Dr Suldan Abdullahi

03/12/2025

🧵𝐏𝐞𝐫𝐢𝐨𝐩𝐞𝐫𝐚𝐭𝐢𝐯𝐞 𝐀𝐧𝐭𝐢𝐜𝐨𝐚𝐠𝐮𝐥𝐚𝐭𝐢𝐨𝐧

This is one of the hardest decisions in medicine.
Stopping too early increases clots.
Stopping too late increases bleeding.
This post simplifies everything.

1️⃣ 𝐒𝐭𝐚𝐫𝐭 𝐰𝐢𝐭𝐡 𝐭𝐡𝐞 𝐟𝐮𝐧𝐝𝐚𝐦𝐞𝐧𝐭𝐚𝐥 𝐪𝐮𝐞𝐬𝐭𝐢𝐨𝐧

Perioperative AC is about preventing two dangers
• Surgical bleeding
• Thrombosis when AC is stopped
Every patient needs BOTH risks assessed before making any move.

2️⃣ 𝐒𝐭𝐞𝐩 𝟏. 𝐂𝐥𝐚𝐬𝐬𝐢𝐟𝐲 𝐭𝐡𝐞 𝐩𝐫𝐨𝐜𝐞𝐝𝐮𝐫𝐞 𝐛𝐥𝐞𝐞𝐝𝐢𝐧𝐠 𝐫𝐢𝐬𝐤 🩸

Three levels guide the entire plan
• Minimal
• Low to moderate
• High
This determines whether AC is continued, temporarily held, or fully reversed.

3️⃣ 𝐌𝐢𝐧𝐢𝐦𝐚𝐥 𝐛𝐥𝐞𝐞𝐝𝐢𝐧𝐠 𝐫𝐢𝐬𝐤 (𝐀𝐂 𝐮𝐬𝐮𝐚𝐥𝐥𝐲 𝐜𝐨𝐧𝐭𝐢𝐧𝐮𝐞𝐝)

Examples
• Dental procedures
• Minor dermatology
• Pacemaker implantation
• Cataract surgery
• Arthrocentesis
• Diagnostic endoscopy
These have extremely low procedure-related bleeding even if AC is continued.

4️⃣ 𝐋𝐨𝐰 𝐭𝐨 𝐦𝐨𝐝𝐞𝐫𝐚𝐭𝐞 𝐛𝐥𝐞𝐞𝐝𝐢𝐧𝐠 𝐫𝐢𝐬𝐤 (𝐀𝐂 𝐮𝐬𝐮𝐚𝐥𝐥𝐲 𝐢𝐧𝐭𝐞𝐫𝐫𝐮𝐩𝐭𝐞𝐝)

Common examples
• Laparoscopic cholecystectomy
• Hernia repair
• Most abdominal and thoracic surgeries
• Coronary angiography
These procedures typically need short DOAC hold or warfarin interruption.

5️⃣ 𝐇𝐢𝐠𝐡 𝐛𝐥𝐞𝐞𝐝𝐢𝐧𝐠 𝐫𝐢𝐬𝐤 𝐩𝐫𝐨𝐜𝐞𝐝𝐮𝐫𝐞𝐬 (𝐬𝐭𝐫𝐢𝐜𝐭 𝐀𝐂 𝐜𝐨𝐧𝐭𝐫𝐨𝐥 𝐧𝐞𝐞𝐝𝐞𝐝)

Examples
• Neurosurgery
• Major vascular surgeries
• Major cancer surgeries
• Total hip or knee replacement
• Surgeries with neuraxial anesthesia
These require near-complete anticoagulant clearance and controlled restart.

6️⃣ 𝐒𝐭𝐞𝐩 𝟐. 𝐀𝐬𝐬𝐞𝐬𝐬 𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬 𝐫𝐢𝐬𝐤 🧠

You must stratify thrombosis risk from
• Mechanical valves
• Atrial fibrillation
• VTE

This step decides whether interruption is safe and whether bridging is required.

7️⃣ 𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐜𝐚𝐥 𝐯𝐚𝐥𝐯𝐞 𝐩𝐚𝐭𝐢𝐞𝐧𝐭𝐬 = 𝐡𝐢𝐠𝐡𝐞𝐬𝐭 𝐫𝐢𝐬𝐤 𝐠𝐫𝐨𝐮𝐩

High-risk features
• Mitral mechanical valve
• Caged-ball or tilting-disk valves
• Valve placed ❤ months
• Prior stroke
• AF or LV dysfunction
Mitral mechanical valves have up to 22 percent annual stroke risk without AC.

8️⃣ 𝐀𝐭𝐫𝐢𝐚𝐥 𝐟𝐢𝐛𝐫𝐢𝐥𝐥𝐚𝐭𝐢𝐨𝐧 𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬 𝐫𝐢𝐬𝐤 (𝐂𝐇𝐀𝟐𝐃𝐒𝟐-𝐕𝐀𝐒𝐜)

Risk levels
• 0 to 3 → low
• 4 to 6 → moderate
• ≥7 or recent stroke → high
BRIDGE trial: low and moderate AF patients bleed more if bridged without any reduction in stroke.

