Fluid and electrolyte imbalnce

1. FLUID AND ELECTROLYTE
IMBALNCE .

2. INTRODUCTION
 Fluid & electrolyte balance is a dynamic
process i.e. crucial for life, as fluid &
electrolyte help to maintain health & function
in all body system. Water is found everywhere
on earth including human body
 In an adult 60% of the weight is water
 Two third of the body’s water is found in the
cell

3. FUNCTION OF WATER

4. DISTRIBUTION OF BODY FLUID
 The body fluid is distributed into two
compartment
 1) Intracellular fluid
 2) Extra cellular fluid

5. 1)INTRACELLULAR FLUID
 It is found within the cells of
the body.
 It constitute of approximately
2/3 of the total body fluid in
adult i.e approx. 40% of body
weight.
 It is vital to normal cell
functioning.
 It contains solute such as O2,
electrolyte, &glucose.
 It provides a medium in
which metabolic process of the
cell take place.

6. EXTRACELLULAR FLUID
 It is found out side the cell & account for about
1/3 of total body fluid.
 It is transport system that carries nutrients &
waste products from the cell .
It is subdivided into three compartments
 1) Interstitial fluid
 2) Intravascular fluid
 3) Tran cellular fluid

7.  1) INTERSTITIAL FLUID:-
- It contains lymph is a fluid between cells
& outside the blood vessels.
- Accounting for approximately 75% of
ECF surrounds the cells.
 2) INTRAVASCULAR FLUID
- It accounts for approximately 20% of ECF
& found within the vascular system.
- It is blood plasma.
 3) TRANSCELLULAR FLUID
- It includes cerebrospinal fluid,
pericardial, pancreatic, pleural,
intraocular, biliary, peritoneal &
synovial fluid.

8. COMPOSITIONS OF BODY FLUID
 The fluid circulating throughout the body in
extra cellular & intracellular fluid spaces
contain:-
 Electrolyte
 Mineral
 Cells.

9. DEFINITION OF ELECROLYTE
 An ELECTROLYTE is an element or compound that when
melted or dissolved in water or another solvent, dissociate
into ions and carry electrical current.
 There are positively charged ions & negatively charged ions.
 Positively charged ions
 Sodium ( Na+)
 Potassium ( K+ )
 Calcium (Ca+)
 Negatively charged ions:-
 Chloride ( Cl-)
 Bicarbonate ( HCo3-)
 Sulfate ( So2-)
 Phosphate ( HPo4-)

10. MOVEMENT OF FLUID.
 The method by which electrolyte & other solutes
move are as follows.
 1) Osmosis
 2) Diffusion
 3) Filtration
 4) Active transport

11. 1) OSMOSIS
 It is the
movement of
water across cell
membrane from
low concentrated
solution to more
Concentrated
solution.

12. 2) DIFFUSION
 It is continual
intermingling of
molecule in liquid ,
gases or solid
brought about by
random movement of
molecule .
 Eg. Two gases
become mixed by the
constant motion of
their molecule

13. 3) FILTRATION
 It is process where
by fluid & solutes
move together
across a membrane
from one
compartment to
another
compartment. The
movement is from
area of higher
pressure to one of
lower area.

14. 4) ACTIVE TRANSPORT
 Substance can move across cell membrane from
less concentrated solution to more concentrated
one by active transport.

15. REGULATION OF FLUID
 The body fluid is regulated by:-
1) Fluid Intake
2) Fluid Output
 1) Fluid intake:-
The adult drinks about 1500 ml of fluid in a
day but need 2500ml/day.
This remaining 1000 ml added from food &
Oxidation of food from metabolic process i.e.
750 ml &200 ml respectively

16. REGULATION OF WATER INTAKE
 The hypothalamic thirst center is
stimulated:
 By a decline in plasma volume of 10%–15%
 By increases in plasma osmolality of 1–2%
 Via baroreceptor ,osmoreceptors and other stimuli.
 Feedback signals that inhibit the thirst centers
include:
 Moistening of the mucosa of the mouth and throat
 Activation of stomach and intestinal stretch receptors

17. REGULATION OF OUTPUT.
 ANTI DIURETIC HORMONE.
 ALDOSTERONE.

19.  2) Fluid output :-
 Fluid losses from body 2500ml .There are
following routes of fluid output
 e.g.- urine, insensible loss through skin,
perspiration & through lungs & feces.

