NCM 112 cellular aberrations
FLUID VOLUME EXCESS
TOPIC OUTLINE
1 Global new covid-19 cases
2 Global healthcare situation
3 Causes of death
4 Categories of diseases
5 National healthcare situation
6 Local healthcare situation
Objectives:
- Differentiate the two types of fluid volume excess in
terms of pathophysiology, signs and symptoms,
treatments, and nursing interventions.
- Utilize nursing process in the care and management of
specific problems in homeostasis
DEFINITION
- Retention of excess fluid in the body
- It often occurs in conjunction with renal failure
 Because renal system is chief regulator of
water and electrolytes
- Electrolytes may also be out of balance
 Sodium concentrations can be decreased
as well as the osmolality because there is
more water than sodium; the hematocrit
will be reduced from the dilution of excess
water
- The problem here would be too much water that dilutes
the solutes that affects the concentration of the plasma,
which reduces the serum osmolality
TYPES
a. EXTRACELLULAR FVE
- Also called edema formation (peripheral or pulmonary)
- it occurs in the periphery (peripheral edema), usually the
lower parts of the body, and it may also occur in the
lungs (pulmonary edema)
- Abnormal retention of fluids in the interstitial space
- Secondary to increase in body sodium (sodium draws
water)
- Percentage of adult body weight that is water can
increase from 60% (normal) to 69% - 72 % (edema)
 Increases water to 9-12%, this increase is
considered edema formation
- Interstitial fluid increases from about 15% (normal) to
about 28% of body weight
PATHOPHYSIOLOGY
Edema – abnormal accumulation of excess fluid in the tissue, it
manifests as:
 External swelling (face, hands, arms, feet, ankles, legs)
 Enlarged internal organs
Three principle groups it causes:
 Increased filtration either from increased blood
pressure or increased capillary permeability
 Decreased reabsorption due to reduced blood
albumin concentration
 Obstruction of lymphatic drainage
 Excess fluid hinders the exchange of nutrients and gases
and may lead to tissue necrosis
 Severe edema may also be accompanied by critically
reduced blood volume which may result to circulatory
shock
PULMONARY EDEMA
- Refers to build-up of fluid in the lungs including the
airways, alveoli (tiny air sacs), interstitium (lung tissue
that is sandwiched between alveoli and capillaries)
o Interstitium is usually full of proteins, when it
starts filling up with fluid, it can make it hard
for oxygen to cross from alveoli to capillary,
making the body hypoxic (deprived with
oxygen)
UNDERLYING CAUSES
 Cardiogenic
 Result of a heart disease
CAUSES
 LEFT SIDED HEART FAILURE
The left ventricle becomes unhealthy and can’t
pump effectively. The blood backs up in left
atrium, then in pulmonary vein, then in
pulmonary capillaries. The extra blood in the
pulmonary capillaries causes pulmonary
hypertension, which increases the hydrostatic
pressure of the pulmonary blood vessels. And
it pushes fluid in the interstitial spaces of the
lungs, causing pulmonary edema.
 SEVERE SYSTEMIC HYPERTENSION
A blood pressure greater than 180/110mmHg. In
this case, the left ventricle is healthy but can’t
effectively pump blood with a high afterload.
This situation has high systemic pressure.
Blood backs up at the left atrium, pulmonary veins,
pulmonary capillaries, resulting to pulmonary
hypertension then pulmonary edema.
 Non-cardiogenic
 Damage to pulmonary capillaries or alveoli
CAUSES
 PULMONARY INFECTIONS,
INHALATION OF TOXIC SUBSTANCE, &
TRAUMA TO THE CHEST
o these cause direct injury to alveoli.
When this happens there is usually
inflammatory process that makes
nearby capillaries more permeable, as
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 a result, protein and fluid enter the
interstitial space
 SEPSIS
o The key difference is that in sepsis,
the inflammatory process happens
throughout the body, rather than just
in the lungs. So, in addition to
pulmonary edema, sepsis can cause
extra fluid in interstitial space and
tissues throughout the body.
 LOW ONCOTIC PRESSURE
o Can result from not taking enough
proteins like albumin due to
malnutrition or liver failure. It can
also result from losing proteins too
quickly in nephrotic syndrome.
Regardless of the cause, low oncotic
pressure causes fluid to goes from
