Transcript Renal failure

Fluids, Electrolytes, and
Intravenous Therapy
Brian Mitu, FNP, PA-C, FAAPA
Internal Medicine
Instructor Basic/Advance EKG
National/Community Speaker
Chronic Hepatitis B
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Learning Objectives
Theory
1. Recall the various functions fluid performs in
the body.
2. Identify the body’s mechanisms for fluid
regulation.
3. Review three ways in which body fluids are
continually being distributed among the fluid
compartments.
4. Distinguish the signs and symptoms of
various electrolyte imbalances.
5. Discuss why the elderly have more problems
with fluid and electrolyte imbalances.
6. Recognize the disorders that cause specific
fluid and electrolyte imbalances.
7. Compare the major causes of acid-base
imbalances.
8. State correct interventions to correct an
acid-base imbalance.
9. Discuss the steps in managing an
intravenous infusion.
10. Describe the measures used to prevent the
complications of intravenous therapy.
11. Identify intravenous fluids that are isotonic.
12. Discuss the principles of intravenous
therapy.
Clinical Practice
1. Assess patients for signs of dehydration.
2. Correctly assess for and identify edema and
signs of overhydration.
3. Apply knowledge of normal laboratory
values in order to recognize electrolyte
imbalances.
4. Carry out interventions to correct an
electrolyte imbalance.
5. Determine if a patient has an acid-base
imbalance.
6. Carry out measures to prevent the
complications of Intravenous therapy.
7. Compare interventions for the care of a
patient receiving total parenteral nutrition
with one undergoing intravenous therapy.
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Basic Concepts of Fluid and
Electrolytes
• So why do we care about fluid and
electrolytes?
– Lets start with the fluids
• Over half of our body weight is fluid material
• Body weight of adult male 55-60%, female 5055%, newborn 75-80%
• In adults, a loss of just 1/5 of your body fluid weight
can be fatal.
• That is how marathon runners who are not
adequately hydrated die in mile 21
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Basic Concepts of Fluid and
Electrolytes
• So why do we care about fluid and
electrolytes?
– Elderly patients are even more at risk. Why ?
• They have less muscle mass. This also means
that a smaller amount of fluid loss can and will be
detrimental
– The same can be said to infants. Why?
• Because 80% of their body weight consist of fluids
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Basic Concepts of Fluid and
Electrolytes
• So why do we care about fluid and
electrolytes?
– Electrolytes
• Are substances that become ions in solution
and acquire the capacity to conduct electricity.
• Essential for normal function of our cells and our
organs
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So Where are These Fluids
Kept?
• Body fluid compartments
– Each body fluid compartment has a particular
composition of electrolytes/fluid, which differ
from that of the other compartments
– Extracellular compartment ( 20% BW)
• Tissue fluid (interstitial) ( 15% BW)
• Intravascular compartment ( 4.5% BW)
• Transcellular (1.5% BW)
– Intracellular compartment ( 40% of BW)
• Refers to all the fluid inside the cell (most bodily
fluid are inside the cell)
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Extracellular(ECF)Compartment
• One third ( 20%) of body fluid
• Comprised of 3 major components
– Intravascular
• Fluid within the blood vessels. Plasma accounts
for about half of the total blood volume of the body
– Interstitial
• Fluid that surrounds the cells – an example of
interstitial fluid is lymph
– Transcellular
• Fluid found in the cerebrospinal column,
pericardial envelope, synovial joints, or intraocular
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space
Extracellular(ECF)Compartment
• Extracellular fluids provide
– Nutrients for cell functioning
•
•
•
•
•
•
Na++
Ca++
ClGlucose
Fatty acids
Amino Acids
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ECF: IntravascularComponent
• Plasma
– Fluid portion of blood
• Made of:
– Water
– Plasma proteins
• Albumin, Clotting protein, Immunoglobulins
(Antibodies)
– Small amount of other substances
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ECF: Interstitial Component
• Made up of fluid between cells
– Surrounds cells
– Transport medium for nutrients, gases, waste
products and other substances between blood
and body cells
– Back-up fluid reservoir
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ECF: Transcellular Component
• 1% of ECF
• Located in joints, connective tissue,
bones, body cavities, CSF, and other
tissues
• Potential to increase significantly in
abnormal conditions
– 3rd space
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Intracellular (ICF) Compartment
•
•
•
•
Fluid within the cells themselves
Two thirds of body fluid (40%)
Located primarily in skeletal muscle mass
Provide nutrients for metabolism:
– High in K, Po4, protein
– Moderate levels of Mg, So4
• Assists in cellular metabolism
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Major Players of Fluid and
Electrolyte Balance
• Hypothalamus
– Thirst center
• Stimulated by changes in water loss or increase
extracellular osmolality
– Baroreceptors (carotid/ aortic) and stretch
receptors (atrial) as detectors
• Impulses sent to the thirst control centers in the
hypothalamus
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Major Players of Fluid and
Electrolyte Balance
• Posterior Pituitary
– ADH ( Antidiuretic Hormone or Vasopressin)
– Stimulated by changes in water loss or
increase extracellular osmolality
• Heart
– ANP (Atrial Natriuretic Peptide)
– In response to an increase in blood volume
– Increase sodium excretion by increasing GFR
and inhibiting sodium reabsorption
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Major Players of Fluid and
Electrolyte Balance
• Kidneys/Adrenal glands (RAAS)
– Renin
• Is released in response to decreased blood flow or
decreased renal pressure (sensed by receptors in
the nephrons)
– Aldosterone
• Is produced by the adrenal cortex (in response to
stimulation by angiotensin II) causing the tubules
to excrete K+ while retaining Na 2+, adding to the
reabsorption of water back into the vascular
system.
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Movement of Fluid and
Electrolytes
• Water Steady
State
• Amount Ingested =
Amount Eliminated
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Movement of Fluid and
Electrolytes
•
•
•
•
Electrolyte (Na+, K+, Ca++) Steady State
Amount Ingested = Amount Excreted.
Normal entry: Mainly ingestion in food.
