Draft

209  Locke Summer Bootcamp H2o And Na

209.1 Summary

  • Disturbances of Water and Sodium
  • Roadmap
  • How does hyponatremia cause problems?
  • Hyponatremia: Resident-level algorithm
  • Hyponatremia: Fellow-level algorithm

209.2 Slide outline

209.2.1 Slide 1

  • Disturbances of Water and Sodium
  • Brian Locke, MD
  • 2022 Fellow Bootcamp ### Slide 2
  • Roadmap
  • Disorders of Water
  • Hyponatremia
  • Fellow-level schema
  • When to use DDAVP clamp
  • Hypernatremia
  • Why all our ARDS patients are hypernatremia and why Orme’s approach works
  • Disorders of Sodium
  • Congestion
  • Diuresis vs Natriuresis
  • Inadequate dosing of lasix
  • When to stop ### Slide 3
  • How does hyponatremia cause problems?
  • Why does DKA cause “hyponatremia” on labs, but symptoms of “hypernatremia” (thirst/dehydration, AMS) ### Slide 4
  • How does hyponatremia cause problems?
  • Osmolarity: number of particles in 1L ( that drops the freezing point 1.86 Kelvin; independent of size/weight of particles)
  • Osmolality: number of particles of 1kg of solvent.
  • Tonicity: effective osmolality of solutes that can act across a semi-permeable membrane
  • Osm: property of particle in solution; Tonicity property of solution in relationship to a semipermeable membrane (cell membrane)
  • Na+: exerts osmotic pressure
  • Glu: moves across semipermeable membranes w/ insulin – transient (usually)
  • Urea, ethanol, lactate: passively moves across semipermeable membrane: no osmotic pressure ### Slide 5
  • Hyponatremia: Resident-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • Serum Osm ### Slide 6
  • Hyponatremia: Resident-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Serum Osm
  • Urine Osm
  • Serum too dilute, urine should be ultra-dilute ### Slide 7
  • Hyponatremia: Resident-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (0.75l/hr max UOP)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (100 mOsm-> 2L max)
  • Impaired Range (~100 mOsm/kg)
  • AKI, CKD, Old Age…
  • Serum Osm
  • Urine Osm
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 8
  • Hyponatremia: Resident-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (0.75l/hr max UOP)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (100 mOsm-> 2L max)
  • Impaired Range (~100 mOsm/kg)
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Serum Osm
  • Urine Osm
  • Urine Na
  • (Why not FENa?)
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 9
  • Hyponatremia: Resident-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (0.75l/hr max UOP)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (100 mOsm-> 2L max)
  • Impaired Range (~100 mOsm/kg)
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • Serum Osm
  • Urine Osm
  • Urine Na
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 10
  • TODO: No text extracted from this slide. ### Slide 11
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Are they hyperosmolar?
  • Lab error? (lipemic, m-prot)
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • Clinical Situation (IVIG?)
  • Low USpec Grav: specific, not sensitive
  • What happened with 1L NS in ED? ### Slide 12
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • What happened with 1L NS in ED?
  • 1542 MEqmOsm Na Cl allows 6L free water loss if ADH gone
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 13
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • What happened with 1L NS in ED?
  • 1542 MEqmOsm Na+Cl allows 6L free water loss if ADH gone!
  • What if ADH to cause min Uosm:
  • 150? 300? 600?
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 14
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • What happened with 1L NS in ED?
