Na Imbal Ë most abundant elect in ECF 135 -145 mEq/L š when âNa is d/t SIADH, the urinary Na >

nary Na > 20 mEq/L, &

š determins ECF osmolality.
š â Na = r in osmolality.
š controls H20 distrib bc doesn’t easily cross cell wall memb
& bc of its abundance & high concent in the body.
Na reg by ADH, thirst, & RAAS.
š prim. Reg of ECF vol .
š A loss /gain of Na accomp by a loss/ gain of H20.
š Na estab electrochemical statemusc contraction &
transmiss nerve impulses.
Na Deficit (â Na)
Plasma Na concentratio of total body Na 2 total body H20. hrs, to avoid neuro damage d/t osmotic demyelination
š â ratiolow quantity of total body Na w/ lesser reduction
in total body H20,
© norm total body Na content w/ excess H20
© excess Na w/ an even greater excess of H20
© can be superimposed on an existing FVD or FVE.
Ë Lost V*, D*, fistulas, or sweat, diuretics (mainly w/ a
low-Na diet combo)
š Aldosteroneadrenal insufficiency âNa
¶dilutional âNa (H20 intox~hypotonic overhydr) ¶
 Na is diluted  á ratio of H20 to Na á ECF vol &
norm or á total Na
© SIADH; áBS; & áH20 intake  admin of elect-
poor parenteral fluids, tap-water enemas, or irrigation the medullary collecting tubule.
of NG w/ H20 instead of NS.
š H20 gained abnormally
© exces IV- dextrose & H20 sol., (usually stressed)
© compulsive H20 drinking (psychogenic polydipsia).
©SIADH  excess ADH activity, w/ H20 reten &âoverhy
¶SXdepend on the cause, magnitude, & speed of deficit
š Poor skin turgor, dry mucosa, HA*, âsaliva, orth-BP-fall,
*N & abd cramping.
š Neuro rî alt mental status, status epilepticus, coma, &
obtundation r/t cell swell & cerebral edema
ø As Na level â , cell fluid  more concentrated & pulls
H20  cells.
š acute â Na- have more cerebral edema & higher mortality
rates than do those w/ more slowly developing âNa.
ø Acute â in Na develop in < 48 hrs, may be assoc w/ brain
herniation & compression of midbrain structures.
ø Chronic â in Na over 48 hrs or more status epilepticus The nurse needs to identify patients at risk âNa so that they
& cerebral pontine myelinolysis.
ø assoc w/ Na loss & H20 gain  anorexia, cramps, &
exhaustion.
š severity á w/ the degree & the speed it develop.
ø < 115  sx of á ICP î lethargy, confusion, twitching, focal V*, *N, abd cramp. The nurse must be particularly alert for
weakness, hemiparesis, papilledema, & seizures
Assessment & Diagnostic Findings
ø SIADH can be 100 or less
© Serum osmolality â, except in azotemia or toxin ingestion
© when Na loss, the urinary Na content is < 20 mEq/L,
suggesting á proximal reabsorpt of Na 2nd to ECF vol
depletion, & the specific gravity is low (1.002 to 1.004).
Detecting & Controlling HypoNa
urine specific gravity > 1.012
retains H20 abnorm  gains body weight, no
peripheral edema; instead, fluid á inside the cells
“fingerprinting” finger is pressed over a bony
prominence like the sternum.
Medical Management
ø Key tx is assesspeed it occurred & Na value
Na Replacement
ø careful admin of Na by mouth, NG tube, or IV î LR or
isotonic saline (0.9% NS)
© Serum Na must not be á by more than 12 mEq/L in 24
overcorrected (exceeding 140 mEq/L) too rapidly or in
hypoxia or anoxia
Osmot. demylmay produce lesions in the pons 
paraparesis, dysarthria, dysphagia, & coma.
š daily Na requirement 100 mEq
ø In SIADH, the admin of hypertonic saline solution alone
cannot r the plasma Na concent. š excess Na would be
excreted rapidly  highly concentrated urine. W/ the addition
of Lasix, urine is not concentrated & isotonic urine is
excreted to effect a r in H20 balance.
In SIADH, ( H20 restriction is difficult), lithium or
demeclocycline can antagonize the osmotic effect of ADH on
H20 Restriction
øNorm/excess fluid vol tx fluid restrict- 800 mL in 24 hrs.
 safer than Na admin
ø If Neuro sx admin small vol of a hypertonic Na î3% or
5% NS.
š Incorrect use  extremely dangerous,
1 L of 3% NS solution contains 513 mEq of Na
 1 L of 5% NS  855 mEq of Na
© edema exists alone, Na is restricted
© edema & âNa together, both Na & H20 restrict.
