chapter 24 · 2015-03-12 · medical & nursing managements: •the medical managements is...
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Neonate course kamlah olaimat
lecture 4fluid and electrolyte
implance4\7\2010
Fluid and Electrolyte
manegment• At birth :-
• Term infant -75% water
• Premature infant – great
• ECF – 35%
• ICF – 65%
• ECF – easy to lose fluid
from so the neonate high
risk for dehydration
Water Movement in Fluid Compartments
• Electrolytes play principle role in water
distribution and total water content
Facts about fluid
• At first day 5-10 % lose of body weight that is
water
• Premature neonate increased total body water and
ECF volume which increased lose ( 15% )
• Negative water and sodium palance during 5-10
day ( represent adaptation to extra uterine life , not
to give fluid or Na supplement
Insensible water loss (IWL)
• Water that evaporates in an invisible manner via
skin and respiratory tract
• Newborn ( -1\3 of loss through respiratory tract
• - 2\3 through skin )
• IWL=( fluid intake – urine out put )+weight loss
(150 – 70) + 300=380cc
1gm=1cc
Factors affect insensible water loss in
neonate Factors Effect on IWL
Level of maturity Birth weight and GA
Environmental temperature Increased 30% at rectal temperature above 37,2c
High ambient or inspired humidity Reduced by 30%
Skin break downs( burn) Increased ( extend of lesion)
Congenital skin defect ( large omphalocele)
Increased (size of defect)
Radiant warmer Increased 50%
Phototherapy Increased 20-30%
Plastic heat shield Reduced by 10-30%
Factors affect fluid requirement
1. Infant dependent:-
- Gestational age
- Respiratory distress
- Fever
- Prolonged crying
- Renal condition
2. Environmental influences :-
- Radiant warmer
- Plastic head shields
- Phototherapy
3. Clinical condition:-
Diarrhea and dehydration
Chest tube
Surgical wound drainage
Excessive urinary loss
Important to measure the volume of abnormal fluid loss to replace volume per volume
Clinical management
• 1. day of life 1-3 (stabilization period):-
- A urine output of approximately 1-3 ml\kg\hou
- Urine specific gravity 1.008- 1.012
- Weight loss 5-15%in term and very low birth
weight infant
- Normal serum electrolyte
Calculation of fluid in first 3 day
Weight (gm) Dextrose
(Gm/100ml)
First day fluid
Cc\kg
Second day fluid
Cc\kg
Third day fluid
Cc\kg
<1,000 5-10 100 110 120
1,000 – 1,500 10 90 100 110
1,500-2,00 10 80 90 100
2,000- 2,500 10 70 80 90
> 2,500 10 60 70 80
Assessment of hydration status1. Physical exam:-- Body weight\daily- Skin , fontanelle ,mucous ,edema,- Cardiovascular ,tachycardia ,delayed capillary reffel
,hepatomegally2. laboratory evaluation:-- Serum electrolytes and plasma osmolarity- Urine electrolytes and specific gravity - Urine output decreased with ECF depletion (less than
1ml\kg\hours)but in neonates with immature kidney function , urine output may not decrease despite ECF volume depletion
Other consideration
• If the infant start phototherapy , increase the total fluid
intake by 20cc \kg\day .
• Glucose infusion should be started at a rate of 4-6mg\min
and adjusted to keep plasma glucose level between 50-
120mg\dl .
• Do not infuse a concentration higher than D12.5Win a
peripheral vein .
CONTENUE
• GFR mg\kg\min=fluid rate cc\h*dextrose concentration
• 6*weight kg
Example:-what is the GFR in an infant weighing 1500gm a
total fluid of 120cc\kg\day using the D10Wsolution?
