Oliver Vasconcelos

La unidad es la variedad, y la variedad en la unidad es la ley suprema del universo. 💡

[NEJM @NEJM]

A 61-year-old man with prolonged neutropenia after chemotherapy for AML was evaluated for persistent fever despite antimicrobial therapy. Physical examination was notable for a skin macule with central necrosis on the chest.

Read the full case details in the Images in Clinical Medicine article “Disseminated Fusariosis”: https://t.co/zjZ0oMCrHN

[NEJM @NEJM]

Leishmaniasis is a parasitic infection that is transmitted by sand flies and caused by multiple leishmania species, with different species capable of causing cutaneous, visceral, or mucosal forms of the disease. 👉 https://t.co/ezm9gi6ZM8

Cutaneous leishmaniasis usually manifests as slowly progressing nodules that can evolve to painless ulcers at the site of the sand-fly bite. Lesions can heal spontaneously or be treated with local cryotherapy or thermotherapy (such as a “hot metal”), topical agents, or systemic therapy. In either case, they usually leave a residual scar. Cases can occur among family members who share the same environment and exposures.

Certain species of leishmania can persist in a latent state after apparent resolution of cutaneous disease and can later lead to mucosal leishmaniasis. This manifestation is most commonly associated with, although not exclusive to, 𝘓𝘦𝘪𝘴𝘩𝘮𝘢𝘯𝘪𝘢 𝘣𝘳𝘢𝘻𝘪𝘭𝘪𝘦𝘯𝘴𝘪𝘴 and other members of the viannia subgenus, which are endemic in parts of Latin America, particularly Bolivia, Brazil, and Peru (seen in figure). Because local therapies may not completely eradicate the parasite, systemic treatment is recommended for known or suspected cutaneous infections with these species in order to reduce the risk of subsequent mucosal disease. Mucosal leishmaniasis may occur concurrently or emerge months to decades after inadequately treated cutaneous infection.

Learn more in “A 37-Year-Old Woman with Persistent Nasal Ulceration,” a Case Record of the Massachusetts General Hospital (@MassGeneralNews), by Stacey T. Gray, MD, Carolina D. Geadas, MD, and Peter M. Sadow, MD, PhD: https://t.co/ezm9gi6ZM8

[NEJM @NEJM]

𝗜𝗺𝗺𝘂𝗻𝗼𝗽𝗮𝘁𝗵𝗼𝗴𝗲𝗻𝗲𝘀𝗶𝘀 𝗼𝗳 𝗛𝗲𝗽𝗮𝗿𝗶𝗻-𝗜𝗻𝗱𝘂𝗰𝗲𝗱 𝗧𝗵𝗿𝗼𝗺𝗯𝗼𝗰𝘆𝘁𝗼𝗽𝗲𝗻𝗶𝗮 (𝗛𝗜𝗧)

The pathogenesis of HIT is summarized in the figure. Platelet factor 4 (PF4) undergoes conformational changes when binding to polyanions, thereby expressing neoantigens. The rapid formation (approximately 5 days after an immunizing heparin exposure) of anti–PF4–heparin antibodies of IgG class to these neoantigens — even in a patient who has never previously received heparin — suggests presensitization, perhaps through exposure to PF4 bound to polyanions on bacteria. Many healthy persons have natural, polyreactive IgM antibodies that recognize PF4–heparin complexes and bind complement factor C3. The PF4–heparin–natural IgM–C3 complexes bind to nearly all B cells at their complement receptors. This action stimulates preexisting B cells bearing the cognate anti–PF4–polyanion receptor, which results in production of anti–PF4–polyanion antibodies of IgG, IgA, and IgM classes, in various combinations, but only a subset of IgG anti-PF4 antibodies induce the platelet activation that is responsible for development of clinically evident thrombocytopenia and thrombosis (iceberg model). Some of these pathogenic HIT antibodies are monoclonal.

Learn more about HIT and other anti–platelet factor 4 disorders in the Review Article “Platelet-Activating Anti–Platelet Factor 4 Disorders” by Theodore E. Warkentin, MD, and Andreas Greinacher, MD: https://t.co/5mnvrPal1Z

[Aravind Palraj @Rheumat_Aravind]

A special milestone for me.

I’m deeply grateful to Dr. John Cush (@RheumNow) for the opportunity to contribute to RheumNow. He invited me to create two educational infographics on gout, and seeing one of them published on RheumNow and shared on his X account is truly an honour.

