗶𝗻𝗱𝗶𝗰𝗮𝗱𝗼 𝗮𝗻𝘁𝗶𝗯𝗶𝗼́𝘁𝗶𝗰𝗼?

👉 𝘾𝙧𝙞𝙩𝙚𝙧𝙞𝙤𝙨 𝙙𝙚 𝘼𝙣𝙩𝙝𝙤𝙣𝙞𝙨𝙚𝙣

Se evalúan 𝙩𝙧𝙚𝙨 𝙨𝙞́𝙣𝙩𝙤𝙢𝙖𝙨 𝙘𝙖𝙧𝙙𝙞𝙣𝙖𝙡𝙚𝙨:

1️⃣ 𝘼𝙪𝙢𝙚𝙣𝙩𝙤 𝙙𝙚 𝙡𝙖 𝙙𝙞𝙨𝙣𝙚𝙖
2️⃣ 𝘼𝙪𝙢𝙚𝙣𝙩𝙤 𝙙𝙚𝙡 𝙫𝙤𝙡𝙪𝙢𝙚𝙣 𝙙𝙚𝙡 𝙚𝙨𝙥𝙪𝙩𝙤
3️⃣ 𝘼𝙪𝙢𝙚𝙣𝙩𝙤 𝙙𝙚 𝙡𝙖 𝙥𝙪𝙧𝙪𝙡𝙚𝙣𝙘𝙞𝙖 𝙙𝙚𝙡 𝙚𝙨𝙥𝙪𝙩𝙤 (el más específico de infección bacteriana)

𝙀𝙨𝙩𝙧𝙖𝙩𝙞𝙛𝙞𝙘𝙖𝙘𝙞𝙤́𝙣:
•𝙏𝙞𝙥𝙤 𝙄 (𝙜𝙧𝙖𝙫𝙚): 3/3 criterios → ✅ Antibiótico obligatorio
•𝙏𝙞𝙥𝙤 𝙄𝙄 (𝙢𝙤𝙙𝙚𝙧𝙖𝙙𝙖): 2/3 criterios
•Si 𝙪𝙣𝙤 𝙚𝙨 𝙥𝙪𝙧𝙪𝙡𝙚𝙣𝙘𝙞𝙖 → ✅ 𝘼𝙣𝙩𝙞𝙗𝙞𝙤́𝙩𝙞𝙘𝙤 𝙞𝙣𝙙𝙞𝙘𝙖𝙙𝙤
•𝙏𝙞𝙥𝙤 𝙄𝙄𝙄 (𝙡𝙚𝙫𝙚): 1 criterio ± fiebre/tos/taquipnea → ❌ 𝙉𝙤 𝙖𝙣𝙩𝙞𝙗𝙞𝙤́𝙩𝙞𝙘𝙤 𝙙𝙚 𝙧𝙪𝙩𝙞𝙣𝙖

🔹 𝗣𝗔𝗦𝗢 𝟮. 𝗜𝗱𝗲𝗻𝘁𝗶𝗳𝗶𝗰𝗮𝗿 𝗲𝘀𝗰𝗲𝗻𝗮𝗿𝗶𝗼𝘀 𝗱𝗲 𝗮𝗹𝘁𝗼 𝗿𝗶𝗲𝘀𝗴𝗼

🚨 𝘼𝙀𝙋𝙊𝘾 𝙢𝙪𝙮 𝙜𝙧𝙖𝙫𝙚
•𝙁𝙀𝙑₁ ≤ 𝟯𝟬%
•Alto riesgo de gramnegativos y 𝙋𝙨𝙚𝙪𝙙𝙤𝙢𝙤𝙣𝙖𝙨 𝙖𝙚𝙧𝙪𝙜𝙞𝙣𝙤𝙨𝙖
•Tratar 𝙖𝙣𝙩𝙚 𝙘𝙪𝙖𝙡𝙦𝙪𝙞𝙚𝙧 𝙨𝙞𝙜𝙣𝙤 𝙙𝙚 𝙞𝙣𝙛𝙚𝙘𝙘𝙞𝙤́𝙣

🫁 𝘼𝙀𝙋𝙊𝘾 + 𝙣𝙚𝙪𝙢𝙤𝙣𝙞́𝙖
•Fiebre persistente
•Crepitantes
•Infiltrado radiológico
👉 Tratar como 𝙉𝘼𝘾, no como AEPOC simple
(S. pneumoniae como patógeno clave)

