Hyponatremia in critical ill patients Hypertonic saline

1. Hyponatremia

2. Manisha sahay
Definition of Hyponatremia
Normal serum sodium level
: 135 – 145mEq/L
Hyponatremia is defined as a serum sodium
level less than 135mEq/L
Severe - serum Na < 120mEq/L

3. SYMPTOMS

4. Manisha sahay
Clinical Manifestations
 Hyponatremia not a disease but a manifestation of
a variety of disorders.
Clinical symptoms
 hyponatremia itself
 Disease causing hyponatremia
recognition of hyponatremia incidental.

5. Acute
Low serum Na
More Na in brain
Water enters
brain cells
Cerebral
oedema
Chronic
Adaptation
Pathogenesis

6. Manisha sahay
S [Na] > 125 mmol/L
or
Gradual onset
Asymptomatic
GI sym
Headache
Lethargy
Confusion
Obtundation
Stupor
Seizures
Coma
Rhabdomyolysis
Brain stem compressiom
Pulm oedema
Na+ level <120mEq/L
or
Rapid decrease(<48hr)
Symptoms depend on
magnitude of the hyponatremia
rapidity of its development.

7. Manisha sahay
Symptoms & signs
Gait disturbances
Fractures
• reduction in total hip bone mineral
density of 0.037 g/cm2 for every 1
mmol/l drop in plasma sodium
concentration.
European Jr Endocrinology 2010
Manisha Sahay

8. Etiology -Hyponatremia
Hyperglycemia
Mannitol
Hyperlipidemia
Hyperproteinemia
SIADH
GC def
Hypothyroid
Exercise ind
Psychogenic
CHF
NS
Cirrhosis
CRF
GI loss
3rd space loss
Salt wasting dz
RTA
Diuretics
Cerebral salt
wasting
?
? ?
?
?

9. Manisha sahay
Determine if true Hyponatremia?
IA Pseudohyponatremia/Normal plasma osmolality
(275-295)
1. Hyperlipidemia - ion-specific electrodes avoid this
2. Hyperproteinemia-Multiple myeloma
IB Increased plasma osmolality /Translocational/redistributive
(osmo > 295)
A. Hyperglycemia 1.6 mEq/L for every 100 mg/dL [glucose)
B. Mannitol
II. Hypoosmolal hyponatremia (serum
osmolality<275mOsm/kg)

10. Manisha sahay
Manisha Sahay

11. Manisha sahay
Manisha Sahay
IB Increased plasma osmolality
/Translocational/redistributi
ve
(osmo > 295)
A. Hyperglycemia 1.6
mEq/L or 2.4 mmol for every
100 mg/dL [glucose)
B. Mannitol

12. Manisha sahay
Hypovolemic
Hypervolemic
Euvolemic
2 step
check volume status

13. Hypovolemic- Low CVP
Responds to NS
Low urine Na(<20 mmol/l)
 Non renal
• Volume Depletion
• GI, lung or skin
losses -burns
• Third space
sequestration
• CSW
• Excess water
intake
High urine Na >20 mmol/l
Renal
• Salt wasting
nephropathy
• Mineralocorticoid
deficiency-primary
adrenal insuficiency
• Osmotic diuresis-KB
• Cerebral salt
wasting
Manisha Sahay
Step 3
Check renal
or non renal
Urine Na

14. Renal salt wasting
 Renal salt wasting can also occur in kidney dysfunction.
The so-called salt-losing nephro pathies, such as
tubulopathy after chemotherapy or in analgesic
nephropathy, medullary cystic kidney disease and
certain pharmacological compounds can inhibit the
kidney’s ability to re-absorb appropriate amounts of
sodium
Manisha Sahay

15. Hypervolemic -High CVP
Increased total body water that
exceeds the increase in total body Na+
Low urine Na <20 mmol/l
• CHF
• Cirrhosis with
ascites
• Nephrotic
syndrome
High urine Na >20 mmol/l
• Advanced renal
failure
Manisha Sahayin
Step 3
Check urine
Na