9️⃣ 𝐕𝐓𝐄 𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬 𝐫𝐢𝐬𝐤 𝐝𝐞𝐩𝐞𝐧𝐝𝐬 𝐦𝐚𝐢𝐧𝐥𝐲 𝐨𝐧 𝐭𝐢𝐦𝐢𝐧𝐠

• VTE ❤ months → high risk
• VTE 3 to 12 months → moderate
• VTE >12 months → low
Strong thrombophilias (APS, protein C/S, AT deficiency) push the patient into high-risk category irrespective of timing.

🔟 𝐒𝐭𝐞𝐩 𝟑. 𝐃𝐞𝐜𝐢𝐝𝐞 𝐢𝐟 𝐀𝐂 𝐦𝐮𝐬𝐭 𝐛𝐞 𝐢𝐧𝐭𝐞𝐫𝐫𝐮𝐩𝐭𝐞𝐝

Simple rule
• Minimal bleeding risk → continue AC
• Low/moderate → interrupt safely
• High bleeding risk → interrupt and ensure INR normalization or full DOAC washout before incision

This step prevents intraoperative bleeding catastrophes.

1️⃣1️⃣ 𝐒𝐭𝐞𝐩 𝟒. 𝐁𝐫𝐢𝐝𝐠𝐢𝐧𝐠 𝐝𝐞𝐜𝐢𝐬𝐢𝐨𝐧𝐬 (𝐟𝐨𝐫 𝐰𝐚𝐫𝐟𝐚𝐫𝐢𝐧 𝐨𝐧𝐥𝐲) 🧩

Bridging = giving LMWH or UFH during warfarin interruption.
Modern evidence: bridging should be used only in very high thrombosis risk patients because it increases bleeding without reducing thrombosis in most others.
(PERIOP2 + BRIDGE trials)

1️⃣2️⃣ 𝐖𝐡𝐨 𝐭𝐫𝐮𝐥𝐲 𝐧𝐞𝐞𝐝𝐬 𝐛𝐫𝐢𝐝𝐠𝐢𝐧𝐠 (𝐫𝐚𝐫𝐞 𝐛𝐮𝐭 𝐜𝐫𝐮𝐜𝐢𝐚𝐥)

Use bridging only when stopping AC is extremely unsafe:
• Mechanical mitral valve
• Caged-ball or tilting-disk valve
• CHA2DS2-VASc ≥7
• Recent stroke or TIA
• VTE ❤ months
• APS or multiple thrombophilias

These are the ONLY groups where bridging has a favorable risk–benefit ratio.

1️⃣3️⃣ 𝐖𝐚𝐫𝐟𝐚𝐫𝐢𝐧 𝐩𝐞𝐫𝐢𝐨𝐩𝐞𝐫𝐚𝐭𝐢𝐯𝐞 𝐩𝐥𝐚𝐧 (𝐜𝐥𝐞𝐚𝐫 𝐚𝐧𝐝 𝐝𝐞𝐭𝐚𝐢𝐥𝐞𝐝) 🟡

Stopping
• Stop 5 days before surgery
• Check INR 7–10 days before, then again night before
• If INR >1.5 → give 1.25–2.5 mg vitamin K
Restarting
• Low/mod risk → restart 12 hours post-op
• High bleed risk → restart 24–36 hours post-op
Bridging ONLY if patient is very high thrombosis risk.

1️⃣4️⃣ 𝐁𝐫𝐢𝐝𝐠𝐢𝐧𝐠 𝐩𝐫𝐨𝐭𝐨𝐜𝐨𝐥 (𝐢𝐟 𝐢𝐧𝐝𝐢𝐜𝐚𝐭𝐞𝐝)

• Start LMWH 36 hours after last warfarin dose
• Last LMWH dose 24 hours before procedure
• If CrCl

02/12/2025

𝐒𝐭𝐚𝐫𝐭𝐢𝐧𝐠 𝐈𝐧𝐬𝐮𝐥𝐢𝐧 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐢𝐧 𝐓𝐲𝐩𝐞 𝟐 𝐃𝐢𝐚𝐛𝐞𝐭𝐞𝐬 (𝐓𝟐𝐃𝐌)
By Dr. Suldan Abdullahi

1: 𝐖𝐡𝐲 𝐈𝐧𝐬𝐮𝐥𝐢𝐧 𝐢𝐬 𝐍𝐞𝐞𝐝𝐞𝐝 𝐢𝐧 𝐓𝟐𝐃𝐌
• Diabetes is 𝐩𝐫𝐨𝐠𝐫𝐞𝐬𝐬𝐢𝐯𝐞; most patients will eventually require insulin.
• Pancreatic beta-cell decline is genetically determined.
• Not caused by prior medications (e.g., sulfonylureas).
• Patients should understand that insulin may be required at some stage.

“𝐏𝐫𝐨𝐠𝐫𝐞𝐬𝐬𝐢𝐯𝐞 𝐥𝐨𝐬𝐬 𝐨𝐟 𝐛𝐞𝐭𝐚 𝐜𝐞𝐥𝐥𝐬 → 𝐧𝐞𝐞𝐝 𝐟𝐨𝐫 𝐞𝐱𝐨𝐠𝐞𝐧𝐨𝐮𝐬 𝐢𝐧𝐬𝐮𝐥𝐢𝐧”

2: 𝐖𝐡𝐞𝐧 𝐭𝐨 𝐒𝐭𝐚𝐫𝐭 𝐈𝐧𝐬𝐮𝐥𝐢𝐧

1. 𝐔𝐫𝐠𝐞𝐧𝐭 / 𝐀𝐛𝐬𝐨𝐥𝐮𝐭𝐞 𝐈𝐧𝐝𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬:
• A1C ≥ 10%
• Fasting BG ≥ 300 mg/dL
• Glucose toxicity: high glucose suppresses endogenous insulin
• Clinical instability: hyperglycemia with dehydration, moderate-large ketones

These patients need immediate insulin, even if newly diagnosed T2DM.

