@omogaderrick

MD|MPH|

Joined February 2014
Si Tcha 🔥! #MachokaAt50
1
3
1
5
511
Oloo Omoga retweeted
At first, I thought of a JT with exit block (clear grouped beating), but the patient has AF, and previous ECGs consistently show AF. Therefore, I believe it is AF + CHB and JT with RBBB, LAFB, and exit block. I agree with @abdelqader_LL
Interesting case. 88-year-old patient admitted to Pulmonology for pneumonia. History of aortic valve replacement with a biological prosthesis, AF, PM and heart failure. The patient was about to be discharged, but reported asthenia. Therefore, this ECG was taken
2
1
5
502
Belhassen VT (idiopathic left fascicular VT) is a verapamil-sensitive ventricular tachycardia seen in young patients with structurally normal hearts, presenting as a relatively narrow complex tachycardia with right bundle branch block morphology and left axis deviation.
🩺 ECG Challenge | European Heart Journal – Case Reports A clue hidden in plain sight How much can a single ECG reveal? This educational ECG Challenge walks readers through a step-by-step diagnostic approach, demonstrating how careful interpretation of subtle electrocardiographic findings can uncover the underlying diagnosis and guide appropriate management. A great reminder that the ECG remains one of the most powerful tools in cardiovascular medicine. 📖 Test your diagnostic skills: ow.ly/XlIi50ZWIao #EHJCaseReports @KardiologieHH @aayshacader @ANazmiCalik @TJ_Yeo @FarhanaAra @cfcamm
1
4
34
3,265
Your take?
Interesting case. 88-year-old patient admitted to Pulmonology for pneumonia. History of aortic valve replacement with a biological prosthesis, AF, PM and heart failure. The patient was about to be discharged, but reported asthenia. Therefore, this ECG was taken
1
33
What's the reason behind a PVC that restores normal conduction? ⚡️🫀
6
4
1
26
3,640
Thoughts on this 😳
35
40
5
239
41,776
ASYMPTOMATIC HYPERURICAEMIA: WHAT THE EVIDENCE SAYS (Evidence on treating high Uric acid without having gout or uric acid stones) A routine health check shows high uric acid 8.6 mg/dL. No joint has ever swollen. The patient leaves on febuxostat. Should they? A thread on 6 RCTs, 6 meta-analyses and every major guideline. #Rheumatology #MedTwitter
6
19
73
6,915
Your diagnosis ?
12
11
68
7,915
Subaortic VSD with an Unruptured Right Sinus of Valsalva Aneurysm in 23 y.o patient. • Subaortic VSD partially overridden by the aortic root • Rightward displacement of the aortic root • Elongated, unruptured aneurysm arising from the right coronary sinus
8
28
1
123
6,514
Diagnosis ?
23
22
153
27,266
Diagnosis??
13
20
2
161
28,708
Thoughts on this ?
7
9
1
62
11,941
Oloo Omoga retweeted
For ECG Nerds only..... Sent to me from Medical OPD without history except for that it belongs to a young man !
25
10
83
25,377
Understanding peripheral arterial disease in the current era: a must-read review in The Lancet thelancet.com/journals/lance… @TheLancet
1
32
134
7,393
Oloo Omoga retweeted
For Fellows ➖Patient in ED 🚨after Stroke⚡️- Can ECG tell us the cause of CVA ⁉️
2
5
22
1,964
One calculation answers it. Urinary anion gap = (urine Na + urine K ) minus urine Cl. Here's why it works. Ammonium is how the kidney dumps acid, and it leaves paired with chloride. But ammonium is a cation nobody measures. So when a healthy kidney is working hard, urine chloride quietly climbs above Na+ and K+, and the gap turns negative. Negative gap: kidney is doing its job, the acid is being lost somewhere else. Diarrhoea. Positive gap: kidney cannot make ammonium. That is RTA. Remember it as neGUTive. Negative means gut. 2/2
4
30
1,237
Oloo Omoga retweeted
#Thiamine in the ICU: 10 high-yield pearls 1. Unexplained lactate? Think thiamine. Thiamine is required for pyruvate dehydrogenase. Deficiency blocks conversion of pyruvate to acetyl-CoA, shunting pyruvate toward lactate and impairing mitochondrial aerobic metabolism. Thus, thiamine deficiency belongs in the differential diagnosis for otherwise unexplained lactic acidosis. 2. Thiamine deficiency in the ICU is not rare. ~30-70% of critically ill patients are thiamine-deficient. Many arrive deficient; others develop deficiency during critical illness because of increased metabolic demand, inadequate intake, or losses. 3. The bedside phenotype is more important than waiting for a thiamine level. High-risk situations include malnutrition, alcohol-related liver disease, bariatric surgery, renal replacement therapy, polyuria/DKA, chronic diuretic therapy, unexplained encephalopathy, unexplained lactate elevation, and sepsis. 4. Starting nutrition can unmask the deficiency. Glucose administration increases carbohydrate metabolism and thiamine utilization. A malnourished patient may therefore develop rising lactate after initiation of enteral/parenteral nutrition. Refeeding syndrome is not simply a phosphorus/potassium problem; thiamine deficiency can be central to its pathophysiology. 5. Dialysis and polyuria are major clues. Thiamine can be lost during continuous RRT, hemodialysis, and peritoneal dialysis. Renal losses also rise with polyuria, including the diuretic phase of AKI, post-transplant polyuria, DKA, and chronic diuretic therapy in heart failure. 