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NURSING MANAGEMENT
C. CALCIUM IMBALANCES
NORMAL TOTAL SERUM CALCIUM:
8.6 to 10.2 mg/dL (2.2 to 2.6 mmol/L)
Calcium is found in the ECF but less than 1% of
total body Calcium is there.
Major component of bones and teeth; 99% of
body’s Calcium is located in
skeletal system
MEDICAL MANAGEMENT Plays a major role in TRANSMITTING NERVE
Obtain ECG tracing IMPULSES, helps regulate MUSCLE
Repeat serum potassium levels without IV CONTRACTION AND RELAXATION including
infusing potassium solution Cardiac muscle
Plays a role in BLOOD COAGULATION
Calcium is absorbed from foods in the presence
of normal gastric acidity and
vitamin D
Controlled by PTH and calcitonin
CAUSES:
Malignancies and hyperparathyroidism MEDICAL MANAGEMENT
Immobility ( multiple fractures and spinal injury) • Treating the underlying cause is very important
(e.g. hyperparathyroidism, chemotherapy for
Thiazide diuretics- potentiate action of PTH
malignancy)
Vitamin A and D intoxication
Pharmacologic Therapy
Hypophosphatemia, hyperthyroidism
• Administration of fluids to dilute serum calcium
Digoxin toxicity
such as 0.9% Sodium Chloride Solution →
increases urinary Ca+ secretion
• IV phosphate- also drops serum Calcium
• Furosemide- together with saline solution→
increases Ca+ excretion
• Calcitonin- useful for patients with heart and
kidney disease; reduces bone resorption ; given
IM
ASSESSMENT AND FINDINGS • Bisphosphonates e.g Pamidronate disodium
SIGNS AND SYMPTOMS (Aredia) and Ibandronate sodium (Boniva)-
Muscle weakness, nausea, vomiting abdominal inhibits osteoclast activity; often used for
cramps, constipation, bone pain, polyuria and malignant disease
polydipsia, dehydration, Flank pain, calcium • Plicamycin: cytotoxic antibiotics that decreases
stones, bradycardia bone resorption. Used with neoplastic
Hypercalcemic crisis: acute rise in serum Ca+ disorders
level to 17mg/dl or • Corticosteroids: competes with Vitamin D for
more – severe thirst and polyuria absorption in small intestine→ decreases
ECG findings: shortening QT interval and ST calcium absorption
segment, prolonged PR interval. more severe:
ventricular dysrhythmia. NURSING MANAGEMENT
XRAY: Bone cavitation, urinary calculi • Monitor for patients at risk of hypercalcemia:
s/s
• Increase patient mobility
• Ambulate as possible (for hospitalized patients)
• Encourage fluids; fluids containing sodium
assists with Calcium excretion (2.8 to 3.8 L of
fluid daily) unless contraindicated
• Adequate fiber in diet : for constipation
• Cardiac rate and rhythm are monitored for any
abnormalities
D. PHOSPHORUS IMBALANCES Low serum magnesium levels
Normal serum phosphorus (HPO4) level: Increased Alkaline Phosphatase – due to
2.5 to 4.5 mg/dl (0.8 to 1.45mmol/L) increased osteoblastic activity Xray: changes in
Phosphorus is the main anion of the cell bone density; osteomalacia(softening of bones)
Stored with Calcium in bones and teeth or rickets
Regulated by Parathyroid hormone: phosphate
reabsorption in the kidney
and allows shift of phosphate from bone to
plasma
FUNCTION OF PHOSPHORUS:
• Nerve and muscle function and red blood cells
• Acid/base balance
• Component of ATP
• CHO, CHON, and fat metabolism
• Part of structure of bones and teeth
MEDICAL MANAGEMENT
Treating the underlying cause
IV preparation of phosphorus: sodium or
potassium phosphate
(IV site should be monitored: may cause tissue
sloughing and necrosis due to infiltration
Avoid phosphate binders such as aluminum,
magnesium and calcium
antacids
NURSING MANAGEMENT
Gradually introduce parenteral solutions (for
HYPOPHOSPHATEMIA malnourished patients)- to avoid rapid shifts of
Value < 2.5mg/dl (0.8 mmol/L) phosphorus into the cells.