🔹 𝗣𝗔𝗦𝗢 𝟯. 𝗦𝗲𝗹𝗲𝗰𝗰𝗶𝗼́𝗻 𝗱𝗲𝗹 𝗮𝗻𝘁𝗶𝗯𝗶𝗼́𝘁𝗶𝗰𝗼

🟢 𝟭ª 𝙡𝙞́𝙣𝙚𝙖 – 𝘼𝙀𝙋𝙊𝘾 𝙨𝙞𝙢𝙥𝙡𝙚, 𝙨𝙞𝙣 𝙛𝙖𝙘𝙩𝙤𝙧𝙚𝙨 𝙙𝙚 𝙧𝙞𝙚𝙨𝙜𝙤
•𝘼𝙢𝙤𝙭𝙞𝙘𝙞𝙡𝙞𝙣𝙖/𝘼́𝙘𝙞𝙙𝙤 𝙘𝙡𝙖𝙫𝙪𝙡𝙖́𝙣𝙞𝙘𝙤
•875/125 mg c/8 h o
•2000/125 mg c/12 h
•Duración: 𝟱–𝟳 𝙙𝙞́𝙖𝙨

Cobertura adecuada para:
•𝘏. 𝘪𝘯𝘧𝘭𝘶𝘦𝘯𝘻𝘢𝘦
•𝘚. 𝘱𝘯𝘦𝘶𝘮𝘰𝘯𝘪𝘢𝘦
•𝘔. 𝘤𝘢𝘵𝘢𝘳𝘳𝘩𝘢𝘭𝘪𝘴

🟠 𝟮ª 𝙡𝙞́𝙣𝙚𝙖 – 𝙁𝙖𝙡𝙡𝙤 𝙥𝙧𝙚𝙫𝙞𝙤 𝙤 𝙛𝙖𝙘𝙩𝙤𝙧𝙚𝙨 𝙙𝙚 𝙧𝙞𝙚𝙨𝙜𝙤

(FEV₁ < 50%, edad > 65 años)
•𝙇𝙚𝙫𝙤𝙛𝙡𝙤𝙭𝙖𝙘𝙞𝙣𝙤 𝟱𝟬𝟬 𝙢𝙜/𝙙𝙞́𝙖
•𝙈𝙤𝙭𝙞𝙛𝙡𝙤𝙭𝙖𝙘𝙞𝙣𝙤 𝟰𝟬𝟬 𝙢𝙜/𝙙𝙞́𝙖
⏱️ 5–7 días

📌 Mayor espectro, usar con criterio (QT, C. difficile).

🔴 𝟯ª 𝙡𝙞́𝙣𝙚𝙖 – 𝙍𝙞𝙚𝙨𝙜𝙤 𝙙𝙚 𝙋𝙨𝙚𝙪𝙙𝙤𝙢𝙤𝙣𝙖𝙨

(FEV₁ ≤ 30%, bronquiectasias, aislamientos previos)
•𝘾𝙞𝙥𝙧𝙤𝙛𝙡𝙤𝙭𝙖𝙘𝙞𝙣𝙤 𝟱𝟬𝟬–𝟳𝟱𝟬 𝙢𝙜 𝙘/𝟭𝟮 𝙝
•Duración: 𝟳–𝟭𝟬 𝙙𝙞́𝙖𝙨

⚠️ Indicado 𝙨𝙤𝙡𝙤 𝙨𝙞 𝙝𝙖𝙮 𝙧𝙞𝙚𝙨𝙜𝙤 𝙧𝙚𝙖𝙡 𝙤 𝙖𝙞𝙨𝙡𝙖𝙢𝙞𝙚𝙣𝙩𝙤 𝙥𝙧𝙚𝙫𝙞𝙤.