2. 𝐑𝐞𝐥𝐚𝐭𝐢𝐯𝐞 𝐈𝐧𝐝𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬:
• Clinically stable but BG above target:
• Pre/post-surgery
• Infection
• Steroid-induced hyperglycemia
• Persistent high A1C/BG despite maximal non-insulin therapy (>3 months)
• Target: Fasting 80–130 mg/dL, post-meal

02/12/2025

𝐅𝐢𝐫𝐬𝐭-𝐋𝐢𝐧𝐞 𝐚𝐧𝐝 𝐂𝐨𝐦𝐛𝐢𝐧𝐚𝐭𝐢𝐨𝐧 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐂𝐡𝐨𝐢𝐜𝐞𝐬
𝐅𝐢𝐫𝐬𝐭-𝐋𝐢𝐧𝐞 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 (𝐀𝐃𝐀/𝐄𝐀𝐒𝐃 𝐜𝐨𝐧𝐬𝐞𝐧𝐬𝐮𝐬)

𝐌𝐞𝐭𝐟𝐨𝐫𝐦𝐢𝐧 + 𝐋𝐢𝐟𝐞𝐬𝐭𝐲𝐥𝐞

Unless contraindicated or not tolerated.

𝐖𝐡𝐞𝐧 𝐭𝐨 𝐒𝐭𝐚𝐫𝐭 𝐰𝐢𝐭𝐡 𝐎𝐭𝐡𝐞𝐫 𝐅𝐢𝐫𝐬𝐭-𝐋𝐢𝐧𝐞 𝐎𝐩𝐭𝐢𝐨𝐧𝐬

(Instead of, or in addition to, metformin)

A. 𝐀𝐒𝐂𝐕𝐃 𝐨𝐫 𝐡𝐢𝐠𝐡 𝐂𝐕 𝐫𝐢𝐬𝐤

𝐒𝐆𝐋𝐓𝟐 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫 (empagliflozin, canagliflozin, dapagliflozin)

OR 𝐆𝐋𝐏-𝟏 𝐑𝐀 (e.g., semaglutide)

B. 𝐇𝐞𝐚𝐫𝐭 𝐅𝐚𝐢𝐥𝐮𝐫𝐞 (𝐇𝐅)

𝐒𝐆𝐋𝐓𝟐 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫 preferred

C. 𝐂𝐡𝐫𝐨𝐧𝐢𝐜 𝐊𝐢𝐝𝐧𝐞𝐲 𝐃𝐢𝐬𝐞𝐚𝐬𝐞

𝐒𝐆𝐋𝐓𝟐 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫 if eGFR adequate

If not: 𝐃𝐏𝐏-𝟒 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫 (𝐞.𝐠., 𝐥𝐢𝐧𝐚𝐠𝐥𝐢𝐩𝐭𝐢𝐧) 𝐨𝐫 𝐆𝐋𝐏-𝟏 𝐑𝐀

D. 𝐒𝐢𝐠𝐧𝐢𝐟𝐢𝐜𝐚𝐧𝐭 𝐎𝐛𝐞𝐬𝐢𝐭𝐲

GLP-1 RA (oral/SC)

SGLT2 inhibitor

E. 𝐄𝐥𝐝𝐞𝐫𝐥𝐲 / 𝐇𝐢𝐠𝐡 𝐫𝐢𝐬𝐤 𝐨𝐟 𝐡𝐲𝐩𝐨𝐠𝐥𝐲𝐜𝐞𝐦𝐢𝐚

DPP-4 inhibitors

TZDs (with caution in HF/edema)

𝐀𝐯𝐨𝐢𝐝 sulfonylureas

𝐂𝐨𝐦𝐛𝐢𝐧𝐚𝐭𝐢𝐨𝐧 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐂𝐡𝐨𝐢𝐜𝐞𝐬

𝐃𝐮𝐚𝐥 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐄𝐱𝐚𝐦𝐩𝐥𝐞𝐬

Metformin + DPP-4 inhibitor

Metformin + SGLT2 inhibitor

Metformin + Sulfonylurea (cheap but hypoglycemia risk)

Metformin + TZD

Metformin + GLP-1 RA

𝐈𝐟 𝐀𝟏𝐂 ≥𝟏.𝟓% 𝐚𝐛𝐨𝐯𝐞 𝐭𝐚𝐫𝐠𝐞𝐭 → 𝐬𝐭𝐚𝐫𝐭 𝐝𝐮𝐚𝐥 𝐭𝐡𝐞𝐫𝐚𝐩𝐲 𝐢𝐧𝐢𝐭𝐢𝐚𝐥𝐥𝐲.