22. REGULATION OF ELECTROLYTES.
 SODIUM.
 CALCIUM.
 POTTASSIUM

23. FACTORS AFFECTING FLUID AND
ELECTROLYTE IMBALANCE.

24. FLIUD IMBALANCES
 The two types of fluid imbalances
that may occur are:
 fluid volume excess(FVE)
 fluid volume deficit(FVD)

25. 1) EXTRACELULLAR FLUID VOLUME DEFICIT
(HYPOVOLEMIA)
 An ECFVD, commonly called as dehydration , is a
decrease in intravascular and interstitial fluids
 An ECFVD can result in cellular fluid loss if it is
sudden or severe .

26. TYPES OF ECFVD
 A) Hyperosmolar fluid volume deficit- water loss
is greater than the electrolyte loss
 B) Isosmolar fluid volume deficit – equal
proportion of fluid and electrolyte loss
 C) Hypotonic fluid volume deficit – electrolyte
loss is greater than fluid loss

27.  In Mild ECFVD, 1to 2 L of water or 2% of the
body weight is lost
 In Moderate ECFVD, 3 to 5L of water loss or
5%weight loss
 IN Severe ECFVD , 5 to 10 L of water loss or 8%
of weight loss

28. ETIOLOGY AND RISK FACTORS
 Lack of fluid intake.
 Excess fluid loss.

29. CLINICAL MANIFESTATION
 Thirst
 Muscle weakness
 Dry mucus membrane; dry cracked lips or furrowed
tongue
 Eyeballs soft and sunken (severe deficit)
 Apprehension , restlessness, headache , confusion,
coma in severe deficit
 Poor skin turgor.
 Fatigue.
 Elevated temperature
 Tachycardia, weak thready pulse

30.  Peripheral vein filling> 5 seconds
 Postural systolic BP falls >25mm Hg and
diastolic fall > 20 mm Hg , with pulse
increases > 30
 Narrowed pulse pressure, decreased
CVP&PCWP
 Flattened neck veins in supine position
 Weight loss
 Oliguria(< 30 ml per hour)

31. LABORATORY FINDINGS
 Increased osmolality(> 295 m Osm/ kg)
 Increased or normal serum sodium level (> 145mEq/ L
)
 Increase BUN (>25 mg / L )
 Hyperglycemia ( >120 mg /dl )
 Elevated hematocrit (> 55%)
 Increased specific gravity ( > 1.030)

32. MANAGEMENT
 Mild fluid volume loss can be corrected with oral
fluid replacement
 -if tolerates solid foods -1200 ml to 1500ml of oral
fluids
 -if takes only fluids, increase the total intake to 2500
ml in 24 hours
 Management of Hyperosmolar fluid volume
deficit
 Hypotonic IV solution, such as D5% in 0.2 %saline
 If the deficit has existed for more than 24 hours, avoid
rapid correction of fluid [sodium solution to be infused
at the rate of 0.5 to 0.1m Eq/ L/ hr]

33.  If hemorrhage is the cause -Packed red cells
followed by hypotonic IV fluids is administered
 In situations where the blood loss is less than 1 L
normal saline or ringer lactate may be used

34. 2) EXTRACELLULAR FLUID VOLUME
EXCESS
 ECFVE is increased fluid retention in the intravasular and
interstitial spaces