Thank you, Dr. Cush, for your trust, encouragement, and support. Looking forward to contributing more to rheumatology education.

#Rheumatology #Gout #MedEd #FOAMed #MedicalEducation

[Internal Medicine @pgMedicine]

Amiodarone Side Effects You Should Know

[Aravind Palraj @Rheumat_Aravind]

Erythema Nodosum:
#MedTwitter @IhabFathiSulima @docakx

[Dr.Marlon Villanueva™ 🩺 𝕏 @MarlonVFZR]

🫁⚙️𝗩𝗲𝗻𝘁𝗶𝗹𝗮𝗰𝗶𝗼́𝗻 𝗺𝗲𝗰𝗮́𝗻𝗶𝗰𝗮 𝗲𝗻 𝗽𝗮𝗰𝗶𝗲𝗻𝘁𝗲 𝗰𝗼𝗻 𝗼𝗯𝗲𝘀𝗶𝗱𝗮𝗱🚨
@SpringerNature
👇🏼👇🏼👇🏼👇🏼
📑🔗🔑🔓
https://t.co/89ht2mBRSA
⬇️⬇️⬇️⬇️
🧵👇

La obesidad cambia de forma profunda la fisiología respiratoria en UCI.
📌 ↑ presión pleural
📌 ↓ capacidad residual funcional
📌 ↑ cierre de vía aérea y atelectasias
📌 ↑ riesgo de hipoxemia, hipercapnia y VILI
El exceso de tejido adiposo aumenta la elastancia de pared torácica y reduce los volúmenes pulmonares.

🧠 𝙇𝙖 𝙧𝙚𝙜𝙡𝙖 𝙢𝙖́𝙨 𝙞𝙢𝙥𝙤𝙧𝙩𝙖𝙣𝙩𝙚: 𝙚𝙡 𝙫𝙤𝙡𝙪𝙢𝙚𝙣 𝙘𝙤𝙧𝙧𝙞𝙚𝙣𝙩𝙚 𝙉𝙊 𝙨𝙚 𝙘𝙖𝙡𝙘𝙪𝙡𝙖 𝙘𝙤𝙣 𝙥𝙚𝙨𝙤 𝙧𝙚𝙖𝙡
✅ el VT 𝙙𝙚𝙗𝙚 𝙞𝙣𝙙𝙚𝙭𝙖𝙧𝙨𝙚 𝙖 𝙥𝙚𝙨𝙤 𝙘𝙤𝙧𝙥𝙤𝙧𝙖𝙡 𝙥𝙧𝙚𝙙𝙞𝙘𝙝𝙤 (𝙋𝘽𝙒)
✅ objetivo habitual: 𝟲–𝟴 𝙢𝙇/𝙠𝙜 𝙋𝘽𝙒
porque el tamaño pulmonar no aumenta proporcionalmente con el peso corporal real.
👉 Usar el peso real en estos pacientes puede llevar a sobredistensión y más riesgo de lesión pulmonar inducida por ventilador.

🌬️ 𝙋𝙀𝙀𝙋: 𝙥𝙧𝙤𝙗𝙖𝙗𝙡𝙚𝙢𝙚𝙣𝙩𝙚 𝙨𝙚 𝙣𝙚𝙘𝙚𝙨𝙞𝙩𝙖 𝙢𝙖́𝙨, 𝙥𝙚𝙧𝙤 𝙣𝙤 “𝙢𝙖́𝙨 𝙥𝙤𝙧 𝙧𝙪𝙩𝙞𝙣𝙖”
En obesidad, la combinación de:
📉 FRC baja
📈 presión pleural alta
📉 presión transpulmonar al final de la espiración
favorece colapso alveolar.
Por eso, estos pacientes muchas veces requieren 𝙋𝙀𝙀𝙋 𝙢𝙖́𝙨 𝙖𝙡𝙩𝙖 𝙚 𝙞𝙣𝙙𝙞𝙫𝙞𝙙𝙪𝙖𝙡𝙞𝙯𝙖𝙙𝙖 para prevenir cierre de vía aérea y atelectasia.
El mejor enfoque es personalizarla con herramientas como:
🔹 presión esofágica
🔹 EIT
🔹 driving pressure
más que aplicar una PEEP fija para todos.

