This document discusses hyponatremia and hypernatremia. It defines hyponatremia as a sodium concentration below 135 mEq/L, generally caused by increased water retention. The types of hyponatremia are depletional and dilutional. Causes, symptoms, diagnostic workup and treatment approaches are described for hyponatremia. Hypernatremia is defined as a sodium level above 145 mEq/L. Causes, symptoms, and treatment focusing on calculating and correcting water deficit are covered for hypernatremia.

1. Dr. Saroj K. Suwal
MO, Oncosurgery Department,
Bhaktapur Cancer Hospital

2. Na + (Sodium)
 90 % of total ECF cations, Low in ICF
 Normal range : 135 -145 mEq / L
 Pairs with Cl- , HCO3
- to neutralize charge
 Most important ion in regulating water balance
 Important in nerve and muscle function

3. Hyponatremia
 Defined as sodium concentration < 135
mEq/L
 Generally considered with disorder of water
as opposed to disorder of salt
 Results from increased water retention

4. Types of Hyponatremia
depletional and dilutional
 Depletional Hyponatremia
Na+ loss:
 diuretics, chronic vomiting
 Chronic diarrhea
 Decreased aldosterone
 Decreased Na+ intake
4

5.  Dilutional Hyponatremia:
 Renal dysfunction with ↑ intake of hypotonic fluids
 Excessive sweating→ increased thirst → intake of excessive
amounts of pure water
 Syndrome of Inappropriate ADH (SIADH) or oliguric renal
failure, severe congestive heart failure, cirrhosis all lead to:
 Impaired renal excretion of water
Hyperglycemia – pulls interacellular water to
ECF translocation of water lowers sodium
(also called translocational hyponatrimia)-
 serum sodium concerntraion falls 2mEq/L for
every 100mg/dl when glucose concerntration is
between 200 to 400 mg/dl
 Falls to 4mEq/L when greater than 400mg/dl of
Glucose
5

6. Cause Hyponatremia
can be classified based on
 volume status,
 Serum /Plasma Osmolality
 ADH level inappropireatly suppressed
or appropriately elevated

7. Hypovolemic, Euvolemic or Hypervolemic

8. Volume status helps predict cause
 Hypovolemia
 True Volume Depletion
 Adrenal insufficiency
 Thiazide overdose
 Exercised induced Hyponatremia
 Euvolemia
 SIADH
 Primary Polydipsia
 Hypervolemia
 Cirrhosis and CHF

9. Isotonic(280-295mosm/kg),Hypotonic and
Hypertonic Hyponatremia

10. ADH-Antidiuretic Hormone
 Release by the postrior pitutary
 Function :is water retension, Raise BP by peripheral
vasoconstrictions
 Vasopressin has two effects 1. increased urine osmolarity
(increased concentration) and decreased water excretion.
These are:
 Increasing the water permeability of distal tubule and
collecting duct cells in the kidney, thus allowing water
reabsorption and excretion of more concentrated urine,
i.e., antidiuresis
 Increasing permeability of the inner medullary portion of the
collecting duct to urea which facilitates its reabsorption into
the medullary interstitiumm as it travels down the concentration
gradient created by removing water from the connecting
tubule, cortical collecting duct, and outer medullary collecting duct

11. ADH inappropriately elevated or appropriately
suppressed

12. ADH suppression
 Conditions which ADH is suppressed
 Primary Polydipsia or psychogenic Polydipsia
(associated with a patient's increasing fluid intake due
to the sensation of having a dry mouth ,generally
>10L/day, )
 Low dietary solute intake or “Beer Potomania”
 Advanced Renal Failure

13. ADH elevation
 Conditions which ADH is elevated
 Volume Depletion
 True volume depletion (i.e. bleeding)
 Effective circulating volume depletion (i.e. heart failure and
cirrhosis)
 Exercised induced Hyponatremia
 Thiazide Diuretics
 Adrenal insufficiency
 SIADH

14. Causes
 Psuedohyponatremia –, Serum Sodium Level
falsely depressed due to Hyper lipidemia or protein
level (multiple myeloma). In this Serum
Osmolality is Normal as protien and lipid doesn’t
alter serum osmolatiyalso called isotonic
hyponatrimia
 High blood sugar (esp. DKA) Hypertonic
hypernatrimia

15. Symptoms of Hyponatremia
 Neurological symptoms
 Lethargy, headache, confusion, apprehension, depressed
reflexes, seizures and coma
Muscle symptoms
 Cramps, weakness, fatigue
 Gastrointestinal symptoms
 Nausea, vomiting, abdominal cramps, and diarrhea

16. Workups For Hyponatremia
 3 mandatory lab tests
 Serum Osmolality- solute concerntration
 Urine Osmolality
 Urine Sodium Concentration

17. Interpretations :
 Serum Osmolality
 Can differentiate between true Hyponatremia,
pseudohyponatremia and hypertonic Hyponatremia
 Urine Osmolality
 Can differentiate between primary Polydipsia and
impaired free water excretion
 Urine Sodium concentration
 Can differentiate between Hypovolemia Hyponatremia
and SIADH