Clinical entry: Can include parenteral
administration
• Just a remember that each fluid
compartment has constant amount of fluid,
and constant amount of electrolytes
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Exact Mechanism of Fluid and
Electrolyte Shift
• Passive transport
– Diffusion
– Osmosis
– Filtration
– Hydrostatic pressure
– Oncotic pressure
• Active transport
– Sodium pump and ATP
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Passive Transport
• Diffusion
– Movement of solutes from an area of higher
concentration to an area of lower
concentration in a solution and/or across a
permeable membrane (permeable for that
solute)
– Movement occurs until near equal state
• Note: solutes can not free move needs
channels and transport
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Passive Transport
• Osmosis
– Movement of water through a selectively
permeable membrane from an area of low
solute concentration to a higher concentration
until equilibrium occurs
– Movement occurs until near equal
concentration found
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Passive Transport
• Osmolality
– Concentration of body fluids
• Affects movement of fluid by osmosis
– Reflects hydration status
– Measured by serum and urine
– Solutes measured
• Mainly urea, glucose, and sodium
– Measured as solute concentration/Kg
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Passive Transport
• Osmolality
– Serum Osm/L = (serum Na x 2) + BUN/3 +
Glucose/18
– Normal serum value: 280 - 300 mOsm/Kg
– Serum <240 or >320 is critically abnormal
– Normal urine Osm: 250 – 900 mOsm / kg
• Increase means dehydrated
• Decrease means excess fluid
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Osmolality of a Solution
• Hypertonic solution
– A solution has higher concentration of
sodium or solutes than the intracellular
space
– Increases sodium in the blood, but sodium is
a charged ion so it can not pass the cell
membrane ( high to low concentration)
– Water will diffuse out of the cell into the blood;
intravascular volume increases
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Osmolality of a Solution
• Hypertonic solution
• 3%, 5% NaCl, D10%w, D5% with 0.9% NaCl,
D5% with 0.45% NaCl, D5% LR
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Osmolality of a Solution
• Hypotonic solutions
– Means lower concentration of salt or solute
than the intracellular space
– Water will move out of the intravascular space
into the cells
– Less salt or > water than isotonic
– 0.45% NaCl, 0.226%, 0.33% Nacl
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Osmolality of a Solution
• Isotonic solutions
– Means same concentration of solute or
sodium as what is in the cells
– Thus no fluid shifts
– Intravascular volume simply increases
– 0.9% NaCl, 5% dextrose water, 5%
dextrose in 0.225% saline, LR
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Passive Transport
• Filtration
– Movement of solutes and solvents through
semipermeable membrane
– Influenced by hydrostatic pressure
• Hydrostatic pressure is created by the pumping action
of the heart
• Think of arterial end of the capillary
• Supplying fluid to tissue cells
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Passive Transport
• Oncotic /osmotic pressure
– Think of the venous end
– Getting back the excess fluid and solutes that
are in the tissue and returned to the vascular
compartment via lymph
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Active Transport
• Ion moves through a membrane from an
area of lower to higher concentration
• Sodium pump and ATP
• Substances that are transported actively
through the cell membrane
– Sodium
– Potassium, calcium, iron
– Hydrogen, sugars, amino acids
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Basic Concept
• Most substances can not pass freely
across cell membranes, but water can
(also gases, steroid hormones which
nonpolar substances)
• Ions and solutes can pass across
membranes via transporters and channels,
but regulated
• Thus we can predict the effects of various
disturbances in electrolytes on the
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intravascular EC
volume
Fluid Volume deficit
• Dehydration
– Occurs when the fluid intake of the body
is not sufficient to meet the fluid needs
of the body
• Goal of treatment
– Is to restore fluid volume, replace
electrolytes PRN, find the cause
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Fluid Volume deficit
• Types
– Isotonic Flood Volume Deficit
– Hypotonic dehydration
– Hypertonic dehydration
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Isotonic Dehydration
• Description
– Both water and electrolytes are lost equally
– Known as hypovolemia → ↓circulating
blood volume, tissue perfusion
– Stimulates ADH
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Hypertonic Dehydration
• Description
– Water loss exceeds electrolyte loss
– Fluid moves from the intracellular
compartment into the plasma and tissue
fluid compartment → cellular dehydration
and shrinkage
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Hypotonic Dehydration
• Description
– Electrolyte loss exceeds water loss
– Fluids from the plasma and tissue
compartment moves into the cells →
swelling
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Causes of Fluid Volume Deficit
• Isotonic dehydration
– Third spacing: peritonitis, intestinal
obstruction, ascites, burns, Hemorrhage
– Altered intake, such as nothing by mouth
(NPO)
• Hypertonic dehydration
– Excessive perspiration, Ketoacidosis
– Prolonged fevers, Diarrhea
– ESRD, Diabetes Insipidus, Diuretic therapy
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Causes of Fluid Volume Deficit
• Hypotonic dehydration
– Chronic illness
– Excessive fluid replacement (hypotonic)
– Renal Failure, Chronic malnutrition
– Gastrointestinal (GI) losses: vomiting,
nasogastric suctioning
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Fluid Volume Deficit:
Assessment
• Cardiovascular
–
–
–
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Thready, increase pulse rate
Decrease BP, Orthostatic hypotension
Flat neck and hand veins in dependent position
Diminished peripheral pulses
• Respiratory
– Increase rate and depth of respiration
• Neuromuscular
– Lethargy and coma
– Fever
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Fluid Volume Deficit:
Assessment
• Renal
– Decrease urine output, increase specific
gravity
• Integumentary
– Dry skin, poor turgor, tenting
– Dry mouth
• GI
– Wt loss, thirst
• Hypotonic dehydration
– Muscle weakness
• Hypertonic dehydration
– Pitting edema, hyperactive DTR
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Fluid Volume Deficit:
Assessment
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Fluid Volume Deficit:
Interventions
• Place client in shock position
– On back with legs elevated
• Fluid replacement
– Mild cases can be corrected via PO route
– Significant losses (hemorrhage, anemia, 3rd
space)
• Blood transfusion
• Colloid solution (albumin, dextran)
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Fluid Volume Deficit:
Interventions
• Fluid replacement
– Significant losses (hemorrhage, anemia, 3rd
space)
– 0.9% NaCl or 154mEq/L Na+
• Solution of choice for normonatremic and mildly
hyponatremic, hypotensive or shock pts
– Severe hyponatremia
• Hypertonic saline (3.0% NaCl or 513 mEq/L)
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Fluid Volume Deficit: Nsg
Interventions
• Monitor I&O
– Alert the primary care provider to urine
output less than 30 mL/hr for 2
consecutive hr
• Monitor vital signs and heart rhythm
• Monitor level of consciousness and
maintain client safety
• Treat underlying cause of fluid volume
deficit
• Encourage the client to change
positions slowly
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Fluid Volume Deficit:
Complications
• Hypovolemic Shock
– This can lead to vital organ hypoxia/anoxia
decreased hemoglobin, oxygen saturation,
and pulse pressure (systolic-diastolic blood
pressure).
– Administer oxygen.
– Perform hemodynamic monitoring.