𝐓𝐫𝐢𝐩𝐥𝐞 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐄𝐱𝐚𝐦𝐩𝐥𝐞𝐬

Metformin + SGLT2i + DPP-4i

Metformin + SGLT2i + sulfonylurea

Metformin + GLP-1 RA + SGLT2i

𝐈𝐟 𝐀𝟏𝐂 >𝟏𝟎% 𝐨𝐫 𝐬𝐲𝐦𝐩𝐭𝐨𝐦𝐚𝐭𝐢𝐜 𝐡𝐲𝐩𝐞𝐫𝐠𝐥𝐲𝐜𝐞𝐦𝐢𝐚 → 𝐜𝐨𝐧𝐬𝐢𝐝𝐞𝐫 𝐢𝐧𝐬𝐮𝐥𝐢𝐧.

3. 𝐒𝐢𝐝𝐞-𝐄𝐟𝐟𝐞𝐜𝐭 𝐏𝐫𝐨𝐟𝐢𝐥𝐞𝐬 𝐛𝐲 𝐃𝐫𝐮𝐠 𝐂𝐥𝐚𝐬𝐬

𝐀. 𝐁𝐢𝐠𝐮𝐚𝐧𝐢𝐝𝐞𝐬 (𝐌𝐞𝐭𝐟𝐨𝐫𝐦𝐢𝐧)

GI upset (most common)

Vitamin B12 deficiency

Lactic acidosis (rare; ↑ risk in renal/hepatic/cardiac failure)

B. 𝐒𝐮𝐥𝐟𝐨𝐧𝐲𝐥𝐮𝐫𝐞𝐚𝐬

Hypoglycemia (major)

Weight gain

SIADH (rare)

C. 𝐌𝐞𝐠𝐥𝐢𝐭𝐢𝐧𝐢𝐝𝐞𝐬

Hypoglycemia (less than SU)

Weight gain

Frequent dosing burden

D. 𝐓𝐙𝐃𝐬

Weight gain

Edema

Heart failure exacerbation

Bone fractures

Pioglitazone: ↑ bladder cancer risk (controversial)

Rosiglitazone: CV risk concerns

E. 𝐀𝐥𝐩𝐡𝐚-𝐆𝐥𝐮𝐜𝐨𝐬𝐢𝐝𝐚𝐬𝐞 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬

Flatulence, diarrhea, abdominal discomfort

Elevated LFTs (high doses)

F. 𝐃𝐏𝐏-𝟒 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬

Weight neutral

Nasopharyngitis

Headache

Joint pain

Saxagliptin: possible ↑ HF risk

G. 𝐒𝐆𝐋𝐓𝟐 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬

Ge***al mycotic infections

UTIs

Dehydration, hypotension

Euglycemic ketoacidosis

Canagliflozin: ↑ amputation risk, ↓ bone density (dose-dependent)

H. 𝐆𝐋𝐏-𝟏 𝐑𝐀 (𝐎𝐫𝐚𝐥 𝐒𝐞𝐦𝐚𝐠𝐥𝐮𝐭𝐢𝐝𝐞)

Nausea, vomiting

Delayed gastric emptying

Weight loss

Rare: pancreatitis

02/12/2025

𝐎𝐫𝐚𝐥 𝐇𝐲𝐩𝐨𝐠𝐥𝐲𝐜𝐞𝐦𝐢𝐜 𝐃𝐫𝐮𝐠𝐬 – 𝐓𝐲𝐩𝐢𝐜𝐚𝐥 𝐀𝐝𝐮𝐥𝐭 𝐃𝐨𝐬𝐞𝐬

1. Biguanides
𝐌𝐞𝐭𝐟𝐨𝐫𝐦𝐢𝐧

Immediate-release (IR):
• Start: 500 mg once or twice daily
• Titrate: Increase by 500 mg weekly
• Usual dose: 1500–2000 mg/day in divided doses
• Max: 2550 mg/day

Extended-release (XR):
• Start: 500–750 mg once daily
• Max: 2000 mg/day

2. 𝐒𝐮𝐥𝐟𝐨𝐧𝐲𝐥𝐮𝐫𝐞𝐚𝐬
𝐆𝐥𝐢𝐩𝐢𝐳𝐢𝐝𝐞

IR: 2.5–20 mg/day, single or divided

ER: 2.5–20 mg once daily

Max: 40 mg/day

𝐆𝐥𝐲𝐛𝐮𝐫𝐢𝐝𝐞 (𝐆𝐥𝐢𝐛𝐞𝐧𝐜𝐥𝐚𝐦𝐢𝐝𝐞)

2.5–5 mg/day, max 20 mg/day

𝐆𝐥𝐢𝐜𝐥𝐚𝐳𝐢𝐝𝐞

Regular: 40–80 mg once or twice daily, max 320 mg/day

MR (modified-release): 30–120 mg once daily

3. 𝐌𝐞𝐠𝐥𝐢𝐭𝐢𝐧𝐢𝐝𝐞𝐬
𝐑𝐞𝐩𝐚𝐠𝐥𝐢𝐧𝐢𝐝𝐞

0.5–4 mg before meals, 2–4 times/day

Max: 16 mg/day

𝐍𝐚𝐭𝐞𝐠𝐥𝐢𝐧𝐢𝐝𝐞

60–120 mg before meals, 3 times/day

4. 𝐓𝐡𝐢𝐚𝐳𝐨𝐥𝐢𝐝𝐢𝐧𝐞𝐝𝐢𝐨𝐧𝐞𝐬 (𝐓𝐙𝐃𝐬)
𝐏𝐢𝐨𝐠𝐥𝐢𝐭𝐚𝐳𝐨𝐧𝐞

15–45 mg once daily

Rosiglitazone

4–8 mg/day, once or divided

5. 𝐀𝐥𝐩𝐡𝐚-𝐆𝐥𝐮𝐜𝐨𝐬𝐢𝐝𝐚𝐬𝐞 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬
𝐀𝐜𝐚𝐫𝐛𝐨𝐬𝐞