Abnormally low content of phosphorus in lean Encourage patient to take in foods rich in
tissues Phosphorus such as milk and milk products,
CAUSES: organ meats, fish, poultry and whole grains
Inadequate intake: TPN with inadequate
phosphorus HYPERPHOSPHOTEMIA
Refeeding after starvation, alcohol withdrawal, Serum Phosphorus levels
respiratory and metabolic alkalosis, burns, o >4.5mg/dl (1.45 mmol/L)
diarrhea CAUSES:
Medications: phosphate binding hypoparathyroidism, acute or chronic renal
antacids(aluminum,calcium,magnesium),diureti failure
cs, laxative abuse Excessive Vitamin D intake and phosphorus
Low magnesium levels and low Potassium levels supplements, excessive use of laxatives and
Hyperparathyroidism enemas (absorbs phosphorus)
respiratory acidosis and metabolic acidosis,
ASSESSMENT AND DIAGNOSTIC FINDINGS diabetic ketoacidosis, infection
SIGNS AND SYMPTOMS Neoplastic disease (leukemia, lymphoma),
Paresthesia, muscle weakness, bone pain, increased tissue catabolism (trauma, crush
seizures, tissue hypoxia. injury), tumor lysis syndrome, chemotherapy,
Confusion, respiratory failure, nystagmus rhabdomyolysis (breakdown of striated muscle)
( repetitive uncontrolled movement of SIGNS AND SYMPTOMS
the eyes) Tetany (low calcium; high phosphorus): inverse
Insulin resistance and hyperglycemia- causes relationship
slight decrease in serum phosphorus levels Signs and symptoms of hypocalcemia
LABORATORY FINDINGS:
Increased PTH levels
Muscle weakness (pulls Calcium out of your AVOID phosphate containing laxatives and
bones),Tachycardia, nausea and vomiting enemas (absorbs phosphates; also causes
Soft tissue calcifications in lungs, heart, kidneys hypocalcemia)
and cornea Monitor for changes in urine output
LAB FINDINGS:
BUN, Creatinine: to assess renal status
PTH levels are low: hypoparathyroidism
XRAY: Skeletal changes with abnormal
development
Low serum Calcium levels
MEDICAL MANAGEMENT
Treatment of underlying disorder
Vitamin D preparation: calcitriol, which is E. MAGNESIUM IMBALANCES
available in both oral (Rocaltrol) and parenteral normal serum magnesium level is
(Calcijex, paricalcitol [Zemplar]) formscan help o 1.3 to 2.3 mg/dL (0.62 to 0.95 mmol/L)
reduce PTH levels. Magnesium (Mg++) is an abundant intracellular
Phosphate binders: Sevelamer (Renvela) ;binds cation
to Phosphorus in the GI tract to decrease Activator for many intracellular enzyme systems
absorption; prevents hypocalcemia Carbohydrate and protein metabolism
Calcium binding Antacids: calcium carbonate or Important in neuromuscular function; sedative
calcium citrate effect at neuromuscular junction
o binds phosphorus and decreases is controlled by Vitamin D; regulated by kidneys
absorption Excretion is affected by 3 things:
Loop diuretics (Lasix) ↑ PTH → ↓ Mg Excretion
Dialysis - severe ↓ Sodium and Calcium excretion → ↓ Mg
Excretion
NURSING MANAGEMENT ↓ blood volume → ↓ Mg Excretion
Monitor patients at risk for hyperphosphatemia
Low phosphorus diet as prescribed (refined oils:
sunflower oil, palm oil), fruits, vegetables,
eggwhite: good low phosphorus source of
CHON, soymilk; no meat (more phosphorus is
easily absorbed)
AVOID phosphorus-rich foods, such as hard
cheeses, cream, nuts, meats, whole- grain
cereals, dried fruits, dried vegetables, sardines,
sweetbreads, and foods made with milk
HYPOMAGNESEMIA
• <to normal serum Mg of
• 1.3 mg/dl/0.62 mmol/L
• Associated with HYPOKALEMIA and
HYPOCALCEMIA
CAUSES:
• Decreased intake: decreased GI absorption-
malabsorption
• Increased magnesium excretion: diuretics
• Excess GI loss (vomiting, diarrhea, nasogastric MANAGEMENT
suction, fistula) • Diet: green leafy vegetables, nuts, seeds,
• alcoholism, cirrhosis, hyperthyroidism, legumes, whole grains, seafood, peanut butter,
hypothyroidism, pancreatitis, preeclampsia, and cocoa
hemodialysis, hypercalcemia, hypothermia, • IV or IM Magnesium Sulfate: must be given via