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Fluid Volume Deficit:
Complications
• Hypovolemic Shock
– Administer vasoconstrictors, coronary
vasodilators, and/or positive inotropes
•
•
•
•
•
dopamine (Inotropin)
Epinephrine
dobutamine (Dobutrex)
norepinephrine (Levophed)
phenylephrine (Neo-Synephrine)
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Nausea and Vomiting
• “Sick to my stomach"
• Pallor, mild diaphoresis, cold clammy skin,
excessive salivation, and attempts to
remain quiet and motionless
• Vomitus odor, color, contents
(e.g., undigested food), and amount
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Medical Treatment
• Antihistamines, sedative-hypnotics,
anticholinergics, and phenothiazines
• Complementary and alternative therapy
• NPO, then progressing slowly to a regular
diet
• Carbonated drinks
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Diarrhea
• Frequent watery bowel movements, abdominal
cramping, and general weakness
• Watery stools often contain mucus and are
blood-streaked; frequency could be as high as 15
to 20 liquid stools.
• Acute diarrhea and local irritation
• Chronic and prolonged diarrhea in ulcerative
colitis, irritable bowel syndrome, allergies, lactose
intolerance, and nontropical sprue
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Diarrhea
• Dehydration, malnutrition, and anemia
• Bowel sounds likely to be loud gurgling and
tinkling sounds that come in waves and are
hyperactive
• Note and record the number of stools
during the shift and the characteristics of
each stool and associated pain
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Acute Diarrhea
• Limit the intake of food
• Progress to clear, bland liquids and to solids with
increased calories and high-protein,
high-carbohydrate content
• Give rehydrating solutions containing glucose and
electrolytes
• Avoid iced fluids, carbonated drinks, whole milk,
roughage, raw fruits, and highly seasoned foods
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Medications for Diarrhea
• Cause of the disorder and the length of time the
condition
Mild cases:
– Kaolin and bismuth preparations, (e.g., Kaopectate)
• Antispasmodic drugs such as belladonna or paregoric
• Bismuth and "traveler's diarrhea"
• Codeine, diphenoxylate (Lomotil), or loperamide
(Imodium)
• Drugs and causative organisms
• Metabolic acidosis and buffer solutions
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Nursing Management
• Provide physical and mental rest, prevent
unnecessary loss of water and nutrients,
protect the rectal mucosa, and replace
fluids
• Maintain a calm and dignified manner,
accept and understand the patient's
behavior, and provide privacy and a restful
environment
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Home Care: Fluid Volume Deficit
• Log of intake and output
• Small amounts of liquid every hour while
awake
• Emergency department and intravenous
fluids
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Fluid Volume Excess
• Description
– Fluid intake or fluid retention exceeds the fluid
needs of the body or extracellular
compartment
– Aka: fluid overload or overhydration
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Fluid Volume Excess
• Types
– Isotonic overhydration
– Hypertonic overhydration
– Hypotonic overhydration
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Isotonic Overhydration
• Hypervolemia
• Only the EC compartment expands
• Results in circulatory overload and
tissue edema
– When severe it can worsen CHF and lead
to pulmonary edema
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Hypertonic Overhydration
• Rare
• Caused by excessive Na intake
• Fluid is drawn from the ICF compartment
and the EC volume expands
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Hypotonic Overhydration
• Water intoxication
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Causes Fluid Volume Excess
• Isotonic overhydration
– Inadequate control of IV
– Renal Failure
• ↓ excretion of sodium and water
– Long-term corticosteroid therapy
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Causes Fluid Volume Excess
• Hypertonic overhydration
– Excessive sodium ingestion
– Rapid infusion of hypertonic solution
– Excessive sodium bicarbonate therapy
– Interstitial to plasma fluid shifts
(hypertonic fluids, burns)
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Causes Fluid Volume Excess
• Hypotonic overhydration
– Early Renal Failure
– CHF, SIADH
• Chronic stimulus to the kidney to conserve sodium
and water (heart failure, cirrhosis,
glucocorticosteroids)
– Irrigation of wounds and body cavities with
hypotonic fluids
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Fluid Volume Excess: Risk
Factors
• Overhydration
– Water replacement without electrolyte
replacement such as strenuous exercise
with profuse diaphoresis
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Fluid Volume Excess:
Assessment
• Cardiovascular
– Bounding, increase pulse rate
– ↑ BP, elevated JVP or distended neck vein, CVP
• Respiratory
– Dyspnea, crackles
• Neuromuscular
– ALOC, HA, visual disturbance, muscle weakness,
paresthesia
• Integumentary
– Pitting edema in dependent areas
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Fluid Volume Excess:
Assessment
• GI
– Hepatojugular reflux, ascites, liver
enlargement
• Labs
– ↓ serum osmolality, hct, BUN, sodium,
urine specific gravity
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Fluid Volume Excess:
Assessment
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Excess Fluid Volume
• Hematocrit:
– 35% to 54%, depending on age and sex
• Urine concentration:
– Specific gravity: 1.003 to 1.030 (average range
is 1.010 to 1.025)
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Fluid Volume Excess:
Interventions
• Assess/monitor for signs of respiratory distress
– including breath sounds and arterial blood gases
(ABGs).
•
•
•
•
•
Position the client in semi-Fowler’s position.
Administer oxygen as needed.
Reduce IV flow rates.
Administer diuretics (osmotic, loop) as ordered.
Monitor daily I&O and weight.
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Fluid Volume Excess:
Interventions
• Limit fluid and sodium intake as ordered.
• Assess/monitor and document peripheral vascular
system including
– skin color, presence of edema (pretibial, sacral,
periorbital), and circulation to extremities.
• Turn and position the client at least every 2 hr.
• Support arms and legs to decrease dependent
edema and promote venous return as appropriate.
• Monitor for/treat skin breakdown.
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Fluid Volume Excess:
Complications
• Pulmonary Edema
– Signs and symptoms include ascending
crackles, dyspnea at rest, and confusion.
– Position the client in Fowler’s position.
– Administer IV morphine. Why?
• ↑ pulmonary venous capacitance, ↓ left atrial
pressure and anxiety → better ventilation
– Administer IV diuretic.
– Prepare for possible intubation and
mechanical ventilation.
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Edema
• Localized edema and generalized edema
• General causes of edema:
– An increase in capillary hydrostatic pressure
– A loss of plasma proteins
– An obstruction of lymphatic circulation
– An increase in capillary permeability
• Dependent edema
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Figure 17-3 Mechanisms of edema formation. Na+, Sodium; H2O, water. From Huether
SE, McCance KL: Understanding pathophysiology, ed 3, St Louis, 2004, Mosby.
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Treatment
•
•
•
•
•
•
•
Correct the underlying cause
Assist the body to rebalance fluid content
Restrict fluids
Give diuretic drugs
Allow bed rest
Provide low-sodium diet
Use elastic stockings or sequential
compression devices
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Home Care: Fluid Excess
• Weigh daily
• Assess edema
• Know when to notify physician
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Electrolytes
• Electrolytes are minerals (sometimes
called salts) that are present in all body
fluids.