  • 1542 MEqmOsm Na+Cl allows 6L free water loss if ADH gone!
  • What if ADH to cause min Uosm:
  • 150? (2L, Na up) 300? (1L, na unchanged) 600? (500 cc, na down)
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 15
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • What will happen if we restore EABV to kidneys?
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 16
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • What will happen if we restore EABV to kidneys?
  • All the way off: 6L of UOP for 1L NS
  • Part of the way off: 1L-5L off
  • Uosm, Una reflect a physiologic state, not a diagnosis – can cycle them
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L
  • Δ Urine Osm
  • Δ Urine Na ### Slide 17
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • Your intern gave 1L IVF and the patient’s UOP is now 400 cc/hr. What category were they in?
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 18
  • Hyponatremia: Fellow-level algorithm
  • Na+ low enough to care?
  • Kidneys appropriate?
  • ADH present
  • No ADH present
  • Uosm: 50 – 1200 mOsm/kg
  • < 50 osm per L H2O
  • Polydipsia (H2O up)
  • Beer: EtOH, C6H12O6
  • Tea/Toast (osm down)
  • Impaired Range
  • AKI, CKD, Old Age…
  • Appropriate?
  • Not Appropriate:
  • SIADH etc.
  • ADH like a vasopressor (decreased EABV)
  • Hypovolemic
  • Hypervolemic
  • Maldistributed
  • Your intern gave 1L IVF and the patient’s UOP is now 400 cc/hr. What category were they in?
  • How could we stop this?
  • Do not wait for next Na
  • 60kg -> 600 mOsm/d solute
  • 50 mOsm: max 12L
  • 1200 mOsm: min 0.5L ### Slide 19
  • DDAVP clamp:
  • ALL of the risk of over-correction comes from solute being given when ADH is low ( body can now dump free water at Uosm 50 osm/L)
  • Adrogue-Madias equation: 1L NS in 70kg w/ Na 105 -> 107.5
  • 2 options:
  • D5W to match the urine output (that’s a lot of D5; ‘iatrogenic polydipsia’)
  • Give ADH back (useful whenever UOP high or might become high)
  • DDAVP 2 mcg IV q8hr, continued until Na at target
  • Give 3% Saline to increase
  • Do nothing to keep unchanged
  • Give D5w to decrease ### Slide 20
  • Hyponatremia: summary
  • Tools for residents: Serum Osm, Urine Osm, Urine Na (FENa)
  • Tools for fellows: UOP, response to solutes, clinical circumstance, cycling the labs prn
  • If the ED gave 1L IVF and the [Na] didn’t budge or worsened:
  • SIADH etc., or appropriate ADH presence from hypervol/maldistributed
  • If the ED gave 1L IVF and the patient is making more than 250+ cc/hr
  • They either had no ADH to start, or reason for ADH is gone (hypovol)
  • Start DDAVP 2 mcg IV q8h ### Slide 21
  • Hypernatremia
  • 60kg -> 600 mOsm/d solute; 50 mOsm: max 12L; 1200 mOsm/L: min 0.5L
  • With normal solute intake and less than 500cc water, you’d get hypernatremic
  • If you have Diabetes Insipidus, your maximum concentration drops. If max Uosm 600 mOsm/L, then <1L leads to hypernatremia. If Uosm 300, <2 L leads to hypernatremia, etc.
  • High urine output, CNS tumor, long term lithium and hypernatremic? Check Uosm
  • 1200 mOsm minimum of 1L of maximally concentrated UOP ### Slide 22
  • Does someone who eats 2g of Na/d drink the same H2O as someone who eats 4g of Na/d?
  • Yes – at steady state – in out.
  • Over a large range of sodium intake, urine production and thus fluid intake will be constant
  • More natriuresis occurs in people who eat more salt. ### Slide 23
  • Physiology Review
  • Large bolus of free water?
  • ADH shuts off. Kidneys produce dilute urine. Electrolytes and volume status unchanged.
  • For avg (10 mOsm/kg/day) diet, ADH fully off 50 mmol/L (maximally dilute) 70 kg person > 700 mmol load > 50 mmol/L excretion > 14L of free water can be excreted per day without perturbing sodium balance.
