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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

Slide3

Under 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

Slide5

Notes

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

Slide7

Determining 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.

Slide8

Here,

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

Slide9

Hypovolaemia

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)

Slide10

Hyponatraemia

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

Slide13

Paradoxical 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

Slide14

symptoms

 

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.

Slide15

History, 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

,

Slide16

History, 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

Slide17

History, 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

Slide18

Pseudohyponatraemia

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).

Slide19

Hyponatraemia

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).

Slide20

Management of

hyponatraemia

Slide21

Management 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

Slide22

Management 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

Slide23

demeclocycline

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

Slide24

Management 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

.

Slide25

Osmotic 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.

Slide26

Management 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)

.

Slide27

Management 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

Slide28

Hyponatremia

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

.

Slide29

Hyponatremia

Slide30

Hyponatremia

#

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

Slide31

Hyponatremia

# 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 .

Slide32

Hypernatremia

Slide33

Hypernatremia

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

.

Slide35

History, examination, and investigation

Measurement

of

urine

osmolality

plasma

osmolality and the

urine

sodium

concentration

Slide36

Box 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

*

Slide37

Hypervolaemia

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

Slide38

Management

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

Slide39

Management

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

.

Slide41

Calculation 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

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