16. Manisha sahay
Euvolemic – Normal CVP
Normal sodium stores (N ECF) & total
body excess of free water.
 SIADH/Reset osmostat
 Primary polydipsia
 Hypothyroidism
 Glucocorticoid deficiency2ndry adrenal insu
 Exercise induced
 Beer potomania
 Post op
Step 3
All have high urine Na
U osm <100 in PP, BP

17. Manisha sahay
Secondary adrenal insufficiency is caused by
reduced or absent secretion of
adrenocortico trophic hormone, resulting in
hypocortisolism. Under normal circumstances,
cortisol suppresses both pro duction of
corticotrophin-releasing hormone and
vasopressin in the hypothalamus. In secondary
adrenal insufficiency, persistently low
concentrations of cortisol fail to suppress
vasopressin and hyponatraemia results from
impaired free water excretio
Manisha Sahay

18. Manisha sahay
European clinical practice on
mangement ò hyponatremia
Manisha Sahay

19. Manisha sahay
Manisha Sahay

20. Manisha sahay
Manisha Sahay

21. Manisha sahay
Manisha Sahay

22. Manisha sahay
Manisha Sahay

23. Manisha sahay
Acute hyponatremia without sever
syptoms
Manisha Sahay

24. Manisha sahay
Chronic asyptomatic hyponatremia
with increased ECF
Restrection of fluid intake
Loop diuretics
May úse anti ADH antagonist
Manisha Sahay

25. Manisha sahay
Chronic asyptomatic hyponatremia
with ECF depletion
Manisha Sahay
† A sudden increase in urine output to O100 ml/h signals
increased risk of overly rapid rise in serum sodium concentration.
If vasopressin activity is sud denly suppressed, as happens when
intravascular volume is restored in hypovolaemia, free water
clearance can dramatically increase, resulting in serum sodium
concentrations rising more rapidly than expected.

26. Manisha sahay
Chronic asyptomatic hyponatremia
with euvolemic state
As a means of increasing solute intake, we suggest daily intake of
0.25–0.50 g/kg urea can be used. The bitter taste can be reduced by
combining it with sweet-tasting substances. The pharmacist may be
asked to prepare the following as sachets: urea 10 gCNaHCO3 2 gC
citric acid 1.5 gCsucrose 200 mg to be dissolved in 50–100 ml water.
This will result in a more palatable,

27. Serum Osmolality
History & volume status
Urine Osmolality/sp gr
Urine Na
S Cr/urea/K
T3/T4/TSH
CXR
CT Scan
Manisha Sahay
Investigations

28. Manisha Sahay
Treatment Acute hyponatremia
Syptomatic hypertonic saline Asyptomatic normal saline
Symptomatic hypertonic saline with F.U Volume Asyptomatic fluid
Status pat. May need lasix restrectioin
intake low than U.O.P by 500 ml
Syptomatic hypertonic saline with furosemide Asyptomatic fluid
resterction ưith furosemide
Hypertonic saline
hypovolemic
euvolemic
hypervolemic

29. Manisha Sahay

30. Manisha Sahay

31. Manisha sahay
Cerebral Salt Wasting
 Causes: Head injury, surgery, tumors, Infections
 Signs/symptoms:
• Polyuria, Dehydration/hypovolemia/Hypotension
• High urine Na > 20 mmol/L
 Pathogenesis:
•  renal Na loss d/t plasma ANP, BNP 
• Volume depletion could be protective for ICP
 Treatment:
• Volume replacement - large volumes of NS
• Oral Na supplementation for a period of time
• fludrocortisone
Berendes Lancet 1997, Isotani Stroke 1994, Wijdicks Stroke 1991
Mather J Neuro Nsurg Psych 1981; Wijdicks Ann Neuro 1985