ETIOLOGY AND RISK FACTORS
 Heart failure
 Renal disorders
 Cirrhosis of liver
 Increased ingestion of high sodium foods
 Excessive amount of IV fluids containing sodium
 Electrolyte free IV fluids
 SIADH,Sepsis
 decreased colloid osmotic pressure
 lymphatic and venous obstruction
 Cushing’s syndrome & glucocorticoids

35.  CLINICAL MANIFESTATION
 Constant irritating cough
 Dyspnea & crackles in lungs
 Cyanosis, pleural fffusion
 Neck vein obstruction
 Bounding pulse &elevated BP
 S3 gallop
 Pitting & sacral edema
 Weight gain
 Increased CVP& PCWP
 Change in level of consiousness

36.  LAB INVESTIGATION
 serum osmolality <275mOsm/ kg
 Low , normal or high sodium
 Decreased hematocrit [ < 45%]
 Specific gravity below 1.010
 Decreased BUN [< 8mg/ dl]
 MANAGEMENT
 Diuretics [combination of potassium sparing
and potassium depleting diuretics]
 In people with CHF, ACE inhibitors and low
dose of beta blockers are used
 A low sodium diet

37. 
ELECTROLYTE
IMBALANCES.

38. ELECTROLYTE IMBALANCE
 1) HYPONATREMIA (SODIUM DEFICIT):-
 It means a plasma sodium level is less than 135 mEq/lit
 It is one of the most common electrolyte disorder in adult.
 It is usually associated with changes in fluid volume status.
 Type of Hyponatremia
 1)Hypovolemic hyponatremia:-
In this sodium loss is greater than water loss.
 2)Euvolemic hypoatremia:-
 When total body water is moderately increased & the total
 body sodium at normal level.
 3)Hyervolemic hyponatremia:-
 Greater increased in total body water in total ody sodium.
 4) Redistributed hyponatremia:-
 No changes in total body water or sodium, water
merely shifted between the Intracellular & extra cellular compartment
relatively to the sodium concentration

39.  ETIOLOGY:-
 Hypovolemic hyponatremia:-
 Renal loss of sodium from diuretic use
 Diabetic glycosuria
 Aldostreron deficiency Intrinsic
 Vomiting
 Diarrhea
 Increased sweating
 Iliostomy
 Euvolemic hyponatremia:-
 Increase secretion of ADH Pain ,Emotion ,Medication ,Some cancer ,CNS
disorder
 Hypervolemic hyponatremia:-
 Edematous disorder such as
 Congestive heart failure
 Cirrhosis of liver
 Nephrotic syndrome
 Acute & chronic renal failure
 Redistributive Hyponatremia:-
 Hyperglycemia
 Hyperlipidemia

40.  OTHER CAUSES:-
 - Prolonged diuretic therapy
 - Excessive diaphoresis
- Insufficient Na intake
 - GI losses – suctioning, laxatives, vomiting
 - Administration of hypotonic fluids
 - Compulsive water drinking
 - Labor induction with oxytocin
- Cystic fibrosis
 - alcoholism

41. CLINICAL MANIFESTATIONS
Clinical manifestation of hyponatremia vary with cause type & rate
of onset of sodium or fluid imbalance.
CNS:-
 Confusion
 Lethargy
 Hallucination
 Seizures
 Muscles twitching/cramping
 Focal weakness
 Hemi paresis
 Papiledema
 Behavioral changes
 Convulsion
 Faintness
 Brain herniation
 Coma
 Death
 Headache

42.  CVS:
 Decrease systolic & Diastolic BP
 Orthostatic hypotension
 Weak & thready pulse
 Tachycardia
RS:-
 Crackles in lung.
 Tachypnea
 Dyspnea
 Orthopnea
 Cheyne stoke respiration
 Apneustic breathing
Ataxic breathing
GI:-
 Nausea
 Vomiting
 Hyper active bowel sound
 Abdominal cramping
 Diarrhea
Other:-
 Dryness of skin, tongue, & mucous membrane