18. Conditions that increased osmolality3
Serum Urine
•Dehydration/sepsis/fever/sweating/bur
ns
•Diabetes mellitus (hyperglycemia)
•Diabetes insipidus
•Uremia
•Hyponatremia
•Ethanol, methanol, or ethylene glycol
ingestion
•Mannitol therapy
•Dehydration
•Syndrome Inappropriate ADH
secretion (SIADH)
•Adrenal insufficiency
•Glycosuria
•Hyponatremia
•High protein diet
Conditions that decrease Osmolality
Serum Urine
•Excess hydration
•Hyponatremia
•Syndrome Inappropriate ADH
secretion (SIADH)
•Diabetes insipidus
•Excess fluid intake
•Acute renal insufficiency
•Glomerulonephritis

19. Additional Tests
TSH, (Hypothyroidism or Adrenal insufficiency)
Albumin, triglycerides and SPEP –serum protein
electrophoresis (pseudohyponatremia, cirrhosis, MM
Cortisol – low in adrenal insufficiency, though may be
inappropriately normal in infection/stressful state, therefore
should get Corti-Stim test to confirm
Head CT and Chest Xray – may see evidence of cerebral salt
wasting or small cell carcinoma which can both cause
Hyponatremia
)

20. not so common test
 Iatrogenic infusion of hypotonic fluids (“Surgeon
sign”)
 Ecstasy use – increased water intake with
inappropriate ADH secretion
 Underlying infections
 Test for SIADH
 Reset Osmostat – Occurs in elderly and pregnancy
where regulated sodium set point is lowered

21. SIADH: concept to understand
 Caused by various etiologies
 CNS disease – tumor, infection, CVA, SAH,GBS,Meningitis,
 Pulmonary disease – TB, Bacterial pneumonia,
Aspergilosis, Bronchiaectiasis, Neoplasm,positive pressure
ventilation
 Cancer – Lung ca, pancreas ca, thymoma, ovary ca,
lymphoma, adenocarcinoma of colon, Prostatic ca.Renal
Cell ca,Osteosarcoma ,Lymphoma, Leukemia
 Drugs – NSAIDs, SSRIs, diuretics, TCAs,
Antineopalastic(cyclophosphomide, vincristine,
Carbamazapine,),Neuroleptics-haloperidol, thiothixene,
thioridazine
 Postoperative,Pain,Stress, AIDS, Pregnancy(Physiologic),
Hypokalemia

22. Diagonositc criteria for SIADH
 Clinicaly –Euvolemia, Hypotonic Hyponatremia
 Normal hepatic, renal and cardiac function
 Normal thyroid and adrenal function
 plasma sodium concentration <135 mmol/l
 plasma Osmolality <280 mOsmol/kg
 urine Osmolality > 100 mOsmol/kg
 urinary sodium concentration >30mmol/L
 no diuretic use (recent or past)
The following investigations could be carried out in SIADH
 urea and electrolytes
 plasma and urine Osmolality
 urinary sodium
 thyroid function tests short , corti-stim test
 chest and skull radiographs may be useful in excluding other causes of
SIADH.

23. Treatment :Hyponatremia
 Patients with serum sodium above 120 are generally
asymptomatic
 Symptoms tend to occur at serum sodium levels lower
than 120 or when a rapid decline in sodium levels
occur
 Patients can have mild symptoms at sodium
concentrations of 110-115 mEq/L when this level is
reached gradually. nausea and malaise (earliest) or
headache and lethargy as mild symptoms

24. With No severe symptoms & fluid restriction
started, next step is to assess volume status to
help determine cause
 Hypovolemic – urine output, dry mucous
membranes, sunken eyes
 Euvolemic – normal appearing
 Hypervolemic – Edema, past medical history,
Jaundice (cirrhosis), (CHF)

25. What if little to no symptoms are
present?
 Oral fluid restriction is the first step
 No more than 1500 mL per day
(NOTE: This only pertains to oral fluid, isotonic IV fluids
do not count towards fluid intake )
 If volume depletion is present, isotonic (0.9%) saline can
be given intravenously
 Careful monitoring should be used whether symptoms are
present or not
 Other non pharmacological practices:Salt added
diet,ORS,Salt Capsule – salt powder inside b-complex
capsule layer

26. When Severe symptoms(coma,
seizures present
starting bolus of 100 ml of 3% hypertonic saline which
generally raise serum sodium level by 2-3 mEq/L
(moniter serum sodium –2 hrly in ICU setup or 4-6
hrly as per need)
 Goals for correction:
 1.5 to 2 mEq/L per hour for first 3-4 hours until
symptoms resolve
 Increase by no more than 10 mEq/L in first 24 hrs
 Inscrease by no more than 18 meq/L in first 48 hrs
(half correction approach after serum sodium =>120

27. How much sodium does the
patient need?
Sodium deficit = Total body water x
(desired Na – actual Na)
Total body water is estimated as lean
body weight x 0.5 for women or 0.6 for
men