Nursing Alert
admin fluids to ♥ disease ~ assess sx circ overload (cough,
dyspnea, puffy eyelids, dependent edema, weight gain in
24 hrs). lungs î crackles. Extreme care is taken when
admin highly hypertonic Na fluids (3% or 5% NS) î lethal
if infused carelessly.
Nursing Management
can be monitored.
Early detection & tx necessary to prevent serious comp.
For at/r ~ nurse : I&O, weight. It is also necessary to note
ab norm losses of Na or gains of H20, as well as GI sx î A*,
ø CNS rlethargy, confusion, musc twitching, & seizures.
š sev neuro sx assoc w/ very low Na that fallen
rapidly bc of fluid overloading.
ø âNafreq overlooked cause of confusion in elderly, who
have an á risk for âNa bc of r in renal fx & subsequent â
ability to excrete excessive H20 loads. š meds  Na loss or
H20 retention is a predisposing fx.
For a pat. who is experiencing abnormal losses of Na & can
consume a general diet, the nurse encourages foods & fluids
w/ a high Na content. For example, broth made w/ one beef
cube contains approximately 900 mg of Na ; 8 oz of tomato
juice contains approximately 700 mg of Na . The nurse also
needs to be familiar w/ the Na content of parenteral fluids
(see Table 14-4). For the pat.taking lithium, the nurse
observes for lithium toxicity, particularly when Na is lost by
an ab norm route. In such instances, supplemental salt &
fluid are administered. Because diuretics promote Na loss,
the pat.taking lithium is instructed not to use diuretics w/out
close medical supervision. For all patients on lithium therapy,
adequate salt intake should be ensured.
Excess H20 supplements are avoided in patients receiving
isotonic or hypotonic enteral feedings, particularly if ab norm
Na loss occurs or H20 is being ab norm ly retained (as in
SIADH). Actual fluid needs are determined by evaluating
fluid I&O, urine specific gravity, & serum Na levels.
Returning the Na Level to norm
ø If primary problem is H20 retention, it’s safer to restrict
fluid
ø Admin Na to a pat. w. norm /ávol predispose the pat. to
fluid vol overload. As stated previously, the nurse must
monitor the pat.w/ ♥ disease very closely.
In severe hypoNa, the aim of therapy is to elevate the serum
Na level only enough to alleviate neurologic signs &
symptoms. It is generally recommended that the serum Na
concent be increased to no greater than 125 mEq/L (125
mmol/L) w/ a hypertonic saline solution.
Na Excess (HyperNa)
HyperNa is a higher-than- norm serum Na level (exceeding
145 mEq/L [145 mmol/L]) (Kee, Paulanka & Purnell, 2004).
It can be caused by a gain of Na in excess of H20 or by a
loss of H20 in excess of Na . It can occur in patients w/
norm fluid vol or in those w/ FVD or FVE. W/ a H20 loss,
the pat.loses more H20 than Na ; as a result, the serum Na
concent increases & the increased concent pulls fluid out of
the cell. This is both an extracellular & an intracellular FVD.
In Na excess, the pat.ingests or retains more Na than H20.
A common cause of hyperNa is fluid deprivation in
unconscious patients who cannot perceive, respond to, or
communicate their thirst (Porth, 2005). Most often affected
are very old, very young, & cognitively impaired patients.
Admin of hypertonic enteral feedings w/out adequate H20
supplements leads to hyperNa, as does H20y diarrhea &
greatly increased insensible H20 loss (eg, hyperventilation,
denuding effects of burns).
Diabetes insipidus, a deficiency of ADH from the posterior
pituitary gland, leads to hyperNa if the pat.does not
experience, or cannot respond to, thirst, or if fluids are
excessively restricted. Neurogenic or nephrogenic causes of
diabetes insipidus should be considered in the assessment
(Olson, Meek & Lynch, 2004).
Less common causes of hyperNa are heat stroke, near-
drowning in sea H20 (which contains a Na concent of
approximately 500 mEq/L), & malfunction of either
hemodialysis or peritoneal dialysis proportioning systems. IV
admin of hypertonic saline or excessive use of Na
bicarbonate also causes hyperNa (Porth, 2005).
Clinical Manifestations
The clinical manifestations of hyperNa are primarily
neurologic & are the consequence of increased plasma
osmolality caused by an increase in plasma Na concent.