• They regulate fluid balance, hormone
production, and strengthen skeletal
structures, as well as act as catalysts in
nerve response, muscle contraction, and
the metabolism of nutrients.
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Electrolytes
• Electrolytes are distributed between
intracellular (ICF) and extracellular (ECF) fluid
compartments.
• When dissolved in fluids, separate in to ions
and conduct either
– Cations: Positively charged ions
• magnesium, potassium, sodium, calcium
– Anions: Negatively charged ions
• phosphate, sulfate, chloride, bicarbonate
• Measured in milliequivalents (mEq)
• Serum levels indicate extracellular
concentration not inside the cells
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Electrolytes
• Creation of an electrical impulse:
– Transmission of nerve impulses
– Contraction of muscles
– Excretion of hormones and other substances
from glandular cells
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Sodium
• Main extracellular Cation
• The body’s goal is to maintain a constant
concentration of sodium. How?
– By altering the amount of water via
• Excreting or retaining water via kidneys
• Shifts of water from cells to the extracellular
space or vice versa
• Normal serum sodium levels are 135 to
145 mEq/L.
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Hyponatremia
• Plasma Na+ of < 135 mEq/L
• Causes
– Increased sodium excretion (Hypovolemic
Hyponatremia)
• Renal
– Diuretics; Renal disease
• Extrarenal
– Excessive diaphoresis, Vomiting, Diarrhea
– Wound drainage ,especially GI
– Burns , nasogastric suctioning
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Hyponatremia
• Causes
– Inadequate sodium intake
• NPO
• Low-salt diet
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Hyponatremia
• Causes
– Loss of sodium with minimal change in water
(euvolemic hyponatremia)
• Primary polydipsia due hypothalamic lesion or
psychogenic polydipsia
• SIADH due to paraneoplastic syndrome,
pulmonary disease such as TB or pneumonia,
cyclophosphamide toxicity, SSRI
• Adrenal insufficiency. How? Remember
aldosterone
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Hyponatremia
• Causes
– Dilution of serum sodium (Hypervolemic
Hyponatremia)
• Excessive irrigation/ ingestion of hypotonic fluids,
tap water enemas
• Renal failure
• Freshwater drowning
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Hyponatremia
• Causes
– Dilution of serum sodium (Hypervolemic
Hyponatremia)
• CHF
– Due to ↓ forward flow by the failing heart, the kidney
senses hypoperfusion and tries to ↑ percieved
diminished intravascular volume via RAAS
– Furthermore, ADH gets activated also
• Cirrhosis
– Pooling of blood in the mesenteric veins which leads
to decrease amount of blood seen by the kidneys
• Nephrotic syndrome
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Hyponatremia
• Causes
– Pseudohyponatremia (Hyperosmolar
Hyponatremia)
• Hyperglycemia
– When BG becomes acutely elevate, water is drawn from
the cells into the extracellular space, diluting the serum
sodium
– Plasma sodium falls by 2 meq/L for every 100 mg/dL rise
of BG
• Hyperlipidemia, hyperproteinemia, increase
urea
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Hyponatremia
• Classification
– Hypotonic hyponatremia < 280 mOsm/kg
• Fluid volume deficit (Hypovolemic) : Sodium loss
greater than water loss
• Fluid volume excess (Hypervolemic): Water gain
greater than sodium gain
• Normal fluid volume ( Euvolemic): Pure water
gain
– Isotonic hyponatremia 280-290 mOsm/kg
– Hyper hyponatremia > 290 mOsm/kg
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Hyponatremia: Assessment
• Manifestations
– Asymptomatic to nonspecific
• Nausea, HA, seizure
• Weakness
– Hyponatremia delays and slows the depolarization of
membranes.
• Muscle cramps
• Orthostatic hypotension, Decreased blood
pressure
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Hyponatremia: Assessment
• Manifestations
– Symptoms are primarily neurologic (Na+
115 to 118 meq/L)
•
•
•
•
Mental status change, seizure
Lethargy
Disorientation
Obtundation,coma
– Water moves from ECF into the ICF, which causes cells
to swell (e.g., cerebral edema).
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Hyponatremia
• Diagnosis
– H&P
– Plasma osmolality (decrease)
– Urine osmolality and volume
• Specific gravity
– Urine Na+ concentration ( increase or
decrease depending on the cause)
– CT scan of the brain is done if SIADH is
suspected
– C-XRAY to r/o lung pathology
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Hyponatremia: Assessment
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Hyponatremia: Interventions
• Fluid overload: Restrict water intake as ordered
(Hypervolemic)
• Acute Hyponatremia
– Administer hypertonic oral and IV fluids as ordered.
– Encourage foods and fluids high in sodium (cheese,
milk)
• If pt is taking lithium, check lithium level
because hyponatremia causes lithium
toxicity
• Give demeclocycline (Declomycin) if the
cause is d/t excess ADH
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Hyponatremia: Interventions
• Foods high in sodium
– Bacon, butter, canned food, american/cottage
cheese
– Frankfurters, ketchup, milk, soy sauce,
processed foods
– White and whole-wheat bread
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Hyponatremia:Interventions
• Restoration of normal ECF volume
– Administer isotonic IV therapy (0.9% normal saline,
Ringer’s lactate solution).
– If the cause is hypovolemic hypotonic hyponatremia
• Serum sodium level must be check hourly
• Monitor I&O and daily weight.
• Monitor vital signs and level of consciousness –
report abnormal findings.
• Encourage the client to change positions slowly
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Hyponatremia: Complications
• Seizures, Coma, and Respiratory Arrest
– Seizure precautions and management
– Life support interventions
• Note:
– Avoid too rapid correction, because osmotic
imbalance may cause water to enter the
brain cells → cerebral edema and potentially
severe neurologic impairment (central
pontine myelinolysis)
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Hypernatremia
• Serum sodium level of > 145 meq/L
• Water content of body fluid is deficient in
relation to sodium content
• Hypernatremia causes significant neurological,
endocrine, and cardiac disturbances.
• Increased sodium causes hypertonicity of the
serum.
• This causes a shift of water out of the cells,
making the cells dehydrated.
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Hypernatremia
• Causes
– Decrease sodium excretion (hypervolemic
Hypernatremia)
•
•
•
•
Corticosteroid
Cushing’s syndrome
Renal Failure
Hyperaldosteronism
– Increase sodium intake (PO/IV), sodium
bicarbonate intake (iatrogenic)
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Hypernatremia
• Causes
– Increase water loss ( hypovolemic
Hypernatremia)
• Renal disease or diuretics
• Insensible losses
– Fever, Exercise
– Heat exposure, Severe burns
– Mechanically ventilated pts, Diarrhea
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Hypernatremia
• Causes ( Euvolemic Hypernatremia)
– Decrease water intake (NPO)
– Central Diabetes Insipidus
• Impaired ADH
– Causes: destruction of posterior pituitary from trauma,
neurosurgery, granulomatous dz, neoplasm, vascular
accident, infxn, idiopathic, hereditary
– Nephrogenic Diabetes Insipidus
• Resistance to the action of ADH
– Causes: acquired or inherited
» Lithium toxicity, hypercalcemia, hypokalemia,
conditions that impair medullary hypertonicity
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Hypernatremia
• How to diagnose if DI is central or
nephrogenic?
