Name: dr Iqra Rasool

Help maintain
body temperature
and cell shape
Helps

transport
nutrients gases
and wastes
 It is an abnormally decreased or
increased fluid volume or rapid shift
from one compartment of body
fluid to another
Hypovolemia

Hypervolemia
• May occur as a result of:
• Reduced fluid intake
• Loss of body fluids
• Sequestration (compartmentalizing) of body fluids
Pathophysiology

DECREASED FLUID VOLUME

Stimulation of ↑ ADH Secretion Renin-Angiotensin-

thirst center Aldosterone
System Activation
in ↑ Water resorption
Person complains of
hypothalamus
thirst ↓ Urine Output
↑ Sodium and
Water Resorption

↑ Urine specific gravity except

with osmotic diuresis
acute weight loss
Oliguria

Low bp

Sunken eyes

Dizziness

 Weakness

Decreased skin turgor

Concentrated urine
• Fluid Management
• Oral rehydration therapy – Solutions
containing glucose and electrolytes.

• IV therapy – Type of fluid ordered depends on

the type of dehydration and the
cardiovascular status.

• Diet therapy – Mild to moderate dehydration.

Correct with oral fluid replacement.
It refers to an isotonic expansion of
the ECF caused by abnormal
retention of water and sodium in
approximately the same proportion
in which they normally exist in the
ECF.
It is most often secondary to
an increase in total body
water.
 Common Causes:
Congestive Heart Failure
Early renal failure
IV therapy
Excessive sodium ingestion
SIADH

Corticosteroid
 Signs/Symptoms

Increased BP
Weight gain
Bounding pulse
Venous
distention
Pulmonary
edema
 Dyspnea

 Orthopnea (diff. breathing when

 Pharmacological therapy
Diuretics such as thiazide diuretics and loop
diuretics
Thiazide diuretics: hydrochlorothiazide
Loop diuretics: furosemide, torsemide
 Potassium supplement
 DIALYSIS
Sodium disorders
HYPONATREMIA
Introductio
n
Defined as a serum [Na] below 135 mmol/L.

Most common disorder of electrolytes encountered in

clinical practice, occurring in 22% of hospitalized

patients.
Important clinically because:

1)acute severe hyponatremia can cause substantial

morbidity and mortality;

2)adverse outcomes are higher in

hyponatremic patients with a wide range of underlying

diseases;

3)overly rapid correction of chronic hyponatremia can

cause severe neurological deficits and death.

ETIOLOGIES AND PATHOPHYSIOLOGIES OF
HYPOTONIC HYPONATREMIAS
Hypovolemic Hyponatremia(↓H2O,
↓↓Na+)
Gastrointestinal and Third-Space
Sequestered Losses
Vomiting or
Diarrhoea
Burns
Peritonitis
Bowel
lumen ileus

Loss water &

Na+, Cl --
Diuretic therapy

Loop diuretics

In TALH
Blocks sodium
reabsorption

interferes with the

generation of a hypertonic
medullary interstitium

More free water excretion,

inspite of vasopressin
Cerebral Salt Wasting
syndrome
 Is a syndrome described following SAH, head injury,
or

neurosurgical procedures, as well in other settings.

 Primary defect is salt wasting from the kidneys(?

role of BNP) with subsequent volume contraction,

which stimulates vasopressin release.

 Uncommon.
Mineralocorticoid (Aldosterone) Deficiency

Characterized by hyponatremia with ECF volume

contraction (provides the nonosmotic stimulus for

vasopressin release).

Urine [Na+] above 20 mmol/l, and high serum

K+.
Euvolemic Hyponatremia(↑H2O,
←→Na+)
SIADH (Syndrome of Inappropriate ADH Secretion)

 A defect in osmoregulation causes vasopressin to be

inappropriately stimulated, leading to urinary concentration.

