Dehydration

What is dehydration.?

A condition that occurs when the loss of body fluids, mostly water, exceeds
the amount that is taken in.

We loss water everyday when we:

Breathe and humidified air leaves the body

Sweat

Eliminate waste by urinating or having bowel movement

What causes dehydration.?

Dehydration occurs because there is too much water lost, not enough water taken
in, or most commonly a combination of two.

Diarrhea

Vomiting

Sweat

Diabetes

Burns

Inability to drink fluids

Body Fluid Compartments
Total body water distributed to two major compartments

Intracellular: Fluid within the cell

K+, Mg2+, proteins and organic phosphates

Extracellular: Fluid outside the cell

Na+, Cl- and HCO3-

. Plasma: Aqueous component of blood

. Interstitial fluid: Fluid that bathes the cells (Ultra-filtrate of plasma)

Transcellular: Small includes peritoneal, pleural, cerebrospinal and

digestive fluid

Shifting of Water
Intracellular and extracellular osmorality must be kept in equilibrium
Disturbances that alters solute or water balance Shifting of water between
fluid compartments
Classified based on ECF osmorality:
1) . Isosmotic: No change in ECF osmorality
2) . Hyposmotic: Decrease in ECF osmorality
3) . Hyperosmotic: Increase in ECF osmorality
Dehydration States

 Dehydration is characterized by loss of ECF volume (Volume contraction) and

subsequently a decrease in blood volume (Hypovolemic)
1) . Isonatremic: ECF sodium within normal range (130-150 mEq/L)
2) . Hyponatremic: Decrease in ECF sodium (< 130 mEq/L)
3) . Hypernatremic: Increase in ECF sodium (> 150 mEq/L)
Isonatremic Dehydration
Loss of fluid and salt in equal amount with no change in ECF sodium (130-150
mEq/L)
ECF osmorality remains unchanged Fluid does not shift between two
compartments
Causes

Extrarenal

Renal

Extrarenal Causes
1) . Inadequate fluid intake
2) . Loss through GI tract (vomiting, diarrhea)
3) . Skin loss (sweating, fever)
4) . Third space loss: Trapping of fluid in transcellular space (edema, ascites)
Renal Causes
1) Osmotic diuresis
2) . Diuretic therapy
3) . Addison disease
Osmotic Diuresis

Glucose, mannitol and urea

Hyperglycemia in diabetic patients

Increase osmolarity of tubular lumen Retention of water

Water reabsorption is prevented Increase urine output

Diuretic Therapy

Use to increase urine output

Such as thiazide diuretics

Inhibit activity of Na+- Cl- co-transporter of epithelial cells of early distal

tubule Prevent NaCl absorption

Addison Disease

Autoimmune disease of all zones of adrenal cortex

Zona glomerulosa: Produces aldosterone

Release in response to decrease arterial blood pressure

Stimulate Na+ reabsorption in late distal and collecting duct

Involves synthesis of ENaC onto the apical surface of principal cells

Clinical Manifestation

Weight loss

Mild fluid deficit: 2% (of body weight)

Moderate fluid deficit: 2-5%

Severe fluid deficit: 8% or greater

Compensatory mechanism

Loss of isotonic fluid Stimulate thirst and release of ADH

Increase water reabsorption from collecting duct

Decrease urine output and increase urine osmolarity

Decreased Vascular volume

Decline in both arterial and venous volume

Arterial pressure decreases with increase in heart rate (Tachycardia)

Weak pulse

Postural hypotension (Drop in blood pressure when standing)

Veins less prominent

Decreased ECF volume

Sunken eyes and softer eyeball as fluid in anterior chamber decreases

Impaired temperature regulation

Reduced blood flow to skin Impairs heat dissipation

Elevated body temperature

Hyponatremic Dehydration
More salt is lost than water (loss of hypertonic fluid) ECF sodium falls (<
130 mEq/L)
Decrease ECF osmorality Water shifts from ECF to ICF
ICF volume increases Swelling of cells
Causes