32. Manisha sahay
Manisha Sahay

33. SIADH (Bartter’s Criteria)
60% of all euvolemic hyponatremia
 F
Essential criteria
 Hyponatremia
 pl osm<275
 Euvolemia clinical
 u osmolality > 100 mOsm/kg
 N renal, cardiac, hepatic,
adrenal, pituitary, thyroid
 No H/o antidiuretic drugs
 No emotional or physical
stress
 Urinary sodium > 30 mEq/l
 Cr N, N ABG, K+ handling
Supplemental features
 uric acid<4
 BUN<10
 failure to correct
hypoNa after NS
infusion
 correction of hypoNa
after fluid
restriction
 Fractional sodium excretion
more.5% Fractional urea
excretion more 55%
Fractional uric acid
excretion more 12%
U SP gravity can be used if u osm not possible, U osm 100= u sp gr 1.005

34. Disorders associated with SIADH
CNS-ADH secr
Encephalitis /Meningitis , trauma
Brain abscess/Brain tumors
GBS/Acute intermittent porphyria
Subarachnoid/subdural hematoma
Cerebellar and cerebral atrophy
Cavernous sinus thrombosis
Neonatal hypoxia
Hydrocephalus
Delirium tremens
CVA, Acute psychosis
Peripheral neuropathy
Multiple sclerosis
PULMONARY
CANCERS
CNS

35. Manisha Sahay

36. SIADH CSW
CNS problem yes yes
Urine Na High (renal) High (renal)
Urine osm High >100 mosm/kg < 100 mosm/kg
Urine Output decreased polyuric
CVP High (Euvolemic) Low (Hypovolemic)
BUN N or ↓BUN ↑BUN

37. Manisha sahay
Primary Polydipsia
 Psychiatric disorder,  thirst with antipsychotics
 ±Hypothalamic lesions
 No hyponatremia unless intake >10-15 L/d, or acute
3-4 L water load
 Urine osm below 100
 Rx: Restrict free water ;classically rapid correction

38. Manisha sahay
Beer protomania
Low Dietary Solute Intake
 Elderly, malnourished (“tea and toast” diets) -poor in
solutes (Na/K)
 Beer drinkers (high water intake, low protein)
 Pathogenesis
• Minimum urine osmolarity- 60 mosm/l
• At least 600-900 msom/kg/d solute load needed to excrete
water >4 l
• Beer protomania- daily solute excretion < 250 mosmol /kg,
hence maximum urine output can be <4 L day ,if more water
ingested -hyponatremia
• Urine appears dilute (osm of< 100)
 Rx: NS, increased dietary solute

39. AVP
Receptor
antagonists
–
•
Mechanism of action
Bind to the V2 receptors in renal
collecting tubules/ducts
Vasopressin antagonist
Uses
 Euvolemic/ hypervolemic hypo Na+;
Contraindicated in hypovolemia
 Chronic hyponatremia
not in acute hyponatremia or in
patients with sNa < 115 mmol/L
as slow aquaresis
Adverse effects:
Thirst ; dry mouth
SALT NEJM 2006

40. Manisha sahay
Vasopressin Receptor Location
& Functions (KI 2006)

41. Vasopressin Receptor Antagonists
Tol-
vaptan*
Lixi-Vaptan Sata-
vaptan
Coni-
vaptan
Receptor V2 V2 V2 V1a/V2
Route of
administration
Oral Oral Oral IV
Urine Volume
UOSM
24 h Na
excretion
No ∆ No ∆ low Dose
High Dose
No ∆ No ∆
*SALT I and SALT II Trials.

42. Manisha sahay
Central Pontine Myelinolysis
Osmotic demyelination
 Pathogenesis
• rapid correction / overcorrection of ch hyponatremia.
• hypoxic encephalopathy / complication of therapy
 Prevention
• Adequate oxygenation
• Gradual increase in serum sodium level to 120-125 mEq/L.
 Symptoms
• Dysarthria, dysphagia, seizures, altered mental status,
quadriparesis, hypotension ,locked in syndrome, extrapontine
• Begin 1-3 days after correction of S Na
• Irreversible , devastating
• MRI diagnostic < 24 h
 Risk factors- Hypokalemia, females,alcoholism, liver transplant
 Treatment- Relowering S Na - hypotonic fluids, Desmopressin