Hourly rate =weight*volume\24
= 1.5*120\24
= 7.5cc\h
GFR=7.5cc\h*10DW\6*1.5
= 8.3MG\KG\MIN
PLAN
• Start an amino acid infusion .5- 1.0gm\kg\day
• Start intravenous lipids ( 20% ) over 20-24 hours
( in I.V line)
• Appropriate intravenous vitamin requirement
• Start enteral feeding 3 day
Day of life 4-6 ( transitional period)
• Infant should be removed from the radiant warmer to an isolate to minimize evaporative losses
• Daily measurement of hydration ( wt, Na , urine output , skin condition )
• Adjust electrolyte intake to correct for urine losses
k= 2-4 mEq\kg\day
Na = 4-8 mEq\kg\day
• advance feeding as protocol
• If infant not start feeding as follow:-
- glucose : 1-2 mg\kg\min.maximum12-15mg\kg\min
-amino acids:0.5 gm\kg\day. maximum 3-3.5mg\kg\min
- lipid : 0.5 gm\kg\day maximum 3-3.5mg\kg\min
Day of life > 7 (nutritional period)
• If the infant is on parenteral nutrition, the goal is to provide:
- Total fluid : 120-150cc\kg\day
- Total calories: 90-100 kcal\kg\day
• If infant is on enteral feeding:-
- total fluid :150cc\kg\day
- Total calories:120cc\kcal\kg\day
- Daily weight gain:20-30 gm
- Maximum volume increase : 10- 20 cc\kg\day
- When advancing enteral feeding , the rate of parenteral nutrition is reduced gradually
Continue
• Total caloric intake can be calculated as follow:
- Each gram of glucose = 3.4 kcal
- Each gram of protein = 4 kcal
- Each gram of lipid = 9 kcal
Miss.kamlah ahmed17
Electrolyte Imbalance
Electrolyte refer to the electrolytes that are presents in the body fluid ( Extracellular or intracellular).
Serum electrolyte value which reported from laboratory; provides information about electrolyte concentration in the blood.
But not necessarily reflect concentration in the other body compartments.
Electrolytes
• Chemically reactive in metabolism, determine cell
membrane potentials, osmolarity of body fluids,
water content and distribution
• Major cations
– Na+, K+, Ca2+, H+
• Major anions
– Cl-, HCO3-, PO4
3-
• Normal concentrations
Miss.kamlah ahmed19
Electrolyte Concentration in Body Compartments
Intravascular Extravascular
Interstitial Vascular Components
LowHighHigh Na+
HighLowLow K+
LowLowLowCa++
HighLowHighProteins
Miss.kamlah ahmed20
Electrolyte Imbalances
• Several types will be discussed which are:
1- Sodium imbalances.
• Hyponatremia.
• Hypernatremia.
2- Potassium imbalances:
• Hypokalemia.
• Hypercalcemia.
3- Calcium imbalances:
• Hypercalcemia.
• Hypercalcemia.
Sodium - Homeostasis
• Deficiency rare
– 0.5 g/day needed, typical diet has 3 to 7 g/day
• Aldosterone - “salt retaining hormone”
– primary effects: NaCl and K+ excreted in urine
• ADH - blood Na+ levels stimulate ADH release
– kidneys reabsorb more water (without retaining more Na+)
• ANF (atrial natriuretic factor) released with BP
– kidneys excrete more Na+ and water, thus BP
• Others - estrogen retains water during pregnancy
– progesterone has diuretic effect
Sodium - Imbalances
• Hypernatremia
– plasma sodium > 140 mEq/L
– water retension, hypertension and edema
manage –restrict Na ,diuretic
Complication CNS damage
• Hyponatremia
– plasma sodium < 130 mEq/L
– result of excess body water, quickly corrected by excretion of excess water
Manage by restrict of fluid
Complication - seizures
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Causes of Hypernatremia
Gain of relatively more Sodium than water
Loss of relatively more water than Sodium
• inability to communicate thirst.
• limited or no access to water.
• high solute intake without adequate water (tube feeding).
• intravenous hypertonic saline.
• Diabetes insipidus ( not enough antidiuritichormone).
• Diarrhea or vomiting without fluid replacement.
