bu Rashed Disorders of plasma sodium are the most common electrolyte disturbances in clinical medicine Distinguishing the causes of hyponatraemia may be challenging
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Slide1
Sodium Disorder
Aisha
A
bu
Rashed
Slide2
Disorders of plasma sodium are the most common electrolyte disturbances in clinical
medicine
Distinguishing the cause(s) of
hyponatraemia
may be challenging in clinical practice, and controversies surrounding its management remain
Slide3Under normal conditions, plasma sodium concentrations are finely maintained within the narrow range of 135-145
mmol
/l despite great variations in water and salt
intake.
Slide4
Sodium and its accompanying anions, principally chloride and bicarbonate, account for 86% of the extracellular fluid osmolality, which is
normally 285-295
mosm
/kg
and calculated
as
The equation:
Posm
= 2 [Na+] + glucose (mg/
dL
)/18 + BUN (mg/
dL
)//2.8 i
The
main determinant of the plasma sodium concentration is the plasma water content, itself determined by water intake (thirst or habit), “insensible” losses (such as metabolic water, sweat), and urinary dilution
Slide5Notes
The causes of sodium imbalance are often iatrogenic and therefore avoidable
Assessing hydration status and measuring sodium in plasma and urine are key to diagnosing the cause of
hyponatraemia
The cause of
hypernatraemia
will usually be evident from the history
Slide6
Hyponatremia
Slide7Determining the cause of
hyponatraemia
may be straightforward if an obvious precipitating cause is
vomiting
or
diarrhoea
, when both sodium and total body water are low, and
elderlytaking
diuretics.
Slide8Here,
hyponatraemia
almost always reflects an excess of water relative to sodium, commonly by dilution of total body sodium secondary to increases in total body water (water overload) and sometimes as a result of depletion of total body sodium in excess of concurrent body water losses
Slide9Hypovolaemia
Extrarenal
loss, urine sodium <30
mmol
/l
Dermal losses, such as burns, sweating
Gastrointestinal losses, such as vomiting,
diarrhoea
Pancreatitis
Renal
loss, urine sodium >30
mmol
/l
Diuretics
Salt wasting nephropathy
Cerebral salt wasting
Mineralocorticoid deficiency (Addison's disease)
Slide10Hyponatraemia
with
hypovolaemia
This
is due to salt loss in excess of water loss. In this situation, ADH secretion is initially suppressed (via the hypothalamic
osmoreceptors
); but as fluid volume is lost, volume receptors override the
osmoreceptors
and stimulate both thirst and the release of ADH. This is an attempt by the body to defend circulating volume at the expense of osmolality. With
extrarenal
losses and normal kidneys, the urinary excretion of sodium falls in response to the volume depletion
Slide11
Hypervolaemia
*
Urine sodium <30
mmol
/l
Congestive cardiac failure
Cirrhosis with ascites
Nephrotic
syndrome
Urine sodium >30
mmol
/l
• Chronic renal failure
Slide12
Euvolaemia
Urine sodium >30
mmol
/l
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)†
Hypothyroidism
Hypopituitarism (glucocorticoid deficiency)
Water intoxication:
Primary polydipsia
Excessive administration of parenteral hypotonic fluids
Post-transurethral prostatectomy
Slide13Paradoxical retention of sodium and water despite a total body excess of each; baroreceptors in the arterial circulation perceive
hypoperfusion
, triggering an increase in arginine vasopressin release and net water retention.
†Remember that SIADH is a diagnosis of exclusion
Slide14symptoms
Patients with mild
hyponatraemia
(plasma
sodium 130-135
mmol
/l
) are usually asymptomatic.
Nausea
and malaise are typically seen when plasma sodium concentration falls
below 125-130
mmol
/l
.
Headache, lethargy, restlessness, and disorientation follow, as the sodium concentration falls
below 115-120
mmol
/l.
With
severe and rapidly evolving
hyponatraemia
, seizure, coma, permanent brain damage, respiratory arrest, brain stem herniation, and death may occur.