 Excess vasopressin: CNS disturbances such as hemorrhage,
tumors, infections, and trauma.
Ectopic vasopressin: Small cell lung cancers, cancer of the
duodenum and pancreas, and olfactory neuroblastoma.

Idiopathic: seen in elderly(10%).


Criteria for Diagnosing SIADH

Decreased effective osmolality of the extracellular fluid.

Inappropriate urinary concentration (Uosm >100 mOsmol/kg

H2O) with normal renal function) at some level of plasma hypo-
osmolality.
Clinical euvolemia.

Elevated urinary sodium excretion (>20 mmol/L) while on

normal salt and water intake.
Absence of other potential causes of euvolemic hypo-
osmolality

Normal renal function and absence of diuretic use, particularly

thiazide diuretics.
 Postoperative
Exercise-Associated
Hyponatremia(EAH)
hyponatremia
•Long-distance marathon runners.
increased risk:
• BMI below 20 kg/m2,
• Running time exceeding 4 hours
• Excessive infusion of free • Consumption of fluids every
water (5% dextrose) and mile
• ↑Vasopressin due to pain

↑vasopressin
 Drugs Causing Hyponatremia

Vasopressin analogues Drugs that potentiate renal action of

vasopressin

Desmopressin Cyclophosphamid
Oxytocin e NSAIDs
Acetaminophen

Drugs that enhance vasopressin release Drugs that cause hyponatremia by

unknown mechanisms

Clofibrate Haloperidol
Carbamazepine Amitryptyline
Vincristine Fluoxetine
Nicotine Fluphenazine
Narcotics IVIG)
SSRI
ifosfamide
Hypervolemic Hyponatremia (↑↑H2O,
↑Na+)
Failure
↓MAP, ↓CO

Reduced effective
intravascular volume

↑vasopressin RAAS ↑Norepinephrine

(non osmotic baroreceptor
stimulation)

↑Thirst ↓GFR
 Cirrhosis
In pts of advanced cirrhosis

↑extracellular volume (ascites, edema).

↑ plasma volume (splanchnic venous dilation)

↑plasma renin,
↑ norepinephrine,
↑ vasopressin

↓GFR, ↑free water retention

Dilutional hyponatremia
 Advanced Chronic kidney disease

•Urine output is relatively fixed and water intake in

excess of urine output and insensible losses will cause

hyponatremia.

•Edema usually develops when the Na+ ingested exceeds

the kidneys capacity to excrete.

Clinical Manifestations of
Hyponatremia
Acute Hyponatremia – <48 hours

chronic hyponatremia - > 48 hours

General principles of treatment
.Primarilydetermined by the severity of symptoms and
the cause of the hyponatremia

• Symptomatic hyponatremia (seizures, or coma)

o likely to occur with an acute case and marked
reduction in the plasma sodium
concentration
o Aggressive therapy is required.
o Chronic but significant hyponatremia
where less severe neurologic symptoms occur
fatigue, nausea, dizziness, gait disturbances,
confusion, lethargy, and muscle cramps
These symptoms typically do not
mandate aggressive therapy
Treatment of hypovolemic hyponatremia

Diuretic related- Discontinuation of thiazides and

correction of volume deficits.

Mineralocorticoid deficiency- Volume repletion with

isotonic saline, Fludrocortisone chronically for

mineralocorticoid replacement.
 Treatment of euvolemic hyponatremia
SIADH - For most cases of mild-to moderate SIADH, fluid

Restriction. Failure to water restriction

- Vaptans

- Glucocorticoid Deficiency-glucocorticoid
replacement

 Severe Hypothyroidism-thyroid hormone

replacement
Treatment of hypervolemic
hyponatremia
Heart Failure-for patients with mild to
moderate

symptoms, begin with fluid restriction (1 L/d total) and,

if signs of volume overload are present, administer

loop

diuretics.