43.  MANAGEMENT OF HYPONATREMIA.
- Monitor for - Restrict fluids
- Monitor Vital sign
- Monitor serum Na levels
- Oral intake of sodium
- IV normal saline or Lactated Ringers
- If Na is below 115, mEq/L hypertonic saline is ordered
- May give a diuretic eg- Furosemide to prevent pulmonary
fluid overload or increasing H2O loss
- Encourage a balanced diet
- I/O monitoring
- Safety for weakness or confusion
- Assist with ambulation if low B/P

44. 2) Hypernatremia:-_
 Plasma sodium level is
greater than 145mEq/ lit
 It occurs with excess
loss of H2O or excessive retention of Na
 Can lead to death if not treated

45.  Type of Hypernatremia
 1) Hypovolemic hypernatremia:-
In it total body water(TBW) is greatly
decreased relatively to sodium (loss of
hypotonic fluid)
2) Euvolemic hypernatremia:-
 In it TBW is decreased relative to the normal
total body sodi
 3) Hypervolemic hypernatremia:-
 In it TBW is increased but the Na+ gains
exceed the water gain.

46.  Etiology:-
 1) Hypovolemic hypernatremia:-
Renal loss
Osmotic diauresis
Sev.hyperglycemia
Profuse diaphoresis
Decrease thirst
Diarrhea
Inadequate fluid volume replacement
Inadequete water intake
Excessive water loss due to fever, vomiting, excess
drainage, polyurea
Burn

47.  2) Evolumic hypernatremia:-
Excess fluid loss from skin& lungs
Hypodipsia in older adult & infant
Diabetic incipidus
 3) Hypervolemic hypernatremia:-
Administration of concentrated saline solution
Hypertonic feeding (tube feeding)
Accidental or intentional salt ingestion
Commercially prepared soup
Retention of sodium occur in heart ,renal, or liver
disease, Cushing syndrome,hyperaldesterone
Corticosteroid therapy
 Inadequate ADH

48.  SIGN & SYMPTOMS
 CNS:-
Restlessness
Agitation
Irritability
Muscles weakness
Confusion
Seizures
Coma
Muscles twitching
Tremors
Hyperflexia
Hyperactive deep tendon reflexes

49.  CVS:-
 Orthostatic hypotension in hypovolemic hypernatremia
 In hypervolemic hypernatremia
 Increase BP
 Jugular venous distention
 Prolong peripheral vein emptying
 S3 gallop sound
 Edema
 Weight gain
 Tachycardia
 RS:-
- Crackles
- Plural effusion
GI:-
 Anorexia
 Nausea
 Vomiting
 Thirst increase

50.  Renal:-
 Low UOP or Oliguria in hypovolemic hypernatremia
 Kidney excreta some of excess water in hypervolemic
hypernatremia
 Other:-
 Dry & flushed skin
 Mucous membrane become dry & sticky
 Tongue furrows

51.  Managment -
 Hypo-osmolar electrolyte solution -(o.2% or 0.4% NaCl)
- D5W & furosemide – in hypernatremia
 Encourage H2O consumption
 Low Na diet.
 Monitor fluid intake on patients with heart or renal disease.
 Monitor serum Na levels
 Assess respiratory for crackles
 Weigh daily
 Assess skin and mucus membranes
 Assist with oral hygiene
 Check neurological status.
 Safety precautions

52. POTASSIUM DISORDERS
 1) Hypokalemia:- Serum potassium level is less
than 3.5 mEq/lit
 A serum K+ level below 2.5 or above 7.0 can cause
cardiac arrest

53.  Causes
 Prolonged diuretic therapy
 Inadequate intake
 Restricted K+ diet
 Weight reduction diet
 Use of osmosis diuretics.
 Potassium wasting diuretics e.g.- Thiazide loop, & osmotic
diuretics, steroid, amino glycosides, amphotericine B , digital
preparation, Beta adrenergic drug, Cisplastin & bicarbonate
 Increase level of Na+ intake promotes K+ loss
 Alkalosis
 Healing phase of sev. Injury or burn – as a result of the
shifting of K+ into the cell.

