Fluids and Electrolytes Sp 09
Transcript of Fluids and Electrolytes Sp 09
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Fluids and Electrolytes
Vesta Fairley RNC, MSN, OCN
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Fluid and Electrolyte Balance
Internal equilibrium
Balanced body systems
Steady state
Fluids, electrolytes
osmolarity are maintainedwithin narrow limits
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We Are in Fluid Balance
Maintain blood volume
Transport nutrients
Medium for chemicalfunction
Cushions, lubricates, gives
structureMaintain body temperature
Eliminates waste
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What Influences the Amount of
Body Fluid?
Body fat / elderly
Age
Gender
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Body Fluid Compartments
Extracellular Intracellula
Interstitial
intravascular
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Body Fluid Compartments
xtracellularIntracellula
Interstitial
intravascular
Third space
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Fluid and Electrolyte Balance
Intracellular
Potassium (k+)
Proteins ( -) Magnesium (mg++)
Phosphates (PSO4
=)
Sulfate (SO4 =)
Extracellular
Sodium(Na+)
Organic Acids Chloride (Cl-)
Bicarbonate
(HCO3-)
Calcium (Ca++)
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Electrolyte Balance
Intracellular Cations Potassium 150 Magnesium 40 Sodium 10
Intracellular Anions Phosphate/ sulfate 150
Bicarbonate10 Proteinate 40
Extracellular Cations
Sodium 142
Potassium 5
Calcium 5
Magnesium 2
Extracellular Anions
Chloride 103
Bicarbonate 26
Phosphate 2, Sulfate 1
Organic acid 5
Proteinate 17
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Electrolyte Functions
Neuromuscular activity
Maintain body fluid volume and
osmolality
Regulates acid base
Distribute body water between
compartments
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Assessment of Imbalance
Change in behavior
LOC, VS
Skin turgor Muscle strength
Condition of mucous membrane
Monitor Intake and output Daily weight
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Evaluation of Fluid Status
Creatinine
Hematocrit
Urine sodium
Blood urea nitrogen
Specific gravity of urine
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Dont Disturb Me Right Now
Routes of Gains
Eating and Drinking Parenteral fluids
Enteral fluids
Total Parenteral Nutrition
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Enteral Feeds
Normal GI motility and absorption arerequired
Pancreatic enzymes and insulinproduction are required
High protein feeds can cause waterdeficit through osmosis. Additional wateris needed
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Routes of Gains and Losses
Output is approximately 1 ml of urine/ kg / hr in
all age groups
300 to 400 ml of water vapor is eliminated bythe lungs every day
100 - 200 ml per day is lost from the GI tract
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Parenteral Fluids
Isotonic - (0.9 %) NS, D5NS, D5 W, LR,
Ringers solution
Hypotonic - Normal saline, Normal
saline
Hypertonic - 3% and 5% sodium solution,
Concentrated dextrose solutions, Whole
blood, albumin, TPN, lipids
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Normal Saline ( 0.9% )
Isotonic, Osmolality of 308 mOsm / L
Used to treat extracellular fluid deficit
Supplies only sodium and chloride Can cause fluid volume excess and
hyperchloremic acidosis if given in
excessive amounts Only solution administered with blood
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5% Dextrose in Water ( D5W )
Isotonic - Osmolality of 252 mOsm / L
Hypotonic when administered
Supplies free water to aid in renalexcretion
Corrects increased serum osmolality
Caloric value about 170 kcal / L
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Ringers Solution
Contains electrolytes (NA, Cl, K, Ca)
Lactated ringers contain lactate which is
bicarbonate precursors
Used in the treatment of hypovolemia(fluid loss,burns,diarrhea)
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Ringers Solution
No calories, dehydration, sodium
depletion, replacement of GI loss
Check urine output before infusing
potassium
Continually assess for electrolyte or
fluid imbalance
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Half Strength Normal Saline
( 0.45% NS )
Hypotonic is used to replace cellularfluid
Provide free water for excretion ofbody waste
Used to treat hypernatremia or otherhyperosmolar conditions
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Half Strength Normal Saline
( 0.45% NS )
Excessive infusion of hypotonic
solutions can lead to intravascular
fluid depletion, decreased blood
pressure, cellular edema and cell
damage
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Dextrose Solutions
(2.5%, 5%, 10%, 20%, 50%)
Hypertonic, Supplies calories as carbs
May cause peripheral circulatory collapse
and anuria in patients with sodiumdeficiency
May aggravate hypokalemia
May irritate veins.
