fluid and electrolyte imbalances

2. Fluid
&
electrolyte imbalances
PRINCY FRANCIS M
IST YR MSC NURSING
JMCON

3. DEFINTIONS AND TERMINOLOGIES
• Osmosis
Diffusion of fluid through a semipermeable membrane from a solution
with a low solute concentration to a solution with a higher solute
concentration until there is an equal concentration of fluid on both sides
of the membrane.
• Osmolarity
The concentration of solution in terms of osmoles of solutes per litre of
solution.
• Osmolality
The number of osmosis ( standard unit of osmotic pressure) per
kilogram of solution.

4. • Diffusion
The process by which solutes move from an area of higher
concentration to one of the lower concentration, without any
expending extra energy.
• Filtration
Passage through a filter or through a material that prevents
passage of certain molecules. Eg: capillary wall, blood brain
barrier, radiographic grid.

5. FLUID IMBALANCES
•EXTRACELLULAR FLUID VOLUME DEFICIT (ECFVD)
•EXTRA CELLULAR FLUID VOLUME EXCESS (ECFVE)
•EXTRA CELLULAR FLUID VOLUME SHIFT : THIRD
SPACE FLUID
•INTRAVASCULAR FLUID VOLUME EXCESS (ICFVE)

6. EXTRACELLULAR FLUID VOLUME DEFICIT (ECFVD)
• An ECFVD is a decrease in intravascular and interstitial
fluids.
• ECFVD is a common and serous fluid imbalance that
results in vascular fluid volume loss(hypovolemia).
• It occurs when loss of ECF volume exceeds the intake of
fluid.

7. Etiology
Severe vomiting or diarrhea
Traumatic injuries with excessive blood loss
Third space fluid shifts
Insufficient water or fluid intake

8. Risk Factors
In Diabetic Ketoacidosis
•loosing large volume of blood
•experiencing severe vomiting or diarrhea
•having difficulty in swallowing
•elderly, confused persons.

9. Clinical Manifestation
FVD develop rapidly and can be mild, moderate and severe.
•Mild: ECFVD – 1 to 2L of water and 2% of bodyweight is
lost.
•Moderate ECFVD – 3- 5L of water loss and 5% of weight
loss.
•Severe ECFVD – 5 to 10L of water loss and 8% weight
loss.

10. •Postural hypotension, Weight loss
•Decreased skin turgor, Dry mucus membrane, Dry cracked
lips or tongue
•Eyeballs sunken or soft
•Restlessness, coma in severe deficit
•Elevated temperature, tachycardia, postural systolic
BP>15mm Hg, Diastolic Fall <10 mm Hg
•Oliguria(<30ml/hr), concentrated urine, Thirst

11. Assessment and Diagnostic Finding
•Increased osmolality
•Increased or normal serum sodium level
•BUN >25mg/dl
•Hyperglycemia (>120mg/dl)
•Elevated hematocrit(>55%)
•Increased specific gravity

12. Medical Management
Pharmacologic management
•An intravenous solution of 5% dextrose in water(d5w) or 5%
Dextrose in 0.2% saline (D5/0.2% NaCl)
•If hemorrhage is the case of ECFVD blood replacement may
be necessary if blood losses greater than 1L
•In situation in which the blood losses are less than 1L,
normal saline and Ringer’s lactate may be used to restore
blood volume.

13. Diet Management
Client experiencing fluid loss from diarrhea
should avoid fatty or fried food and milk
products
Nursing Diagnosis
Fluid volume deficit related to insufficient
fluid intake, vomiting, diarrhea, hemorrhage1.

14. EXTRA CELLULAR FLUID VOLUME EXCESS (ECFVE)
ECFVE is increased fluid retention in the intravascular
and interstitial spaces.
It refers to an isotonic expansion of the ECF caused by
the abnormal retention of water and sodium in
approximately the same proportion in which they
normally exist in the ECF.

15. Etiology
• Increase in the total body sodium content
• Excessive amount of IV fluid containing Sodium
• Increased ingestion of foods that contain high amount of
sodium
• Contributing factors include heart failure, renal failure,
cirrhosis of liver and excessive amount of table salts.