burns, sepsis, wound debridement Infusion pump
• Vital signs must be assessed frequently : cardiac
rate, hypotension and respiratory distress
• Monitor urine output
• Seizure precaution
HYPERMAGNESEMIA
• > 3.0 mg/dl (1.25 mmol/L)
Causes:
• Kidney injury: common cause (kidneys
normally excrete magnesium)
SIGNS AND SYMPTOMS
• Diabetic ketoacidosis
• paresthesia, insomnia, loss of appetite, mood
• Use of Mg antacids (Maalox, Riopan, Mylanta)
changes, confusion, fatigue, weakness,
or laxatives (Milk of Magnesium)
hallucinations
• Opioids and anticholinergics
LABORATORY FINDINGS:
Lab findings: ECG: AV block, prolonged PR interval, tall T
• ECG: may see changes related to magnesium,
waves and
potassium or calcium deficiencies. flat or
widened QRS and high serum Mg levels
inverted T waves; depressed ST
segment.Prolonged PR interval and widened
MANAGEMENT
QRS
• Treat underlying cause: if magnesium is high
• Serum Albumin: if albumin is decreased it may
due to medication,
cause decreased magnesium level
• d/c the medication (antacids or laxatives that
• Serum Calcium and Potassium: decreased ( Mg
have magnesium: Maalox, Mylanta, Mag
helps to transport Ca and K in and out of the
Citrate, Milk of Magnesia, Mag-Sulfate)
cells)
• Loop diuretics and NSS/PLR IV solution will help
• Serum Ionized Mg: decreased – tends to reflect
intracellular magnesium increase magnesium excretion, as long as
• Serum Magnesium: decreased (can be normal patient has adequate renal function.
despite low intracellular magnesium) • IV Ca gluconate: counteract neuromuscular
• Serum Potassium: decreased – hypokalemia effects of Mg if
• Hypermagnesemia is severe.
may be resistant to replacement if the cause is
• Dialysis with a low magnesium dialysate (pt
a problem with the sodium-potassium pump –
with severe renal impairment)
magnesium may need to be repleted first
NURSING MANAGEMENT
• Low Urine Magnesium
• STRICT intake and output
• Place patient under cardiac monitoring
• Watch for hypotension, bradycardia and
respiratory depression (shallow respiration)
• Assess neuromuscular function: decreased deep Instruct to avoid drinking free water without
tendon reflex and change in LOC electrolytes (excretes large amounts of
chloride)
F. CHLORIDE IMBALANCES
Normal range: 97-107 mEqs/L (97-107 mmol/L) HYPERCHLOREMIA
Found more in interstitial and lymph fluid >108 mEqs/L
compartments than in blood; also contained in SIGNS AND SYMPYOMS:
gastric, pancreatic juices, sweat, bile and saliva Associated with:
Largest electrolyte composition of the ECF and Hypernatremia; dehydration
assist in determining osmotic pressure Corticosteroids, resp. alkalosis, metabolic
Produced in the stomach; combines with HCL acidosis
Dependent with sodium Head injury (causes water retention)
SIGNS/SYMPTOMS:
-tachypnea, lethargy, weakness , decrease cardiac
output, lethargy, dyspnea
LABORATORY FINDINGS:
Increased CL, increase K+ and Na+, low pH, low
HCO3, increase urinary chloride level
MANAGEMENT
Hypotonic solutions may be given
PLR solution may be prescribed: corrects
acidosis
IV sodium bicarbonate: excretes excess
HYPOCHLOREMIA chloride ions
<96 mEq/L Diuretics
CAUSES: Parallel to hyponatremia Vital signs, I & O, blood gas values
Diarrhea and prolonged vomiting Maintain adequate hydration
Excessive sweating
Loop, osmotic diuretics
Addison’s disease
SIGNS/SYMPTOMS
- agitation, irritability, muscle cramps
- Dysrhythmias, seizures and coma
- s/s of hyponatremia ang hypokalemia,
metabolic acidosis
LABORATORY FINDINGS:
Decrease serum chloride, decrease serum
sodium, increase pH, increase serum
bicarbonate, increase total CO2 content,
Decrease urine Chloride level and decrease
potassium
MANAGEMENT
0.9% NSS or 0.45% NaCl IV for replacement
Discontinue diuretics
Ammonium chloride- treats met. Alkalosis
Diet rich in high chloride content: tomato
juice, bananas, dates, cheese, eggs, milk,
salty broth , canned veggies and processed
meats