⚠️ !𝘾𝙪𝙞𝙙𝙖𝙙𝙤 𝙖𝙡 𝙞𝙣𝙩𝙚𝙧𝙥𝙧𝙚𝙩𝙖𝙧 𝙡𝙖𝙨 𝙥𝙧𝙚𝙨𝙞𝙤𝙣𝙚𝙨! 𝙀𝙣 𝙥𝙖𝙘𝙞𝙚𝙣𝙩𝙚𝙨 𝙘𝙤𝙣 𝙤𝙗𝙚𝙨𝙞𝙙𝙖𝙙, 𝙡𝙖 𝙫𝙞́𝙖 𝙖𝙚́𝙧𝙚𝙖 𝙥𝙪𝙚𝙙𝙚 𝙨𝙚𝙧 𝙢𝙖́𝙨 “𝙖𝙥𝙧𝙚𝙩𝙖𝙙𝙖” 𝙦𝙪𝙚 𝙚𝙡 𝙥𝙪𝙡𝙢𝙤́𝙣.
𝙋𝙡𝙖𝙩𝙚𝙖𝙪 𝙥𝙧𝙚𝙨𝙨𝙪𝙧𝙚 y 𝙙𝙧𝙞𝙫𝙞𝙣𝙜 𝙥𝙧𝙚𝙨𝙨𝙪𝙧𝙚 siguen siendo útiles, pero deben leerse con cautela.
👉 En obesidad, la mayor elastancia de pared torácica puede elevar las presiones de vía aérea 𝙨𝙞𝙣 𝙦𝙪𝙚 𝙚𝙨𝙤 𝙨𝙞𝙜𝙣𝙞𝙛𝙞𝙦𝙪𝙚 𝙣𝙚𝙘𝙚𝙨𝙖𝙧𝙞𝙖𝙢𝙚𝙣𝙩𝙚 𝙨𝙤𝙗𝙧𝙚𝙙𝙞𝙨𝙩𝙚𝙣𝙨𝙞𝙤́𝙣 𝙥𝙪𝙡𝙢𝙤𝙣𝙖𝙧𝙣̃.
La presión de vía aérea refleja tanto pulmón como pared torácica, por lo que la 𝙥𝙧𝙚𝙨𝙞𝙤́𝙣 𝙩𝙧𝙖𝙣𝙨𝙥𝙪𝙡𝙢𝙤𝙣𝙖𝙧 puede ser más informativa en casos seleccionados.

🫁 𝙄𝙣𝙩𝙪𝙗𝙖𝙘𝙞𝙤́𝙣 𝙮 𝙚𝙭𝙩𝙪𝙗𝙖𝙘𝙞𝙤́𝙣 𝙩𝙖𝙢𝙗𝙞𝙚́𝙣 𝙧𝙚𝙦𝙪𝙞𝙚𝙧𝙚𝙣 𝙚𝙨𝙩𝙧𝙖𝙩𝙚𝙜𝙞𝙖 𝙚𝙨𝙥𝙚𝙘𝙞́𝙛𝙞𝙘𝙖
Antes de intubar:
✅ posición 𝙧𝙖𝙢𝙥𝙚𝙙 𝙤 𝙘𝙖𝙗𝙚𝙘𝙚𝙧𝙖 𝙚𝙡𝙚𝙫𝙖𝙙𝙖
✅ preferir 𝙥𝙧𝙚𝙤𝙭𝙞𝙜𝙚𝙣𝙖𝙘𝙞𝙤́𝙣 𝙘𝙤𝙣 𝙥𝙧𝙚𝙨𝙞𝙤́𝙣 𝙥𝙤𝙨𝙞𝙩𝙞𝙫𝙖
✅ 𝙫𝙞𝙙𝙚𝙤𝙡𝙖𝙧𝙞𝙣𝙜𝙤𝙨𝙘𝙤𝙥𝙞𝙤 como primera línea
El beneficio absoluto de la preoxigenación con presión positiva aumenta conforme sube el IMC.
Después, en la liberación:
📌 el trabajo respiratorio postextubación puede ser alto
📌 la 𝙉𝙄𝙑 𝙥𝙧𝙤𝙛𝙞𝙡𝙖́𝙘𝙩𝙞𝙘𝙖 tras extubación puede reducir reintubación en pacientes seleccionados con obesidad, especialmente si se aplica durante suficiente tiempo.

