This document discusses the approach to a patient presenting with hyponatremia. It begins by outlining the clinical scenario of a 74-year-old man with recent gastroenteritis, fatigue, headache and a sodium level of 118. It then provides definitions and discusses evaluating hyponatremia by assessing serum osmolality, urine osmolality and volume status. Based on these factors, the patient's hyponatremia is likely due to volume depletion from gastroenteritis. The document concludes by stating the patient should be treated slowly with isotonic saline given mild symptoms, but more rapid correction with hypertonic saline would be needed if seizures were present.

1. Approach to
Hyponatremia
Dr. Hammad Arshi

2. Clinical Scenario
 74-year-old man p/w recent gastroenteritis characterized by
n/v/d x 5 days, in addition to fatigue and headache.
 CT head (-) in ED. No focal neurologic deficits found. He
looks dry on physical exam
 Labs significant for Na+ of 118, baseline unknown. Serum
osmolality is 266. Urine osmolality is 377. Urine sodium is 8.
 How would you approach this patient’s hyponatremia?
 How would your approach be different if this patient
presented with new-onset seizures?

3. Hyponatremia
 Definition: Serum Na+ <135 meq/L
 Most common electrolyte abnormality.
 Seen in 15-30% of hospitalized pnts
 It is the excess of total body water relative to extracellular
Sodium
 The concentration of sodium in ECF is a reflection of the
tonicity of body fluids
 Usually a drop in osmolality will suppress ADH to allow
excretion of the excess water via dilute urine

4. …

5. …

6. Signs & Symptoms
 More profound when the deficit in sodium is very large or
occurs rapidly (i.e. over hours)
 Generally asymptomatic if Na+ level >125

7. …

8. Approach to Hyponatremia
 Step 1 – Is it real?Step 1 – Is it real?
Assess Serum osmolality (hyper, iso, or hypo)Assess Serum osmolality (hyper, iso, or hypo)
 Step 2 – Is water excretion appropriate?Step 2 – Is water excretion appropriate?
Assess urinary osmolality - Is urine concentrated orAssess urinary osmolality - Is urine concentrated or
dilute?dilute?
 Step 3 - assess volume statusStep 3 - assess volume status
Is the patient volume overloaded, depleted, or euvolemic?Is the patient volume overloaded, depleted, or euvolemic?

9. The 3 Questions

10. …

11. Initial HypoNa workup

12. STEP 1 - Serum Osmolality
 Assess osmolality hyper, iso, or hypo
 Hypotonic hyponatremia = warrants further workup, especially when
there is no obvious fluid overload or depletion
 Serum Osmolality: lab value or calculation – in mosm/kg
 =(2 x Na+) + (glucose/18) + (BUN/2.8)
 Hypertonic - >295
 hyperglycemia, mannitol, glycerol
 Isotonic - 280-295
 pseudo-hyponatremia from elevated lipids or protein
 Hypotonic - <280
 excess fluid intake, low solute intake, renal disease, siADH,
hypothyroidism, adrenal insufficiency, CHF, cirrhosis, etc.

13. Isotonic (Pseudo) Hyponatremia
 Normally Plasma contains 93% waterand 7% comprises
of lipids and proteins.
 Indirect potentiometry is used to calculate Serum Na+.
Sample is diluted and measurement assumes that water
constitutes 93%
 Thus if there is increase in either the protein component
(e.g multiple myeloma, macroglobulinemias) or increase
in lipid component (cholestatic jaundice) there is a
falsely low Serum Na+ value.
 Also seen in Drip Arm sample.

14. Hypertonic Hyponatremia
 When plasma contains Osmotically active substances
e.g in hyperglycemia or mannitol administration.
 They induce a concentration gradient and draw water
from ICF to ECF, thus increasing the water component of
plasma and causing hyponatremia.
 IVIg can cause both hyper and isotonic hyponatremia.
Isotonic – increases the protein component of plasma.
Hypertonic – sucrose is used as a carrier in commercial
preparations.

15. …

16. STEP 2 – Urine Osmolality
 When hypotonic hyponatremia is present, urine
osmolality should be measured to determine whether the
urine is maximally dilute
 Urine osmolality <100 - (ADH is NOT a factor) - excess
water intake and/or low solute intake as in psychogenic
polydipsia and beer potomania/ malnutrition
Primary/psychogenic polydipsia - patient drinks water
in excess to the capacity of the kidney to excrete ( > 1
L/h), despite suppression of ADH with an intact ability to
dilute the urine.