– Administer IV DDAVP
– If the urine becomes concentrated, then the
problem is central because the kidney
responded to the vasopressin
– If the urine is still diluted, then the problem is
the kidneys because it did not respond to
vasopressin
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Hypernatremia
• Manifestations
– Thirst, polyuria, polydipsia (likes ice-cold
water for CDI)
– Dry mouth, mucous membranes, decrease
tears, salivation, oliguria
– Orthostatic hypotension
– Major sxs are neurologic
•
•
•
•
AMS (altered mental status)
Weakness
Neuromuscular irritability
Focal neurologic deficits, coma, seizures
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Hypernatremia
• Signs and symptoms:
– Decreased urine output if compensatory ADH
is being secreted
– Increased thirst with dry mucous membranes
– Weakness and agitation
– Good tissue turgor and firm subcutaneous
tissues
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Hypernatremia: Assessment
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Hypernatremia
• Diagnostic studies
– Check serum sodium level and serum
osmolality
– Check urine volume and osmolality
• This determines renal losses to insensible loss ( if
clinical and physical history can not determine the
cause). How?
• If kidneys are working properly, the urine sodium
concentration will be low ( insensible loss)
• If kidneys are not working, the urine sodium will be
increased (renal loss)
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Hypernatremia: Interventions
• Based on serum osmolarity
– Fluid Loss (Hypernatremia with hypovolemia)
• Isotonic (0.9%) saline, followed by 0.45% saline
– Decrease excretion of sodium (Hypernatremia
with euvolemia)
• Water drinking or 5% dextrose in water →
excretion of sodium in the urine
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Hypernatremia: Interventions
Excess Sodium (Hypernatremia with
hypervolemia)
• Encourage water intake and discourage
sodium intake.
• Administer diuretics, such as loop diuretics.
• Monitor level of consciousness and maintain
client safety.
• Provide oral hygiene and other comfort
measures to decrease thirst.
• Monitor I&O, and alert the primary care
provider of inadequate renal output.
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Hypernatremia: Complications
• Cellular Dehydration, Convulsions, and
Death
– Seizure precautions and management
– Life support interventions
• Note
– Avoid rapid correction → pulmonary or
cerebral edema
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Potassium
• Major intracellular cation (150mEq/L)
• Normal plasma 3.5 -5.3mEq/L
– Note: K+ concentration is higher inside the
cells than the serum
• Na-K pump actively transports Na+ out of the
cell and K+ into the cell
• Renal excretion is the major route of
elimination of excess K+
• Vital role in cell metabolism, transmission of
nerve impulses, functioning of cardiac, lung,
and muscle tissues, and acid base balance.
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Hypokalemia
• Serum potassium less than 3.5 mEq/L.
• Causes
– Inadequate potassium intake
• NPO
• Rare cause because body has many mechanisms
of K+ regulation (aldosterone, insulin,
catecholamine)
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Hypokalemia
• Causes
– Increased loss
• Renal loss d/t ↑ flow rate (washing away K+ →
↑ secretion of the tubules)
– Diuretic therapy
– Hyperaldosteronism (adrenal adenoma
or carcinomas)
• GI loss
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Hypokalemia
• GI losses
– Diarrhea
– Vomiting/NGT suctioning
•
•
•
•
•
Direct or indirect K+ loss
Indirect loss via kidneys. Why?
Vomiting →loss of acid from the stomach ( H +)
Loss of acid will →alkalosis (excess HCO3-)
Excess HCO3- makes into the kidneys (more
negative)
• To maintain normal balance, the kidneys will
secrete positively charge k+ which → excretion
of K+
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Hypokalemia
• Causes
– Movement from the blood into the cells
• Insulin excess
• Beta agonist treatment
– Albuterol
• Alkalosis
– Not enough H+ in the blood, so cells release H+ into
the blood in exchange for K+
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Causes and Effects of Hypokalemia
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Hypokalemia
• Manifestation
– Cardiovascular
•
•
•
•
Ventricular arrhythmias
Hypotension
Cardiac arrest
EKG
– Flattened T or inverted T wave
– ST depression
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Hypokalemia
• Manifestation
– Neuromuscular
•
•
•
•
Malaise
Weakness, Flacid paralysis
Cramps
Smooth muscle involvement
– Ileus and constipation, abdominal pain, distention
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Hypokalemia:Interventions
• Treat underlying cause. Usually not an
emergency unless cardiac
manifestations are present
• Replacement of Potassium:
– Encourage foods high in potassium (e.g.,
avocados, broccoli, dairy products, dried fruit,
cantaloupe, bananas).
– Provide oral potassium supplementation
• Liquid potassium chloride has an unpleasant taste
• Should be taken with juice
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Common Food Source for
Potassium
•
•
•
•
•
•
•
Avocado
Bananas
Cantaloupe
Carrots
Fish
Mushrooms
Oranges
•
•
•
•
•
•
•
Potatoes
Pork
Beef, veal
Raisins
Spinach
Strawberries
tomatoes
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Hypokalemia: Interventions
• Precaution with IV potassium
– Never give IV push, IM, SC
– Ensure that IV bag containing potassium is
properly labeled
– Can cause phlebitis
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Hypokalemia: Interventions
– IV potassium supplementation
• Never IV push (high risk cardiac arrest).
• Monitor for phlebitis (tissue irritant).
• Monitor for and maintain adequate urine output.
• Monitor for shallow ineffective respirations
and diminished breath sounds.
• Monitor the client’s cardiac rhythm,
level of consciousness, and bowel
function.
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Hypokalemia: Complications
• Respiratory Failure
– Monitor for hypoxemia and hypercapnia.
– Intubation and mechanical ventilation may be
required.
• Cardiac Arrest
– Perform continuous cardiac monitoring.
– Treat life-threatening dysrhythmias.
