4. Introduction.
Hyponatremia is one of the commonest biochemical
abnormalities in clinical practice.
Reference interval for serum sodium – 135-145mmol/L
(may differ btw Labs)
Hyponatremia is defined as a plasma concentration
less than 135mmol/L.
Occurs in up to 22% of hospitalized patients ( over 1 in
5 patients).
Important to detect; if left untreated ,may be
associated with poor outcomes.
5. INTRODUCTION
Disorders of serum Na+ concentration are caused by
abnormalities in water homeostasis leading to changes
in the relative ratio of Na+ to water body
Water intake and circulating AVP, key effectors in the
defence against serum osmolarity; and defects in one
or both of these defence mechanisms cause most
cases of hyponatraemia and hypernatraemia.
6. INTRODUCTION CTD
May be classified into
Mild hyponatremia: 130-134mmol/L
Moderate hyponatremia : 125-129mmol/L
Severe hyponatremia :<125mmol/L
Clinically significant hyponatremia <130mmol/L
7. Epidemiology
In the US, among hospitalized patient, hyponatremia
had a prevalence of 15-20%.
In Calabar, a study on hyponatremia in patients on
antipsychotics by Olose et al revealed a prevalence of
19.6%.
Pattern of electrolyte profile among admitted children
(1-18 years) at UCTH by Lawson Ekpe et al.- 39.6% had
hyponatremia.
8. Epidemiology.
No racial or sexual predilection exists for
hyponatremia.
However, symptoms are more likely to occur in young
women than in men.
Hyponatremia is more common in elderly persons,
because they have a higher rate of comorbid
conditions (eg, cardiac, hepatic, or renal failure) that
can lead to hyponatremia.
9. Epidemiology ctd.
Severe hyponatremia (< 125 mEq/L) has a high
mortality rate. In patients whose serum sodium level
falls below 105 mEq/L, and especially in alcoholics, the
mortality is over 50%.
Also, hyponatremia is an important predictor of
mortality in several conditions viz liver cirrhosis,
chronic kidney disease and acute STEMI.
10. Pathophysiology.
Sodium is the most abundant extracellular cation.
Alongside its anions determines up to 80-90% of
plasma osmolality.
Plasma osmolality is key in influencing movement of
fluid from the intravascular to interstitial compartment
and between the interstitial and intracellular
compartment.
11.
12.
13. Sodium homeostasis
For a 70 kg adult daily Na + intake is 100-150 mmols in
addition to 1.5-2.5 L of oral daily intake of fluids.
Approximately 8 L more are produced and secreted by
various parts of GIT.
These secretions contain 1200-1400 mmol of Na +
6 to 6.5 L is reabsorbed in the small intestine and the
remainder is reabsorbed in the large intestine
Only 100-200 mL of fluid and 4-5 mmol of Na + are ex-
creted in the stool.
14. Sodium homeostasis –
excretion.
The kidney has two important functions for Na + and
water balance: filtration and reabsorption.
Normally filtration is autoregulated, so it is the
reabsorptive mechanisms that adjust to variable input and
output.
Every minute 125 mL (180 L/day) of filtrate containing 17
mmoL of Na + (daily 25,000 mmoLs) enters the proximal
tubule (PT); 99% is reabsorbed and 1% excreted.
Daily, it can excrete 0.5 to 25 L of urine with osmolality
varying from 40-1400 mosm/L. Thus, depending on the
demands, urine volume can vary 50-fold and urine
osmolality 35-fold.
15. Reabsorption of filtered Na + load varies in the
different parts of the nephron;
65% of filtered Na + is reabsorbed the Prox. Tubule via
Na cotransporters, paracellular pathway and Na-H+
exchanger (stimulated by Ang II)
20%, and thick ascending part of loop of Henle (aLOH),
via Na+K+2Cl cotransporters (loop diuretics)
10% at the distal tubule (DT),via NaCL co transporter
4% at the collecting duct (CD) via epithelial Na
channels .
16. Pathophysiology ctd.
Sodium and water balance is maintained by a system
of ‘sensors’ and ‘effectors’
Sensors include
chemoreceptors (osmoreceptors) found in the brain -
circumventricular organs –lamina terminalis and
subfornical organ and in the kidneys.