17. …

18. …
 Beer potomania and malnutrition results from a
combination of poor solute intake and relatively
excessive fluid intake.
 Isotonic or hypotonic irrigation solutions used during TURP
and hysterectomy can also cause hypotonic
hyponatremia

19. STEP 3 – Assess Volume Status
 Assess volume status (extracellular fluid volume)
 Hypotonic hyponatremia has 3 main etiologies:
 Hypovolemic – both H2O and Na decreased (H20 < Na)
Renal or extrarenal causes
 Euvolemic – H20 increased and Na stable
Consider siADH, thyroid disease, glucocorticoid def
 Hypervolemic – H20 increased and Na increased (H2O > Na)
 Consider obvious CHF, cirrhosis, renal failure

20. Hypovolemic hypoNa
 Obvious signs of volume depletion - decreased skin
turgor, dry mucous membranes, orthostatic hypotension,
and tachycardia.
 detecting hypovolemia in hypoNa can be difficult in the
absence of obvious signs. The patient has a deficit in
serum sodium and total body water but has lost relatively
more sodium.
 Check Urine sodium

21. …
 . A urine sodium concentration >30 mEq/L - renal losses
of sodium and water,- diuretic use, mineralocorticoid
deficiency, salt-wasting nephropathy, and cerebral salt
wasting (CSW).
 A urine sodium <30 mEq/L - non renal losses from
vomiting, diarrhea, third spacing (pancreatitis, burn injury
or trauma).
 Check Urine Chloride – low in hypovolemia.
 Fe Na < 1 % in non renal causes.

22. Euvolemic HypoNa
 Euvolemic hyponatremia occurs with an increased
amount of total body water with normal or reduced
total body sodium
 Iatrogenic - administration of hypotonic fluids without
careful monitoring of serum sodium levels (following
elective surgery- can result in acute onset of
hyponatremia with resulting neurological damage)
 SIADH - most common electrolyte disorder in hospi
talized patients. Occurs when an excess of AVP is
present with continued intake of water.

23. SIADH
 Excretion of sodium in the urine is intact with urine sodium
concentrations >40 mEq/L.
 Urine is NOT maximally diluted but is inappropriately
concentrated - Urine osmolality >100
 Patient is euvolemic with normal renal, adrenal, thyroid,
cardiac, and liver function
 A low serum BUN and uric acid occur in SIADH. Uric acid of 4
mg/dL or less is characteristic of SIADH, while a uric acid of
more than 5 mg/dL occurred in non-SIADH hyponatremia.
The fractional excre- tion of uric acid can be used to
differentiate patients with SIADH who are on diuretics from
patients with hypovolemia

24. SIADH causes

25. Other causes of Euvolemic
HypoNa
 Glucocorticoid deficiency from hypopituitarism,
hypothala- mic dysfunction, Sheehan syndrome,
tumors, or empty sella causes
 Hypothyroidism
 Exercise-associated hyponatremia (EAH)

26. EAH

27. Hypervolemic Hypo Na
 Patients with hypervolemic hyponatremia will have
signs of volume overload, such as peripheral edema,
pulmonary edema, or pleural effusion.
 This condition involves an excess of water and an excess
of sodium.
 Congestive heart failure
 Cirrhosis
 Nephrotic syndrome
 Renal failure.

28. Hyponatremia Flow Sheet

29. Treatment of Hyponatremia
 Acute Hyponatremia - develops over the course of 24 to
48 hours and ( most often results from psychogenic
polydipsia, EAH,, ecstasy/ MDMA use, patients treated
with hypotonic IV fluids postoperatively)
 Rapidly developing hyponatremia causes brain edema,
pro- found neurologic injury, transtentorial herniation
(TTH) and death (if acute hypoNa is not corrected
immediately)

30. Acute Hypo Na (t/t)
 Hypertonic saline is the mainstay of treatment for sympto-
matic acute hyponatremia.
 Target - increase in the serum sodium level of 5 mEq/L
- reduced brain edema, ICP (by 50%) - resolution of
symptoms.
 infusion of 100 mL of 3% NaCl that can be repeated
every 10 minutes for a total of 3 doses as needed
until symptoms resolve
 Less severe symptoms - infusion of 3% NaCl at a rate
of 1 to 2 mL/kg/h. Goal should be to increase the
serum sodium up to 2 mEq/L/h.