• Excessive sweating without fluid replacement.
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Clinical Manifestations
• Diminished urine output.
• Decrease level of consciousness.
• Confusion, lethargy, coma (shrinking of the brain cell).
• Seizures (in sever case).
• Increase Na serum. • Increase urine specific
gravity ( > 1.030).not detectable in newborn
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Treatment:
Administer isotonic solution then hypotonic solution.
Nursing interventions:
1- prevent hypernatremia by:
•Teaching breast feeding mother about signs of adequacy of feeding.
•Teaching mother how to calculate correct dose of formula.
•Instructing mother about normal urine output (7-8wet diapers).
• instructing the mother not to give concentrated formula
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Nursing interventions:
• Instructing the parents to offer extra fluid during hot weather.
2- During hospitalization:
• Monitor serum sodium level, urine specific gravity.
• Intake/output chart.
• Frequent check on responsiveness ( to monitor effect on brain cells).
• Enhance oral intake.
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Hyponatremia
Hyponatremia: • Is a condition of decreased blood osmolarity,
in which contains excess water relative to sodium.
• Na < 130 mmol/L in newborn.
• It results from conditions that cause gain relatively more water than sodium or loss sodium relatively than water.
Hyponatremia
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Causes of Hyponatremia
Loss of relatively more Sodium than water
Gain relatively more water than Sodium
• Diarrhea or vomiting with replacement of tap water only instead of fluid containing sodium.
• excessive sweating.
• Diuretics.
• Excessive intravenous D5W (hypotonic) rather than isotonic fluid.
• irrigation of body cavities with distilled water.
• Excessive antidiuritic hormone (concentrated urine).
•Excessive oral intake of tap water.
•CHF.
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Clinical Manifestations
• Decreased level of consciousness (from edema in brain cells).
• Vomiting, nausea
• Confusion.
• Headache.
• Respiratory distress.
• Mucsle weakness.
• Decreased deep tendon reflex.
the condition progress to:
• Respiratory arrest.
• Dilated pupils.
• Coma.
• Seizures.
In sever cases: it can be fatal.
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Treatment:
Administer hypertonic solution.
Nursing interventions:
• Teaching mother how to calculate correct dose of formula to prevent hyponatremia.
• Teaching mother to give the child the proper formula to prevent hyponatremia.
• monitor the hospitalized child on I.V therapy to prevent hyponatremia.
• Administer hypertonic solution as doctor order, but monitor the child to prevent rebound hypernatremia.
Miss.kamlah ahmed31
Potassium Imbalances
• Potassium is an essential anion (negatively charged particle). Most of the potassium in the body is found inside the cells. It is excreted from the body through urine, feces & sweat.
• The aldesterone hormone increase potassium excretion in the urine.
• Hyperkalemia:
• An excess of potassium in the blood, is reflected by levels above 6 mEq\l in newborn.
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High insulin level
Alkalosis
Burns, cancers
Crush injury
Acidosis
Epinephrine
Beta-adrenergic stimulation
Factors that shifts potassium in or out of cells Hyperkalemia Hypokalemia
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1- increase potassium intake:
is due to intravenous potassium overload. Blood transfusion (multiple units).
2- shifting of potassium outside the cells:
Due to massive cell death (e.g. crush injury, sickle cell anemia, chemotherapy use). Potassium also shifts during metabolic acidosis caused by diarrhea and diabetes mellitus when insulin levels are low.
Causes:
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3- Decreased potassium excretion:
Occur with acute or chronic oligurea during renal failure, sever hypovolemia, and conditions that leads to decrease levels of aldesterone secretion from the adrenal cortex. Such as lead poisoning.
Causes:
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Clinical Manifestations
• All of the clinical manifestations of hyperkalemia are related to muscle dysfunction, because potassium plays an important role in muscle activity.