54. Diuretic phase of renal failure
Hyperaldosteronism.
Severe diaphoresis
Nesogastric suctioning
 laxative use
 Vomiting
Intestinal fistula or iliostemy
Diarrhea.
Excess stress
Acute alcoholism

55. SIGNS AND SYMPTOMS

GI:-
 - Anorexia
 Abdominal distention
 Constipation
 Musculoskeletal:-
 Muscles weakness may
progress paralysis
 Leg cramps
 Parasthesia
 Hyperreflexia
CNS:-
 increase conduction of
nerve impulses
 Fatigue
 Convulsion
 Areflexia
 Coma
 Drowsiness
 Lethargy
 Confusion
 Depression
 Dysphasia

56.  CVS:-
 Decreased myocardial contraction leads Hypotension
 Slow , weakened pulse
 Cardiac dysrhythmias
 Ventricular fibrillation & cardiac arrest due to less K+ level i.e
2.5mEq/li
RS:-
- Shallow respiration
- Shortness of breath
- Apnea
Renal:- Inhibit the ability of kidney to concentrate
urine which leads to:-
 Polyuria
 Nocturia
 Decrease plasma osmolality
 Extreme smooth muscles slowing leads to urinary retention

57.  Treatment & Managment
 To restore potassium level:-
 Administer high K+ food
 - IV or PO replacement.
 Give K+ IV diluted in a large vein.
 Never push K+ as a bolus .
 Monitor site for infiltration
 Monitor patients at risk
 Monitor I/O
 Monitor EKG
 Monitor Serum K+
 Watch urine out put

58.  Watch patients who take Digitalis for toxicity because low
K+ level increases sensitivity of myocardium to digitalis
induce dysrhythmia.
 Monitor for nausea, vomiting, anorexia, diarrhea,
headache, weakness, blurring vision & change in cardiac
rate in pt receiving digitalis.
 Teach family and patient dietary changes

59.  2) Hyperkalemia
 K+ level is greater than 5.0mEq/lit
 Results form impaired renal function
 Metabolic acidosis
 Acts as myocardial depressant; decreased heart rate,
cardiac output
 Muscle weakness
 GI hyperactivity

60.  Etiology
 Increased dietary intake
 Excessive administration of K+
 Excessive use of salt substitutes
 Excessive release of K+ from the cell during 1st 24-27 hrs
after traumatic injury , cell damage, burns, trauma,
acodosis
 Administration of larger quantities of blood that is old
 Hyponatremia
 Renal failure

61.  Signs and Symptoms:-
 - Tachycardia
- Intestinal colic
 Mild to moderate hyperkalemia(K+ near by 6mEq/l) cause
nerve & Muscles irritability resulting in
paresthesia,numbness, tingling
- Diarrhea
- K+ 7MEq/l – Na+ channels become inactivated
&
Cause disturbances in nerve & muscles function
 - Impaired cardiac conduction
 - Ventricular contraction
- Hypotension
 - Cardiac arrest

62.  - Convulsion
- Neuromuscular weakness progressing to
flaccid paralysis & Respiratory muscles
paralysis may develop.
-Apathy
-Confusion
-Numbness/paresthesia ofextremities
-Abdominal cramps
-Nausea
-Oliguria & anuria

63.  Medical mg & Nursing managment:-
 I/V saline to improve urine output
 Calcium gluconate IV - to decrease the antagonistic effect of
K+ excess on myocardium
 Infusion of insulin & glucose or sodabicarb to promote K+
uptake into the cell
 Beta-agonist albuterol (0.5mg iv) – it decrease K+ level within
30 min. lasting for 6 hrs.
 Administer Kayexolate or sodium polystyrene sulfonate
(oral and rectal) – due to that K+ ion is exchanged for Na+
ion in the intestinal tract & K+ ion is excreted in the stool.
 Dialysis .

