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Sodium Management After Stroke

Sodium Management After Stroke

Assessment

Presentation

Health Sciences

Professional Development

Medium

Created by

Anthony Anzivino

Used 4+ times

FREE Resource

22 Slides • 9 Questions

1

Sodium Management After Stroke

Anthony Anzivino, MD
PGY-2

2

  • Quiz Modality Test

  • Overview

  • Hyponatremia

  • Hypernatremia

Outline

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Multiple Choice

Who is the shortest PGY-2?

1

Noah

2

Tommy

3

Heidi

4

Brian

4

Poll

Who is saltiest about that previous question?

Heidi

Brian

Salt King Simran for not being an answer choice

5

Pathophysiology Trigger Warning

6

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7

Multiple Choice

What percent of patients with acute stroke have sodium related abnormalities?

1

5%

2

10%

3

30%

4

50%

8

  • Sodium/Water abnormalities in 50% of stroke cases [1].

    • longer hospitalization

    • increased mortality

    • poorer outcomes

  • Hyponatremia 5x more likely than Hypernatremia

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9

  • Osmoreceptors in hypothalamus monitor serum osmolality changes - sense increased osmolality.

  • Baroreceptors located in the carotid arteries sense decrease in arterial pressure

  • ADH synthesized in hypothalamus and stored in posterior pituitary gland binds V2 receptors in renal collecting ducts leading to passive water resorption

  • Simultaneously, the thirst centre in the lamina terminalis of the third ventricle is stimulated to promote active water consumption.

Normal Homeostasis

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10

Multiple Choice

What kind of receptor is NOT involved in normal water homeostasis?

1

Osmoreceptors

2

Hydroreceptors

3

Baroreceptors

11

  1. Patients not having free access to water

    • low conscious levels, impaired neurocognition --> become dehydrated

  2. Development of Central diabetes insipidus (DI)

    • Impaired ability to produce ADH in order to tell kidneys to reabsorb water

  3. Less likely, primary hypodipsia due to damage directly to thirst center

  4. Medications

    • diuretics

    • lithium

    • colchicine

    • mannitol, sorbitol

Pathogenesis of Hypernatremia

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12

Multiple Choice

In Diabetes Insipidus what will the Urine Osm result?

1

High

2

Low

3

Normal Range

13

  • BMP

  • Urine Osm

  • Serum Osm

​​Evaluation:

  • ​Restore patient to euvolemic state

  • In DI: use water or 5% dextrose solution (correcting a pure water loss)

  • If water loss is from secondary source (infection, GI, etc) use NS to correct for some Na being lost

Treatment:

Management of Hypernatremia

14

Multiple Choice

You are concerned your patient has hypernatremia on the rehab unit, you order a Urine Osm after impressively remembering this lecture. What kind of fluids will you give the patient if the urine Osm returns LOW? (ignore the Code Yellow for now)

1

Isotonic Saline

2

LR (because we love it)

3

Dextrose 5%

4

Hypertonic saline

15

Poll

Do we need a break before continuing on to Hyponatremia?

Yes

No

Very short one as the lamina terminalis of my third ventricle says I must get water

There's no downtime when you're on Uptime

16

  • Admission BMP came back and Sodium is <135

  • ...

Hyponatremia in Stroke Pt

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18

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19

Word Cloud

If your rehab patient's admission BMP comes back with a sodium <135 what will you do?

20

  • Admission BMP came back and Sodium is <135

    • Determine if True or Pseudo (w/ Serum Osm)

      • Once True Hypotonic Hyponatremia is identified

      • *Insert John Cena theme music*

      • Stat page Simran Benipal

Hyponatremia in Stroke Pt

21

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  • Admission BMP came back and Sodium is <135

    1. Determine if True or Pseudo (w/ Serum Osm)

    2. Assess volume status

      1. Hypovolemia

      2. Euvolemia

      3. Hypervolemia

    3. Obtain Urine Sodium

Hyponatremia in Stroke Pt

23

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24

  • In acute stroke, ADH release from the posterior pituitary secretory granules is stimulated by various factors.