H20 moves out of the cell into the ECF, resulting in cellular
dehydration (Rose & Post, 2000). HyperNa leads to a
relatively concentrated ECF (see Fig. 14-4). Clinically, these
changes may be manifested by restlessness & weakness in
moderate hyperNa & by disorientation, delusions, &
hallucinations in severe hyperNa. Dehydration (resulting in
hyperNa) is often overlooked as the primary reason for
behavioral changes in elderly patients. If hyperNa is severe,
permanent brain damage can occur (especially in children).
Brain damage is apparently due to subarachnoid hemorrhages
that result from brain contraction.
A primary characteristic of hyperNa is thirst. Thirst is such a
strong defender of serum Na levels in healthy people that
hyperNa never occurs unless the person is unconscious or
does not have access to H20. However, ill people may have
an impaired thirst mechanism. Other signs include a dry,
swollen tongue & sticky mucous membs. Flushed skin,
peripheral & pulmonary edema, postural hypotension, &
increased muscle tone & deep tendon reflexes are additional
signs & symptoms of hyperNa. Body temperature may
increase mildly, but it returns to norm after the hyperNa is
corrected.
Assessment & Diagnostic Findings
In hyperNa, the serum Na level exceeds 145 mEq/L (145
mmol/L) & the serum osmolality exceeds 300 mOsm/kg (300
mmol/L). The urine specific gravity & urine osmolality are
increased as the kidneys attempt to conserve H20 (provided
the H20 loss is from a route other than the kidneys) (Rose &
Post, 2000).
Medical Management
Treatment of hyperNa consists of a gradual lowering of the
serum Na level by the infusion of a hypotonic elect solution
(eg, 0.3% Na chloride) or an isotonic nonsaline solution (eg,
dextrose 5% in H20 [D5W]). D5W is indicated when H20
needs to be replaced w/out Na . Many clinicians consider a
hypotonic Na solution to be safer than D 5W because it
allows a gradual reduction in the serum Na level, thereby
decreasing the risk of cerebral edema. It is the solution of
choice in severe hyperglycemia w/ hyperNa. A rapid
reduction in the serum Na level temporarily decreases the
plasma osmolality below that of the fluid in the brain tissue,
causing dangerous cerebral edema. Diuretics also may be
prescribed to treat the Na gain.
There is no consensus about the exact rate at which serum Na
levels should be reduced. As a general rule, the serum Na
level is reduced at a rate no faster than 0.5 to 1 mEq/L per
hour to allow sufficient time for readjustment through
diffusion across fluid compartments. Desmopressin acetate
(DDAVP), a synthetic antidiuretic hormone, may be
prescribed to treat diabetes insipidus if it is the cause of
hyperNa (Porth, 2005).
Nursing Management
As in hypoNa, fluid losses & gains are carefully monitored in
patients who are at risk for hyperNa. The nurse should assess
for ab norm losses of H20 or low H20 intake & for lrg gains
of Na , as might occur w/ ingestion of over-the-counter
medications that have a high Na content (eg, Alka-Seltzer).
In addition, the nurse obtains a medication history, because
some prescription medications have a high Na content. The
nurse also notes the patient's thirst or elevated body
temperature & evaluates it in relation to other clinical signs.
The nurse monitors for changes in behavior, such as
restlessness, disorientation, & lethargy.
Preventing HyperNa
The nurse attempts to prevent hyperNa by offering fluids at
regular intervals, particularly in debilitated or unconscious
patients who are unable to perceive or respond to thirst. If
fluid intake remains inadequate, the nurse consults w/ the
physician to plan an alternative route for intake, either by
enteral feedings or by the parenteral route. If enteral feedings
are used, sufficient H20 should be administered to keep the
serum Na & BUN w/in norm limits. As a rule, the higher
the osmolality of the enteral feeding, the greater the need for
H20 supplementation.
For patients w/ diabetes insipidus, adequate H20 intake must
be ensured. If the pat.is alert & has an intact thirst
mechanism, merely providing access to H20 may be
sufficient. If the pat.has a decreased level of consciousness or
other disability interfering w/ adequate fluid intake, parenteral
fluid replacement may be prescribed. This therapy can be
anticipated in patients w/ neurologic disorders, particularly in
the early postoperative period.
Correcting HyperNa
When parenteral fluids are necessary for managing hyperNa,
the nurse monitors the patient's response to the fluids by
reviewing serial serum Na levels & by observing for
changes in neurologic signs. W/ a gradual decrease in the
serum Na level, the neurologic signs should improve. As
stated in the discussion on management, too-rapid reduction
in the serum Na level renders the plasma temporarily hypo-
osmotic to the fluid in the brain tissue, causing movement of
fluid into brain cells & dangerous cerebral edema.