64.  Cardiac monitoring
 Monitor pulse, rate and rhythm, and B/P
 Lung sound
 Vital sing / apical pulse
 Urine output 1 hrly
 Watch for peripheral edema every 4-8 hr
 Assess for hyperactive bowel sounds
 Assess sensory and motor function
 Monitor neurological status
 ECG monitor

65. CALCIUM DISORDER
 1) Hypocalcaemia :-
 Ca++ level less than 8.5 mg/dL
 Common in older adult because of inadequate intake

66. ETIOLOGY
 Decrease intake for several days
 Dieting or weight reduction
 Open wound increase loss of Ca++
 Renal failure,
 Inadequate vitamin D consumption.
 Excess Na+ e.g. in Cushing syndrome – promotes the
excretion of Ca+.
 Client receiving multiple transfusion of store blood are
at risk of binding of the preservatives citrate with the
Ca++
 Hyperparathyroidism

67. Vitamin D deficiency
Inadequate exposure to ultraviolet light
Acute pancreatitis
hyperphosphatemia
Medications like
1) Magnesium sulphate, Colchicin, & Neomycin
inhibit PTH secretion
2) Aspirin, Anticonvulsant & Estrogen after Vit D
metabolism
3) Phosphate preparation impairs reabsorption of
Ca++
4) Steroid increases Ca++ mobilization
 5) Antacids & laxatives decreases Ca++
absorption from the intestine

68.  Signs and Symptoms
 Muscle cramps
 Hyperactive deep tendon reflexes
 Hyper excitability
 Numbness & tingling of fingers, toes, lips and face
 Emotional labiality (e.g. irritability & anxiety)
 Tetany
 Positive Trousseau’s sign/Chvostek’s sign
 Laryngeal spasms
 Confusion
 Memory loss
 Cardiac insufficiency
 Cardiac dysrhythmias
 Hypotension
 Dysrhythmias
 Prolong QT interval
 Trousseau’s & Chvostek’s sign

69. Prolong bleeding time
These abnormalities progress to seizures, laryngeal
stridor, tetany, hemorrhage, cardiac collapse &
eventual death
Cataract – with prolong hypocalemia because of
increase uptake of Na+ & water by lens.
Dry, spare hair & rough skin
Spontaneous fracture can occur when the bone is
depleted of calcium.
Can cause skeletal and neuromuscular
abnormalities
Impairs clotting mechanisms
Affects membrane permeability
Diagnostic findings
Serum Ca++ levels decrease
 - Prolonged PT and PTT

70.  Medical & Nursing managmet:-
 1) Restore calcium balance:
 Asymptomatic hypocalemia is usually corrected with oral
calcium gluconate, calcium lactate or calcium chloride
 For increased calcium absorption it should be given with milk
& meal
 Vit D in the milk promotes calcium absorption
 Treat the cause.
 Seizure precautions
 Administer IV Ca++ slowly; watch for infiltration
 Keep calcium gluconate at bedside
 Assess nutritional intake of Ca++

71.  2) Hypercalcemia
 Increased serum levels of Ca++ greater than 10.5 mg/dl.
 Cause
Hyperthyroidism
 Excessive intake of Ca++ supplement withVit D or calcium
containing antacids
 Excessive use of antacids with phosphate-binding
 Prolonged immobility – reabsorption of calcium in bone
 Metabolic acidosis – it promote hypercalcemia by two
mechanisms.
 Excessive vitamin D intake
 Thiazide diuretics therapy
 Renal failure.

72.  Cancer – most common cause of hypercalcemia are
malignancies
 Thyrotoxicosis
 metastatic cancer are especially at risk
 Signs and Symptoms
 Anorexia
 Nausea
 Vomiting
 Polyuria it leads to dehydration & thirst & further exacerbates
the constipation
 Muscle weakness
 Fatigue
 Dehydration.
 Confusion
 impaired memory.