16. Clinical Manifestation
• Respiratory
• Constant irritating
cough
• Dyspnea, wheezing
• Cyanosis
• Crackled lungs
• Neurologic
• Change in level of
consciousness
• Cardiovascular
• Neck vein engorgement in semi
fowlers position, Head vein
engorgement
• Elevated BP, Tachycardia
• Pitting edema of lower
extremities
• Increased pulse pressure,
Increased CVP
• Sacral edema
• Weight gain

17. Assessment and Diagnostic Findings
• Serum osmolality <275MOSM/kg
• Serum Sodium <135meq/L
• Decreased hematocrit value
• Specific gravity below 1.010
• Chest X-ray - pulmonary congestion
• Low protein

18. Medical Management
Pharmacologic management
• Diuretics
• Loop diuretics- furosemide, torsemide
• Potassium sparing diuretics - spirinolactone
• Thiazide diuretics – hydrochlorothiazide, metolazone
• Digoxin - To increase the force of myocardial contraction
or to slow heart rate
Hemodialysis

19. Dietary Management
Low sodium diet
Nursing management
Fluid volume excess related to compromised regulatory
mechanisms of kidneys.

20. EXTRA CELLULAR FLUID VOLUME SHIFT : THIRD SPACE
FLUID
Third space fluid is a term used to describe the
accumulation of fluids in the interstitial spaces.
A fluid volume shift is basically a change in the location
of extracellular fluid between the intravascular and
interstitial spaces.
The common sites includes pleural cavity, peritoneal
cavity, and pericardial sac.

21. Types of fluid shifts
• Vascular fluid to interstitial space : fluid that shifts into the
interstitial space and remains there is referred to as third
space fluid. Third space fluid occurs in cases of tissue injury
resulting from altered capillary permeability(eg:
inflammation , traumatic injury) and from increased vascular
fluid volumes.
• Increased vascular fluid volume appears in the abdomen
(Ascitis), peritoneal cavity and pericardial sac.

22. Etiology
• Simple blister or sprain
• Crushing injuries
• Extensive burns
• Perforated peptic ulcer
• Intestinal obstruction
• Large venous thrombosis
• Lymphatic obstruction

23. Pathophysiology
• Tissue injury
• release of histamine and bradykinin( increases capillary
permeability)
• allowing fluid, protein and other solutes to shift into the
interstitial spaces.
• The first phase is the fluid shift from vascular to interstitial
spaces leading to a fluid volume deficit(hypovolemia).
• The second phase is the shift from the interstitial to the vascular
space, leading to a fluid Volume Excess (hypervolemia).

24. Clinical Manifestation
• Skin pallor, cold extremities
• Weak and rapid pulse, hypotension
• Oliguria and decreased level of consciousness

25. Assessment and Diagnostic Findings
• Elevated hematocrit and BUN
• Later, decreased hematocrit and BUN due to fluid
returns to blood stream

26. Medical Management
• Determination of cause
• Intravenous isotonic solution
• First phase : amount of fluid infusion is three times
greater than urinary output
• Second phase: less amount of fluid infusion

27. Nursing Management
• Check vital signs q8h.
• Monitor IV Fluid replacement
• Measure abdominal girth of clients with ascites q8h
• Assess breathing difficulty, chest crackle, neck vein engorgement
• Level of consciousness and precaution for seizure
• Frequent skin care to edematous area to prevent skin break down
• Serum levels of BUN and Ammonia should be monitored
• Monitor urine output every hour to ensure atleast 25ml/hr
• If extremities are involved, the circumference of extremities and
the peripheral pulses should be measured every hour.

28. INTRAVASCULAR FLUID
VOLUME EXCESS (ICFVE)
– Water intoxication hypoosmolar disorders results
from either water excess or solute deficit and are
mainly due to sodium loss.
– water excess:- the number of solutes is normal, but
they are diluted by excessive water.
– solute deficit:- the amount of water is normal, but
there are too few particles per litre of water.