  • Large bolus of sodium?
  • Maximal natriuresis ~280 mmol/L (2x serum, roughly).
  • Why? There is NO active sodium excretion along the nephron ### Slide 24
  • The nephron doesn’t have a dedicated method to excrete sodium.
  • Instead, the kidneys concentrate urine by increasing urea concentration in the medulla.
  • Counter-intuitively, to maintain osmolality the major mechanism after an ingestion of salt is not thirst, but free water re-absorption in the kidney (ie. concentration of urine)
  • It takes time to generate this gradient
  • Kidneys retain water (with ADH) to maintain [Na] in serum in the interim
  • Glucocorticoid driven catabolism to generate urea
  • Increase urea in the renal medullary interstitium
  • Increase osmotic gradient to reabsorb free water ### Slide 25
  • If someone who normally eats low Na diet eats high Na diet, do they drink more water?
  • Healthy people randomized to either low sodium (0.5 g) to regular (3.2g) diet, then swap
  • After increased Na load: takes ~3-5 days to reach a new steady state with kidney able to match Na load
  • On the first day: only half of excess Na load excreted
  • The positive sodium balance caused fluid retention and an increase in body weight of over 1 kg.
  • No difference in fluid intake (free-water reabsorption makes up difference) ### Slide 26
  • Na and fluid loading in the ICU
  • 1L of NaCl 3.5gm (154 mmol Na) ~7 gm NaCl
  • Consider COVID-ARDS:
  • ~750 cc/d NS from Ketamine, 350 cc/d from Fentanyl 100 cc/d ciastricurium, 200 from CTX
  • ~4g of sodium just from sedation and NMB ### Slide 27
  • ADH is also a weak Anti-natriuretic Hormone
  • Healthy volunteers drank either:
  • Low hydration: free water 0.25 mL/kg q30m (35 mL/hr for 70kg) or
  • High hydration: water 2.0 mL/kg q30m ( 288 mL/h for 70kg).
  • Then received 250cc 2% NaCl
  • High hydration: excrete the extra sodium immediately.
  • Low hydration cannot (ADH crosstalk, maximal concentration ability of kidneys)
  • Meaning: the kidneys CANNOT create low free water, high Na urine ### Slide 28
  • Physiology Review:
  • The kidneys have mechanisms to quickly adjust free water clearance.
  • The kidney does not have a fast mechanism to increase natriuresis – it takes several days and catabolism to achieve this.
  • Limitation in free water hampers natriuresis due to ADH crosstalk.
  • While the kidney is adapting to a new baseline sodium intake, fluid retention occurs in the kidney (regardless how much fluid they drink).
  • Therefore, it is very hard to achieve balanced I/O during salt loading ### Slide 29
  • Bad ARDS Circle of Life
  • Many Drips
  • (in NS)
  • Lasix & no
  • free H2O
  • Fluid Overload
  • Hypernatremia ### Slide 30
  • Single-day, point prevalence survey: 46 Australian and New Zealand ICUs on 21 September 2011
  • Median sodium admin: 224.5 mmol (IQR, 144.9-367.6 mmol). 2.8 mmol/kg (IQR, 1.6-4.7 mmol/kg).
  • Patients Day 2-10 of ICU admission:
  • maintenance or replacement intravenous (IV) infusions, 69.3mmol; 30.9% of all sodium sources;
  • IV fluid boluses, 36.5 mmol; 16.3%;
  • IV drug boluses, 27.6 mmol; 12.3%;
  • enteral nutrition, 26.5 mmol; 11.8%;
  • IV drug infusions, 19.3 mmol; 8.6%;
  • IV flushes, 16.6mmol; 7.4%;
  • blood products, 13.5 mmol; 6%;
  • IV antimicrobials, 11.2mmol; 5%;
  • parenteral nutrition, 4.3 mmol; 1.9%.
  • Median 5 grams of Na per day
  • Double the usual intake ### Slide 31
  • Why do we dissolve medications in NaCl?
  • ICUs have pre-mixed versions of medications to deliver quickly (ie. antibiotics, fentanyl)
  • Some meds are sodium salts ( any negative ion paired with a sodium cation) – generally more soluble in water than the acid form
  • A few medications must be given in NS