6. Do not wait for the classic Wernicke's triad. Altered mental status, ocular abnormalities, and gait ataxia are rarely all present together. I think I have seen it only a few times. In an at-risk ICU patient with otherwise unexplained encephalopathy, absence of the complete triad should not reassure you. 7. A plasma thiamine concentration is not a great “rule-out” test. Testing is often unavailable and expensive, and blood concentration does not necessarily reflect tissue thiamine status. I don't even remember when I last ordered the test (if ever...). Erythrocyte transketolase activity is physiologically more informative, but its cutoffs are poorly defined. Just recognize the risk population and consider a therapeutic trial rather than wait for laboratory confirmation. 8. The sepsis data are more nuanced than “thiamine works” or “thiamine doesn't work.” Thiamine is not expected to improve hard outcomes in the overall septic-shock population. Some subgroup analyses and meta-analyses suggest signals for improved lactate clearance and organ function, particularly renal outcomes. I don't consider it a magic drug... 9. Thiamine alone ≠ HAT (hydrocortisone + ascorbic acid +thiamine) therapy. Do not interpret negative trials of HAT as proof that correcting thiamine deficiency is useless. Large HAT RCTs failed to demonstrate the dramatic clinical benefit initially claimed, and a VICTAS secondary analysis raised concerns about longer-term outcomes. That is a different question from replacing thiamine in a patient likely to be deficient. 10. The kidney may be an important target organ. Renal tubular cells are highly energy dependent. Across secondary analyses, observational data, and meta-analytic evidence, thiamine supplementation -particularly in deficient patients- shows a signal toward less AKI progression, better renal recovery, and less need for RRT, although individual RCTs have not consistently demonstrated significant benefit in unselected populations. Rule of thumb: “⬆️ lactate + risk factor + no good explanation" → think B1 deficiency” Especially think about it when you see malnutrition/refeeding, alcoholism/cirrhosis, dialysis, polyuria/DKA, chronic diuretics, unexplained encephalopathy, sepsis, or otherwise unexplained persistent hyperlactatemia. I usually include it in the admission orders for most of my ICU patients along with DVT and GI prophylaxis...! Thiamine deficiency behaves less like an obscure vitamin deficiency and more like a potentially reversible form of mitochondrial energy failure. Or that's how I like to think about it. #foamed #foamcc #meded
13
158
7
636
77,130
🧠 Acute ischemic stroke in 2026: the treatment window is becoming a tissue window The management of acute ischemic stroke has changed dramatically. This useful 2026 review brings together the evolving evidence for thrombolysis, thrombectomy and early antithrombotic therapy. Thrombolysis: tenecteplase is changing practice Alteplase established IV thrombolysis as standard therapy, but tenecteplase has important practical and pharmacological advantages: greater fibrin specificity, a longer half-life and, importantly in emergency stroke workflows, administration as a single IV bolus. The reviewed evidence supports tenecteplase 0.25 mg/kg, maximum 25 mg, and a 2024 meta-analysis found a higher likelihood of excellent functional outcome and less disability at 90 days compared with alteplase. Tenecteplase was FDA-approved for acute ischemic stroke in 2025. But perhaps the bigger conceptual change is that 4.5 hours is no longer an absolute biological boundary. MRI DWI-FLAIR mismatch and CT/MR perfusion can identify selected patients with potentially salvageable tissue beyond conventional time windows. WAKE-UP and EXTEND established this principle, while more recent studies have continued exploring thrombolysis as far as 24 hours in carefully selected patients. Thrombectomy: even a large core does not necessarily mean “too late” Mechanical thrombectomy transformed large-vessel-occlusion stroke, and DAWN and DEFUSE 3 subsequently demonstrated that carefully selected patients can benefit 6-24 hours after onset. Now another boundary is disappearing: the large ischemic core. Multiple randomized trials have demonstrated benefit from thrombectomy in patients previously considered to have too much established infarction. Across these studies, thrombectomy plus medical therapy was associated with better 90-day functional outcomes, with a combined OR of 1.57 (95% CI 1.40-1.76). The review highlights current consideration of thrombectomy for proximal MCA/ICA occlusion with ASPECTS 3-5 and, in selected patients, even ASPECTS 0-2. Posterior circulation treatment has also evolved. For basilar artery occlusion with moderate-to-severe deficits, thrombectomy can be considered up to 24 hours. In contrast, the role of thrombectomy for medium and distal vessel occlusion remains unsettled, with recent trials producing conflicting signals. And reperfusion is only the beginning Recurrent ischemic events cluster early after stroke. Aspirin initiated within 48 hours reduces recurrence and produces a small mortality benefit. For minor ischemic stroke or high-risk TIA, appropriately selected patients benefit from early, short-term dual antiplatelet therapy, rather than simply continuing aspirin alone. Time is brain... Reference 📚 Leon Guerrero CR. 2026. Thrombolysis, Thrombectomy, and Antithrombotic Therapy for Acute Ischemic Stroke. Continuum (Minneap Minn). 32(3):775–790. DOI: 10.1212/cont.0000000000001701
96
266
8,207