29. ETIOLOGY
– administration of excessive amounts of hypo-
Osmolar fluids such as 0.45% Saline or 5% Dextrose
in water.
– clients who receive continuous D5% IV fluids
– in those with brain injury or disease that causes an
increased production of ADH, which increases water
reabsorption from renal tubules

30. Clinical Manifestation
– Headache, nausea and vomiting
– Pupillary changes
– Behavioural changes, irritability, disorientation
– Confusion, drowsiness, decreased co-ordination
– Weight gain
– Bradycardia with increased systolic BP
– Increased respiration, projectile vomiting
– Convulsions

31. Assessment and Diagnostic findings
– Serum Sodium level <125meq/L
– Decreased hematocrit value
Management
– Addition of solutes to IV fluids
– D5 0.45%NaCl will help to correct ICFVE when the cause is
water excess
– Oral fluids : juices, soft drinks, water and ice chips
– Antiemetics

32. Nursing Management
– Assess reflexes and pupillary response
– Monitor vital signs and intake , output every 1-8 hrs.
– IV therapy should be monitored every hour
– Weight should be checked daily to measure fluid gain or
loss
– Safety measures are necessary when client displays
behavioural changes

33. ELECTROLYTE IMBALANCE
Cations
Sodium
Potassium
calcium
magnesium
Anions
Chloride
Phosphate
Bicarbonate

34. HYPONATREMIA
A serum sodium level that is below normal (less than 135 mEq
/L).

35. ETIOLOGY
 Occurs when total body water is decreased (vomiting diarrhea Fistula)
 Kidney’s inability to excrete sufficiently diluted urine.
 Diuresis (increased urine excretion)
 Diuretics
 Gastrointestinal suction
 Excessive perspiration followed by increased water intake.
 Low salt diet.
 Aldosterone deficiency.
 Predisposing condition SIADH, Hyperglycemia, Use of tap water enema,
poor administration of electrolyte parenteral fluids.

36. CLINICAL MANIFESTATION
 Gastro Intestinal : Nausea, vomiting, diarrhea, bowel sounds,
abdominal cramps.
 Cardiovascular : Decrease in diastolic pressure, tachycardia,
orthostatic hypotension, weak pulse.
 Pulmonary : changes in rate of respirations
 Neurologic : headache, lethargy, confusion, clowed problem solving,
diminished muscle tone on extremities, weakness and tremor.
 Integumentary : Dry Skin, pale, dry mucous membrane.

37. MEDICAL MANAGEMENT
 Determine cause and correct it
 Correct body Osmolality
 Sodium replacement
 Water restriction
Pharmacologic Management
 Hyponatremia (125meq/L) IV Saline solution (0.9% NaCl) or
lactated Ringer’s solution
 Na 115meq/L or less, a concentrated saline solution such as
3%NaCl.

38. DIETARY MANAGEMENT
A balanced diet is usually adequate for mild
hyponatremia( 126-135meq/L)
Fluids restricted to 800 -1000ml/day
Common food sources of Sodium are cold cereal, corn
ships, potato chips, cheeses, meats, ham, Pizza, soups,
canned food items5.

39. NURSING MANAGEMENT
Detection and controlling hyponatremia
Returning sodium level to normal

40. HYPERNATREMIA
Hypernatremia is a serum sodium level over 145meq/L
Etiology
Diabetes insipidus
Excess NaCl IV fluid intake
Accidental or increased salt intake
Hypertonic feedings
Canned vegetables
Renal losses

41. Clinical Manifestations
 Gastro Intestinal : Anorexia, Nausea and vomiting
 Integumentary: Dry & flushed skin, mucous
membranes dry and sticky, thirst.
 Neurologic: Restlessness agitation, irritability,
lethargy, coma, tremor, seizures
 Cardiovascular: Tachycardia, hypotension or
hypertension.
 Renal: Oliguria

42. Laboratory Findings
Serum Sodium>145 meq/L.
Urine specific gravity and urine
osmolality

43. Management
Medical Management
To decrease total body sodium and replace fluid loss either a
hypo-osmolar electrolyte solution (0.2 % or 0.45 % NaCl) or
D5w is administered.
Hypernatremia caused by solution excess can be treated with
D5w ad diuretic such as furosemide.
Dietary Management
Dietary restriction of sodium are useful to prevent
hypernatremia un high risk clients
Clients with renal diseases may need to have their sodium
intake restricted to 500 to 2000mg/day.