Electrolyte free solution increases body
fluid loss
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Saline Solutions
(0.45%, 0.9%, 3%, 5%)
No calories, fluid replacement,
dehydration, sodium depletion or
hyponatremia
Use chloride solution with caution in
edematous patients with heart, renal or
hepatic disease
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Dextrose Saline Solutions(5% Dextrose in 0.45% or 0.9% NS)
Fluid replacement, calorie feeding, dehydration,
sodium depletion
Use chloride solution with caution in patientswith compromised cardiovascular or pulmonary
status
Continually assess for crackles, edema, and skin
turgor
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I Got the Lytes Knocked Out of Me
Routes of Losses
Kidneys
Skin
Lungs
GI Tract
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He Said Something About a FluidImbalance
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Hypovolemia Sounds Bad
Fluid and electrolytes are lost in the same
proportions
Causes
Vomiting and Diarrhea GI suctioning
Sweating
Decreased intake
Fever, fistulas
Blood loss, burns
Fluid shifts
Diabetes
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Manifestations of Hypovolemia
Acute wt loss and Decr skin turgor
Oliguria / concentrated urine
Postural hypotension and Weak rapid
pulse. Flattened neck veins Increased temp
Cold clammy skin
Thirst and Anorexia
Muscle weakness and Cramps
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Diagnosis of Hypovolemia
Increased
blood urea nitrogen
hematocrit
sodium and potassium level
urine specific gravity
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Management of Hypovolemia
Give oral fluids or IV isotonic fluids
Give hypotonic solution, when
normotensive
Assess I&O, weight, VS, LOC, breath
sounds, skin color
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Nursing Measures of Hypovolemia
Measure I & O every 8 hrs (1 hr)
Daily weight
Vital signs Monitor skin and tongue
Urinary concentration
Mental function
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Hypovolemia Sounds Bad
Fluid Is Lost and Electrolytes Are in
Excess
Osmotic diuresis
Cellular dehydration
Circulation failure
Buildup of waste products
Mental changes. Disruption of brain cells
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Signs of Hypovolemia
Weight loss
Thirst
Increased body temperature due to less
water for temp regulation
Dry mouth and throat
M t f H l i
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Management of Hypovolemia
Give one liter of fluid / kg wt loss plusan additional 1.5 liters of fluid to
supply current daily need.
Replace fluid over a period of several
days
Give IV glucose and water to replace
water loss and increase urinary flow to
excrete excess electrolytes 2
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Hypervolemia Sounds Bad Too
Sodium and water are retained in thesame proportions
Causes CHF Cirrhosis of the liver
Regulation Problem Renal failure Fluid overload Increased table salt
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Manifestations of Hypervolemia
Weight gain
Polyuria
Distended neck
veins
Elevated blood
pressure
Full bounding
pulse
Dyspnea
Tachypnea Ascites
Peripheral edema
Change in mentalstatus
Diagnostic - Decreased BUN and hematocrit
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Nursing Assessment
Hypervolemia
MonitorDaily weight
Intake and output
Blood pressureRespiratory rate
Lab values
Sacral edema in bedriddenpatients
Auscultate lung sounds
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Management of Hypervolemia
Treat causative factors
Restrict fluids and sodium
Diuretics
Dialysis
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Hypervolemia
Water Excess or Water Intoxication
Causes Sodium deficit
Water intake excessive
Intake of electrolyte free fluids Increased secretion of antidiuretic
hormone
Inadequate output of urine
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Signs of Hypervolemia
Change in behavior
Hyperventilation
Sudden weight gain Warm, moist skin
Increased intracranial pressure
Peripheral edema, usually not marked
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Management of Hypervolemia
Water restriction
Lasix and hypertonic saline (5%)
Obtain hourly intake and output Obtain body weight
Auscultate breath sounds
Obtain serum sodium levels
Assess neurological status
Assure patient safety
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Have you lost
your
electrolytes?