73.  Weakness
 Depression
 Difficulty in concentration
 Osmotic diuresis
 Ca++ precipitation tends to urethral or kidney stones which
result in urinary blockage & sev. Colicky pain
 Excess Ca++ also impairs glomerular blood flow , which can
lead to renal failure
 Bone pain – often associated with Ca bone & is due to
pressure on nerve ending from the tumor cells
 Pathological # are due to decalcification of bony matrix & can
occur with Ca of bone or any condition that causes
reabsorption of Ca++
 Calcium deposit can also occur on the skin
 Progressive neurological depression from increase in
hypercalcemia & is manifested by
 Lethargy

74. Depressed sensorium
Confusion
Coma
Sev hypercalcemia may result in hypercacemia
crisis, Ca++ reach 7.1 mEq/lit or 15 mg/dl
The resultant increased conduction transmission,
shortened repolarization(shorten QT interval widen
T waves
Sev. Cardiac depression can cause cardiac
dysrhythmias, ECG changes & cardiac arrest
 Personality changes
Calcifications in the skin and cornea

75.  Diagnostic Findings
 Serum Ca++ > 10.5 mg/dl
 ECG changes
 Medical &Nursing Managment:-
 I/V NS given rapidly with furosimide.
 Antitumour antibiotics – that inhibit the action of PTH on
osteoclasts in bone tissue which reduce decalcification & the
plasma calcium level
 Calcitonin - decrease Ca++ level by inhibiting the effect of
PTH on osteoclast & increases urinary calcium excretion
 Corticosteroid drug decrease the Ca++ level by competing Vit
D, resulting in decreased the intestinal absorption of Ca++ &
by inhibiting prostaglandins , resulting in decreased bone
reabsorption
 Restrict calcium food

76. PHOSPHATE DISORDERS;
(2.5-4.5MG/DL)
 1) HYPOPHOSPETEMIA:-
 Phosphorus level is less than 2.5 mg/dl.
 It can occur from loss of phosphate ions in the urine
or intestine from decreased absorption from the
intestine or from intracellular shift of phosphate ions.

77.  Etiology:-
Low intake of phosphorous containing foods such as
milk, meat, vegetables due to anorexia,
starvation,vomiting, prolong diarrhea
Poor absorption from the GIT
Increase renal excretion of phosphate .
Excessive ingestion of phosphate-binding antacids,
such as magnesium-aluminium
hydroxide(Amphogel,Gelusil, Maaloxetc)

78.  SIGN & SYMPTOMS:
CNS:-
Mental irritability
Apprehension
Malaise
Paresthesias around the mouth
Dysarthria
Confusion
 seizures
Coma.

79.  Treatment:-
 Antacid containing aluminium or magnesium that bind
phosphate should be avoid
 Milk and other dietry suppliments.
 I/V phosphorous as a potassium phosphate or sodium
phosphate

80.  2) HYPERPHOSPHATEMIA:-
Phosphate level greater than 4.5 mg/dl.
 Etiology:-
Excessive intake of high phosphate food
Excess vit D (especially with renal insufficiency)
Impaired colonic motility causing increased
absorption
Hypo parathyroidism.
Menopause
Addisons disease
Renal failure

81.  Sign & symptoms:-
Tachycardia
Palpitation
Restlessness
Anoresia
Nausea
Vomitting
Hyper-reflexia
Tetany
 Treatment:-
Limit high phosphate food especially milk, ice
cream, cheese, large amount of meat & fish &
carbonate beverages or giving calcium aluminium
products that promotes the binding & excretion of
phosphate
Dialysis for renal failure

82. MAGNESIUM DISORDER
 1) Hypomagnesaemia
 Magnesium level is less than 1.5 mEq/l or 1.8 mg/dl.

83. ETIOLOGY:-
 Excess Mg loss from GI – Nasogastric suction ,
diarrhea, vomiting
 Chronic Alcoholism
 Pancreatitis
 Burn
 Chronic malnutrition
 Malabsoption syndrome – crohn’s or celiac disease or
pancreatitis
 High volume iliostomy
 Fistulae
 Laxatives abuse.
 Diuretic therapy with loop or thiazide diuretics, or
ammonium chloride

