A ๐งต on chest Xray signs in pulmonary thromboembolism.
The ๐๐น๐ฒ๐ถ๐๐ฐ๐ต๐ป๐ฒ๐ฟ ๐๐ถ๐ด๐ป is a prominent central artery that can be caused either by pulmonary hypertension or by distension of the vessel by a large pulmonary embolus seen on chest x ray.
๐๐ฎ๐บ๐ฝ๐๐ผ๐ป ๐ต๐๐บ๐ฝ refers to a dome-shaped, pleural-based opacification in the lung most commonly due to pulmonary embolism and lung infarction (it can also result from other causes of pulmonary infarction (e.g. vascular occlusion due to angioinvasive aspergillosis)
The focal area of increased translucency due to oligaemia is caused by impaired vascularisation of the lung due to primary mechanical obstruction or reflex vasoconstriction.
The ๐๐ป๐๐ฐ๐ธ๐น๐ฒ ๐๐ถ๐ด๐ป refers to the abrupt tapering or cutoff of a pulmonary artery secondary to a pulmonary embolus (PE).
This is an important ancillary finding in pulmonary embolism, and often associated with the Fleischner sign of dilated central pulmonary arteries.
A summary of things till now๐
๐ฃ๐ฎ๐น๐น๐ฎ's ๐๐ถ๐ด๐ป :
Clinical sign in which an enlarged right descending pulmonary artery is seen on the chest x-ray in patients with pulmonary embolism
๐๐ต๐ฎ๐ป๐ด ๐๐ถ๐ด๐ป on CXR describes a dilated left or right descending pulmonary artery with an abrupt change in calibre, with an amputated appearance.
This sign is most commonly associated with with pulmonary infarction and pulmonary hypertension following pulmonary embolism
"Doctor, my vitamin D levels are only 9. I am always tired"
Frequent scenario in my clinic and this is how I approach this . A๐งต
1,25(OH)2 VitD is the active form of vitD in our body. But the levels of 1,25(OH)2 is almost always normal in vitD deficiency. This is why we doctors always recommend checking serum levels of 25(OH) vitamin D to evaluate vitamin D deficiency.
You see, 25(OH) vitamin D is the primary form that circulates and gets stored in your body. On the other hand, levels of 1,25(OH)2 vitamin D, which is the active form, are seldom requested by physicians because they're not meant for diagnosing deficiency. Instead, they're useful for investigating elevated calcium levels due to conditions like granulomatous diseases, but let's keep our focus on vitamin D deficiency for now. Most crucially, remember that 1,25(OH)2 assays are available in labs, so avoid mistakenly ordering them just to screen for vitamin D deficiency.
I want to ascertain something here. There are myriad causes of tiredness, and I will not jump the gun here just by seeing a low serum vitamin D report and calling it. I would definitely rule out other causes of fatigue, but now will stick to vitamin D deficiency for the sake of our discussion here. Read onโฆ.
Vitamin D deficiency is mainly diagnosed by measuring serum 25-hydroxyvitamin D (25(OH)D), the key biomarker for vitamin D status, as it reflects skin production, diet, and supplementation effects.
Thresholds generally classify deficiency below 20 ng/mL (50 nmol/L), insufficiency at 20-30 ng/mL (50-75 nmol/L), and sufficiency at 30-50 ng/mL (75-125 nmol/L), though these lack full agreement and stem from observational studies rather than trials.
Routine checking isn't recommended for symptom-free people, but it's advised for high-risk groups like those with malabsorption, chronic kidney disease, obesity (BMI >30 kg/mยฒ), dark skin, low sun exposure, or symptoms such as bone/muscle pain.
๐ธWhy is vitamin D important to our body?
Vitamin D plays a pivotal role in regulating calcium and phosphorus homeostasis by enhancing their intestinal absorption, promoting renal reabsorption, and supporting bone mineralization, which helps prevent conditions like rickets in children or osteomalacia/osteoporosis in adults. It also modulates your immune response by fine-tuning immunity, potentially reducing susceptibility to infections and chronic inflammation. On top of that, its pleiotropic effects extend to cardiovascular protection and lowering all-cause mortality, while optimizing maternal-fetal outcomes during pregnancy through various signaling pathways in cells.
๐ธWhat causes vitamin D deficiency?
There are many causes of low vitamin D levels in the body. Here, I am strictly sticking to nutritional and lifestyle-related causes to avoid the risk of overwhelming you.
Older people often ask me this question: "Vitamin D deficiency was not common in our times. Why is it so common now? What changed?
Well, the short answer is nutritional choices and low sun exposure. You can understand this answer if you compare your lifestyle and food choices with the older generation.
๐ธHow does our body get vitamin D?