capillary to interstitial space
throughout the body, and in the lung
which result in pulmonary edema.
 Pulmonary edema can be just severe shortness of breath
 In left-sided heart failure can lead to orthopnea (shortness of
breath when lying flat), this is due to increased pulmonary
congestion when lying down. In left-sided ventricular heart
failure the pulmonary circulation is already overloaded. As a
result, the extra blood can’t be pumped out efficiently and causes
shortness of breath. This pulmonary congestion and shortness of
breath decrease/improves when the person wits up.
DIAGNOSIS OF PULMONARY EDEMA
 Chest x-ray/chest CT scan
o It shows fluid in the interstitial space
TREATMENT
 Typically involve supplemental oxygen
 Other treatments are dependent on the underlying
cause
 Those cardiogenic in nature require medications
which boost heart’s performance, or lowering
blood pressure
 Those caused by inflammation or low oncotic
pressure, managing illness will help resolve the
problem
b. INTRACELLULAR FVE
- Also called water intoxication; there’s build-up of water
into cells
- Abnormal retention of fluid within cells
- Water usually comes from extracellular compartments
because of the difference in the concentration of
solutions/fluids between two compartments, through
osmosis water is drawn into the cells
- Results from an excess of water and/or decrease in
solutes (electrolytes or non-electrolytes) in vascular
system
- Serum osmolality of vascular fluid is decreased, related
to dilution because of massive buildup of water in the
system
- Hypo-osmolar fluid in vascular system moves by
osmosis into cells
WATER INTOXICATION
- Also called dilutional hyponatremia
- A potentially fatal disturbance in brain functions when
the normal balance of electrolytes is not properly
replenished
- Kidneys flush out excess water through urination, but if
a lot of water is coming in and not being excreted, then
this creates a large concentration difference
- Water is then drawn into cells to dilute the concentration
causing cells to swell
- The brain has no room in the skull for the newly
pumped cells
- This can result in: severe headaches, confusion,
seizures, comas, respiratory arrest, and death
PATHOPHYSIOLOGY OF FVE
Venous stasis  Increased plasma hydrostatic pressure  fluid
is forced into interstitial space  Decreased albumin in plasma
(liver cirrhosis/malnutrition/nephrosis )  Decreased plasma
osmotic pressure  Fluid flows out into interstitial space
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Increased capillary permeability (inflammatory response) 
Albumin escapes into the interstitial space leading to decreased
PCOP  Fluid leaks out of the capillaries  Decreased
lymphatic drainage (lyphadenectomy, lymphadenitis, Hodgkin’s
disease  Reduced return of albumin to the bloodstream and
decreased PCOP  Fluid flows into interstitial space
Body’s response to tissue injury is inflammatory response, that
response trigger the release of potent chemicals regulators like
histamines, bradykinin, and prostaglandin. These promotes
increased capillary permeability. As a result of the of the
released of these potent chemicals regulators from damaged
mass cells, the lining of the capillary or capillary wall makes it
stretched and the endothelial cells makeup the membrane may
widen, or the gaps between these endothelial cells may widen,
allowing non-diffusible substances to escape, like albumin.
Normally, considering the molecules of these colloid or plasma
protein, they do not pass through the membrane of the capillary,
but under this condition or increased capillary permeability,
these proteins may escape into interstitial space leading to
decreased plasma colloid osmotic pressure. So, when they
escape, the level in the blood may decrease and the pons that
supposed to keep water inside the cells may disappear. As a
result, there is fluid leakage out of the capillaries.
The plasma proteins in the form of albumin that may have
escaped into interstitial space are supposed to be absorbed back
into the general circulation by the lymphatic system, but if
there’s decreased lymphatic drainage as a result of:
 surgical removal of lymph nodes (lymphadenectomy),
or
 inflammatory condition of lymph nodes (lymphadenitis)
usually a result of systemic lymphatic disease or cancer
