good way of presenting hyponatremia

1. Hyponatremia in focus
Mahmoud khalid
Nephrology & kidney
transplantation

2. References
 Clinical comprehensive nephrology.
 Up to date.
 Medscape.
 USMLE.
 MRCP.

3. Case 1

4. 1: Definition ?
• Hyponatremia is defined as a serum sodium
level of less than 135 mEq/L.

5. Describe ?
 severity:
 Mild - Serum sodium concentration 130-134
mmol/L.
 Moderate - Serum sodium concentration 125-
129 mmol/L.
 Profound - Serum sodium concentration <125
mmol/L.

6. Describe?
 Signs and symptoms:
 Mild: nausea and malaise.
 lethargy, decreased level of consciousness and headache.
 Sever: seizures and coma.
 Very low serum sodium levels (usually <115 mEq/L), resulting
in intracerebral osmotic fluid shifts and brain edema. This
neurologic symptom complex can lead to tentorial herniation
with subsequent brain stem compression and respiratory
arrest, resulting in death in the most severe cases.
 Acute/chronic:
 Acute hyponatremia (ie, with a known duration of <24-48
hours).
 Chronic hyponatremia (known duration >48 hours)

7. Describe?
 The severity of neurologic symptoms:
 Correlates well with the rate and degree of the drop in
serum sodium.
 A gradual drop in serum sodium, even to very low levels, may
be tolerated well if it occurs over several days or weeks,
because of neuronal adaptation.
 The presence of an underlying neurologic disease, like a
seizure disorder, or nonneurologic metabolic abnormalities,
like hypoxia, hypercapnia, or acidosis, also affects the severity
of neurologic symptoms.

8. Hints
 renal handling of water is sufficient to excrete as much as 15-
20 L of free water per day.
 hyponatremia is of clinical significance only when it reflects a
drop in the serum osmolality (ie, hypotonic hyponatremia),
which is measured directly via osmometry or is calculated as
2(Na) mEq/L + serum glucose (mg/dL)/18 + BUN (mg/dL)/2.8.
 Acute hyponatremia (duration < 48 h) can be safely corrected
more quickly than chronic hyponatremia.
 Severe hyponatremia (< 125 mEq/L) has a high mortality rate.
 when the serum sodium level is less than 105 mEq/L, the
mortality is over 50%.

9. Interpretation
 Serum osmolarity: The reference range of serum
osmolality is 275–295 mosm/kg (mmol/kg).
 Urine osmolarity: The normal 24-hour urine osmolality
is, on average, 500-800 mOsm/kg of water. Random urine
osmolality should average 300-900 mOsm/kg of water.
 Volume status.
 Urinary sodium: The reference range for urine sodium
is 40-220 mEq/L/24 hours.

10. Differential diagnosis

11. Causes
Hypertonic hyponatremia:
 Normal total body sodium.
 Dilutional drop in the measured serum sodium due to the
presence of osmotically active molecules in the serum, which
causes a water shift from the intracellular compartment to the
extracellular compartment.
 Glucose: drop in the serum sodium level of 1.6 mEq/L for each
100 mg/dL of serum glucose greater than 100 mg/dL.

12. Causes
 Normotonic hyponatremia:
 Severe hyperlipidemia and paraproteinemia can lead to low
measured serum sodium concentrations with normal serum
osmolality.
 Artifactual low sodium (so-called pseudohyponatremia) is
secondary to measurement by flame photometry. It can be
avoided by direct ion-selective electrode measurement.
 Hyponatremia post-transurethral resection
of the prostate (TURP) or hysteroscopy :
 glycine, sorbitol, or mannitol.
 Use of isotonic saline as an irrigant instead of glycine.

13. Causes
 Hypotonic hyponatremia:
 Hypovolemic hypotonic hyponatremia:
 Cerebral salt wasting (CSW):
o Intracranial disorders, such as subarachnoid hemorrhage,
carcinomatous or infectious meningitis, and metastatic
carcinoma, but especially after neurologic procedures.
o Disruption of sympathetic neural input into the kidney.
o Plasma renin and aldosterone levels fail to rise appropriately.
o Volume depletion leads to an elevation of plasma vasopressin
levels and impaired free water excretion.
 Salt-wasting nephropathy:
o interstitial nephropathy, medullary cystic disease, polycystic
kidney disease, partial urinary obstruction) with low salt intake.

14. Causes
 Diuretics:
o thiazide diuretics, in contrast to loop diuretics, impair the
diluting mechanism without limiting the concentrating
mechanism, thereby impairing the ability to excrete a free
water load. Thus, thiazides are more prone to causing
hyponatremia than are loop diuretics.
 Hypervolemic hypotonic hyponatremia:
 liver cirrhosis, congestive heart failure, nephrotic syndrome,
and severe hypoproteinemia (albumin level <1.5-2 g/dL).
 decrease in the effective circulating volume, critical for tissue
perfusion, stimulates the same pathophysiologic mechanism of
impaired water excretion by the kidney that is observed in
hypovolemic hypotonic hyponatremia.

15. Causes
 Euvolemic hypotonic hyponatremia:
 SIADH:
o Medications : chlorpropamide (potentiating renal action of ADH),
carbamazepine (possesses antidiuretic property),
cyclophosphamide , vincristine, vinblastine, amitriptyline,
haloperidol, selective serotonin reuptake inhibitors (particularly in
elderly patients), and monoamine oxidase (MAO) antidepressants.
o diagnostic criteria for SIADH:
1. Normal hepatic, renal, and cardiac function - clinical euvolemia
(absence of intravascular volume depletion).
2. Normal thyroid and adrenal function.
3. Hypotonic hyponatremia.
4. Urine osmolality greater than 100 mOsm/kg.
5. Urinary sodium concentrations are also typically greater than 20
mEq/L.