84. alcoholism
Administration of fluids without Mg
Starvation
Ulcerative colitis
Hypercalcemia. Hypoaldosteronism
High dose steroid use
Insufficient dietary intake
Essential for neuromuscular integration;
hypomagnesaemia increases muscle irritability and
contractility
Causes decreased blood pressure and cardiac
dysrhythmias
Often mistaken for hypokalemia, which can occur
simultaneously
Cancer chemotherapy

85.  Signs and Symptoms
 Anorexia
 Nausea
 Abdominal distention
 Depression Psychosis
 Confusion
 Agitation
 Hallusination
 Convulsion
 Increases reflexes, clonus , a positive babinski sign
 Tachycardia

86. Ataxia
Nystagmus
Tetany with chvostek sign
Muscles fasciculation
Muscles cramps
Paresthesias of feet & legs
Abnormal electrocephalogram.
Vasomotor changes such as painful cold hands &
feet or increased perspiration, & nonspecific T wave
changes in ECG
Dysphagia

87.  Cardiac dysrhythmias
 Tremor
Hyperactive deep tendon reflexes
Positive Chvostek’s and Trousseau’s signs
Memory loss
Emotional liability
Seizures
Diagnostic Findings
Serum Mg level < 1,5 mEq/liter
Hypocalcaemia
Hypokalemia
EKG changes

88. Medical & Nursing
Management.
Inj. Magnesium sulphate IM/IV/orall
Green vegetables
Nuts
Beans
Fruits
legumes

89.  2) Hypermagnesemia
 Mg level greater than 2.5 mEq/lit .
Causes
 Renal failure
 Excessive use of Mg containing antacids
 Untreated diabetic ketoacidosis
 Hypoadrenalism
 Frequent magnesium sulphate enemas used in congenital
megacolon
 Hypocalcemia
 Many potassium sparing diuretics conserve magnesium

90.  Signs and Symptoms
 Lethargy and drowsiness
 Sev. Muscles weakness
 Loss of deep tendon reflexes respiratory paralysis
 Loss of conciousness
 Cardiac sign – wide QRS complex, elevated T wave
 Heart block
 Premature ventricular contraction
 Depress neuromuscular activity
 Depresses respirations
 Sensation of warmth throughout the body
 Hypotension
 BradycardiaCardiac arrest

91. 
Medical Managment
Saline infusion with diuretics increase
the renal elimination of mg
I/V calcium may be given to
antagonize the effect of
hypermagnesemia
Albuterol also used to reduce mg level
In Respiratory distress require
ventilator support
In renal failute hemodialysis.
Avoid constant use of laxatives.

92. CHLORIDE.
 EQUILIBRIUM IN BODY.

93. HYPOCHLOREMIA.
 GI DRAINAGE.
 SALT RESTRICTED DIET.
 SEVERE DIARRHEA.
 VOMITING.

94. CLINICAL FEATURES.
 HYPER EXCITABILITY OF MUSCLES.
 TETANY.
 HYPERACTIVE DTR.
 WEAKNESS
 TWITCHING.
 MUSCLE CRAMPS.

95. MANAGEMENT.
 CORRECT THE CAUSE
 IV NS OF 0.45%.
 DIET.
-TOMATO JUICE.
-SALTY BROTH.
-PROCESSED MEAT.
-FRUITS.

96. HYPERCHLOREMIA.
 MORE THAN 106 Meq/ liter.
Causes
 Increased intake
 Reduced elimination by urine.

97. CLINICAL FEATURES.
 Tachypnoea.
 Weakness.
 Lethargy.
 Deep rapid respirations.
 Reduced cognition.

98. TREATMENT.
 IVF RL.
 IV SODIUM BICARBONATE.
 DIURETIC
 SODIUM AND WATER RESTRICTION.

99. 
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