  • It’s the default ### Slide 32
  • TODO: No text extracted from this slide. ### Slide 33
  • Clinical impact - TOPMAST trial
  • Blind randomization of 70 patients undergoing major thoracic surgery to [Na] 154 mmol/L vs [Na] 54 mmol/L fluid
  • Primary: Net fluid balance: Na154 +4.5L vs Na54 3.12L despite identical fluid infused
  • Secondary:
  • Pulmonary Edema: Na154 17%, Na54 3%
  • Electrolyte abnormalities:
  • Na154 – n3 had Na above 145.
  • N24 had Cl- above ULN
  • Na54 – n4 patients had Na
  • below 135. ### Slide 34
  • The patient is hypernatremic and congested:
  • Reduce Na intake (The Orme approach- is the patient on Nepro?)
  • Wait – their kidneys will adapt in 3-5 days
  • Give them more D5w – this will allow natriuresis by decreasing ADH
  • Maybe we should default to meds in D5w instead of NS?
  • If you give 2L D5w… say next day the ins 3L, outs 3L – have you made progress? Stay tuned… ### Slide 35
  • Bad ARDS Circle of Life
  • Many Drips
  • (in NS)
  • Lasix & no
  • free H2O
  • Fluid Overload
  • Hypernatremia
  • Use D5W instead
  • Driven By Na Overload
  • Liberal free water can allow natriuresis ### Slide 36
  • Congestion
  • Disorders of H2O homeostasis: Hypernatremia and Hyponatremia
  • Disorders of Na homeostasis: Congestion and Hypovolemia
  • Yet
  • On rounds, we present “(mLs) in and out” and not ”Na in and Na out”
  • Why? ### Slide 37
  • “Despite hospitalization for HF being exceptionally common, expensive, and morbid, we have not a single Class I Level of Evidence: A guideline recommendation to guide our care of these patients” ### Slide 38
  • A patient is congested: what initial orders are important?
  • Na restriction of 2g per day? Yes or No
  • Fluid restriction of 2L per day? Yes or No
  • Strict I/Os and Daily weights? Yes or No ### Slide 39
  • Salt and Fluid Restriction ### Slide 40
  • Salt and Fluid Restriction causes… thirst ### Slide 41
  • What is the problem with I/O and Kg?
  • Assumptions:
  • For I/O to be a surrogate of net natriuresis:
  • [Na] intake constant
  • D5 / NS
  • [UNa] constant
  • Breaking phenomenon
  • Recording is accurate.
  • In reality, it is not ### Slide 42
  • Natriuresis varies widely during diuresis
  • Why might the Na concentration of urine vary between patients?
  • Depends on ADH presence (among other other reasons).
  • Tight water restriction ADH increase, natriuresis unchanged.
  • Loose water restriction ADH decrease, natriuresis unchanged ### Slide 43
  • Urine composition by time
  • “the sodium content of diuretic-induced urine is highly variable and correlates only modestly with fluid and weight loss” ### Slide 44
  • Braking Phenomenon (of natriuresis)
  • Assume a patient makes no dietary changes
  • Sodium clearance increases with ECF (true)
  • Off diuretics, a patient takes in 3g of Na in 24h. They are at steady state. 3g of Na must be excreted in 24h. They are congested.
  • If you start a diuretic, initially their ECF is unchanged (congested), but natriuresis increases.
  • They eventually reach a new steady state (inout), but at a lower ECF ### Slide 45
  • Discordant Diuresis and Natriuresis
  • Net Na drops a little
  • Net Na drops a lot
  • Net I/O drops a little
  • Not much response, normal [UNa]
  • Good natriuresis, high [UNa]
  • Net I/O drops a lot
  • Good diuresis,
  • Low [UNa]
  • Good response, normal [Una] ### Slide 46
  • Natriuresis based decongestion
  • Simple: Spot urine Na > 100 2h after dose was probably effective (will lead to net 2g+ natriuresis in BID dosing)
  • Complex: ### Slide 47
  • Does it work?
  • NCT04481919 RCT with hard outcome end-points ongoing ### Slide 48
  • TODO: No text extracted from this slide. ### Slide 49
  • How to dose:
    1. DOSE trial: 2.5x home dose and IV
    1. Assess:
  • UOP should be 150 hr+ within 2h of IV dose (don’t wait 6 to see)
  • UNa should be 50-70+
  • Why are you not giving a higher dose?
  • Would respond to
  • low dose
  • Needs high dose
  • Give low dose
  • Delayed in needed care
  • Give high dose
  • What’s the harm? ### Slide 50
  • Toxicity without volume depletion?
  • 1985: Patient with oliguric AKI were given “1 g furosemide was given as a single injection over four hours. In the test group, frusemide was then continued either intravenously or orally in a dose of 3 g/24 hr until a urine output of 200 ml/hr was sustained or until the plasma creatinine fell …The serious complication of deafness occurred in two of 28 patients and in one of them this was permanent.”
  • 2021: Yale Diuretic Protocol: “automated, nurse-driven, and called for administration of 2 to 12.5 mg IV bumetanide up to 3 times daily.” “rapidly escalated toward a peak of 1,500 mg IV furosemide equivalents per day that was reached in the first 2 days of the protocol in 86% of patients.” “No cases of ototoxicity (n409)
  • Meta-analysis: OR 3 of developing ototoxicity when dose excess 1 GRAM daily (~40 mg/hr)
  • NOT A NEPHROTOXIN ### Slide 51
  • “Suspect near euvolemia due to contraction alkalosis”
  • Loop diuretics create Chloride (and Sodium)-Rich urine
  • Loosing Cl- rich, ‘bicarbonate poor’ urine will lead to development of alkalosis at ANY extracellular volume.
  • Pendrin: Chloride – Bicarbonate exchanger to maintain neutrality
  • Not “contraction” (albumin will not fix it), but “chloride depletion” (saline will). ### Slide 52
  • Diurese until sCr clearly increases: No intrinsic renal injury from diuretic caused creatinine increase ### Slide 53
  • Congestion: Review
  • Realize that I/O’s are a surrogate for what we care about (Na flux)
  • Salt and Fluid restrictions are TWDFNR in patients with normal [Na+]
  • Give higher doses of loop diuretics
  • Do not use elevated [HCO3-] as a reason to stop diuresing ### Slide 54
  • Key References
  • Hyponatremia:
  • https://www.coreimpodcast.com/2021/02/10/5-pearls-on-hyponatremia-episode-1/
  • Desmopressin to Prevent Rapid Sodium Correction in Severe Hyponatremia: A Systematic Review: DOI: 10.1016/j.amjmed.2015.04.040
  • Hypernatremia:
  • Fluid-induced harm in the hospital: look beyond volume and start considering sodium. From physiology towards recommendations for daily practice in hospitalized adults: https://doi.org/10.1186/s13613-021-00851-3
  • Congestion:
  • The use of diuretics in heart failure with congestion - a position statement from the Heart Failure Association of the European Society of Cardiology: https://onlinelibrary.wiley.com/doi/10.1002/ejhf.1369
  • It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis: https://doi.org/10.1681/ASN.2011070720

209.3 Learning objectives

  • Disturbances of Water and Sodium
  • Roadmap
  • How does hyponatremia cause problems?
  • Hyponatremia: Resident-level algorithm
  • Hyponatremia: Fellow-level algorithm

209.4 Bottom line / summary

  • Disturbances of Water and Sodium
  • Roadmap
  • How does hyponatremia cause problems?
  • Hyponatremia: Resident-level algorithm
  • Hyponatremia: Fellow-level algorithm

209.5 Approach

  1. TODO: Outline the initial assessment or decision point.
  2. TODO: Outline the next diagnostic or management step.
  3. TODO: Outline follow-up or escalation criteria.

209.6 Red flags / when to escalate

  • TODO: List red flags that require urgent escalation.

209.7 Common pitfalls

  • TODO: Capture common errors or missed steps.

209.8 References

TODO: Add landmark references or guideline citations.

209.9 Slides and assets

209.10 Source materials