16. Causes
 Severe hypothyroidism: nonosmotic vasopressin release and
impaired sodium reabsorption, leading to hypotonic
hyponatremia.
 adrenal insufficiency.
 Increased release of ADH: malignancy, Pneumocystis carinii.
 Other causes:
 Hyponatremia in patients after surgery: hypotonic fluids.
 Compulsive intake of large amounts of free water .
 NSAID.
 Nephrogenic syndrome of inappropriate antidiuresis (or NSIAD):
SIADH-like , undetectable plasma arginine vasopressin (AVP)
levels, mutations in the V2 vasopressin receptor.

17. Check serum osmolarity

18. SIADH

19. Ask 3 questions ?

20. Answer

21. Case 2

22. Case 2

23. Case 2

24. Answer

25. Case 3

26. Case 3

27. Case 3

28. Case 3

29. Answer

30. Case 4

31. Case 4

32. Answer

33. Case 5

34. Case 5

35. Case 5

36. Case 5

37. Answer

38. Case 6

39. Answer

40. Hints
 A liter of normal saline contains 154 mEq NaCl.
 A liter of 3% saline has 513 mEq NaCl.
 Expected change in serum sodium (Na):
 Change in serum Na = [(infusate Na + infusate K) - serum Na] /
[Total body water +1].
 Acute hyponatremia (duration < 48 h) can be safely corrected
more quickly than chronic hyponatremia.
 A severely symptomatic patient with acute hyponatremia is in
danger from brain edema.
 A symptomatic patient with chronic hyponatremia is more at
risk from rapid correction of hyponatremia.
 Rapid correction of serum sodium can precipitate severe
neurologic complications, such as central pontine myelinosis:
spastic quadriparesis, swallowing dysfunction, pseudobulbar
palsy, and mutism

41. Hints
 Acutely symptomatic (duration <48 h, such as after surgery),
the treatment goal is to increase the serum sodium level by
approximately 1-2 mEq/L/h for 3-4 hours, until the neurologic
symptoms subside or until plasma sodium concentration is over
120 mEq/L.
 chronic, severe symptomatic hyponatremia, the rate of
correction should not exceed 0.5-1 mEq/L/h, with a total
increase not to exceed 8-12 mEq/L/d and no more than 18
mEq/L in the first 48 h.
 The sodium concentration must be corrected to a safe range
(usually to no greater than 120 mEq/L) rather than to a normal
value.

42. Guidelines for TT
 factors guide treatment:
 Patient's volume status.
 Duration and magnitude of the hyponatremia.
 Degree and severity of clinical symptoms.
 asymptomatic patient:
 Hypovolemic hyponatremia: isotonic saline.
 Hypervolemic hyponatremia: salt and fluid restriction, plus loop
diuretics, and correction of the underlying condition. The use of
a V2 receptor antagonist may be considered .
 Euvolemic hyponatremia: free water restriction (<1 L/d) is
generally the treatment of choice.
 Symptomatic hyponatremia (eg, seizures, severe neurological
deficits): hypertonic (3%) saline should be used.

43. Guidelines for TT
 The European Society of Intensive Care Medicine, the
European Society of Endocrinology, and the European Renal
Association–European Dialysis and Transplant Association:
 serious symptomatic hyponatremia: first line of treatment is
prompt intravenous infusion of hypertonic saline, with a target
increase of 6 mmol/L over 24 hours (not exceeding 12 mmol/L).
 SIADH and moderate or profound hyponatremia: First-line
treatment is fluid restriction, second-line treatments include
increasing solute intake with 0.25–0.50 g/kg per day of urea or
combined treatment with low-dose loop diuretics and oral
sodium chloride.
 reduced circulating volume: intravenous infusion of 0.9%
saline.

44. Aquaresis
 AVP receptor antagonists.
 aquaresis (ie, electrolyte-sparing excretion of free water).
 The first agent to be approved was conivaptan, a V1A and V2
vasopressin receptor antagonist. It is available only for
intravenous use and is approved for use in the hospital setting
for euvolemic and hypervolemic hyponatremia.
 It is contraindicated in hypovolemic patients.
 Tolvaptan, a selective V2 receptor antagonist.

45. TT
 SIADH:
o fluid restriction (with a goal of 500 mL/d below the 24-hour urine
volume) is generally first-line therapy.
o if the serum sodium concentration does not correct after 24-48
hours of fluid restriction: demeclocycline, vasopressin receptor
antagonists (vaptans).
o demeclocycline, and vaptans are not recommended for patients
with moderate or profound hyponatremia.

46. Guidelines for TT
 United States experts guidelines 2013:
 Symptomatic patients with acute hyponatremia (ie, with a
known duration of <24-48 hours):
o Severe symptoms: 100 mL of 3% NaCl infused intravenously
over 10 minutes × 3 as needed.
o Mild to moderate symptoms, in patients at low risk for
herniation: 3% NaCl infused at 0.5–2 mL/kg/h.
 chronic hyponatremia (known duration >48 hours):
o Minimum correction of serum sodium by 4-8 mmol/L per day.