Start: 25 mg once or twice daily with meals

Titrate: Up to 50–100 mg three times/day

Max: 300 mg/day

𝐌𝐢𝐠𝐥𝐢𝐭𝐨𝐥

25 mg three times/day, max 100 mg TID

6. 𝐃𝐏𝐏-𝟒 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬 (𝐆𝐥𝐢𝐩𝐭𝐢𝐧𝐬)

(Usually once daily)

Drug Typical Dose
𝐒𝐢𝐭𝐚𝐠𝐥𝐢𝐩𝐭𝐢𝐧 100 mg daily (adjust in renal impairment)

𝐕𝐢𝐥𝐝𝐚𝐠𝐥𝐢𝐩𝐭𝐢𝐧 50 mg twice daily

𝐒𝐚𝐱𝐚𝐠𝐥𝐢𝐩𝐭𝐢𝐧 2.5–5 mg daily

𝐋𝐢𝐧𝐚𝐠𝐥𝐢𝐩𝐭𝐢𝐧 5 mg daily

𝐀𝐥𝐨𝐠𝐥𝐢𝐩𝐭𝐢𝐧 25 mg daily

7. 𝐒𝐆𝐋𝐓𝟐 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬

Drug Typical Dose

𝐄𝐦𝐩𝐚𝐠𝐥𝐢𝐟𝐥𝐨𝐳𝐢𝐧 10–25 mg daily

𝐃𝐚𝐩𝐚𝐠𝐥𝐢𝐟𝐥𝐨𝐳𝐢𝐧 5–10 mg daily

𝐂𝐚𝐧𝐚𝐠𝐥𝐢𝐟𝐥𝐨𝐳𝐢𝐧 100–300 mg daily

𝐄𝐫𝐭𝐮𝐠𝐥𝐢𝐟𝐥𝐨𝐳𝐢𝐧 5–15 mg daily

8. 𝐎𝐫𝐚𝐥 𝐆𝐋𝐏-𝟏 𝐑𝐞𝐜𝐞𝐩𝐭𝐨𝐫 𝐀𝐠𝐨𝐧𝐢𝐬𝐭

𝐎𝐫𝐚𝐥 𝐒𝐞𝐦𝐚𝐠𝐥𝐮𝐭𝐢𝐝𝐞

Start: 3 mg once daily for 30 days

Increase to 7 mg once daily

Max: 14 mg once daily

01/12/2025

“𝐓𝐡𝐞 𝐌𝐢𝐬𝐬𝐢𝐧𝐠 𝐇𝐮𝐦𝐚𝐧 𝐓𝐨𝐮𝐜𝐡 𝐢𝐧 𝐌𝐨𝐝𝐞𝐫𝐧 𝐌𝐞𝐝𝐢𝐜𝐢𝐧𝐞” by By Dr. Abhijeet Shinde (Thinking Healer, 2025).

🩺 – 𝐂𝐥𝐢𝐧𝐢𝐜𝐚𝐥 𝐏𝐞𝐚𝐫𝐥𝐬

The Missing Human Touch in Modern Medicine

1. 𝐓𝐞𝐜𝐡𝐧𝐨𝐥𝐨𝐠𝐢𝐜𝐚𝐥 𝐩𝐫𝐨𝐠𝐫𝐞𝐬𝐬 𝐡𝐚𝐬 𝐨𝐮𝐭𝐩𝐚𝐜𝐞𝐝 𝐡𝐮𝐦𝐚𝐧 𝐜𝐨𝐧𝐧𝐞𝐜𝐭𝐢𝐨𝐧.

Despite unmatched diagnostic capability, patients increasingly experience healthcare as impersonal, fragmented, and rushed—a paradox at the heart of modern medicine.

2. 𝐄𝐦𝐩𝐚𝐭𝐡𝐲 𝐞𝐫𝐨𝐬𝐢𝐨𝐧 𝐢𝐬 𝐬𝐲𝐬𝐭𝐞𝐦𝐢𝐜, 𝐧𝐨𝐭 𝐢𝐧𝐝𝐢𝐯𝐢𝐝𝐮𝐚𝐥.

It is driven by bureaucratic overload, regulatory pressures, EHR-centric workflows, medico-legal fear, and hyper-specialisation—not because clinicians “care less.”

3. 𝐃𝐨𝐜𝐮𝐦𝐞𝐧𝐭𝐚𝐭𝐢𝐨𝐧 𝐡𝐚𝐬 𝐫𝐞𝐩𝐥𝐚𝐜𝐞𝐝 𝐝𝐢𝐚𝐥𝐨𝐠𝐮𝐞.

Clinicians now spend twice as much time with computers as with patients, shrinking narrative listening and disrupting the doctor–patient bond.

4. 𝐇𝐲𝐩𝐞𝐫-𝐬𝐩𝐞𝐜𝐢𝐚𝐥𝐢𝐬𝐚𝐭𝐢𝐨𝐧 𝐟𝐫𝐚𝐜𝐭𝐮𝐫𝐞𝐬 𝐩𝐚𝐭𝐢𝐞𝐧𝐭 𝐢𝐝𝐞𝐧𝐭𝐢𝐭𝐲.