  • Water retention or (less often) loss of effective solutes (sodium and potassium) in excess of water can also lead to hyponatremia.

  • Medications

    • antibiotics

    • AEDs

    • Antiarrhythmics

    • Diuretics

    • Benzos

Pathogenesis of Hyponatremia

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  • CSWS first described by Peter et al.in 1950 is defined by the development of excessive natriuresis and subsequent hyponatremia, dehydration in patients with intracranial disease.

  • Though many hypotheses have been given, but the exact mechanism of CSWS is not known

CSWS

SIADH

  • Ordinarily, it is a physiological response to a drop in plasma volume or an increase in serum osmolality that causes the release of ADH.

  • In SIADH, there is a persistent production of ADH despite body fluid hypotonicity and an expanded effective circulatory volume so that the negative feedback mechanism that normally controls ADH fails and ADH continues to be released.

27

CSWS
vs
SIADH

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28

Multiple Choice

Which condition would benefit from water restriction?

1

Cerebral Salt Wasting

2

SIADH

29

  • BMP

  • Serum Osm

  • JVP

  • Urine Na

​​Evaluation:

  • Discontinue offending drugs

  • Treat underlying conditions (infection, adrenal insufficiency)

  • If Hypovolemic - restore with 0.9% isotonic saline

  • If Euvolemic - restrict H2O, vaptans (ADH antagonists), salt tabs, hypertonic saline

  • If Hypervolemic - restrict H2O and Na, vaptans, diuretics may be appropriate

Treatment:

Management of Hyponatremia

30

Hyponatremia

  • Dehydration vs DI

  • Measure Urine Osm

  • Address medication culprits

  • Treat DI w/ 5% dextrose

  • Rarely can see primary hypodipsia

Hypernatremia

Conclusions

  • Rule out True vs Pseudo w/ serum Osm

  • Determine volume status, get Urine Na

  • Address medication culprits

  • Hypovolemic (CSWS) 0.9% isotonic saline

  • Euvolemic (SIADH) - restrict H2O, vaptans, salt tabs, hypertonic saline

  • Hypervolemic - restrict H2O and Na, vaptans, diuretics

31

1.Yuen KCJ, Sharf V, Smith E, et al. Sodium and water perturbations in patients who had an acute stroke: clinical relevance and management strategies for the neurologist. Stroke and Vascular Neurology 2022;7:doi: 10.1136/svn-2021-001230
2. https://now.aapmr.org/hematological-metabolic-and-endocrine-complications/
3. Barkas F, Anastasiou G, Liamis G, Milionis H. A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke. Ther Adv Endocrinol Metab. 2023 Apr 3;14:20420188231163806. doi: 10.1177/20420188231163806. PMID: 37033701; PMCID: PMC10074625.

4. El-Fawal BM , Badry R , Abbas WA , et al. Stress hyperglycemia and electrolytes disturbance in patients with acute cerebrovascular stroke.Egypt J Neurol Psychiatr Neurosurg2019;55:86.doi:10.1186/s41983-019-0137-0
5. Robben JH, Knoers NVAM , Deen PMT. Regulation of the vasopressin V2 receptor by vasopressin in polarized renal collecting duct cells.Mol Biol Cell2004;15:5693–9.doi:10.1091/mbc.e04-04-0337
6. McKinley MJ , Johnson AK.The physiological regulation of thirst and fluid intake.News Physiol Sci2004;19:16.doi:10.1152/nips.01470.2003
7. Saleem S, Yousuf I, Gul A, Gupta S, Verma S. Hyponatremia in stroke. Ann Indian Acad Neurol. 2014 Jan;17(1):55-7. doi: 10.4103/0972-2327.128554. PMID: 24753660; PMCID: PMC3992770.
8. Peters JP, Welt LG, Sims EA, et al. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians. 1950;63:57–64

References

Sodium Management After Stroke

Anthony Anzivino, MD
PGY-2

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