Vitamin D is more of a hormone than a vitamin if you have understood its action. The body is capable of creating its own vitamin D in the skin if it gets exposed to UV rays. When the skin is exposed to UV rays, an intermediate of cholesterol metabolism called 7-dehydrocholesterol, which is present in the skin cells, gets converted to vitamin D3 (cholecalciferol). This vitamin D3 then gets hydroxylated in the liver and finally in the kidneys to form the active form, 1,25(OH)2 vitamin D. Medical societies have come to the conclusion that merely sunlight exposure may not be enough for meeting the daily vitamin D requirements. Read on....
The other source of vitamin D is from the diet. It is obvious that if the diet is not proper and there is low sunlight exposure, the chances of vitamin D deficiency increases, as the daily recommended intake is 600-800 IU/day. So, supplementation may be required.
So by now, you have become familiar with the various forms of vitamin D.
๐ฅ๐๐ฟ๐๐ด๐ฎ๐ฑ๐ฎ ๐ฆ๐๐ป๐ฑ๐ฟ๐ผ๐บ๐ฒ (BrS)
is a rare arrhythmogenic cardiac channelopathy characterised by ECG findings of โก๏ธ
๐ด โฅ0.2mV of ST segment elevation
โ๏ธ
๐ด Negative T-wave in more than one anterior precordial leads (v1 v2, v3)
BrS is associated with risk of sudden cardiac death resulting from lethal arrythmias (VF/VT).
It is caused by mutation in cardio-myocyte voltage channels.
Various mutations are implied resulting in BrS.
Most common is the mutation in SCN5A, a Na channel encoding gene.
๐ฅSmith ๐ฆ๐ต ๐ข๐ญ. reported draining a world record of 41 ๐น๐ถ๐๐ฟ๐ฒ๐ of ascitic fluid in a single paracentesis session of a patient with decompensated cirrhosis.
How much Albumin would be needed in this case to prevent post paracentesis circulatory dysfunction ? ๐งต Read on๐
A ๐งต on important points to consider while performing Large Volume Paracentesis (LVP)
๐Large Volume Paracentesis(LVP)
is arbitrarily defined as a paracentesis with >5 L of ascitic fluid drained.
In patients undergoing LVP, the use of albumin is crucial to prevent a further reduction of effective arterial blood volume, which may precipitate postparacentesis circulatory dysfunction (PPCD).
The clinical manifestations of PPCD include renal impairment, including HRS, dilutional hyponatremia, hepatic encephalopathy and death.
Albumin infusion is particularly important if more than 5 L of ascites are removed to prevent the development of PPCD.
Paracenteses of a smaller volume(<5L) are not associated with significant hemodynamic changes and albumin infusion may not be required.
Although there has not been a doseโresponse study on albumin use with LVP, the administration of 6โ8 g of albumin per liter of ascites removed has been recommended.
๐ฅFor example, after the fifth liter, approximately 40 g of albumin should be infused, and after 8 L removal, the amount of albumin given should be approximately 64 g.
It has been held that there is no limit for the amount of ascites that can be removed in a single session, provided an appropriate amount of albumin is administered.
However, the risk of PPCD increases with >8 L of fluid evacuated in one single session.
A study showed that by limiting the LVP volume to <8 L per session and providing a higher than recommended dose of albumin (9.0 ยฑ 2.5 g per liter of ascites removed), renal function and survival may be better preserved over a mean period of 2 years despite the development of PPCD in 40% of patients.
In patients with hemodynamic instability (systolic blood pressure <90 mm Hg), hyponatremia (serum sodium <130 mmol/L), and/or the presence of AKI, albumin infusion should be strongly considered for paracentesis of a smaller volume.
LVP is a safe procedure even in the presence of coagulopathy. In a study that included patients with an international normalized ratio of >1.5 and a platelet count of <50 ร 109/L, only 1% of patients experienced minimal cutaneous bleeding after LVP.
Therefore, elevated prothrombin time or thrombocytopenia is not a contraindication for paracentesis, nor is transfusion of clotting factors or platelets recommended.
Possible exceptions may include patients with disseminated intravascular coagulation or uremia with thrombocytopenia.
1/3 ๐ ๐พ๐ค๐ฃ๐ฉ.
๐ฅIdeal site for needle insertion in abdominal paracentesis
๐ธ๏ธMalar rash is classically described in SLE as a "butterfly" shaped erythematous rash in the malar distribution, which includes the cheeks and crosses the nasal bridge but spares the nasolabial folds.
Let's look at the mimickers๐
Do read the whole๐งต
๐ Systemic Lupus Erythematosus
๐ธ๏ธClassic finding in SLE
๐ธ๏ธThe ORIGINAL Malar Rash๐ฆ
From Kelley's Textbook of Rheumatology, 9e
๐ ACNE ROSACEA
A common chronic inflammatory acneiform disorder of the facial pilosebaceous units.
An increased reactivity of capillaries leading to flushing and telangiectasia.
May result in rubbery thickening of nose, cheeks, forehead, or chin due to sebaceous hyperplasia.