Organ-based silos divide responsibility and disrupt continuity. Without a clinician who maintains the whole-person narrative, empathy becomes structurally difficult.

5. 𝐓𝐞𝐜𝐡𝐧𝐨𝐥𝐨𝐠𝐲 𝐦𝐞𝐝𝐢𝐚𝐭𝐞𝐬, 𝐛𝐮𝐭 𝐜𝐚𝐧 𝐚𝐥𝐬𝐨 𝐝𝐞𝐡𝐮𝐦𝐚𝐧𝐢𝐬𝐞.

AI tools and telemedicine alter the phenomenology of care—reducing non-verbal cues, context, and intuitive reasoning.
👉 Technology is not the problem; absence of relational counterbalances is.

6. 𝐌𝐞𝐝𝐢𝐜𝐨-𝐥𝐞𝐠𝐚𝐥 𝐚𝐧𝐱𝐢𝐞𝐭𝐲 𝐬𝐡𝐚𝐩𝐞𝐬 𝐛𝐞𝐡𝐚𝐯𝐢𝐨𝐮𝐫 𝐦𝐨𝐫𝐞 𝐭𝐡𝐚𝐧 𝐜𝐥𝐢𝐧𝐢𝐜𝐚𝐥 𝐰𝐢𝐬𝐝𝐨𝐦.

Fear of litigation pushes clinicians toward defensive medicine, excessive tests, and exhaustive documentation, shifting focus from meaning to risk-avoidance.

7. 𝐄𝐚𝐫𝐥𝐲 𝐢𝐧𝐭𝐞𝐫𝐫𝐮𝐩𝐭𝐢𝐨𝐧 𝐢𝐬 𝐜𝐨𝐦𝐦𝐨𝐧—𝐚𝐧𝐝 𝐜𝐨𝐬𝐭𝐥𝐲.

Studies show clinicians interrupt patient narratives within 18–20 seconds. This weakens rapport, reduces accuracy, and compromises care outcomes.

8. 𝐄𝐦𝐩𝐚𝐭𝐡𝐲 𝐢𝐦𝐩𝐫𝐨𝐯𝐞𝐬 𝐜𝐥𝐢𝐧𝐢𝐜𝐚𝐥 𝐨𝐮𝐭𝐜𝐨𝐦𝐞𝐬—𝐢𝐭'𝐬 𝐧𝐨𝐭 𝐬𝐞𝐧𝐭𝐢𝐦𝐞𝐧𝐭𝐚𝐥.

High-empathy physicians demonstrate better diabetes, lipid, and adherence outcomes. Empathy is a measurable, evidence-based clinical competency.

9. 𝐄𝐦𝐩𝐚𝐭𝐡𝐲 𝐝𝐞𝐜𝐥𝐢𝐧𝐞 𝐛𝐞𝐠𝐢𝐧𝐬 𝐢𝐧 𝐦𝐞𝐝𝐢𝐜𝐚𝐥 𝐭𝐫𝐚𝐢𝐧𝐢𝐧𝐠.

Without intentional cultivation, empathy consistently drops across medical school and residency.
👉 Curriculum must include narrative medicine, reflective writing, bedside observation, uncertainty training, and digital empathy skills.

10. 𝐇𝐞𝐚𝐥𝐢𝐧𝐠 𝐭𝐡𝐞 𝐬𝐲𝐬𝐭𝐞𝐦 𝐢𝐬 𝐚𝐬 𝐢𝐦𝐩𝐨𝐫𝐭𝐚𝐧𝐭 𝐚𝐬 𝐡𝐞𝐚𝐥𝐢𝐧𝐠 𝐩𝐚𝐭𝐢𝐞𝐧𝐭𝐬.

Sustainable empathy requires:

Documentation-light workflows

Protected patient-interaction time

EHRs designed for narrative capture

Institutional metrics that value patient experience
👉 Empathy must be 𝐬𝐭𝐫𝐮𝐜𝐭𝐮𝐫𝐚𝐥𝐥𝐲 𝐬𝐮𝐩𝐩𝐨𝐫𝐭𝐞𝐝,, not individually demanded.

𝐓𝐚𝐤𝐞-𝐇𝐨𝐦𝐞 𝐌𝐞𝐬𝐬𝐚𝐠𝐞

Modern medicine needs recalibration—not less technology, but more humanity. Empathy is both a clinical skill and a moral commitment, and restoring it requires systemic redesign, narrative integration, and renewed human presence.

thinkinghealer.com/author/thinkin…

30/11/2025

The kindest person in the room is often the the smartest

29/11/2025

https://medium.com//how-and-where-to-study-internal-medicine-7505c286b25d

How and where to study Internal Medicine? This question might seem a bit confusing because Internal Medicine is such a vast field, and there are so many sources! But keep in mind that thousands of …

26/11/2025

🟢 𝐅𝐨𝐫𝐠𝐨𝐭𝐭𝐞𝐧 𝐋𝐞𝐬𝐬𝐨𝐧𝐬 𝐢𝐧 𝐊𝐢𝐝𝐧𝐞𝐲 𝐌𝐞𝐝𝐢𝐜𝐢𝐧𝐞 (𝐍𝐃𝐓, 𝟐𝟎𝟐𝟓)

“𝐒𝐮𝐩𝐞𝐫𝐢𝐨𝐫 doctors 𝐩𝐫𝐞𝐯𝐞𝐧𝐭 CKD — 𝐌𝐞𝐝𝐢𝐨𝐜𝐫𝐞 doctors 𝐭𝐫𝐞𝐚𝐭 CKD — 𝐈𝐧𝐟𝐞𝐫𝐢𝐨𝐫 doctors treat kidney 𝐟𝐚𝐢𝐥𝐮𝐫𝐞.”