🎯 𝙏𝙖𝙠𝙚-𝙝𝙤𝙢𝙚: 𝙚𝙣 𝙚𝙡 𝙥𝙖𝙘𝙞𝙚𝙣𝙩𝙚 𝙘𝙧𝙞́𝙩𝙞𝙘𝙤 𝙘𝙤𝙣 𝙤𝙗𝙚𝙨𝙞𝙙𝙖𝙙, 𝙡𝙖 𝙫𝙚𝙣𝙩𝙞𝙡𝙖𝙘𝙞𝙤́𝙣 𝙙𝙚𝙗𝙚 𝙨𝙚𝙧 𝙥𝙧𝙤𝙩𝙚𝙘𝙩𝙤𝙧𝙖, 𝙧𝙚𝙘𝙡𝙪𝙩𝙖𝙙𝙤𝙧𝙖 𝙚 𝙞𝙣𝙙𝙞𝙫𝙞𝙙𝙪𝙖𝙡𝙞𝙯𝙖𝙙𝙖
Enfoque escalonado muy útil:
1️⃣ optimizar preintubación
2️⃣ VT 𝟲–𝟴 𝙢𝙇/𝙠𝙜 𝙋𝘽𝙒
3️⃣ PEEP individualizada
4️⃣ interpretar presiones con fisiología de pared torácica
5️⃣ considerar 𝙥𝙧𝙤𝙣𝙤 y 𝙀𝘾𝙈𝙊 si corresponde
6️⃣ planear bien la extubación y soporte postextubación

🔥 Mensaje final: en obesidad, el error clásico es tratar las presiones de vía aérea como si reflejaran solo pulmón y usar volúmenes guiados por peso real; el enfoque correcto es 𝙥𝙚𝙣𝙨𝙖𝙧 𝙚𝙣 𝙥𝙧𝙚𝙨𝙞𝙤́𝙣 𝙥𝙡𝙚𝙪𝙧𝙖𝙡, 𝙥𝙧𝙚𝙨𝙞𝙤́𝙣 𝙩𝙧𝙖𝙣𝙨𝙥𝙪𝙡𝙢𝙤𝙣𝙖𝙧, 𝙧𝙚𝙘𝙡𝙪𝙩𝙖𝙢𝙞𝙚𝙣𝙩𝙤 𝙮 𝙋𝘽𝙒.

‼️Si te sirve: ❤️ Me gusta | 🔁 Repost | ➕ Follow para más👇🏼👇🏼👇🏼👇🏼
📚📖#ClubCrit👨🏻‍⚕️👨🏻‍🏫🧠🫶

📚📖 Más en 𝕏 @MarlonVFZR y en el blog 👉 [https://t.co/zr4n2uQVCK]

#MechanicalVentilator #UCI #FOAMed #FOAMcc #CriticalCare #CriticalCare #CuidadoCrítico #MedTwitter #CritCare #icu #intensivecare #diagnosis #management #MedicinaBasadaEnEvidencia #MedEd #MedX #IntensiveCare #MedIntensiva #MedXCommunity #MedED #ICUmanagement #MustRead #LecturaRecomendada

[Aravind Palraj @Rheumat_Aravind]

The greatest challenge in Rheumatology isn’t recognizing disease. It’s recognizing when a disease is pretending to be something else.

SLE, vasculitis, sarcoidosis, IgG4-related disease, Adult-onset Still’s disease, and antiphospholipid syndrome can present across multiple organ systems and mimic infection, malignancy, neurological disorders, endocrine disease, and many other conditions.

🩺 Clinical Pearl:
When a patient has unexplained multisystem involvement, constitutional symptoms, elevated inflammatory markers, or unusual combinations of organ manifestations, think beyond the obvious diagnosis.

The diagnosis often lies in connecting seemingly unrelated clinical clues.

Which rheumatologic masquerader has fooled you the most in clinical practice?

#Rheumatology #ClinicalImmunology #AutoimmuneDisease #Vasculitis #SLE @IhabFathiSulima

[Internal Medicine @pgMedicine]

Renal Tubular Acidosis (RTA): Approach to NAGMA

[Aravind Palraj @Rheumat_Aravind]

VASCULITIS MIMICS

Not every purpura is vasculitis.

Before labeling a patient as having primary vasculitis and initiating immunosuppression, consider important mimics such as infective endocarditis, cholesterol embolization syndrome, antiphospholipid syndrome, thrombotic microangiopathy, calciphylaxis, atrial myxoma, fibromuscular dysplasia, levamisole-associated vasculopathy, septic emboli, and malignancy-associated vasculitis-like syndromes.

Recognizing the red flags can prevent diagnostic errors, unnecessary immunosuppression, and potentially life-threatening consequences.

Which vasculitis mimic have you found most challenging in clinical practice?