44. Nursing Management
Preventing hypernatremia
Correcting hyponatremia

45. HYPOKALEMIA
Hypokalemia is a serum potassium level of less than 3.5
mEq/l
Etiology
•Diarrhea, vomiting, nasogastric suctioning.
•Malnutrition, starvation, potassium free diet.
•Potassium wasting diuretics
•Diabetic acidosis

46. CLINICAL MANIFESTATIONS
a. Gastro intestinal :Anorexia, vomiting, diarrhea.
b. Musculoskeletal: Music weakness, paralysis, leg cramps.
c. Cardiovascular: Dysrhythmias, vertigo, postural
hypertension, flattened T wave
d. Respiratory: shallow respiration, shortness of breath.
e. Neurologic: Fatigue , lethargy , decreased tendon reflexes ,
confusion

47. LABORATORY FINDINGS
•Serum potassium <3.5 meq/L
•ECG – flat T wave or inverted T wave, depressed ST
segments

48. MANAGEMENT
Medical Management
• Determining & correcting the cause of imbalance
• Extreme hypokalemia requires cardiac monitoring.
Pharmacologic management
• Oral potassium replacement therapy is usually prescribed for mild
hypokalemia (serum potassium 3.3 to 3.5 meq/L)
• Potassium is extremely irritating to gastric mucosa; therefore, the drug
must be taken with glass of water or jute or during meals.

49. •Potassium chloride can be administered intravenously for
moderate or severe hypokalemia & must diluted in IV fluids.
•Administration of potassium by IV push may result
in cardiac arrests. Potassium can be given in doses
of 10 to 20 meq / hour diluted in IV fluids if the
client is on heart monitor.
•High concentration of potassium is irritating to
heart muscle. Thus correcting a potassium deficit
may take several days.

50. DIETARY MANAGEMENT
•The adult recommended allowance of potassium is 1875
to 5625 mg.
• Common food source containing potassium cabbage,
carrot, cucumber, mushrooms, Spinach, Tomato, Fruits-
banana, Guava, Orange .

51. NURSING MANAGEMENT
• Preventing hypokalemia
• Correcting hypokalemia
• Administering IV Potassium
• Hypokalemia R/t vomiting, diarrhea, Cushing’s syndrome, or
decreased intake.
• Risk for injury R/t muscle weakness & hypotension.
• Imbalanced nutrition less then body requirement R/t insufficient
intake of foods rich in potassium.

52. HYPERKALEMIA
Hyperkalemia is an elevated potassium level over 5.0
meq/L.
Etiology
• Retention of potassium -Renal insufficiency, renal failure,
decreased urine output, Potassium sparing diuretics.
• Excessive release of cellular potassium – Severe traumatic
injuries. Severe burns, severe infection, metabolic acidosis.
• Excessive IV infusion or oral administration of potassium

53. CLINICAL MANIFESTATION
• Cardiovascular: First tachycardia then bradycardia, ECG
changes like Peaked narrow T waves , wide QRS complex,
depressed ST Segment , Widened PR interval
• Gastrointestinal: Nausea, diarrhea, hyperactive bowel sounds.
• Neuromuscular: Muscle weakness, Muscle cramps, tingling
sensation (Paresthesia)
• Renal: Oliguria & later anuria.

54. LABORATORY FINDINGS
• Serum potassium > 5.0 meq /L
• Serum osmolality > 295 Mosm/kg.
• Serum creatinine > 1.5mg.dl.
• BUN >25 mg/dl(Blood Urea Nitrogen ).