🔹 𝗣𝗔𝗦𝗢 𝟰. 𝗔𝗹𝘁𝗲𝗿𝗻𝗮𝘁𝗶𝘃𝗮𝘀 𝗲𝗻 𝗰𝗮𝘀𝗼 𝗱𝗲 𝗮𝗹𝗲𝗿𝗴𝗶𝗮

🟡 𝘼𝙡𝙚𝙧𝙜𝙞𝙖 𝙡𝙚𝙫𝙚 𝙖 𝙗𝙚𝙩𝙖𝙡𝙖𝙘𝙩𝙖́𝙢𝙞𝙘𝙤𝙨 (𝙣𝙤 𝙖𝙣𝙖𝙛𝙞𝙡𝙖𝙭𝙞𝙖)
•𝘾𝙚𝙛𝙙𝙞𝙩𝙤𝙧𝙚𝙣𝙤 𝟮𝟬𝟬–𝟰𝟬𝟬 𝙢𝙜 𝙘/𝟭𝟮 𝙝

🔴 𝘼𝙡𝙚𝙧𝙜𝙞𝙖 𝙜𝙧𝙖𝙫𝙚 (𝙖𝙣𝙖𝙛𝙞𝙡𝙖𝙭𝙞𝙖)
•𝙇𝙚𝙫𝙤𝙛𝙡𝙤𝙭𝙖𝙘𝙞𝙣𝙤 𝙤 𝙢𝙤𝙭𝙞𝙛𝙡𝙤𝙭𝙖𝙘𝙞𝙣𝙤
•𝘼𝙯𝙞𝙩𝙧𝙤𝙢𝙞𝙘𝙞𝙣𝙖 (𝟯 𝙙𝙞́𝙖𝙨)
•𝘿𝙤𝙭𝙞𝙘𝙞𝙘𝙡𝙞𝙣𝙖

🔹 𝗣𝗔𝗦𝗢 𝟱. 𝗠𝗼𝗻𝗶𝘁𝗼𝗿𝗶𝘇𝗮𝗰𝗶𝗼́𝗻 𝘆 𝗱𝗲𝗿𝗶𝘃𝗮𝗰𝗶𝗼́𝗻

📈 𝙍𝙚𝙚𝙫𝙖𝙡𝙪𝙖𝙧 𝙖 𝙡𝙖𝙨 𝟰𝟴–𝟳𝟮 𝙝
•Mejoría clínica esperada: disnea, esputo, fiebre

🏥 𝘾𝙧𝙞𝙩𝙚𝙧𝙞𝙤𝙨 𝙙𝙚 𝙙𝙚𝙧𝙞𝙫𝙖𝙘𝙞𝙤́𝙣 𝙝𝙤𝙨𝙥𝙞𝙩𝙖𝙡𝙖𝙧𝙞𝙖
•Empeoramiento clínico
•Fiebre persistente
•Insuficiencia respiratoria
•Necesidad de 𝙑𝙉𝙄, 𝙑𝙈𝙄 𝙤 𝙖𝙣𝙩𝙞𝙗𝙞𝙤́𝙩𝙞𝙘𝙤 𝙄𝙑

🧠 𝗠𝗘𝗡𝗦𝗔𝗝𝗘𝗦 𝗖𝗟𝗔𝗩𝗘

✔️ No toda AEPOC requiere antibiótico
✔️ 𝙀𝙫𝙖𝙡𝙪𝙖𝙧 𝙋𝙪𝙧𝙪𝙡𝙚𝙣𝙘𝙞𝙖
✔️ Ajustar antibiótico al 𝙧𝙞𝙚𝙨𝙜𝙤 𝙢𝙞𝙘𝙧𝙤𝙗𝙞𝙤𝙡𝙤́𝙜𝙞𝙘𝙤, no por inercia
✔️ Duraciones cortas (5–7 días) son suficientes en la mayoría
✔️ Uso prudente de fluoroquinolonas

👇🏼👇🏼👇🏼👇🏼
📚📖#ClubCrit

#EPOC #AEPOC #MedTwitter #CritCare #UCI #ICU #CriticalCare #Diagnóstico #icu #intensivecare #MedTwitter #diagnosis #management #Riesgo #ICU #POCUS #UCI #Tratamiento #MedicinaBasadaEnEvidencia #Emergencia #Terapia #MedEd #Medicina #Emergencias #FOAMed #FOAMcc #MedTwitter #CriticalCare #MedEd #CuidadoCrítico #MedX #IntensiveCare #EducaciónMédica #MedIntensiva #MedXCommunity #MedicinaCrítica #MedED #CritCare #ICUManagement #MustRead #LecturaRecomendada

[MEDICINE MADNESS @Doctors_GUILD]

In which of the following nerve injuries is the instrument shown below used?

A). Radial nerve
B). Median nerve
C). Ulnar nerve
D). Volkmann's ischemic contracture

[Mo Imam @MoAImam]

Shoulder anatomy and injuries

[David Palacio Parra @DPalacioParra]

Músculos del cuerpo humano

[David Palacio Parra @DPalacioParra]

Osteotomia valguizante subtrocanterica en coxa vara congénita

[David Palacio Parra @DPalacioParra]

Coxa valga subluxada. Osteotomia varizante y desrotadora

[David Palacio Parra @DPalacioParra]

Genus valgo pos traumático. Osteotomia varizante supracondilea

[David Palacio Parra @DPalacioParra]

LDC infante 18 m. Se realizo reducción y osteotomia femoral desrotadora

[David Palacio Parra @DPalacioParra]

Braqumetapodia en niña de 11 años

[David Palacio Parra @DPalacioParra]

Genus valgo y Enfermedad de Morquio

[David Palacio Parra @DPalacioParra]

Escafoides accesorios TIPO II