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Sodium
Imbalance
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Sodium
(135 - 145 meq/ L)
Extracellular
Regulates fluid balance Essential for glucose to be
transported into the cells
Necessary for muscle and nerveaction
Helps maintain acid base balance
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Causes of Sodium Imbalance
Diuretics
Restricted sodium intake
GI or biliary drainage, draining fistulas
Disease interfering with aldosterone
secretions
Third spacing, heavy perspiration, fever
Chronic renal disease
Manifestations of Sodium
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Manifestations of Sodium
Imbalance
Hyponatremia Headache
Anorexia and N &V
Muscle cramps Exhaustion
Postural HTN
Weight loss
Hypernatremia Swollen tongue and
thirst
Sticky mucous
membranes
Deep tendon reflexes
Peripheral edema
Manifestations of Sodium
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Manifestations of Sodium
Imbalance
Hyponatremia Increased
pressure
Mental
confusion Delirium
Shock
Coma
Hypernatremia Pulmonary edema
Postural hypotension
Increased muscle tone Flushed skin
Neurological changes
related to cellular
dehydration
Di ti f S di I b l
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Diagnostic of Sodium Imbalance
Hyponatremia
Decreased sodium level135 / L
Decreased serumosmolality
Urinary sodium content
changes depending oncause
Hypernatreamia
Serum level greaterthan 145 meq / l
Serum osmolalitygreater than 295mOsm/kg
Increased urinaryspecific gravity
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Management of Sodium ImbalanceHyponatremia Shock rapid infusion of normal saline
Replacement of potassium, calcium
bicarbonate Increase sodium PO, GA, IV
Safety measures
Fluid restriction (treatment of choice)
If neurologic symptoms, administers
hypertonic solution
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Management of Sodium Imbalance
Hypernatremia - Increase fluid, Hydratecautiously, Diuretics, Dialysis
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Potassium
Imbalance
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Potassium Normal value 3.5 - 5.5 meq / l
98% inside cell, 2% outside cell
80 % excreted by kidneys
20% excreted in bowels and sweatglands
Responsible for muscle and cardiacactivity
Potentiates digitalis
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Causes of Potassium Imbalance
Hypokalemia Decreased food and
fluids intake
Failure to replace
losses
Alterations in acid
base
Hyperaldosteronism
Hyperkalemia Decreased renal
function
Corticosteroids
deficiency
NSAIDS, captopril, K
sparing diuretics,
aged blood
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Causes of Potassium Imbalance
Hypokalemia
Potassium losing
diuretics
Digitalis toxicity, if
person becomes
hypokalemic Kidney and heart
damage
Hypokalemia
Acidosis
Tissue damage and
trauma, infection
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Clinical Signs of Potassium Imbalance
Deficit Nausea and
Vomiting Excessive urination Cardiac arrest Respiratory arrest Dysrythmias
Excess EKG changes
Cardiac arrest
Skeletal muscle
weakness
Muscle spasms
C S f
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Clinical Signs of Potassium Imbalance
Deficit Fatigue, muscle
weakness Paralytic ileus Abdominal
distention Anorexia
Leg cramps
Excess Paralysis
Nausea
Intestinal colic
Diarrhea
Diagnostics of Potassium
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Diagnostics of Potassium
Imbalance
Hypokalemia Potassium is less than 3.5 meq / L
Sensitivity to digitalis
Alkalotic (metabolic)
Hyperkalemia Elevated potassium level EKG changes
Acidotic (Metabolic)
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Rapid rise in
potassium canbe lethal
Management of Hypokalemia
Oral or IV potassium IV must be on a pump
Schlerose and burns veins
20 meq / hr rate
Concentration < 40 meq/ l
Agitate solution to mix well Must have adequate urine
output
Monitor potassium level
M t f P t i E
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Management of Potassium Excess
EKG and serum potassium level
No oral intake of foods high in
potassium
D 10 with regular insulin Kayexelate
Dialysis
Calcium gluconate IV or sodium
bicarbonate
Bedrest
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Calcium
Imbalance
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Calcium
Serum calcium level 9.0 11.0 mg / dl
Functions
Blood coagulation
Smooth skeletal functions
Cardiac muscle function
Nerve function Bone and teeth formation
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Hypocalcemia
Causes
Inadequate intake or vitamin D deficiency
Hypoparathyroidism
Pancreatic disease
Excess loss through intestinal fistulas
Hyperphosphatemia
Magnesium deficiency
Medications
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Hypocalcemia
Clinical Manifestations
Tetany
Numbness and tingling of the nose, fingers, andtoes
Muscle spasm and muscle pain
Seizures Mental changes such as depression, confusion,
hallucinations
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Trousseaus Sign
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Hypocalcemia
Diagnostics
Decreased corrected calcium
Increased ph
Decreased parathyroid hormone
Decreased magnesium
Decrease phosphorus
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Hypocalcemia
Management
Increase calcium in diet or oral calciumsalts
10 % calcium gluconate IV
Vitamin D or parathyroid hormone
Give aluminum hydrate
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Hypercalcemia
Serum calcium level > 11mg / dl
Causes Malignant neoplastic disease
Hyperthyroid disease
Immobilization
Thiazide diuretics
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Hypercalcemia
Mild
Polyuria
Severe thirst
Anorexia
Nausea and vomiting Constipation
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Hypercalcemia