28. Case example:
 A 60 kg woman with sodium level of 116mEq/L.
How much sodium will bring him up to 124 in the
next 24 hours?
 Sodium Deficit(Needed) = 0.5 x 60 x (124-116) =
240 mEq
 The patient needs 240 mEq in next 24 hours

29. Na Concerntration in IV Fluid
Nacl 0.9%  154mEq/L
Ringer lactate130 mEq/L
3 % Nacl513 mEq/L
5% Albumin130-160 mEq/L
Hestarch 154 mEq/L
Dextran154 mEq/L

30. What if the sodium increases too
fast?
 Central Pontine Myelinolysis which is a form of
osmotic demyelination
 Symptoms generally occur 2-6 days after elevation of
sodium and usually either irreversible or only partially
reversible
 Symptoms include: dysarthria, dysphagia, paraparesis,
quadriparesis, lethargy, coma or even seizures

31. Risk Factors for Demyelination
 Rate of correction over 24 hours more important than
rate of correction in any one particular hour
 More common if sodium increases by more than 20
mEq/L in 24 hours
 Very uncommon if sodium increases by 12 mEq/L or
less in 24 hours
 CT but preferably MRI to diagnose demyelination if
suspected, though imaging studies may not be positive
for up to 4 weeks after initial correction

32. Summary of Hyponatremia
 Hyponatremia has variety of causes
 Treatment is based on symptoms
 Severe symptoms = Hypertonic Saline
 Mild or no symptoms = Fluid restriction
 Overcorrection, more than 12 mEq increase in 24
hours must be avoided with monitoring
 Serum Osmolality, Urine Osmolality and Urine
sodium concentration are initial tests to order

33. Hypernatremia
Serum Na >145 mEq/L [deficit of (TBW)
relative to Na]
 Incidence >1% in hospitalized patients.
 Can have normal,hypo and hyperosmolality
 Generally hypovolumic due to free water
loss , also hypervolumic is seen as itragenic
treatment with free accesses of water in
hospitals

34. Causes
 Insensible and sweat losses
 GI losses
 Diabetes Insipidus (both central and nephrogenic)
 Osmotic Diuresis – DKA
 Hypothalamic lesions which affect thirst function
– Causes include tumors, granulomatous diseases
or vascular disease
 Sodium Overload – Infusion of Hypertonic sodium
bicarbonate for metabolic acidosis

35. Symptoms of Hypernatremia
 Initial symptoms include lethargy, weakness and
irritability Can progress to twitching, seizures,or
coma
 Resulting decrease in brain volume can lead to rupture
of cerebral veins leading to hemorrhage
 Severe symptoms usually occur with rapid increase to
sodium concentration of 158 mEq or more..
(hyperthermia, delirium , sizure and coma)
 Sodium concentration greater than 180 mEq are
associated with high mortality

36. Lab findings
 Urine Osmolaity >400 mosm/kg
 Renal losssevere hyperglacemiatranslocatinal hyponatrimia
progressive volume depletion from glucosuria lead to
Hypernatrimia
 Non Rneal LossFluid Loss from excessive sweating, respirator
tract or bowel movements. Lactulose cause osmotic diarrohea with
loss of free water
Urine Osmolaity <250 msom/kg
 Hypernatrimia with dilue urine is charactersitc of DI.
 Central DI results from Inadequate ADH release
 Nephrogenic DI results from renal insensitivity to ADH

37.  If urine Osmolality is lower than serum Osmolality
then DI is present
 Administration of DDAVP(desmopressin) will
differentiate
 Urine Osmolality will increase in central DI, no response in
nephrogenic DI
DDAVGreatly enhanced ADH activity. Less vasopressor
activity. Longer DOA. (Synthetic analog of vasopressin-
posterior pituitary hormone).

38. Treatment of Hypernatremia
 First, calculate water deficit
 Water deficit = CBW x ((plasma Na/desired Na level)-
1)
 CBW = current body water assumed to be 50% of body
weight in men and 40% in women

39. •60 kg woman with 168 mEq/L
•How much water will it take to
reduce her sodium to 140 mEq/L
sample calculation:
Water deficit =
0.4 x 60 ([168/140]-1) = 4.8 L

40. Calculation continued
But how fast should I correct it?
 Same as Hyponatremia, sodium should not be lowered
by more than 12 mEq/L in 24 hours
 Overcorrection can lead to cerebral edema which can
lead to encephalopathy, seizures or death
 So what does that mean for our patient?
 The 4.8 L which will lower the sodium level by 28 should
be given over 56-60 hours, or at a rate of 75-80 mL/hr
 Typical fluids given in form of D5 water

41. Summary of Hyponatremia
 Loss of thirst usually has to occur to produce
hypernatremia
 Rate of correction same as Hyponatremia
 D5 water infusion is typically used to lower sodium
level
 Same diagnostic labs used: Serum Osmolality, Urine
Osmolality and Urine sodium
 Beware of overcorrection as cerebral edema may
develop

42. Thank you .