55. MEDICAL MANAGEMENT
• When serum potassium level is 5.0 to 5.5 meq/l restriction of dietary potassium
intake
• If potassium excess is due to metabolic acidosis, correcting the acidosis with
sodium bicarbonate promotes potassium uptake into the cells.
• Improving urine output decreases elevated serum potassium level.
• When hyperkalemia is severe, immediate actions are needed to be taken to
avoid severe cardiac disturbance.
• Intravenous calcium gluconate infusion to decrease the antagonistic effect of
potassium excess on the myocardium.
• Infusion of insulin and glucose or sodium bicarbonate to promote potassium
update into the cells.

56. NURSING MANAGEMENT
• Preventing hyperkalemia
• Correcting hyperkalemia
• Hyperkalemia related to renal dysfunction, shock from
traumatic injuries or burns.
• Potential for dysrhythmias related to hyperkalemia.

57. HYPOCALCEMIA
Hypocalcemia is serum calcium below 8.5mg/dl.
Etiology
 Inadequate dietary calcium intake, Vitamin D deficiency.
 Malabsorption of fat in intestine.
 Metabolic alkalosis. (less ionized calcium)
 Renal failure with hyperphosphatemia, acute pancreatitis.
Burns, Cushing’s disease, hypoparathyroidism.
 Medications – Magnesium Sulphate

58. Clinical Manifestations
a. Neuromuscular-Tetany symptoms: Twitching around
mouth, tingling and numbness of fingers, facial spasm,
convulsion, Trousseau’s sign and chvostek’s sign
b. Respiratory-Dyspnea, laryngeal spasm.
c. Gastrointestinal -increased peristalsis, diarrhea,
d. Cardiovascular- dysrhythmias, palpitations
e. Hematologic-prolonged bleeding time.

59. Chvostek’s sign and Trousseau’s sign

60. Medical Management
 Determining and correcting the cause of hypocalcemia.
 Asymptomatic hypocalcemia is usually corrected with oral calcium gluconate
calcium lactate or calcium chloride.
 Administer calcium supplements 30 minutes before meals for better
absorption and with glass of milk because of vitamin D is necessary
absorption of calcium from the intestine.
 Intravenous calcium chloride or calcium gluconate (10%) is given slowly to
avoid hypertension, bradycardia & other arrhythmias.

61.  Dietary Management
 Chronic or mild hypocalcemia can be treated in part by having the client
consume a diet high in calcium: Eg :cheese ,milk, Spinach
 If hypocalcemia is secondary to parathyroid deficiency the client must
avoid high phosphate foods(Eg: milk products, Carbonate beverages)
 Nursing Management
 Hypocalcemia related to diarrhea, pancreatitis, renal failure or decrease
intake.
 Risk of injury related to increased neuromuscular irritability resulting
from hypocalcemia
 Altered health maintenance related to knowledge deficits regarding foods
high in calcium

62. HYPERCALCEMIA
Hypercalcemia is a serum calcium level over 5.5 meq/ L or 11mg/L
Etiology
• Metastatic malignancy-lung, breast, ovarian, prostatic, bladder,
kidney, Leukemia.
• Hyperparathyroidism.
• Thiazide diuretic therapy.
• Prolong immobilization.
• Excessive intake of calcium supplements and vitamins.

63. Clinical Manifestations
• Gastrointestinal- Anorexia, vomiting, constipation, decreased
peristalsis.
• Neuromuscular- Mild to moderate hypercalcemia – weakness, fatigue,
depression, difficulty to concentrate. Severe hypercalcemic state-
extreme lethargy confusion and coma.
• Cardiovascular-Dysrhythmias, heart block.
• Electro-cardiographic changes -shortened ST segment and lengthened
QT interval.
• Renal-Polyuria, kidney stones, renal failure.
• Musculoskeletal- Bone pain, fracture.