Slide15History, examination, and investigation
An accurate history may reveal a clue to the cause of the
hyponatraemia
and establish the rapidity of the
symptoms
Plasma
osmolality is almost always low in
hyponatraemia
,
Slide16History, examination, and investigation
Evaluation of volume status
Skin turgor
Pulse rate
Postural blood pressure
Jugular venous pressure
Consider central venous pressure monitoring
General
examination for underlying illness
Congestive cardiac
failure ,Cirrhosis,
Nephrotic
syndrome, Addison's disease ,Hypopituitarism
Hypothyroidism
Slide17History, examination, and investigation
Investigations
Urinary sodium
Plasma glucose and lipids
*
Renal function
Thyroid function
Peak cortisol during short
synacthen
test†
Plasma and urine osmolality‡
If indicated: chest
x
ray, and computed tomography and magnetic resonance imaging of head and thorax
Slide18Pseudohyponatraemia
due to
artefactual
reduction in
= hyperlipidemia +
hyperprotenmia
.
artificially lowers
the plasma
sodium concentration measurement via laboratory artifact, but
the amount
of sodium in plasma is normal
Pseudohyponatremia
= ====This
occurs in
hyperlipidaemia
or
hyperproteinaemia
where there is a
spuriously low
measured sodium concentration, the sodium being confined to the aqueous phase but having its concentration expressed in terms of the total volume of plasma. In this situation, plasma osmolality is normal and therefore treatment of ‘
hyponatraemia
’ is unnecessary
hyperglycaemia
causes true
hyponatraemia
, irrespective of laboratory method.
For
SIADH: plasma osmolality < 270
mosm
/kg with inappropriate urinary concentration (> 100
mosm
/kg), in a
euvolaemic
patient after exclusion of hypothyroidism and glucocorticoid deficiency).
Slide19Hyponatraemia
with
hypervolaemia
The
common causes of
hyponatraemia
due to water excess
.
there
is usually an element of reduced glomerular filtration rate with avid reabsorption of sodium and chloride in the
proximal tubule
.
This leads to reduced delivery of chloride to the ‘diluting’ ascending limb of
Henle’s
loop and a reduced ability to
generate ‘free water’, with a consequent inability to excrete
dilute urine. This is commonly compounded by the administration of diuretics that block chloride reabsorption and interfere with the dilution of filtrate either in
Henle’s
loop (loop diuretics) or distally (thiazides).
Slide20Management of
hyponatraemia
Slide21Management of
hyponatraemia
Treatment
This is directed at the primary cause whenever possible.
In a healthy patient:
# Give
oral electrolyte-glucose mixtures
# Increase
salt intake with slow sodium 60–80
mmol
/day.
In a patient with vomiting or severe volume depletion:
#
Give intravenous fluid with potassium supplements, i.e.
1.5–2 L 5% glucose (with 20
mmol
K+
) and 1 L 0.9% saline over 24 h PLUS measurable losses
Slide22Management of
hyponatraemia
Hyponatraemia
with
euvolaemia
#
The most common iatrogenic cause is overgenerous
infusion of 5% glucose into postoperative patients; in
this situation it is exacerbated by an increased ADH
secretion in response to stress.
# Postoperative
hyponatraemia
is a common clinical
problem (almost 1% of patients) with symptomatic
hyponatraemia
occurring in 20% of these patients.
#
Marathon runners drinking excess water and ‘sports
drinks’ can become
hyponatraemic
.
#
Premenopausal females are at most risk for developing
hyponatraemic
encephalopathy postoperatively, with
postoperative ADH values in young females being 40
times higher than in young males
Slide23demeclocycline
It is widely used (though off-label in many countries including the United States) in the treatment of
hyponatremia
(low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) when fluid restriction alone has been ineffective
.
Physiologically, this works by reducing the responsiveness of the collecting tubule cells to ADH
.
The use in SIADH actually relies on a side effect;
demeclocycline
induces
nephrogenic
diabetes
insipidus
(dehydration due to the inability to concentrate
urine.