• Hypokalemia potentiates digitalis
intoxication
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Hyperkalemia
• Plasma K+ >5.3mEq/L
• 3 basic mechanism/Etiology
– ↑ intake
• Iatrogenic infusion of K+
• Ingestion via eating would be quite difficult
unless there is a problem with the kidneys
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Hyperkalemia
• Three basic mechanism/Etiology
– ↓ urinary excretion
• Renal failure
• ↓ inflow rate in the distal nephron → a perceived
high concentration of K+ in the nephron, thus
inhibiting further secretion of K+ in the nephron
(CHF, cirrhosis)
• Hypoaldosteronism/Addison’s disease
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Hyperkalemia
• Three basic mechanism/Etiology
– ↑ movement of K+ from the cells into the
blood stream
• Processes that → breakdown of cells will
cause the release of k+
– Crushing Injuries, Rhabdomyolysis
– Tumor lysis after chemotherapy
– Pseudohyperkalemia
» Due to improper blood drawing technique
– Acidosis
» To maintain homeostasis the body will trade K+ for
H+
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Hyperkalemia
• Three basic mechanism/Etiology
– ↑ movement of K+ from the cells into the
blood stream
• Insulin deficiency or resistance
– Insulin causes k+ to move into cells
• Beta-blockers
– Like insulin, catecholamines causes K+ entry into cells
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Causes and Effects of Hyperkalemia
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Hyperkalemia
• Manifestation
– Muscle weakness
– Hypotension
– Paresthesia
– Paralysis
– Cardiac dysrhythmia
• EKG > 6mEq/L
–
–
–
–
Peak T wave
Flattening of P wave
Prolongation of PR interval
Widening of QRS complex → V.tach, fib
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Hyperkalemia: Interventions
• Decrease potassium intake.
– Stop infusion of IV potassium.
– Withhold oral potassium.
– Provide potassium-restricted diet. Avoid foods
high in potassium (e.g., avocados, broccoli,
dairy products, dried fruit, cantaloupe,
bananas).
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Hyperkalemia: Nsg
Interventions
• Increase potassium excretion.
– Administer potassium-losing diuretics, such
as furosemide (Lasix), if renal function is
adequate.
– Administer cation exchange resins such as
sodium polystyrene sulfonate (Kayexalate).
– Perform dialysis.
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Hyperkalemia: Interventions
• Promote movement of potassium from ECF to
ICF.
– Administer IV fluids with dextrose (glucose) and
regular insulin.
– Administer sodium bicarbonate (reverse
acidosis).
• Monitor the client’s cardiac rhythm, and notify
primary care provider of abnormal findings
– Calcium gluconate to antagonize the effects of
hyperkalemia on the heart
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Hyperkalemia: Complication
• Cardiac Arrest
– Perform continuous cardiac monitoring.
– Treat life-threatening dysrhythmias.
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Calcium
• Normal serum total Ca++ 9-10mg/dL
• Essential for bone and neuromuscular
function, blood clotting
• 99% of body ca++ is bone, 1% is in the ECF
• 50% of serum Ca++ is ionized (free), remainder
is bound to albumin
• Regulated by parathyroid hormone (PTH),
metabolites of vit.D, calcitonin
– Parathyroid hormone serves to increase blood
concentrations of calcium. HOW?
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Calcium
• Parathyroid hormone increases blood
calcium by:
– Stimulating osteoclasts to breakdown bone
– Increasing reabsorption of calcium by the
kidneys
– Increasing conversion of inactive vitamin D to
active vitamin D ( which increases calcium
absorption in the small intestine)
– Decreases reabsorption of phosphate by the
kidneys (urineECloss)
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Calcium
• Vitamin D
– Is absorbed from food and synthesized in skin
after exposure to sunlight
• Liver converts Vit. D to 25-hydroxyvitamin D3,
which in turn converted by the kidney to 1,25D3
• 1,25D3 promotes intestinal Ca++ absorption,
phosphate absorption
– Increases bone resoprtion ( release of
calcium and phosphate into the circulation)
– Increases phosphate reabsorption in the
kidneys
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Calcium
• PTH
– ↑s serum Ca++ but ↓s serum phosphate
• Vitamin D
– ↑s both serum Ca++ and phosphate levels
• Calcitonin
– Antagonistic hormone to PTH and Vit.D
– Little/ minor effect
• Note:
– Diseases that affect the bones or the kidneys
can cause hyperor hypocalcemia
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Hypocalcemia
• serum calcium level less than 9.0 mg/dL.
• Etiology
– Decrease intake
– Hypoparathyroidism
• DiGeorge syndrome (congenital absence of
parathyroid)
• Autoimmune destruction (Rare)
– HAM (hypoparathyroid, adrenal insufficiency, mucocutaneous
candidiasis)
– APECED (autoimmune polyendocrinopathy
candidiasis,ectodermal dystrophy)
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Hypocalcemia
• Etiology
• Hypoparathyroidism
• Familial, Surgical damage/removal
• Magnesium (hypo- or hypermagnesemia
can→hypocalcemia, Metastases
• Pseudoparathyroidism (PTH resistance)
– Albright’s hereditary osteodystrophy
» Obese, short stature, round face
» Resistance to TSH, gonadotropins, and
glucagon
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Hypocalcemia
• Etiology
– Vitamin D deficiency
• Decrease intake, malabsorption, renal dz, liver dz
• Rickets (Children with Vit D deficiency)
• Osteomalacia (adults with Vit D deficiency)
– Increase excretion
• Fanconi syndrome
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Hypocalcemia
• Etiology
– Shift to bone (hungry bone syndrome)
• Happens after surgical correction of the abnormal
PTH
– Binding of ca++
• Hyperphosphatemia (rhabdomyolosis)
• Pancreatitis (fats releases from pancreas bind
ca++)
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Hypocalcemia
• Etiology
– Hypoalbumin
• Recall that ca++ is bound to albumin “factitious
hypocalcemia”
• Caused by: Malnutrition, Burns, Liver disease
– Cirrhosis
– Nephrotic syndrome
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Hypocalcemia
• Etiology
– Hypercalciuric hypocalcemia
• Faulty calcium sensing receptor of the Parathyroid
and the kidney
– Drugs ( ↓s ionized fraction of calcium)
• Chemotherapy, phenytoin, foscarnet
– Sepsis
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Causes and Effects of Hypocalcemia
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Hypocalcemia: Assessment
• Manifestation
– Neuromuscular
•
•
•
•
Muscle twitches/tetany, seizure
Frequent painful muscle spasms at rest
Hyperactive deep tendon reflexes
Positive Chvostek’s sign (tap on facial nerve
triggers facial twitching)
• Positive Trousseau’s sign (hand/finger spasms
with sustained blood pressure cuff inflation)
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Hypocalcemia: Assessment
• Cardiovascular
– Decreased myocardial contractility –
decreased heart rate and hypotension
– Dysrhythmias, prolonged QT interval
• GI – hyperactive bowel sounds, diarrhea,
abdominal cramping
• Respiratory
– Laryngospasm
– Respiratory failure
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Hypocalcemia: Interventions
• Administer oral or IV calcium supplements.