64. Laboratory findings
Serum Calcium > 5.5 meq/L (>11.5 mg/dl).
Arterial blood gasses- PH<7.45 HCO3> 26 meq/L

65. Medial Management
• Treatment consists of correcting the underlying cause.
• Intravenous normal saline (0.9% nacl) given rapidly with furosemide to prevent fluid
overload, promote urinary calcium excretion
• Calcitonin decreases serum calcium level by inhibiting the effects of (Parathyroid
Hormone) PTH on the osteoclasts and increasing urinary calcium excretion.
• Corticosteroid drugs decreases calcium levels by competing with vitamin D thus resulting
in decreased intestinal absorption of calcium.
• If the cause is excessive use of calcium or Vitamin D supplements or calcium containing
antacids these agents should be either avoided or used in reduced dosage.
• A newer form of drug therapy is etidronate disodium. This drug reduces serum calcium by
reducing normal and abnormal reabsorption of calcium and secondarily by reducing bone
formation

66. Dietary management
• Forcing fluids will assist in adequately hydrating the client and
flushing excess calcium through the kidney
Nursing Diagnosis
• Hypercalcemia related to metastatic lesion hyper parathyrodism,
thiazide therapy or increased intake of calcium.
• Altered health maintenance related to excessive ingestion of calcium
supplements and calcium antacids.
• Risk for injury related to potential pathologic fractures, Mental
confusion and immobility

67. HYPOMAGNESEMIA
It refers to a below normal serum magnesium concentration (<
1.3meq/ L or < 1.8mg/dl)
Etiology
• Loss of Mg from GI tract -nasogastric suction, diarrhea or fistula.
• Inflammatory Bowel Disease or intestinal re section.
• Alcoholism.
• Deficit Mg content in parenteral feeding formula.
• Medication -amino glycoside, Cyclosporine, diuretics, digitalis
• Diabetic ketoacidosis, sepsis, burns hypothermia

68. Clinical Manifestation
• Initial manifestation includes lethargy, drowsiness, nausea &
vomiting
• As serum Mg level decrease deep tendon reflects are lost and
respiratory and ultimately cardiac arrest can occur ‘
• Muscle weakness , tremor, athetoid movements (slow, involuntary
twisting and writhing)
• Tetany , generalized tonic- clonic or focal seizures , laryngeal
stridor and positive chvostek’s and trousseaus singed
• Alteration mood- apathy, depression, apprehension, ataxia,
insomnia, confusion, dizziness

69. Assessments and Diagnostic finding
• Serum Mg level <1.3 mEq/L
• ECG -prolonged PR and QT intervals , widened QRS, ST segment
depression, Flattened T wave & prominent U Wave.
• Urine Mg
• Nuclear magnetic resonance and ion selective electrode- newer
diagnostic technique for measuring ionized serum Mg level.

70. Medical Management
Diet management
•green leafy vegetables, nuts, seeds, legumes, whole
grains, sea food, pea nut butter, cocoa
Pharmacological Management
•IV Mg Sulphate , Calcium gluconates
•Mg Gluconate or oxides.

71. Nursing Management
•Assess for dysphagia
•Observe for science and symptoms of hypomagnesemia
•Vital sense must be assessed frequently during Mg
administration to detect to changes in cardiac rate,
rhythm, Hypo tension and respiratory distress. Monitor
Urine output before during and after Mg administration.
•Educate about Mg rich diet.
•Alcohol abstinence program.

72. HYPERMAGNESEMIA
A serum Mg level is elevated to more than 2.3 mEq/L or 3 mg/day
Etiology
 Renal failure
 Pregnant woman who receive MGSO4 for eclampsia
 Diabetic keto acidosis
 Adreno cortical insufficiency, Addison’s disease or hypothermia
 Excessive use of antacids, laxatives
 Lithium intoxication.

73. Clinical manifestation
 Acute elevation of Mg depresses CNS as well as peripheral Neuro
muscular junction
 Nausea, vomiting, weakness, soft tissue calcification , facial
flushing and sensation of warmth
 Hyporeflexia, hypotension, respiratory depression7.
 At higher Mg concentration, lethargic, dysarthria and drowsiness
 Deep tendon reflexes are lost and muscle weakness and paralysis
may develop
 The respiratory center is depressed when Mg level exceeds 10
mEq/L
 Coma , AV heart block , cardiac arrest .