Progressive
Lethargy
ConfusionComatose
Bone pain
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Hypercalcemia
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Hypercalcemia
DiagnosisSerum calcium level > 11 mg / dl
Increased parathyroid hormone
levels
PotassiumSodium
Phosphorus
Urine bun and creatinine Cardiovascular changes
Hypercalcemia
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Hypercalcemia
Treatment Remove the cause
IV saline and diuretics
Calcitonin
Mitramycin, aredia, didronel
Glucocorticoids if cause is cancer
Increase fluid intake to 3 4 L / d to reduce
calculi formation
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Magnesium
Imbalance
Magnesium
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MagnesiumFunctions
Level 1.5 2.5 meq/l
Activates enzyme reaction especially
carbohydrates and proteins
Prevent convulsions in toxemia in pregnancy
Acts as a vasodilator which decreases blood
pressure
Similar to calcium in muscular and nerve
function
Hypomagnesemia
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Hypomagnesemia
Causes Calcium deficit
Loss of intestinal fluids through draining
fistulas, diarrhea, stetorrhea and GI suctioning Alcoholism or prolonged malnutrition Drug therapy with aminoglycosides and loop
diuretics
Endocrine disorders such as increasesecretion of antidiuretic hormone aldosterone
and thyroid hormone
Hypomagnesemia
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yp gClinical Manifestations
Confusion
Hallucinations
Weakness
Convulsions
Depression
Increased reflexes
Tremors
Muscle spasms
Trousseau's sign andchvostek's sign
Hypomagnesemia
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Hypomagnesemia
Diagnostics
Serum albumin < 1.5 meq / l
Decreased potassium and calcium level
Management
Correction of the underlying problem
Mild cases can be corrected by diet alone
Oral magnesium salts
IV magnesium sulfate (calcium gluconate must be
readily available
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Hypermagnesemia
Causes
Can result from frequent use ofmagnesium containing antacids
Can be caused by renal failure
Can be caused by a adrenocortical
insufficiency
Hypermagnesemia
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Clinical Manifestations
Mild
Decreased blood pressure
Facial flushing Sense of heat
Thirst
Nausea and vomiting
Hypermagnesemia
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Hypermagnesemia
Clinical Manifestations
ModerateLethargy
Difficulty speakingDrowsinessLoss of deep tendon reflexes
Muscle weaknessParalysisRespiratory depression
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HypermagnesemiaDiagnostic
Level > 2.5 mg / dl
Management
Calcium gluconate (temporary treatment)
Hemodialysis with a magnesium free
dialysate Duretics and 0.45% NACL to enhance
excretion
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Phosphorus
Imbalance
Ph h
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PhosphorusNormal serum level 2.5 - 4.5 meq / dl
Functions
RBC formation (ATP)
Metabolism of carbohydrates, fats and
proteins
Maintenance of acid base balance
Nerve and muscle function
Support of bones and teeth
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Hypophosphoremia
Causes Overzealous intake of carbohydrates
Anorexia nervosa
Alcoholism or alcohol withdrawal
Poor dietary intake
Thermal burns
Vitamin D deficiency
Diabetic ketoacidiosis
Diagnostics -Level < 2.5 mg / dl
Hypophosphoremia
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Hypophosphoremia
Irritability
Apprehension
Weakness
Numbness
Confusion
Seizures
Coma
Tissue anoxia
Bruising
Bleeding
Clinical manifestations
ManagementOral phosphorus replacement
IV phosphorus
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Hyperphosphoremia
Causes Decreased excretion of phosphorus
Increase phosphorus intake of absorption Muscle necrosis
Diagnostics Level > 4.5 mg / dl
Abnormal bone development
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Hyperphosphoremia
Clinical manifestations
Complication of joint calcification
Tetany - tingling of fingers and toes Anorexia
Nausea
Vomiting Muscle weakness
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Hyperphosphoremia
Management
Treat underlying disorder
Allopurinol Restrict dietary phosphorus
Dialysis
Phosphate binding gels
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Total Parenteral Nutrition
T t l P t l N t iti
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Total Parenteral Nutrition
Method of giving highly concentrated solutions
Intravenously to maintain a patients nutritional
Balance when oral or enteral nutrition is not
Possible
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Total Parenteral N trition
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Total Parenteral Nutrition
Indications Major GI diseases
Fistulas and inflammatory disease
Severe trauma or burns Severe GI side effects from radiation or
chemotherapy
Congenital malformations of the GI tract
Severe malnutrition
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Contents of All TPN
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Contents of All TPN
Water
Proteins
Carbohydrates
Fat Vitamins
Trace elements
Dextrose 25% 35%
Amino acids 3% 5%
Electrolytes Minerals
Vitamins
Fat emulsions 10% 20%
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Total Parenteral Nutrition
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Administration
Must be on a pump
If TPN is stopped for any reason, hang D10 or D5
as ordered Only lipids can be hung with TPN
Lipids are unfiltered, TPN is filtered
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Total Parenteral Nutrition
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Administration
Must be on a pump
If TPN is stopped for any reason, hang D10 or D5
as ordered Only lipids can be hung with TPN
Lipids are unfiltered, TPN is filtered