• Intestinal colic, cramping & diarrhea. • Weak skeletal muscle (start with legs then arms).• Lethargy. • Arrhythmias (tachycardia) is due to weakness of the
heart muscle.• Prolonged QRS complex, Peak in T wave.
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Treatment & nursing interventions:
• restrict potassium intake.
• administer diuretics as order (loop diuretics).
• monitor serum potassium.
• ECG daily to monitor arrhythmias.
• Peritoneal or hemo dialysis.
• administration of intravenous sodium bicarbonate, insulin, glucose and calcium gluconate: to drive potassium ions into the cells.
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Hypokalemia:
low potassium in the blood, is reflected by levels below 3.0 mEq\lin newborn.
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Causes:
1- increase potassium excretion:
Caused by increase excretion of potassium from the GIT (diarrhea). Or it could be due to self-inducing vomiting as in bulimia or nasogastric suctioning.
2- increase urinary potassium excretion:
Caused by osmotic diuretics (manitol), hypomagnesaemia, increased aldesterone.
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Causes:
3- decreased potassium intake:
Caused by anorexia nervosa, bulimia nervosa.
4- shifts of potassium from the extracelluar fluid into cells:
Occur in alkalosis & hypothermia or ingestion of medication such as insulin, systematic antifungal, laxatives, osmotic diuretics (manitol).
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Manifestations
• As in hyperkalemia, the significant symptom s related the muscle dysfunction.
• Decreased GI smooth muscle activity leads to diminished bowel movements, constipation, abdominal distention.
• Skeletal muscle are weak & unresponsive to stimuli. • Deep tendon reflexes are diminished. • Flaccid paralysis in sever cases. • Cardiac arrhythmias occur: inverted or flat T wave. • Decrease urine specific gravity due to kidney changes
related to hypokalemia.
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Medical & nursing managements:
• The medical managements is directed to replace the potassium while treating the underlying cause.
• Monitor potassium level.• Observe muscle weakness. • Assess respiratory rate (to check on respiratory
muscles). • Assess bowel movements (sounds). • Increase intake of food rich in potassium such as
banana, dates, figs, potatoes, strawberries, tomato juice & orange juice.
Potassium & Membrane Potentials
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Calcium Imbalances
• Calcium is important for muscle and nerve function, secretion of hormones, bone formation and in clotting formation.
Calcium - Imbalances
• Hypercalcemia
– alkalosis, hyperparathyroidism, hypothyroidism
– membrane Na+ permeability, inhibits depolarization
– concentrations > 12 mEq/L causes muscular weakness,
depressed reflexes, cardiac arrhythmias
• Hypocalcemia
– vitamin D , diarrhea, pregnancy, acidosis, lactation,
hypoparathyroidism, hyperthyroidism
– membrane Na+ permeability, causing nervous and
muscular systems to be abnormally excitable
– very low levels result in tetanus, laryngospasm, death
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Causes of hypercalcemia Causes of hypocalcaemia
• Vitamin D overdose
• Bone tumors
• Thiazide diuretics
• Familial hypercalcemia
• Low calcium intake.
•Chronic diarrhea.
•Laxative abuse.
•Malabsorption.
•Alkalosis.