Infographic by Dr. Aravind Palraj

#Rheumatology #Vasculitis #ANCA #MedicalEducation #MedEd #FOAMed #InternalMedicine #Nephrology #ClinicalReasoning @IhabFathiSulima @docakx #AutoimmuneDisease #MedTwitter #RheumTwitter #MedX #Medicine #MedEdCommunity

[Internal Medicine @pgMedicine]

Approach to Disseminated Intravascular Coagulation

[Internal Medicine @pgMedicine]

A guide to differentiating osteoporosis, osteomalacia, Paget disease, myeloma, metastasis, parathyroid disorders and CKD using routine biochemical markers.

[Internal Medicine @pgMedicine]

Patterns of Motor Weakness by
Anatomical Site of Lesion

[Aravind Palraj @Rheumat_Aravind]

🧪 RF vs Anti-CCP

🚨 Positive RF ≠ RA

🚨 Anti-CCP is more specific than RF

🚨 Anti-CCP may precede clinical RA

🚨 RF + Anti-CCP positivity predicts more erosive disease

🚬 Smoking is strongly linked to Anti-CCP–positive RA

#RheumatoidArthritis #AntiCCP @IhabFathiSulima @docakx #Rheumatology #MedTwitter #MedicalEducation

[Ahmed S. A. E. @guidelinesMed]

Rheumatologic Serologies

[Aravind Palraj @Rheumat_Aravind]

🧬 ANA Patterns at a Glance

🔵 Homogeneous → Lupus
🟣 Speckled → Mixed autoimmune disease
🟢 Centromere → Limited scleroderma
🟠 Nucleolar → Systemic sclerosis
🔴 Cytoplasmic → Myositis

⚠️ ANA pattern alone does NOT diagnose disease.

#MedTwitter #Rheumatology #ANA #Autoimmunity #MedicalEducation #FOAMed

[Aravind Palraj @Rheumat_Aravind]

🧬 Ferritin in Rheumatology

Ferritin is NOT just an iron marker.

🔵 Low ferritin → Iron deficiency likely

🟠 Moderate elevation → Often inflammation

🔴 Very high ferritin → Think:
• MAS
• HLH
• Adult-onset Still’s disease
• Severe infection/sepsis

⚠️ Red flags:
• Cytopenias
• Fever
• Transaminitis
• Hypertriglyceridemia
• Hypofibrinogenemia
• Rapidly rising ferritin

Ferritin is both:
✔ Iron storage marker
✔ Acute-phase reactant

Normal ferritin does NOT exclude iron deficiency in inflammatory states.

#Rheumatology #MedTwitter #Ferritin #MAS #HLH #AOSD @docakx @IhabFathiSulima @DrNikhilMD #MedicalEducation #FOAMed #InternalMedicine

[Santiago Oquendo MD @rksanti]

🦋 HIPOTIROIDISMO VS HIPERTIROIDISMO 🦋
Guía rápida para consulta y urgencias.
Aprende a identificar sus diferencias clínicas, laboratorios clave y manejo inicial de forma práctica.
🔹 Hipotiroidismo
➡️ TSH ↑ | T4 ↓
➡️ Fatiga, aumento de peso, intolerancia al frío, bradicardia.
➡️ Tratamiento: Levotiroxina.
🔹 Hipertiroidismo
➡️ TSH ↓ | T4/T3 ↑
➡️ Pérdida de peso, taquicardia, ansiedad, intolerancia al calor.
➡️ Tratamiento: Betabloqueadores + antitiroideos.
⚠️ Emergencias endocrinas:
• Coma mixedematoso
• Tormenta tiroidea
📌 Una correcta interpretación clínica y laboratorial permite diagnóstico y manejo oportuno.
👨‍⚕️ Dr. Soquendo
#Hipotiroidismo #Hipertiroidismo #Tiroides #MedicinaInterna #Urgencias #ConsultaExterna #Endocrinología #Medicina #TSH #T4 #EducaciónMédica

[Franklin Loachamin @FranLoachamin]

Excelente imagen de Nefrótico y nefrítico.
Créditos a quien corresponda.

[Aravind Palraj @Rheumat_Aravind]

Sjögren’s disease autoantibodies are clinically predictive — not just diagnostic.

• Anti-SSA/Ro → hallmark antibody
• Isolated anti-SSB has poor specificity
• RF → B-cell hyperactivity
• Low C4 → vasculitis/lymphoma risk

Serology often predicts phenotype, severity & prognosis.

#Rheumatology #Sjogrens #Immunology #MedEd