or bacterial infection or other inflammatory condition.
The nodes may be large, hard, smooth or irregular, and
red and may feel hot. This condition actually alters the
functions of the lymphatic system.
 Hodgkin’s disease – malignant disorder or cancer
characterized by painless, progressive enlargement of
lymph tissues (usually first evidenced in cervical lymph
nodes), and the enlargement and congestion of spleen
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 (a lymphatic organ). Symptoms may include anorexia,  Asses respiration and breath sounds to detect pulmonary
weight loss, generalized pruritus, low-grade fever, night edema
sweats, anemia, and leukocytosis.  Assess peripheral-hand-vein emptying
 Assess skin and tissue for peripheral pitting edema
These conditions and the non-drainage of interstitial fluids
including albumin, may reduce the return of plasma proteins to  Check urine output
the bloodstream and may decrease the plasma colloid osmotic  Make dietary assessment relative to sodium intake
pressure. As a result, fluid flows into the interstitial space,  Assess for behavioral and neurologic changes
hence, edema formation.
-------------- NURSING DIAGNOSIS
Increased sodium retention (kidney failure, excess intake of  FVE: edema related to body fluid overload secondary to
sodium)  Increased retention of water leading to increased heart, renal, or liver dysfunction
hydrostatic pressure  Fluid leaks out of the capillaries  Ineffective breathing patterns related to increased
Sodium attracts water, when there’s increased sodium retention capillary permeability (pulmonary edema)
there’s also build-up or accumulation of water as a result of  Altered skin integrity related to edematous tissue
kidney failure, excess intake of sodium (like high sodium diet, (peripheral edema)
salty diet), and sometimes human error of prolonged  FVE: water intoxication related to excessive infusion of
administration of hypertonic solution which contains a lot of salt
hypo-osmolar solutions
or NaCl, and prolonged administration of steroid as
inflammatory drug which increases reabsorption of water,  High risk for injury related to cerebral edema secondary
sodium, and chloride. These may increase retention of water to intracellular FVE
leading to increased hydrostatic pressure, and then fluid leaks
NURSING INTERVENTIONS
out from capillaries, hence, edema formation
 Monitor vital signs and compare with baseline data
WATER INTOXICATION: INTRACELLULAR FVE  Monitor fluid intake and output
- May result in brain cells that swell, there’s increased in size,  Monitor weight daily for rapid changes
increased volume of the brain inside the skull, so there’s no  Monitor breathing patterns for changes in chest sounds
possibility for expansion therefore can increase intracranial and respiration
pressure.  Administer diuretics, if ordered, monitor client’s
response
 Monitor laboratory test results for changes pertinent to
 Early signs electrolyte balance and fluid status
o headache, nausea, vomiting, rapid weight gain,
 Monitor diet; instruct client in food selection
excessive sweating, and fingerprint edema over
 Monitor for worsening of underlying cause of FVE
flat bony areas such as sternum and sacrum
 Monitor parenteral fluid replacement if given
 Neurologic signs
(intracellular FVE)
o behavioral changes, irritability, disorientation,
 Monitor for changes in behavior indicating changes in
confusion, progressive apprehension,
neurologic status (intracellular FVE)
incoordination, drowsiness, and blurred vision;
caused by swollen cerebral cells and increased
ICP
 Changes in vital signs
o increased BP, ICP, and RR; decreased PR; vital
sign changes are the opposite of those in clients
in shock
 Late signs
o warm, moist, flushed skin; muscle twitching;
projectile vomiting; delirium; and convulsions,
followed by comatose state

TREATMENT AND MANAGEMENT

 Reduce water intake
 Reduce sodium intake
 Increase urine output
 Increase osmolality of extracellular fluid (with
intracellular FVE only)

NURSING PROCESS

NURSING ASSESSMENT
 Assess client history for underlying factors related to
FVE (e.g. renal or cardiac insufficiency, liver damage)
 Check vital signs: BP, PR, and weight; obtain baseline
data

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