Sense changes in circulating osmolality, leading to
release of ADH and thirst.
Baroreceptors located in the carotid sinus and aortic
arch sense changes in MAP and stimulate ADH release
and thirst also.
17. Pathophysiology ctd
Intact sodium and water balance revolves around an
intact thirst mechanism, ADH release and renal
handling of sodium and water.
ADH (AVP) is a peptide hormone synthesized in the
supraoptic and paraventricular nucei of the
hypothalamus.
Secretion is stimulated when systemic osmolality
increases above 285mosm/kg.
Acts on renal V2 type receptors in the THICK asc loop
of henle and principal cells of collecting duct
Stimulating insertion of aquaporin 2 water channels.
18.
19. Classification
According to osmolality
Hypotonic hyponatremia
Isotonic hyponatremia
Hypertonic hyponatremia
According to volume status
Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
20.
21.
22. HYPOVOLAEMIC
HYPONATRAEMIA
Hyponatraemia causes marked neurohumoral
activation, increasing levels of circulating AVP.
The increase in AVP preserves BP via vascular and
baroreceptor V1A receptors and increases water
reabsorption via renal V2 receptors.
Activation of renal V2 receptors can lead to
hyponatraemia in the setting of increased free water
intake.
23. Salt- losing nephropathies
Hyponatraemia with reduced Na+ intake.
Due to impaired renal tubular function
Reflux nephropathy
Interstitial nephropathy
Post obstructive uropathy
Medullary cystic disease
Recovery phase of acute tubular necrosis
24.
25. Thiazides donot inhibit renal concentration mechanisms,AVP retains full effect
Loop diuretics less frequently assoc wth hyponatraemia, blunt countercurrent
26. Increased excretion of osmotically active
nonreabsorbable or poorly reabsorbable solutes
Volume depletion and hyponatraemia
Glycosuria
Ketonuria (starvation, diabetic or alcoholic acidosis)
Bicarbonaturia( RTA or metabolic alkalosis)
27. Mineralocorticoid (aldosterone)
deficiency syndrome
Characterized by hyponatraemia with ECF volume
contraction ( provides a nonosmotic stimulus for
vasopressin release)
Urine[Na+] above 20mmol/l, and high K+.
28. Cerebral salt wasting
syndrome
Follows SAH, head injury, neurological procedures etc
Primary defect is salt wasting from kidneys(? Role of
BNP) with subsequent volume contraction, which
stimulates vasopressin release
Uncommon
Hyponatraemia + hypovolaemia+ intracranial diseases
Responds to aggressive Nacl repletion
30. SIADH
A defect in osmoregulation causes vasopressin to be
inappropriately stimulated, leading to high urinary
concentration
Excess vasopressin: CNS disturbances such as
haemorrhage, tumours, infections, and trauma
Ectopic vasopressin: small cell lung cancers, cancer of
the duodenum and pancreas and olfactory
neuroblastoma
Idiopathic: seen in the elderly(10%)
31.
32.
33.
34.
35.
36.
37.
38. HYPERVOLAEMIC
HYPONATRAEMIA
Increase in total body NaCl accompanied by a
proportionately greater increase in body water leading
to reduced serum Na+
ARF or CRF(UNa>20)
Nephrotic syndrome, cirrhosis, CCF(UNa<20) (arterial
underfilling)
The degree of hyponatraemia provides an indirect
index of associated neurohumoral activation and is an
important prognostic indicator in hypervolaemic
hyponatraemia
39.
40.
41.
42.
43.
44. LOW SALT INTAKE AND
HYPONATRAEMIA- BEER
POTOMANIA
Classically occurs in alcoholics whose sole nutrient is
beer.
Beer is very low in protein and salt content( only 1-
2mM of Na+)
Also in vegetarians
Typically presents with low urine osmolarity(100-
200mOsm/kg) and Na+ concentration of <10-20mM
Low dietary intake of solutes, reduced urinary solute
excretion limits water excretion such that
hyponatraemia ensues after relatively modest
polydipsia
45.
46.
47.
48.