If the serum [Na] does not correct to the desired level, lift the

Cirrhosis-Severe daily fluid
restriction,
Vaptans an alternative choice if fluid restriction has failed to maintain

a serum [Na] 130 mmol/L; however, tolvaptan use should be

restricted to cases where the potential clinical benefit outweighs the

risk of worsened liver function, such as in patients with end-stage

liver disease and severe hyponatremia who are awaiting imminent

liver transplantation.

CKD-Restricting fluid intake. Aquaretics (vaptans

 Role of VAPTANS
 Vaptans have long been anticipated as a more effective

method to treat hyponatremia by virtue of their unique effect

to selectively increase solute-free water excretion by the
kidneys.
HYPERNATREMIA
 Definitio
n
• Hypernatremia is defined as a plasma sodium
>145 mEq/L
• Hypernatremia is seen in about 1% of
hospitalized patients and is more common
(7%) in intensive care unit patients.

• Mortality rate as high as 40% is reported

with hypernatremia, though it is
uncommonly identified as the primary cause
of death.
 Etiolog
y be caused by a primary
• Hypernatremia may
Na gain or a water deficit, the latter being
much more common.
• Impaired thirst response may occur in
situations where access to water is limited,
often due to physical restrictions
(institutionalized, handicapped, postoperative,
or intubated patients) or the mentally
impaired (delirium, dementia).

• Elderly individuals with reduced thirst and/or

diminished access to fluids are at the highest
risk of developing hypernatremia.
Palevsky PM. Hypernatremia. Semin Nephrol. Jan 1998;18(1):20-30.
• Hypernatremia due to water loss
The loss of water must occur in excess of
electrolyte losses in order to raise [Na].

Nonrenal water loss may be due to

evaporation from the skin and respiratory
tract (insensible losses) or loss from the GI
tract.
Diarrhea is the most common GI cause of
hypernatremia.
• Osmotic diarrhea (induced by lactulose,
sorbitol, or malabsorption of carbohydrate)
and viral gastroenteritis, in particular, result in
disproportional water loss.

• Insensible losses of water may increase in the

setting of fever, exercise, heat exposure,
severe burns, or mechanical ventilation.
• Renal water loss results from either
osmotic diuresis or diabetes insipidus (DI).

• Osmotic diuresis is frequently associated

with glycosuria and high osmolar feeds.

In addition, increased urea generation from

accelerated catabolism, high protein feeds,
and stress-dose steroids can also result in an
osmotic diuresis.
• Hypernatremia secondary to nonosmotic urinary
water loss is usually caused by
(a)impaired vasopressin secretion (central
diabetes insipidus [CDI]) or
(b) resistance to the actions of vasopressin
(nephrogenic diabetes insipidus [NDI]).

Partial defects occur more commonly than

complete defects in both types.
Patients with DI generally do not develop
hypernatremia if they are able to maintain fluid
intake adequate to compensate for the water
loss.
• The most common cause of CDI is destruction
of the neurohypophysis from trauma,
neurosurgery, granulomatous disease,
neoplasms, vascular accidents, or infection.

In many cases, CDI is idiopathic.

• NDI may either be inherited or acquired.

The latter often results from a disruption to

the renal concentrating mechanism due to
drugs (lithium, demeclocycline, amphotericin),
electrolyte disorders (hypercalcemia,
hypokalemia), medullary washout (loop
diuretics), and intrinsic renal diseases.
• Gestational diabetes insipidus is a rare
complication of late-term pregnancy in which
increased activity of a circulating placental
protease with vasopressinase activity leads to
reduced circulating AVP and polyuria, often
accompanied by hypernatremia.

DDAVP is an effective therapy for this

syndrome because of its resistance to the
vasopressinase enzyme.
• Hypernatremia due to primary Na gain occurs
infrequently due to the kidney's capacity to
excrete the retained Na.
However, it can rarely occur after repetitive
hypertonic saline administration or chronic
mineralocorticoid excess.