Extrarenal

Renal

Extrarenal Causes
1) Loss through GI tract (vomiting, diarrhea)*
2) . Third space loss: Trapping of fluid in transcellular space (pancreatitis)*
* Replacement fluid are hypotonic compared to loss
Renal Causes
1) Osmotic diuresis
2) . Loop diuretics
3) . Addison disease
4) . Cerebral salt-wasting
Loop Diuretics

Inhibit activity of Na+-K+-2Cl- co-transporter of epithelial cells of TAL Prevent

NaCl absorption

Produces a concentrated (hyperosmotic) urine and body fluid becomes

diluted

Cerebral Salt Wasting

Brain injury causes

1) . Depressed sympathetic stimulation Decrease sodium reabsorption by

proximal tubular cells
2) . Excess secretion of brain natriuretic peptides Increase GFR and decreased
renal sodium reabsorption
Overall excessive loss of salt Decrease plasma osmorality
Clinical Manifestation

Increased ICF volume

Movement of fluid into brain cells

Apathy, lethargy, and headache Progress to disorientation, confusion

and motor weakness

Extremely low plasma sodium Seizure and coma

Neuromuscular tissue

Fingerprint edema (indented fingerprint remains after pressing against

the bony sternum for 15-30 sec)

Muscle cramps, weakness and fatigue

Gastrointestinal manifests

Nausea, vomiting, abdominal cramps and diarrhea

Hypernatremic Dehydration
More water is lost than salt (Loss of hypotonic fluid) ECF sodium rises (>
150 mEq/L)
Fluid initially lost from plasma Increase plasma osmolarity
Water shifts from interstitial fluid to plasma Increase interstitial osmorality
Water shifts from ICF to ECF Both ECF & ICF volume decreases & shrinking
of cells
Causes

Extrarenal

Renal

Extrarenal Causes
1) . Inadequate fluid intake
2) . Excessive skin loss (sweating)
3) . Loss through respiration (fever, exercise)
4) . Increased loss through GI tract (diarrhea, vomiting)
Renal Causes
1) Osmotic diuretics
2) . Central diabetes insipidus
3) . Nephrogenic diabetes insipidus
Central Diabetes Insipidus
Inability of posterior pituitary to secrete ADH

Collecting duct becomes impermeable to water

Produce a large volume of dilute urine and body fluid becomes concentrated

Nephrogenic Diabetes Insipidus

Posterior pituitary gland produce ADH normally

But principal cells of collecting duct becomes unresponsive to ADH

Due to a defect in V2 (Vasopressin 2) receptor

Produce a large volume of dilute urine and body fluid becomes concentrated

Clinical Manifestation

Compensatory mechanism

Increase plasma osmorality Stimulate thirst and release of ADH

Increase water reabsorption from collecting duct

Decrease urine output and increase urine osmolarity

Decreased ICF volume

Dry skin and mucous membrane

Decreased salivation and lacrimation

Decreased ECF volume

Decline in both arterial and venous volume

Arterial pressure decreases with increase in heart rate (Tachycardia)

Weak pulse

Postural hypotension (Drop in blood pressure when standing)

Veins less prominent

Movement of fluid out of brain cells

Headache

Agitation and restlessness

Decreased reflexes

May lead to seizure and coma

Diagnosis
Mental Status Test
to evaluate whether the patient is awake, alert, and oriented
2 .Vital signs
3. Temperature
measured to assess fever
4. Skin
checked to see if sweat is present and to assess degree of elasticity

Laboratory Diagnosis

To help confirm the diagnosis and pinpoint the degree of dehydration

following are the tests are required to perform :
Blood tests. Blood samples may be used to check for a number of factors,

such as the levels of your electrolytes especially sodium and potassium

and how well your kidneys are working.

Urinalysis. Tests done on your urine can help show whether you're
dehydrated and to what degree.