– Aluminum hydroxide ↓s phosphorus levels →
↑calcium levels
– Vit. D to ↑ absorption calcium from the GI tract
• Encourage foods high in calcium including
dairy products and dark green vegetables.
• Be aware of seizure precautions.
• Keep emergency equipment on standby.
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Hypocalcemia:Interventions
• Calcium gluconate IV administration
– Warm solution to body temperature prior to
administration
– Give slowly
– Monitor EKG
– Watch for infiltration
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Food Source for Calcium
•
•
•
•
•
•
•
•
Cheese
Collard greens
Milk and soy milk
Rhubarb
Sardines
Spinach
Tofu
yogurt
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Hypercalcemia
• Calcemia > 10.6 mg/dL
• Causes
– Increase calcium absorption
• Excess ingestion from milk and calcium carbonate antacids
(milk-alkali syndrome)
• Vitamin D
– Decrease excretion
• Decrease renal excretion (thiazide diuretics, lithium)
• Hypocalciuric hypercalcemia (which causes both ↓
excretion and ↑ bone resorption
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Hypercalcemia
• Causes
– Increase bone resorption
• Elevated parathyroid (hyperparathyroidism)
• Elevated vitamin D (lymphoma,
granulomatous disease, milk-alkali syndrome)
• Bone breakdown (secondary to mets to bone,
primary bone tumor, multiple myeloma,
immobilization, hyperthyroidism)
– Hemoconcentration
• Dehydration
• Adrenal insufficiency
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Causes and Effects of Hypercalcemia
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Hypercalcemia
• Manifestation
– “stones, bones, abdominal groans, moans,
and psychiatric overtones” means
•
•
•
•
•
Renal stones
Bone breakdown
Constipation/abdominal pain/ pancreatitis
Fatigue, weakness, arthralgia
Psychiatric disturbance
– Ekg: shorten QT interval
• Mnemonic: Lots of Californians are short QTs
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Hypercalcemia: Interventions
• Calculate corrected calcium level if albumin is low
– Serum calcium+0.8 (4 - albumin)
• Monitor cardiac, respiratory status, neuromuscular,
renal, GI status
• Place pt on cardiac monitor
• D/C IV or PO’s containing calcium, vitamin D,
thiazide diuretic
• Prepare for dialysis if severe levels
• Position pt carefully due to risk of fracture
• Monitor for flank pain, strain urine
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Hypercalcemia: Interventions
• Treatment
– Dilute blood Ca++
• 0.9% NaCl. Infuse 5-10 liters over the 1st 24 hrs
until dehydration is corrected
– Give furosemide IV (40-80mg q 2-4 hrs) to
enhance excretion and prevent volume
overload
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Hypercalcemia: Interventions
• Treatment
– Metastatic bone dz
• Calcitonin (rapid, mild inhibition of bone resorption)
• Pamidronate (delayed onset, but most potent than
calcitonin)
– Sarcoidosis, vit A or D intoxication, multiple
myeloma, leukemia, breast ca
• Glucocorticoid (↑ ca++urinary excretion,↓ GI
absorption of ca++
– Neoplasm
• Resection, irridation
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Magnesium
• Normal 1.8-3.0 mEq/L
• Plays an important role in neuromuscular
function ( same as the effect of calcium )
• One thrid is bound to protein and two
thirds existing as free cation
• Excreted by the kidneys
• Both hyper and hypomagnesemia can
affect calcium by decreasing PTH
secretion or action
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Magnesium
• Hypermagnesemia can decrease PTH
action ( hypocalcemia )
– This is seen in pts being treated due to
preeclampsia
• Hypomagnesemia
– Causes PTH resistance in end-organs and
eventually decreases PTH secretion
• Note: Monitor for neuro and arrhythmias
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Hypomagnesemia
• Serum magnesium level less than 1.8
mg/dL.
• Hypomagnesemia and hypokalemia
shares the same etiologies
– Diuretics, Diarrhea, alcoholism,
aminoglycosides, and amphotericin
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Hypomagnesemia
• Causes
– ↓ intestinal absorption/insufficient intake
• Malnutrition, alcoholism
• Prolonged diarrhea, laxative abuse, small bowel
bypass
• NGT aspiration
• Malabsorption syndrome, Celiac, Crohn’s
disease
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Hypomagnesemia
• Causes
– ↑ renal excretion
•
•
•
•
•
•
•
Hypercalcemia
Osmotic diuresis
Loop diuretics
Aminoglycosides
Amphothericin B
Cisplatin
Cyclosporine
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Hypomagnesemia
• Causes
– Intracellular movement
• Hyperglycemia
• Insulin administration
• Sepsis
– Other
• Post-parathyroidectomy (hungry bone
syndrome)
• Respiratory alkalosis
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Hypomagnesemia
• Diagnosis
– Urine excretion 10-30 mg/ day or fractional
excretion > 2%
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Causes and Effects of Hypomagnesemia
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Hypomagnesemia
• Manifestation: Hypokalemia and
Hypocalcemia, with weakness and muscle
cramps
– Neurologic and neuromuscular
hyperirritability
• Lethargy, Confusion
• Tremor, Fasciculations, Ataxia, Nystagmus,
Tetany, Seizure
– Cardiac: Hypertension and arrhythmia
• Prolonged PR and QT interval → atrial and
ventricular arrhythmia (esp if on digoxin)
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Hypomagnesemia: Assessment
• Neuromuscular :increased nerve impulse
transmission (hyperactive deep tendon
reflexes, paresthesias, muscle tetany),
positive Chvostek’s and Trousseau’s signs
• GI: hypoactive bowel sounds,
constipation, abdominal distention,
paralytic ileus
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Hypomagnesemia: Interventions
• Discontinue magnesium-losing medications, such
as loop diuretics.
• Administer oral or IV magnesium sulfate following
safety protocols.