74. Assessments and diagnostic finding
 Serum Mg level , creatine level , K+ and Ca++
 ECG-prolonged PR interval , tall T wave, Widened
QRS and prolonged QT interval, AV block

75. Medical management
 All parenteral and oral Mg salts are discontinued.
 In emergencies such as respiratory depression or cardiac defective
conduction, ventilatory support and IV Ca Gluconate are indicated
 Hemodialysis with Mg free dialysate
 Administration of loop diuretics and NaCl and RL IV enhances
Mg excretion with adequate Renal function.
 IV Ca Gluconate antagonizes the cardiovascular and neuro
muscular effects of Mg

76. Nursing Management
 Monitor vital signs , hypotension and shallow
respiration
 Observe decreased patellar reflexes and changes in
level of consciousness
 Caution is essential when preparing and
administering Mg containing fluids parentraly

77. HYPOPHOSPHATEMIA
It refers to a below normal serum PO4
3- concentration less than
2.5 mg/dl.
Etiology
◦Malabsorption syndrome
◦Glucose administration
◦Parenteral nutrition
◦Alcoholic withdrawal
◦PO4
3- binding antacids
◦Respiratory alkalosis

78. Clinical manifestation
◦CNS dysfunction (irritability , weakness, numbness ,
paresthesia , seizure, confusion, coma)
◦Muscle weakness including respiratory muscle weakness and
difficulty weaning from ventilator
◦Renal tubular wasting of Mg , Ca, HCO3-
◦Cardiac problems (dysrhythmia, decrease stroke volume)
◦Osteomalacia
◦Rhabdomyolosis

79. Assessment and Diagnostic Finding
◦Serum PO4
3- level
◦X-ray show skeletal changes of Osteomalacia

80. Management
Medical Management
◦IV PO4
3- correction – Sodium or PO4
3- phosphate
◦Oral Phosphorous replacement (Nutra- phos)
◦Phosphorous rich diet (dairy products)
Nursing Management
◦Monitor serum phosphorous level
◦Educate about phosphorous rich diet

81. Serum phosphorous level that exceeds normal
value
Etiology
Renal Failure
Chemotherapeutic agents
Phosphorous containing enema
 large vitamin D intake,
hypoparathyrodism
excessive ingestion (milk, laxatives contacting
phosphate )

82. Hypocalcemia
Muscle problem- tetany
Depositing of calcium phosphate in skin soft tissue
, cornea , viscera , blood vessels
Anorexia , Nausea , vomiting , bone and joint pain ,
muscle weakness , hyperreflexia and tachycardia

83. Serum phosphate , Calcium
X-ray -skeletal changes with abnormal bone
development
Parathyroid hormone level- hypoparathyroidism
BUN and Creatine- assess renal function.
Renal USG-Renal Failure
Bone studies and coronary calcification

84.  Treating underlying disorder
 IV administration of Calcium binding antacids, phosphate binding gels or
antacids, Loop diuretics
 Dialysis
 Restrict dietary phosphate
 Surgery-removal of large calcium phosphorous deposits

85. Avoid Phosphorus rich food such as hard cheese ,
cream , nuts , meats , whole grain cereals , dried
fruits, dried vegetable, kidney, sardine, sweet
bread and dairy products
Monitor for changes in urine output and signs of
hypocalcemia

86. HYPOCHLOREMIA
It refers to below normal serum chlorine level
Etiology
• GI tubed drainage severe vomiting and diarrhea
• Low sodium intake, Chlorine deficient formula, metabolic
alkalosis, diuretic therapy, burns, fever , prolonged therapy
with IV dextrose
• Administration of aldosterone , Corticosteroid , laxatives .