Demeclocycline
used to be the drug of choice for treating SIADH.[13] Meanwhile it might be superseded, now that vasopressin receptor antagonists, such as
tolvaptan
, became available
Slide24Management of
hyponatraemia
S
ymptoms
and their severity should guide the treatment strategy
Acute
hyponatraemia
developing within 48 hours carries a risk of cerebral
oedema
, so prompt treatment is indicated with apparently small risk of central
pontine
myelinolysis
.
A rapid rise in extracellular osmolality, particularly if
there is
an ‘overshoot’ to high serum sodium and osmolality,
will result
in the osmotic demyelination, syndrome (
ODS====central
pontine
demyelination
This
is presumed to occur if the blood-brain barrier becomes permeable with rapid correction of
hyponatraemia
and allows complement mediated
oligodendrocyte
toxicity
.Alcoholics
with malnutrition, premenopausal or elderly women on thiazide diuretics, and patients with
hypokalaemia
or burns are at increased risk of central
pontine
myelinolysis
.
Slide25Osmotic Demylination syndrome
in the phase of rapid correction of
hyponatraemia
, resulting in an hypo-
osmolar
intracellular
compartment and lead to shrinkage of cerebral vascular
endothelial cells.
Consequently
the blood–brain barrier is
functionally impaired, allowing lymphocytes, complement,
and cytokines to enter the brain, damage
oligodendrocytes
,
activate microglial cells and cause
demyelination.
Slide26Management of
hyponatraemia
Neurological injury is typically delayed for two to six days after elevation of the sodium concentration, but the symptoms, which include dysarthria, dysphagia, spastic
paraparesis
, lethargy, seizures, coma, and even death, are generally irreversible, so prevention is key.
raising
the sodium concentration by 1-2
mmol
/l per hour until symptoms have resolved, with close monitoring of plasma
sodium
Therefore
, the rate of correction should not exceed 12
mEq
/L/day (should be <8
mEq
/L in the first 24 hours)
.
Slide27Management of
hyponatraemia
In general, the plasma sodium should not be corrected to
>125–130
mmol
/L. 1 mL/kg of 3% sodium chloride will raise
the plasma sodium by 1
mmol
/L, assuming that total body
water comprises 50% of total bodyweight.
#
Symptomatic
hyponatraemia
in patients with
intracranial pathology should be managed aggressively
and immediately with 3% saline like acute
hyponatraemia
Slide28Hyponatremia
Risk factors for developing
hyponatraemic
encephalopathy.
The brain’s adaptation to
hyponatraemia
initially
involves extrusion of blood and CSF, as well as sodium,
potassium and organic
osmolytes
, in order to decrease brain
osmolality. Various factors can interfere with successful
adaptation. These factors rather than the absolute change in
serum sodium predict whether a patient will suffer
hyponatraemic
encephalopathy.
#
Children under 16 years are at increased risk due to
their relatively larger brain-to-intracranial volume ratio
compared with adults
.
Slide29Hyponatremia
Slide30Hyponatremia
#
To
prevent
hyponatraemia
, avoid using hypotonic fluids
postoperatively and administer 0.9% saline unless
otherwise clinically
contraindicated
.
#
The serum sodium should be measured daily in any patient receiving continuous parenteral fluid.
# Some
degree of
hyponatraemia
is usual in acute
oliguric
kidney injury, while in chronic kidney disease (CKD) it is
most often
due to ill-given advice to ‘push’ fluids
Slide31Hyponatremia
# Chronic/asymptomatic
. If
hyponatraemia
has
developed slowly, as it does in the majority of patients,
the brain will have adapted by decreasing intracellular
osmolality and the
hyponatraemia
can be corrected
slowly (without use of hypertonic saline).
# However
, clinically it can be difficult to know how long the
hyponatraemia
has been present and 3% of hypertonic saline
is still
required .
Slide32Hypernatremia
Slide33Hypernatremia
Hypernatraemia
=
reflects a
water
loss or a hypertonic sodium gain,
,
hyperosmolality
.
Severe
symptoms are usually evident only with acute and large increases in plasma sodium concentrations to above 158-160
mmol
/l
.