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Total Parenteral Nutrition
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Administration
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Must be through a central line
D 10 or less can be administered
through a peripheral IV
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Administration
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Maintain strict aseptic technique
May be unrefrigerated < 30 minutes
prior to admin
Use within 24 hours after mixing
Total Parenteral Nutrition
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Administration
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Dressing change every 72 hours if
central line or every 48 hours if
peripheral line
Total Parenteral Nutrition
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Administration
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Although the bags are
numbered, pay attention to the
expiration date
Total Parenteral Nutrition
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Administration
Start administration slowly about 25 cc / hr
Gradually increase rate about every 4 hrs in
25 cc increments until ordered rate is reached
When discontinuing, gradually taper off over
about 6 hours
Monitor blood glucose levels every 4 hours
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T t l P t l N t iti
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Total Parenteral Nutrition
Mechanical complications
Pneumothorax
Hemothorax Air embolism
Catheter misplacement
Thromboembolism
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Mechanical Complications
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Mechanical Complications
Pneumothorax, hemothorax
Needle tip penetrated the pleura of the lung which
usually occurs in thin malnourished patients
Pneumothorax is characterized by a sudden sharp
pain around the area where the needle was
inserted, coughing, chest pain, cyanosis or
becomes hypotensive
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Mechanical Complications
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Mechanical Complications
Air Embolism
Occurs when changing the
tubing or when the tubing isseparated
100 - 200 cc of air is fatal
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Management of Air Embolism
Place in trendelenburg
Lay on left side
Perform the valsava maneuver, while
disconnecting the tubing
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Mechanical Complications
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Mechanical Complications
Thromboembolism
Predisposition Venous stasis
Hypercoagulable state
Local trauma
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Prevention of
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Prevention of
Thromboembolism Heparin added to the solution
Thrombosis may be asymptomatic
Signs of pulmonary embolism may
be the first sign of thrombosis
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Catheter Related Sepsis
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Catheter contamination is the major sourceof TPN sepsis
Catheter sepsis can be minimized by aseptic
technique in the maintenance as well as
insertion and restricted use of catheter for
nutrition use only
13
Metabolic Complications
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109/119
Metabolic Complications
Glucose intolerance
Hypoglycemia can result from sudden
withdrawal of a prolonged infusion
Symptoms include diaphoresis, confusion
and agitation
Treatment include frequently monitoring ofglucose levels and reinstitution an infusion
of 10% dextrose in water
13
Metabolic Complications
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Metabolic Complications
Glucose intolerance Hyperglycemia infusion rate too fast for
the patient's insulin response
Treatment for a patient with
hyperglycemia is to increase the
percentage of calories provided by fat,infusing glucose infusions slowly, and
providing insulin when necessary
13
Metabolic Compensation
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111/119
Metabolic Compensation
Hypomagnesemia
Symptoms include apathy, weakness,
seizures, arrhythmia hallucinations,hyperreflexia
Symptoms resolve rapidly withmagnesium replacement
13
Metabolic Complications
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Hypophosphatemia Signs and symptoms include tremor,paresthesias. Ataxia, decreased platelet
and erythrocyte survival, impaired
leukocyte function and weakness
Treated with 10 - 15 mmol of phosphate per
liter of solution
13
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113/119
Complication Fluid Imbalance
Volume infused is excessive
Treatment consist of decreasing the
rate of fluid and optimizing cardiac andrenal function
13
Complications Acidosis
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114/119
Complications Acidosis
Acidosis occurs when carbohydrates arebroken down
The increased production of carbondioxide can induce respiratory distress
Abnormal neurological symptoms includedisorientation, lethargy , stupor, and
convulsions which can lead to coma and
death
13
Administration of Lipid
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115/119
Administration of Lipid
Emulsions
Lipids can be piggybacked in the
TPN but it has to be below the
filter preferably close to the
insertion site
13
Administration of Lipid
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116/119
Emulsions
The rate is usually 30 - 60 ml/hr
10% emulsion - 30 ml / hr for 30
min 20% emulsion - 15 ml / hour for 30
min
Gradually increased to prescribeddose if no reaction
Administration of Lipid
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Administration of Lipid
Emulsions
Lipids can be given peripherally
Lipids can be given to a patient who
is glucose intolerant
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