49. Hyponatraemic
encephalopathy
Headache
Confusion and restlessness leading to:
Drowsiness
Myoclonic jerks
Generalised convulsions
eventually, death
Risk factors- children <16yrs,premenopausal
women,hypoxaemia
50.
51. CHRONIC HYPONATRAEMIA
Persistent chronic hyponatraemia results in an efflux of
organic osmolytes(creatine,betaine, glutamate, myoinositol,
and taurine) from brain cells; this response reduces
intracellular osmolality and the osmotic gradient favouring
water entry.
This usually happens after 48hrs
Symptoms include..nausea, vomiting, confusion and
seizures at [Na+] <125mmol/l
Asymptomatic.. Subtle gait and cognitive defects and
hyponatraemia-associated reduction in bone density
52. OSMOTIC DEMYELINATION
SYNDROME
Asymmetric cellular response to correction of chronic hyponatraemia.
Reaccumulation of organic osmolytes by brain cells is attenuated and delayed
resulting in degenerative loss of oligodendrocytes.
Overly correction of hyponatraemia (> 8-10 mmol/l in 24hrs or 18mmol/l in
48hrs) resulting in disruption of the BBB allowing entry of immune mediators
leading to demyelination.
Lesion classically in pons causing central pontine myelinolysis usually 1 or 2
days after over correction of hyponatraemia
Presents with paraparesis or quadriparesis,dysphagia,dysarthria, diplopia, a
locked-in syndrome and loss of consciousness
53. ODS
Extra pontine myelinolysis can occur in the cerebellum,
lateral geniculate body,thalamus, putamen, and cerebral
cortex or subcortex.
Depending on extent and localization of extra pontine
lesions : ataxia, mutism, parkinsonism, dystonia, catatonia.
Lowering [Na+] after overly correction of hyponatraemia
can attenuate ODS
54.
55. DIAGNOSTIC EVALUATION
OF HYPONATRAEMIA
Underlying cause
Detailed drug history/ smoking history
Clinical assessment of volume status
Clinical symptoms and physical examination for signs
Radiological imaging(CXR, CT) for pulmonary or CNS
causes of hyponatraemia
Laboratory investigations
57. LAB INVESTIGATIONS
Urine electrolytes
Urine osmolarity
Urine- plasma electrolytes ratio
Plasma copeptin, apelin and MR-proANP
58.
59. TREATMENT
The European and American guidelines have been
developed
The treatment for hyponatraemia is chosen on the basis of
duration and symptoms.
For acute or severely symptomatic hyponatremia, both
guidelines adopted the approach of giving a bolus of
hypertonic saline
Fluid restriction as first line treatment for chronic
hyponatraemia
60.
61.
62. Hyponatremia correction
Alternatively, another equation for correction
Sodium deficit = (Desired serum sodium- actual serum
sodium) x Total body water.
Alternatively,
Using 3% Hypertonic saline : 1ml/kg of 3% saline is
estimated to raise serum Na by 1mmol/L.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73. CONCLUSION
Hyponatraemia is a common sodium disorder.
Complications of hyponatraemia can result in profound
coma
There is need for urgent intervention when complications
arise.
75. References.
PATTERN OF ELECTROLYTE PROFILE AMONG
ADMITTED CHILDREN (1-18 YEARS) AT THE
UNIVERSITY OF CALABAR TEACHING HOSPITAL,
NIGERIA. Ekpe E. L et al -
https://medrech.com/index.php/medrech/article/view/
410 accessed November 30th, 2020.
Patel S. Sodium balance-an integrated physiological model and
novel approach. Saudi J Kidney Dis Transpl [serial online] 2009
[cited 2020 Dec 9];20:560-9. Available
from: https://www.sjkdt.org/text.asp?2009/20/4/560/53242
76. References
Hyponatremia: A practical approach
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC41
92979/ accessed on November 28th, 2020.
https://emedicine.medscape.com/article/242166-
overview#a2 Accessed on Novenber 26th, 2020.
Hyponatremia – fishing in troubled waters by K.
Sampathkumar. FRCP, India slideshare
presentation.
https://www.aafp.org/afp/2015/0301/p299.html
Accessed on November 29th, 2020.