• Transcellular water shift from ECF to ICF can

occur in circumstances of transient
intracellular hyperosmolality, as in seizures or
rhabdomyolysis.
JAPI Dec 2008 edn
 Cnilcial Presentation
• Hypernatremia results in contraction of brain cells as
water shifts to attenuate the rising ECF osmolality.

• Thus, the most severe symptoms of hypernatremia are

neurologic, including altered mental status, weakness,
neuromuscular irritability, focal neurologic deficits,
and, occasionally, coma or seizures. The presence of
encephalopathy is a poor prognostic sign in
hypernatremia, and carries a mortality rate as high as
50%.
• As with hyponatremia, the severity of the clinical
manifestations is related to the acuity and magnitude
of the rise in plasma [Na].
• The sudden shrinkage of brain cells in acute
hypernatremia may lead to parenchymal or
subarachnoid hemorrhages and/or subdural
hematomas; however, these vascular
complications are encountered primarily in
pediatric and neonatal patients.

• Osmotic damage to muscle membranes also

can lead to hypernatremic rhabdomyolysis.
 Diagnostic Approach
• The history should focus on the presence or absence of
thirst, polyuria, and/or an extrarenal source for water
loss, such as diarrhea.

• The physical examination should include a detailed

neurologic exam and an assessment of the ECFV;
patients with a particularly large water deficit and/or a
combined deficit in electrolytes and water may be
hypovolemic, with reduced JVP and orthostasis.

• Accurate documentation of daily fluid intake and daily

urine output is also critical for the diagnosis and
management of hypernatremia.
• Adequate differentiation between
nephrogenic and central causes of DI requires
the measurement of the response in urinary
osmolality to DDAVP, combined with
measurement of circulating AVP in the setting
of hypertonicity.
Preparation
Please contact the Duty Biochemist at least 24 hours before the test) Normal
dinner and fluids are allowed the night before the test. No alcohol or
caffeine. 7am light breakfast but NO fluids, tea, coffee or smoking.
Supervision is required throughout to assess compliance and safety.
Contraindications
Hypovolaemia or hypernatraemia
Procedure
Print out a worksheet and record results in the table (appendix 1). Please
clearly label all blood and urine samples; the TIME of collection is essential.
1. 8 am:
a) Empty bladder, record the volume, and send urine osmolality
b) Take a serum osmolality
c) Record the patient's weight.
2. Then for the next 8 hours check: Urine osmolality and weight every hour
Serum osmolality every 2 hours
.
.
.
.
• Symptomatic hypernatremia

As in hyponatremia, aggressive correction of

hypernatremia is potentially dangerous.
The rapid shift of water into brain cells
increases the risk of seizures or permanent
neurologic damage.
Therefore, the water deficit should be
reduced gradually by roughly 10 to
12 mEq/L/d.
• Chronic asymptomatic hypernatremia

The risk of treatment-related complication is

increased due to the cerebral adaptation to
the chronic hyperosmolar state, and the
plasma [Na] should be lowered at a more
moderate rate (between 5 and 8 mEq/L/d).
• A 76-year-old man presents with a severe
obtundation, dry mucous membranes,
decreased skin turgor, fever, tachypnea, and a
blood pressure of 142/82 mm Hg without
orthostatic changes. The serum sodium
concentration is 168 mmol per liter, and the
body weight is 68 kg.

• Hypernatremia caused by pure water

depletion due to insensible losses is diagnosed
• A 60-year-old man has received 10 ampules of sodium
bicarbonate over a period of six hours during
resuscitation after recurrent cardiac arrest. He is
stuporous and is undergoing mechanical ventilation.
His blood pressure is 138/86 mm Hg, and peripheral
edema (+++) is present. The serum sodium
concentration is 156 mmol per liter, the body weight is
85 kg, and the urinary output is 30 ml per hour.

• The hypernatremia is caused by hypertonic sodium

gain, and its correction requires that the excess sodium
and water be excreted.