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📢 Tweetorial alert‼️Have you checked out @TheSkeletonKG latest post on Hypophosphatemia? https://www.renalfellow.org/2020/06/17/skeleton-key-group-electrolyte-case-9/

If you have, you must already know that hypophos is bad news⚠️
@kkalra_22 @sopalilla @TheSkeletonKG @NSMCinternship #tweetorial #nephtwitter #FOAMed
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Before we get on with Hypophos, let’s review some Phosphate basics.

Phosphate in the body is present in🤔
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All of the above is correct! Also 85% of Phosphate is present in the skeleton!

📌Serum phosphate(Pi) is regulated by several hormones to maintain a normal range of 2.5-4.5mg/dl.
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Why is phosphate important? Only because it is essential for
💥energy metabolism
🦴 bone formation
📡 signal transduction
It is also an imp. component of phospholipids and nucleic acids🧬

Say what?!
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So what is hypophosphatemia? And how low is too low❓
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But why do we care if Pi is low? What’s the big deal?
Hypophos can cause a lot of complications, sometimes life threatening especially when <1mg/dl.

⚠️⚠️These are dependent on the chronicity & severity of intracellular Pi depletion⚠️⚠️
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Most of the symptoms are due to consequences of intra cellular Pi depletion (<1 mg/dL) which include

📌⏬in red cell DPG levels, thereby ⏫ the affinity of Hb to O2 and ⏬ O2 release at tissue level

📌⏬ in intracellular ATP which impair cell functions
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In the CNS🧠,severe ATP depletion can cause irritability, paresthesias, seizures, encephalopathy, hallucinations, delirium, coma & central myelinolysis 🤯
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In RBCs🩸,🔽 in intracellular ATP 🔼 RBC rigidity & predisposes it to hemolysis.

📌ATP depletion can also 🔽 phagocytosis & chemotaxis of WBCs

📌Defective clot retraction & thrombocytopenia can occur resulting in mucosal bleeding
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In the Heart❤️,ATP depletion can cause impaired myocardial contractility, ⏫ incidence of VT & req. of vasoactive drugs which improves with phos administration

📌Diaphragmatic contractility⏬ in hypophos & may cause prolonged ventilator dependency in critically ill pts
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In the bones 🦴, low Pi can cause osteomalacia, fractures & growth retardation especially in children.

📌This is because initially there is⏫ resorption ➡️ causing release of calcium ➡️ hypercalciuria
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In the muscle💪acute on chronic hypophos can lead to rhabdomyolysis (risk factors-alcoholics & refeeding syndrome)

📌Pi released from damaged muscle may mask actual low Pi & protect against development of symptoms.

⚡️Low Pi before/ after the peak may be the only clue here⚡️
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How does Hypophos occur❓
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And the answer is .. you guessed it..all of them✅

Let look at all the causes of Hypophos👇
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What do we do if we see low Pi?
⚡️Here’s an easy algorithm from @lancet
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Ok so now we know Pi is low and why it is low, What next?
Treat it!

💊Phos is available as Na-phos & K-Phos in both oral & IV forms

⚡️IV preparations 💉are reserved for acute, severe & symptomatic hypophos⚡️
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💉Multiple studies have evaluated the efficacy & safety of IV repletion regimens & generally agree that aggressive Pi supplementation is safe with doses up to 45 mmol with infusion rates up to 20 mmol/ hour.

📌(1mmol of phosphate = 31mg phos)
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⚠️Make sure to check kidney function, Ca & K before correction.

A safe & reasonable approach for IV correction💉 would be
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⚡️Oral Phos 💊is the 1st choice in acute asymptomatic & chronic hypophos⚡️

It is rapidly absorbed in the small intestine & 3-4 daily doses are required to improve the serum levels.

📌Active vit D should be supplemented as needed.
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💊Typical oral dose should be 2-3 times the normal daily intake,i.e 2.5 to 3.5 g (80 to 110 mmol)/ day, divided over 2-3 doses.

⚠️Oral phos causes adverse events like diarrhea & abdominal pain because of which compliance can be a considerable clinical problem.
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Still confused?

⚡Here's a simplified algorithm for the treatment of Hypophos⚡️
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Time to wrap up this tweetorial, here are some🔑points

🔑Severe hypophos (Pi< 1 mg/dl) can be life threatening
🔑Pi can be normal in hypophos induced rhabdomyolysis
🔑Check kidney function, Ca & K before correction
🔑Oral repletion is preferred if asymptomatic & Pi >1 mg/dl
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