– Magoxide 250-500mg qd or bid
– Magnesium sulfate 1-2 g IV, followed by 6g in
1liter/24hrs; repeated for up to 7 days
– Magnesiumsulfate 200-800 mg/d IM in 4 divided
doses
• Encourage foods high in magnesium, including
dairy products and dark green vegetables
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Hypomagnesemia: Interventions
• Monitor cardiac, respiratory,
neuromuscular, GI status
• Place patient on cardiac monitor
• Implement seizure precaution
• Check Deep tendon reflexes
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Hypermagnesemia
• Serum magnesium level of >3.0 mEq/dL
• Etiology
– Decrease renal excretion
• Renal failure
– Increase intake
• After therapy with Antacid or laxatives
– Maalox, Mylanta, Camalox, and Riopan
• During preeclampsia treatment with
magnesium
• Aspiration of sea water
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Hypermagnesemia
• Diagnosis
– Everything will be elevated due to CKD
– Increase BUN, creatinine, potassium,
phosphate, uric acid
– But low calcium
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Causes and Effects of Hypermagnesemia
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Hypermagnesemia
• Manifestation
– s/sx on seen if Mg++ level is > 4 mEq/L
– Impaired neuromuscular transmission
• Areflexia
– Lethargy, weakness, flaccid paralysis,
respiratory failure
– Hypotension, bradycardia
– EKG
• Prolonged PR, QRS widen, peaked T wave
(hyperkalemia) , shorten QT → complete heart
block, asystole
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Hypomagnesemia: Interventions
• Teach pt to avoid abuse of laxatives and
antacids
• Instruct patients with renal problems to avoid
OTC meds that contain Mg++
• Judicious fluid intake
• Monitor I/Os
• Administer diuretics as ordered, calcium
gluconate 10-20ml IV over 10 minutes
(antagonizes effects of magnesium)
• Dialysis
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Food Sources for Magnesium
•
•
•
•
Avocado
• Peanut butter
Canned white tuna
• Peas
Cauliflower
•
Pork,
beef,
chicken
Green leafy vegetables
• Potatoes
– (spinach/broccoli)
• Milk
• Raisins
• Oatmeal
• Yogurt
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Phosphorus
• Critical for bone formation and cellular energy
metabolism
• 85% of body phosphorus is in bone, remainder
is within cells
• Only 1% is in ECF (do not reflect total body
phosphorus stores)
• Phosphorus exists in the body as phosphate
• Normal range 3.0-4.5 mg/dL
• Must be drawn in fasting state (diurnal variation;
nadir in a.m.)
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Phosphorus
• Carbohydrate ingestion and glucose
infusion lower serum phosphorus,
whereas high-phosphate meal raises it
• Major regulatory factors
– PTH (lowers PO4 - via renal excretion)
– Vitamin D ( increase PO4- by enhancing
intestinal absorption)
– Insulin (lowers by shifting PO4- into cells
– Dietary PO4- intake
– Renal function (Most Important)
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Hypophosphatemia
• Serum PO4- level of < 3mg/dL
• Normal 2.7-4.5
• Etiology
– Impaired intestinal absorption
• Alcohol abuse and withdrawal ( beta
adrenergic effect shifts phos into the cell)
• Malabsorption
• Oral phosphate binders
• Refeeding after malnutrition
• Hyperalimentation, Vit D deficiency
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Hypophosphatemia
• Etiology
– Increased renal excretion
• Respiratory alkalosis, alcoholism
• hyperPTH, hyperthyroidism
– Redistribution into cells
• Severe burns
• DKA therapy
• Administration of glucose, Anabolic steroids,
estrogen, OCPs, Beta-adrenergic, xanthine
derivative
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Hypophosphatemia
• Etiology
– Hypercalcemia
– Hypomagnesemia
– Metabolic alkalosis
• Diagnosis
– Urine phosphate or fractional excretion of
phosphate
– Plasma PTH or PTHrP
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Hypophosphatemia
• Manifestation
– Muscular abnormalities
• Weakness
• Rhabdomyolysis
– Affinity of hgb for oxygen through decrease in erythrocyte
2,3 diphophoglycerate concentration
•
•
•
•
Impaired diaphragmatic function
Respiratory failure ( diaphragmatic weakness)
Heart failure
Fractures, decrease reflex
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Hypophosphatemia
• Manifestation
– Neurologic
• Paresthesia, Dysarthria, Confusion
• Stupor, Seizure, Coma
– Hemolysis, platelet dysfunction,
metabolic acidosis (rare)
– Rickets and osteomalacia in chronic
hypophosphatemia
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Hypophosphatemia:Intervention
• Assess for vit D deficiency, hyperPTH
• Assess for overuse of aluminumcontaining antacids
• Elemental phosphorus 0.5-1.0 g bid or tid
– Neutra-phos or neutra-phos K
– Fleet phospho-Soda
• Check crt, phosphorus, ca++
• SE: diarrhea, nausea
– Potasium phosphate or sodium phosphate IV
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TRO 6 hrs
Hypophosphatemia:Intervention
• Check phosphate, calcium, potassium
every 6 hours
• Magnesium deficiency should be treated
• Contraindication to phosphate
replacement
– Hypoparathyroidism, advanced CKD, tissue
damaged and necrosis
– Hypercalcemia
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Hyperphosphatemia
• Serum PO4- > 4.5 mg/dL
• Etiology
– Renal failure
– hypoPTH
– pseudohypoPTH
– Rhabdomyolysis
– Tumor lysis syndrome
– Metabolic and respiratory acidosis
– Excess phosphate administration
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Hyperphosphatemia
• Manifestation
– s/sx are attributable to hypocalcemia and
metastatic calcification of soft tissues
• BVs, cornea, skin, kidney, periarticular tissue
– Please refer to hypocalcemia for s/sx
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Hyperphosphatemia
• Intervention
Administer phosphate-binders that increase
fecal excretion of phosphorus
• Calcium carbonate tid with meals
• Sevelamer (avoids hypermag, calcemia, aluminum
toxicity)
– Also lowers total chol
– SE: GI complaints and metabolic acidosis
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Hyperphosphatemia
• Intervention
– Aluminum hydroxide and aluminum carbonate
• No longer used in dialysis pts because of toxicity
– Calcium citrate should not be use with
aluminum gels because it increases aluminum
toxicity
– Instruct patient to avoid phosphate containing
meds-laxatives and enemas
– Restrict dietary phosphate to 600-900mg/day
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Foods Rich in Phosphorus
•
•
•
•
•
Fish
Organ meats
Nuts
Pork, beef, chicken
Whole-grain breads and cereals
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Anion Imbalances
Imbalances of chloride, phosphate, and
bicarbonate accompany cation imbalances:
• Hypochloremia (below 95 mEq/L) and
hyponatremia
• Hyperchloremia (above 103 mEq/L) with
hypernatremia and metabolic acidosis
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Anion Imbalances
Imbalances of chloride, phosphate, and
bicarbonate accompany cation imbalances
• Hypophosphatemia (below 3.0 mg/dL):
– Aluminum-containing antacids that bind
phosphate
– Vitamin D deficiency
– Hyperparathyroidism
• Hyperphosphatemia (above 4.5 mg/dL) and
renal failure
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Of all of the following patients, the nurse
recognizes that the individual who is most at
risk for a fluid volume deficit is a:
• 6-month-old infant learning to drink from a
cup
• 12-year-old child who is moderately
active in 80° F weather
• 42-year-old patient with severe diarrhea
• 90-year-old patient with frequent
headaches
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Reference
• Berkowitz A: Clinical Pathophysiology
Made Ridiculously Simple. Florida,
MedMaster Inc., 2007