🧠 The Paradigm Shift in Kidney Medicine

🟩 Circa 2030 Kidney Medicine — 𝐏𝐫𝐞𝐯𝐞𝐧𝐭 𝐂𝐊𝐃 (𝐒𝐮𝐩𝐞𝐫𝐢𝐨𝐫 𝐏𝐫𝐚𝐜𝐭𝐢𝐜𝐞)

𝐀𝐢𝐦: 𝐏𝐫𝐞𝐯𝐞𝐧𝐭 𝐝𝐢𝐬𝐞𝐚𝐬𝐞 𝐛𝐞𝐟𝐨𝐫𝐞 𝐨𝐧𝐬𝐞𝐭

Tools available in 2025:

Albuminuria testing

RAS blockers

SGLT2 inhibitors

Non-steroidal MRAs

Statins

GLP-1 receptor agonists

Key Principle: Intervene early—𝐛𝐞𝐟𝐨𝐫𝐞 𝐞𝐆𝐅𝐑 < 𝟔𝟎 𝐦𝐥/𝐦𝐢𝐧/𝟏.𝟕𝟑 𝐦².

🟨 Current 21st Century Kidney Medicine — 𝐓𝐫𝐞𝐚𝐭 𝐂𝐊𝐃 (𝐌𝐞𝐝𝐢𝐨𝐜𝐫𝐞 𝐏𝐫𝐚𝐜𝐭𝐢𝐜𝐞)

We diagnose CKD, but uptake of effective therapies is still suboptimal worldwide.

Treatments are initiated after the disease becomes evident.

🟥 20th Century Kidney Medicine — 𝐓𝐫𝐞𝐚𝐭 𝐊𝐢𝐝𝐧𝐞𝐲 𝐅𝐚𝐢𝐥𝐮𝐫𝐞 (𝐈𝐧𝐟𝐞𝐫𝐢𝐨𝐫 𝐏𝐫𝐚𝐜𝐭𝐢𝐜𝐞)

Focus was on dialysis and ESRD after full-blown disease developed.

Prevention and early treatment were largely ignored.

⭐ 𝐄𝐦𝐞𝐫𝐠𝐢𝐧𝐠 𝐂𝐨𝐧𝐜𝐞𝐩𝐭: 𝐏𝐫𝐞-𝐂𝐊𝐃

Need for a 𝐧𝐞𝐰 𝐝𝐞𝐟𝐢𝐧𝐢𝐭𝐢𝐨𝐧: Individuals with very high CKD risk who still have normal eGFR and UACR.

𝐀𝐧𝐚𝐥𝐨𝐠𝐲: Just like prediabetes precedes diabetes.

𝐏𝐫𝐨𝐩𝐨𝐬𝐚𝐥: Carve out pre-CKD from KDIGO’s current “low-risk (green)” category.

📌 𝐖𝐡𝐲 𝐈𝐭 𝐌𝐚𝐭𝐭𝐞𝐫𝐬 𝐢𝐧 𝟐𝟎𝟐𝟓

We now have strong diagnostic tools and proven medications, but:

Implementation is poor

Early detection is delayed

Prevention is not prioritized

𝐁𝐨𝐭𝐭𝐨𝐦 𝐥𝐢𝐧𝐞:
➡️ The future of nephrology is shifting from treating CKD to preventing it.
➡️ Time to identify high-risk individuals BEFORE CKD appears.

🩺 𝐓𝐚𝐤𝐞𝐚𝐰𝐚𝐲

“Prevent CKD. Detect early. Treat risk, not just disease.”

24/11/2025

https://t.me/sulmedd/1766

24/11/2025

𝐀𝐬𝐲𝐦𝐩𝐭𝐨𝐦𝐚𝐭𝐢𝐜 𝐈𝐧𝐩𝐚𝐭𝐢𝐞𝐧𝐭 𝐇𝐲𝐩𝐞𝐫𝐭𝐞𝐧𝐬𝐢𝐨𝐧 (2025 NEJM Case Debate)

𝐂𝐚𝐬𝐞: 63-year-old man, admitted for diverticulitis, BP persistently high (185/115 → 182/103 mmHg), asymptomatic, no end-organ damage.

𝐊𝐞𝐲 𝐂𝐥𝐢𝐧𝐢𝐜𝐚𝐥 𝐏𝐞𝐚𝐫𝐥𝐬

🔹 Asymptomatic high BP in hospitalized patients is common — often triggered by 𝐩𝐚𝐢𝐧, 𝐚𝐧𝐱𝐢𝐞𝐭𝐲, 𝐚𝐜𝐮𝐭𝐞 𝐢𝐥𝐥𝐧𝐞𝐬𝐬, 𝐢𝐦𝐩𝐫𝐨𝐩𝐞𝐫 𝐜𝐮𝐟𝐟 𝐬𝐢𝐳𝐞, 𝐨𝐫 𝐝𝐢𝐬𝐭𝐮𝐫𝐛𝐞𝐝 𝐬𝐥𝐞𝐞𝐩.