Slide34
Importantly, the sensation of intense thirst that protects against severe
hypernatraemia
in health may be absent or reduced in patients with altered mental status or with hypothalamic lesions affecting their sense of thirst (
adipsia
) and in infants and elderly people. Non-specific symptoms such as
anorexia, muscle weakness, restlessness, nausea, and vomiting
tend to occur early.
More
serious signs follow, with
altered mental status, lethargy, irritability, stupor, or coma
. Acute brain shrinkage can induce vascular rupture, with cerebral bleeding and subarachnoid
haemorrhage
.
Slide35History, examination, and investigation
Measurement
of
urine
osmolality
plasma
osmolality and the
urine
sodium
concentration
Slide36Box 3: Classification of
hypernatraemia
Hypovolaemia
Dermal losses—for example, burns, sweating
Gastrointestinal losses—for example, vomiting,
diarrhoea
, fistulas
Diuretics
Postobstruction
Acute and chronic renal disease
Hyperosmolar non-
ketotic
coma
*
Slide37Hypervolaemia
Iatrogenic (hypertonic saline, tube feedings, antibiotics containing sodium, or hypertonic dialysis)
Hyperaldosteronism
†
Euvolaemia
Diabetes
insipidus
(central,
nephrogenic
, or gestational)
Hypodipsia
Fever
Hyperventilation
Mechanical ventilation
*
Sodium often raised, even after correction for glucose
†Typically mildly elevated sodium ∼147
mmol
/l, so rarely a clinical problem
Slide38Management
1
.
Hypovolemic hypernatremia
—Give isotonic
NaCl
to achieve
euvolemia
and
restore hemodynamics initially. Correction of hypernatremia can wait until the patient is
hemodynamically
stable, then replace the free water
deficit to
determine how much 5% dextrose to give. .
2.
Isovolemic
hypernatremia
—Patients with diabetes
insipidus
require vasopressin
(
nephrogenic
DI, unless hereditary, is rarely complete), low sodium diet, and
thiazide
diuretics or NSAID or both .
Prescribe oral fluids, or if the patient cannot drink, give D5W.
3
.
Hypervolemic
hypernatremia
—Give diuretics (such as
furosemide
and
D5W
(to achieve normal sodium concentration) to remove
excess sodium.
Dialyze
patients with renal failure
Slide39Management
In
patients with
hypernatraemia
that has developed over a period of hours, rapid correction of plasma sodium (falling by 1
mmol
/l per hour) improves the prognosis without the risk of convulsions and cerebral
oedema
.
Patients should be given intravenous 5% dextrose for acute
hypernatraemia
or half-normal saline (0.45% sodium chloride) for chronic
hypernatraemia
if unable to tolerate oral water.
Slide40
Treatment of hypernatremia
Treatment
Treatment is that of the underlying cause, e.g.
#
In ADH deficiency, replace ADH in the form of
desmopressin
, a stable non-
pressor
analogue of ADH
# Remember
to withdraw nephrotoxic drugs where
possible and replace water either orally or, if necessary,
intravenously.
In severe (>170
mmol
/L)
hypernatraemia
, 0.9% saline
(150
mmol
/L) should be used initially. In less severe (e.g. >150
mmol
/L)
hypernatraemia
,
the treatment
is 5% glucose or 0.45% saline; the latter is obviously preferable in hyperosmolar diabetic coma. Very large
volumes – 5 L/day or more – may need to be given in diabetes
insipidus
.
Slide41Calculation of Maintenance Fluids
100/50/20 rule
:
100 mL/kg for first 10 kg, 50 mL/kg for next 10 kg, 20 mL/kg for every 1 kg over 20
Divide total by 24 for hourly rate
For example, for a 70 kg man: 100 × 10 = 1,000; 50 × 10 = 500, 20 × 50 kg = 1,000. Total = 2,500. Divide
by 24 hours: 104 mL/
hr
4/2/1 rule
:
4 mL/kg for first 10 kg, 2 mL/kg for next 10 kg, 1 mL/kg for every 1 kg over 20
For example, for a 70 kg man: 4 × 10 = 40; 2 × 10 = 20; 1 × 50 = 50. Total = 110 mL/
hr