Calcium - Homeostasis
• Calcitriol (vitamin D)
• Calcitonin (in children)
– these hormones affect bone deposition and resorption,
intestinal absorption and urinary excretion
• Cells maintain very low intracellular Ca2+ levels
– to prevent calcium phosphate crystal precipitation
• phosphate levels are high in the ICF
Acids and Bases
• Acids
– strong acids ionize freely, markedly lower pH
– weak acids ionize only slightly
• Bases
– strong bases ionize freely, markedly raise pH
– weak bases ionize only slightly
Buffers
• Resist changes in pH
– convert strong acids or bases to weak ones
• Physiological buffer
– system that controls output of acids, bases or CO2
– urinary system buffers greatest quantity, takes several
hours
– respiratory system buffers within minutes
• Chemical buffer systems
– restore normal pH in fractions of a second
– bicarbonate, phosphate and protein systems
Acid-Base Balance
• Important part of homeostasis
– metabolism depends on enzymes, and enzymes are
sensitive to pH
• Normal pH range of ECF is 7.35 to 7.45
• Challenges to acid-base balance
– metabolism produces lactic acids, phosphoric acids,
fatty acids, ketones and carbonic acids
Bicarbonate Buffer System
• Solution of carbonic acid and bicarbonate ions
– CO2 + H2O H2CO3 HCO3- + H+
• Reversible reaction important in ECF
– CO2 + H2O H2CO3 HCO3- + H+
• lowers pH by releasing H+
– CO2 + H2O H2CO3 HCO3- + H+
• raises pH by binding H+
• Functions with respiratory and urinary systems
– to lower pH, kidneys excrete HCO3-
– to raise pH, kidneys and lungs excrete CO2
Phosphate Buffer System
• H2PO4- HPO4
2- + H+
– as in the bicarbonate system, reactions that proceed to
the right release H+ and pH, and those to the left pH
• Important in the ICF and renal tubules
– where phosphates are more concentrated and function
closer to their optimum pH of 6.8
Protein Buffer System
• More concentrated than bicarbonate or phosphate
systems especially in the ICF
• Acidic side groups can release H+
• Amino side groups can bind H+
Respiratory Control of pH
• Neutralizes 2 to 3 times as much acid as chemical
buffers can
• Collaborates with bicarbonate system
– CO2 + H2O H2CO3 HCO3- + H+
• lowers pH by releasing H+
– CO2(expired) + H2O H2CO3 HCO3- + H+
• raises pH by binding H+
• CO2 and pH stimulate pulmonary ventilation,
while an pH inhibits pulmonary ventilation
Renal Control of pH
• Most powerful buffer system (but slow response)
• Renal tubules secrete H+ into tubular fluid, then
excreted in urine
Limiting pH
• Tubular secretion of H+
– continues only with a concentration gradient of H+
between tubule cells and tubular fluid
– if H+ concentration in tubular fluid, lowering pH to
4.5, secretion of H+ stops
• This is prevented by buffers in tubular fluid
– bicarbonate system
– Na2HPO4 (dibasic sodium phosphate) + H+
NaH2PO4 (monobasic sodium phosphate) + Na+
– ammonia (NH3), from amino acid catabolism, reacts with H+ and Cl- NH4Cl (ammonium chloride)
Buffering Mechanisms in Urine
Acid-Base Balance
Acid-Base & Potassium Imbalances
• Acidosis
– H+ diffuses into cells and drives out K+, elevating K+
concentration in ECF
– H+ buffered by protein in ICF, causing membrane
hyperpolarization, nerve and muscle cells are harder to
stimulate, CNS depression from confusion to death
Acid-Base & Potassium Imbalances
• Alkalosis
– H+ diffuses out of cells and K+ diffuses in, membranes
depolarized, nerves overstimulate muscles causing
spasms, tetany, convulsions, respiratory paralysis
Disorders of Acid-Base Balances
• Respiratory acidosis
– rate of alveolar ventilation falls behind CO2 production
• Respiratory alkalosis (hyperventilation)
– CO2 eliminated faster than it is produced
• Metabolic acidosis
– production of organic acids (lactic acid, ketones),
alcoholism, diabetes, acidic drugs (aspirin), loss of
base (chronic diarrhea, laxative overuse)
• Metabolic alkalosis (rare)
– overuse of bicarbonates (antacids), loss of acid (chronic vomiting)
Compensation for Imbalances
• Respiratory system adjusts ventilation (fast, limited
compensation)
– hypercapnia ( CO2) stimulates pulmonary ventilation
– hypocapnia reduces it
• Renal compensation (slow, powerful compensation)
– effective for imbalances of a few days or longer
– acidosis causes in H+ secretion
– alkalosis causes bicarbonate and pH concentration in
urine to rise