🔹 Do NOT rush to diagnose 𝐜𝐡𝐫𝐨𝐧𝐢𝐜 𝐡𝐲𝐩𝐞𝐫𝐭𝐞𝐧𝐬𝐢𝐨𝐧 based only on inpatient BP. Illness-related elevations may normalize later.

🔹 No evidence supports 𝐚𝐠𝐠𝐫𝐞𝐬𝐬𝐢𝐯𝐞 𝐢𝐧𝐩𝐚𝐭𝐢𝐞𝐧𝐭 𝐁𝐏 𝐜𝐨𝐧𝐭𝐫𝐨𝐥 — randomized trials lacking, and observational data show possible harm.

🔹 𝐑𝐚𝐩𝐢𝐝 𝐁𝐏 𝐥𝐨𝐰𝐞𝐫𝐢𝐧𝐠 (𝐞𝐬𝐩𝐞𝐜𝐢𝐚𝐥𝐥𝐲 𝐈𝐕 𝐝𝐫𝐮𝐠𝐬) may cause hypotension, renal hypoperfusion, myocardial injury, stroke, or AKI.

🔹 If BP is high but patient is 𝐬𝐭𝐚𝐛𝐥𝐞 and 𝐚𝐬𝐲𝐦𝐩𝐭𝐨𝐦𝐚𝐭𝐢𝐜:
👉 First step = 𝐜𝐨𝐧𝐟𝐢𝐫𝐦 𝐩𝐫𝐨𝐩𝐞𝐫 𝐦𝐞𝐚𝐬𝐮𝐫𝐞𝐦𝐞𝐧𝐭 after rest, appropriate cuff size.
👉 𝐑𝐞-𝐜𝐡𝐞𝐜𝐤 𝐁𝐏 𝐭𝐫𝐞𝐧𝐝𝐬 rather than react to a single value.

🔹 𝐄𝐚𝐫𝐥𝐲 𝐭𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐦𝐚𝐲 𝐛𝐞 𝐜𝐨𝐧𝐬𝐢𝐝𝐞𝐫𝐞𝐝 𝐰𝐡𝐞𝐧:

✳️Strong suspicion of chronic untreated hypertension

✳️Poor healthcare access or low likelihood of follow-up

✳️Persistent severe elevation (>180/110 mmHg) despite rest and repeat readings

🔹 𝐇𝐨𝐬𝐩𝐢𝐭𝐚𝐥𝐢𝐳𝐚𝐭𝐢𝐨𝐧 = 𝐨𝐩𝐩𝐨𝐫𝐭𝐮𝐧𝐢𝐭𝐲 𝐟𝐨𝐫:

❇️Diagnosis awareness

❇️Counselling on lifestyle

❇️Arranging follow-up

❇️Considering long-term therapy (oral, low-dose, slow titration) — NOT emergency reduction.

🔹 Discharge prescription alone is not success — 44% of antihypertensive prescriptions started in hospital are never refilled.

🔹 𝐏𝐫𝐢𝐨𝐫𝐢𝐭𝐲 𝐢𝐬 𝐜𝐨𝐧𝐭𝐢𝐧𝐮𝐢𝐭𝐲 𝐨𝐟 𝐜𝐚𝐫𝐞 — connect patient to primary care, pharmacist-led BP management, telemonitoring, or automated reminders.

🔹 𝐅𝐢𝐧𝐚𝐥 𝐫𝐮𝐥𝐞
📌 𝐓𝐫𝐞𝐚𝐭 𝐮𝐫𝐠𝐞𝐧𝐜𝐲 𝐨𝐧𝐥𝐲 𝐢𝐟 persistently very high BP + no reversible trigger + high risk + poor likelihood of follow-up.
📌 𝐎𝐭𝐡𝐞𝐫𝐰𝐢𝐬𝐞, watchful waiting with structured outpatient BP plan is safer.

𝐓𝐚𝐤𝐞 𝐇𝐨𝐦𝐞 𝐌𝐞𝐬𝐬𝐚𝐠𝐞 𝐟𝐫𝐨𝐦 𝐍𝐄𝐉𝐌 𝐜𝐚𝐬𝐞

> Asymptomatic inpatient hypertension is usually not an emergency. 𝐀𝐯𝐨𝐢𝐝 𝐫𝐞𝐟𝐥𝐞𝐱 𝐭𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭, prevent overtreatment harms, and focus on accurate measurement, identifying chronic hypertension, patient education, and arranging reliable follow-up or gradual outpatient initiation of therapy.

This question is a clinical dilemma that debates whether to treat asymptomatic inpatient hypertension with oral antihypertensives or to use watchful waiting, with experts arguing for each approach in short essays. This interactive feature from NEJM highlights the lack of a universally correct answer and seeks community opinion.

https://pubmed.ncbi.nlm.nih.gov/41259762/

19/11/2025

Internal medicine brings together curiosity, expertise, and care. IM physicians navigate complex diagnoses, support patients over time, and lead in shaping the future of health care. See what makes this specialty so unique: f.mtr.cool/zwvgcinnmt