31. …
 The serum sodium level should be checked every 2 hours
and the rate of the infusion adjusted accordingly
 Avoid overcorrection.
 Risk factors for neurologic complications of correction
alcoholism, malnourishment, and nonacute
hyponatremia - corrected at a slower rate once the risk
of brain edema has been overcome.

32. Chronic Hypo Na (t/t)
 Chronic SYMPTOMATIC hyponatremia - treated with
hypertonic saline (3% NaCl) until symptoms resolve
because those symptoms can rapidly worsen.
 Safe rate of correction to avoid ODS – not more than 12
mEq/L over the first 24 hours and 18 mEq/L over
the first 48 hours.
 0.5 meq/L increase per every hour is a safe rate
 Volume of 3% NaCl per hour = Wt in Kg x 0.5
 For a 70 kg pt = 35 ml/hr.

33. …
Treatment varies greatly by etiology of hyponatremia.
 Hypovolemic hyponatremia - treated by volume
repletion with normal saline with serum Na+ monitoring
every 4 to 6 hours. Administration of potassium
supplementation causes a shift of sodium from
intracellular to extracellular space. Diuretics should be
stopped.
 Chronic hyponatremia due to cardiac failure is treated
by fluid restriction to less than 1000 mL/d. Loop
diuretics are also usually added.

34. …
SIADH is usually a chronic process.
 Patients with neurological symptoms should receive
hypertonic saline until symptoms resolve.
 The parenteral and oral fluid intake should be
restricted.
 Drugs known to cause SIADH should be discontinued.
 Treatment of underlying infection or malignancy
 Solute (NaCl tablets, urea) administration and
Demeclocycline
 Vaptans.

35. Vasopressin Receptor
Antagonists
 Vaptans are Vasopressin receptor (V2) blockers. V2
receptors are found in collecting ducts.
 Vaptans block ADH binding to the V2 receptor and
induce an electrolyte- free diuresis (aquaresis).
 Examples – Tolvaptan, Moxavaptan, satavaptan.
 They should not be used in - symptomatic
hyponatremia, hypovolemic hyponatremia, and in
patients with liver injury.

36. …
 Vaptans should not be used together with hypertonic
saline, - danger of overcorrection .
 Vaptans also induce a successful aquaresis in patients
with CHF but do not show any benefit on surviva
 Vaptans are most effective in SIADH. To avoid over-
correction with vaptans, the experts recommend not to
restrict oral fluid in the first 24 to 48 hours of treatment and
to check serum sodium and urine osmolality frequently. If
there is over- correction, the vaptan should be stopped
and IV D5W should be administered as desmopressin
(DDAVP) will not work since the V2 receptor is blocked.

37. Osmotic Demyelination
Syndrome

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39. …

40. Risk Factors for ODS

41. Clinical Scenario - Conclusion
 74-year-old man p/w recent gastroenteritis characterized by n/v/d x 5 days, in
addition to fatigue and headache.
 BMP significant for Na+ of 118, baseline unknown. Serum osmolality is 266. Urine
osmolality is 377.
 How would you approach this patient’s hyponatremia? The steps:
 1) Serum osmolality – 266, decreased (hypotonic)
 2) Urine osmolality –377, increased (>100)
 3) Volume status - hypovolemic
 4) Urine Na, 8, appropriately reabsorbing, likely volume depleted
 5) Treatment: Mild symptoms, correct slowly w/ isotonic saline
 How would your approach be different if this patient presented with new-onset
seizures?
 For symptomatic, severe hyponatremia, more rapid correction using 3%
normal saline

42. TAKE HOME POINTS
 Symptoms: Usually Na <125 or rapid decline
 N/V, headache, lethargy, AMS, seizures, coma
 WORK-UP in 3 important steps (S-U-V):
 1) Assess serum osmolality
 2) Assess urine osmolality
 3) Assess volume status
 Treatment varies by etiology, but cautious correction of
sodium important to prevent demyelination as fluid leaves
the brain