87. CLINICAL MANIFESTATION
• Signs and symptoms of hyponatremia (seizure,
coma), hypokalemia (cardiac dysrhythmia) and
metabolic alkalosis(high pH, high serum
bicarbonate )
• Hyper excitability of muscle, tetany, hyper active
deep tendon reflexes weakness, twitching and
muscle cramps

88. ASSESSMENTS AND DIAGNOSIS FINDING
• Serum chloride, sodium and potassium level
• ABG analysis
• Urine chloride level

89. MEDICAL MANAGEMENT
• Normal saline (0.9% or 0.45 % NaCl)
• Discontinue diuretic (loop, osmotic, thiazide) therapy
• High chloride rich foods (tomato juice, banana ,dates ,
eggs, cheese , milk, salty broth,canned vegetables and
processed meat )
• Avoid Free water(water without electrolytes ) or bottled
water
• Ammonium chloride and acidifying agent for metabolic
alkalosis

90. NURSING MANAGEMENT
• Monitor intake output chart, ABG value, Serum
Electrolyte value, Level of consciousness, Muscle
Strength and movement
• Vital signs and respiratory assessments are
monitored
• Educate about high chloride diet

91. HYPERCHLOREMIA
It refers to serum level of chloride exceeds 107 meq/L
Etiology
•Head trauma, increased perspiration, excess
adrenocortical hormone production, decreased GFR
•Loss of bicarbonate via kidney or GI tract with a
corresponding increase in Chloride ion

92. Clinical Manifestation
•Metabolic acidosis, hypervolemia and hypernatremia
•Tachypnea, weakness, lethargy , deep rapid respiration ,
Hypertension
Assessment and Diagnosis Finding
•Serum chloride level ,sodium ,bicarbonate and pH level
•Urine chloride level

93. MEDICAL MANAGEMENT
• Treating underlying cause of hyperchloremia and restoring
electrolyte , fluid and acid based balanced.
• Hypertonic IV solution to restore balance
• Diuretics
• Restrict sodium, chloride and fluids
• RL solution to convert lactate to bicarbonate level to correct
acidosis
• IV sodium bicarbonate

94. NURSING MANAGEMENT
• Monitor vital signs , ABG & I&O
• Assessment of respiratory neurologic & cardiac systems
• Educate to restrict chlorine containing foods
• Maintain adequate hydration

95. z
JOURNAL ABSTRACT
Hypokalemia from beta2-receptor stimulation by circulating epinephrine
To determine whether epinephrine-induced hypokalemia is due to beta2-
adrenoceptor stimulation, and whether hypokalemia can occur at physiologic
concentrations of the agonist, epinephrine was infused into six normal volunteers at
a rate of 0.1 microgram per kilogram of body weight per minute. This hypothesis
was tested in six subjects given infusions of epinephrine (0.05 micrograms per
kilogram per minute) after administration of either 2.5 or 5 mg of ICI 118551--a
selective beta2-receptor antagonist--or placebo. After placebo, epinephrine infusion
elevated the circulating epinephrine concentration and reduced plasma potassium;
hypokalemia was prevented by the beta2-antagonist. This drug only partially
inhibited the rises in plasma renin and glucose and the shortening of systolic time
intervals; there was no tachycardia. Fifteen-fold to 30-fold increases in circulating
epinephrine concentration appear to cause hypokalemia by a specific beta2-receptor
effect distinct from other actions of epinephrine. This phenomenon may be of
physiologic importance after severe myocardial infarction, when similar increases
in plasma epinephrine have occurred.

96. Effects of
gender and
hypovolemia
on
sympathetic
neural
responses to
orthostatic
stress
• The hypothesis that women have blunted
sympathetic neural responses to orthostatic stress
compared with men, which may be elicited under
hypovolemic conditions. Muscle sympathetic nerve
activity (MSNA) and hemodynamics were measured
in eight healthy young women and seven men under
normovolemic and hypovolemic conditions
(randomly), with approximately 4-wk interval.
Orthostatic tolerance was lower in women,
especially under hypovolemic conditions. The lower
orthostatic tolerance in women is predominantly
because of a smaller stroke volume, presumably due
to less cardiac filling during orthostasis, especially
under hypovolemic conditions

97. ASSIGNMENT
Write an assignment of
care of patients with
electrolyte imbalance
with a nursing process
approach.