Fluid and Electrolytes

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Diabetes Insipidus-Nephrogenic: Nephrogenic- Kidney Malfunction
Diabetes Insipidus- Cerebral: Head trauma or trauma to pituitary. Can result from surgical trauma
Diabetes Insipidus- clinical manifestations-: Increased urine output
Lower specific gravity in urine
Altered thirst mechanism
Dehydration
Diabetes Insipidus resulting from brain trauma- manifestations: Localized swelling blocks the transport of ADH from hypothalamus to pituitary
Diabetes Insipidus- interventions: Administer Fluids
Administer Pitressin (synth ADH)
SIADH (Syndrome Of Inappropriate Diuretic Hormone): Excessive ADH production
SIADH- causes: Stress
Anesthesia
Surgery
Tumors
Aids
Meds- cytoxin, diabenese, elavil
SIADH- clinical manifestations: Water retention
Decreased urine output
Increased specific gravity of urine (more concentrated)
BUN/Creatinine levels decreased.
SIADH- interventions: Administer diuretics
Treat cause
Allow recovery time
Water Excess- causes: Excess water or excess sodium ingestion
Water Excess- clinical manifestations: Weight gain
Edema
Rales- too much fluid in lungs
Nausea, vomitting, diarrhea
Abdominal cramps
Low H&H (hematocrit and hemoglobin)
Low B.U.N.
Orthostatic hypotension
Water Excess- Treatment: Diuretics
Limit fluid intake
Dialysis
Water deficit- causes: Decreased water intake
Losses (vomitting, diarrhea, NGT)
Fever
Excessive use of diuretics
Hyperglycemia (causes osmotic diuresis)
Water deficit- clinical manifestations: Turgor decreased
Dry mucuous membranes
Weight loss
Lethargy
Change in mental status
Water deficit treatment: IV fluids to restore electrolytes and fluids
Third Spacing: shift of fluid from vascular space to another part of the body (interstitial space)
Third spacing- causes: increased hydrostatic pressure- as seen in CHF
Too much fluid in vessels
Decreased plasma proteins
Liver disease
Increased capillary permeability- sepsis, trauma and burns
Third Spacing- clinical manifestations: Weak right sided pressure
Low albumin levels
Protein levels
Third Spacing- interventions: IV albumin
Lasix after IV treatment
In sepsis, treat cause
Electrolytes: substances which when dissolved in water separate into ions (capable of conducting electricity)
Intracellular Electrolytes: potassium and magnesium
Extracellular: Sodium and Chloride
Sodium: most abundant cation (postitive ion) 135-145 mEq/L
Sodium- function: maintain extracellular volume and water balance
aids to transmit nerve impulses
Hypernatremia- causes: Decreased water intake
Fluid loss
Osmotic diuresis
Hyperglycemia
Salt water intake
Profuse diaphoresis accompanied by low water intake
Hyperaldosteronism-too much sodium in blood.
Diabetes Insipidus
Hypernatremia- Clinical manifestations: Mental status decrease
Decreased turgor
Dry Skin and mucous membranes
Thirst
Hypernatremia- interventions: Administer hypotonic IV (0.455% NSS)
Water
Administer oral hygeine
Hyponatremia- causes: Sweating followed by large plain water intake causes dilution of plasma sodium
Increased ADH
Adrenal Insufficiency (decreased aldosterone so Na levels fall)
Hyponatremia- clinical manifestations: Neurological symptoms due to brain swelling
Weight gain
Edema
Rales
Abdominal cramps
Low hematocrit
Low BUN
Orthostatic hypotension
Hyponatremia- Interventions: Administer hypotonic IV
Diuretics
Potassium: 3.5-5 mEq/L
Potassium- function: Cellular metabolism
Transmission of neuromuscular impulses
supports cardiac cycle
Acid base balance
Any condition that increases urinary output decreases potassium
Hypokalemia- Causes: Diuretics
GI Losses
Adrenal Tumor- may cause excess secretion of aldosterone,which then secretes too much Ka
Hypokalemia- clinical manifestations: Malaise
Muscle Weakness
Leg Cramps
Fatigue
Decreased reflexes
Abnormal ECG and disrhythmia
Hypokalemia- interventions: Administer potassium
Oral or IV (NEVER IV PUSH Ka, THIS CAN BE FATAL)
Hyperkalemia- causes: Renal insufficiency
Cellular destruction
Excessive administration of Ka
Adrenal Insufficiency- too little aldosterone.
Hyperkalemia- clinical manifestations: Mental changes
Abnormal ECG
Lethal disrhythmia
Dialysis (#1 cause)
Hyperkalemia- interventions: Glucose and insulin concentrate to move Ka into cells
Sodium Bicarbonate for acidosis
Kayexelate enema or oral
Calcium- function: formation of bone and teeth
blood clotting
myocardial contractility
nerve impulse conduction (suppressant effect)
Calcium: 8.5-10.5mEq/L
Calcium- regulation: Vitamin D
Parathyroid
Hypocalcemia- causes: Hypoparathyroid
Pancreatitis
Low dietary Ca
Alkalosis
Renal disease (kidneys activate V-D, Vit D helps absorb Ca)
Hypocalcemia- clinical manifestations: hyperactive reflexes
tingling in face fingers toes
Muscle spasm
tetany
Decreased blood clotting
Bronchospasms
(assess by checking trousseau's signs)
Trousseaus Signs: BP cuff inflated for 3-4 minutes hand claws up.
Hypocalcemia- interventions: Oral or IV calcium (NEVER IM CALCIUM)
Hypercalcemia- causes: Hyperparathyroidism- causes too much Ca to be retained
Malignancies-some cancers produce pth.
Osteoporosis
Prolonged immobility
Decreased renal function
Hypercalcemia- clinical manifestations: Hypotonicity
Lethargy
Increased blood clotting
Extreme thirst
Decreased neuromuscular function
Kidney Stones
Fractures-too much Ca can cause breaks.
Hypercalcemia- interventions: Parathyroidectomy
Steriods (they decrease GI absorption of Ca)
Mitromycin
Calcitonin
Magnesium- function: Nerve impulse conduction
Chemical metabolism
Cardiac conduction
Magnesium: 1.5-2.5mEq/L
Hypomagnesemia-causes: Decreased Mg intake
Malnutrition
Alcoholism
Hypomagnesemia-clinical manifestations: tremors
hyperactivity
tetany
positive Trousseau's
Confusion
Agitation
Hypomagnesemia- interventions: Replace Magnesium- IV (Mg salts)IV Mg can cause cardiac arrest if given too quickly.
Oral
IM
Hypermagnesemia- causes: Renal failure- may be exacerbated by meds containing magnesium.
Hypermagnesemia- clinical manifestations: Lethargy
Slow/Weak pulse
Low BP
Decreased tonicity
Brachypnea
Hypermagnesemia- interventions: Dialysis
Stop intake of Mg.

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