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Fluid and Electrolytes

Fluid and electrolyte balance is…


• A dynamic process that is crucial for life.
• Potential and actual disorders of fluid and electrolyte balance occur in every setting with every disorder,
and with variety of changes that affect well people.

2 Fluid Compartments of Body Fluid:


Intracellular Space
• Fluids in the cell
• 2/3 of the body fluid is in the ICFLocated primarily in the skeletal muscle mass
Extracellular Space
• Further divided into:
• INTRAVASCULAR
• INTERSTITIAL

Factors that influence the amount of body fluid :


• Gender
• Age
• Body fat

ELECTROLYTES . . .
• These are active chemicals in the body fluids
• These chemicals unite in varying combinations
• It is expressed I terms of mEq per Liter ( a measure of chemical activity rather than mg which is a unit of
weight)

Electrolytes
Cations
• Carry positive charges
• Major cations in the body fluid:
 Sodium
 Potassium
 Calcium
 Hydrogen ions
 Magnesium
Anions
• Carry negative charges
• Major anions
 Chloride
 Bicarbonate
 Phosphate
 Sulfate
 Proteinate ions

3 Types of Extracellular Fluid Spaces:


• Intravascular
• Fluid within the blood vesssels that contain plasma
• Interstitial
• Contains fluids that surrounds the cell
• Lymph is an example of interstitial fluid
• Transcellular
• It is the smallest division of the ECF
• Example: cerebrospinal fluid,synovial, intraocular, pleural fluids, sweats and digestive secretions
Regulation of Body Fluid Compartments
• Osmosis
• The process by which fluid moves an area of low solute concentration to an area of high solute
concentration; the process continues until the solute concentrations are equal on both sides of the
membrane
• Osmolality
• The number of osmoles; the standard unit of osmotic pressure per liter of solution. It is the
concentration of solutes or dissolved particles.
• Diffusion
• The process by which solutes move from an area of higher concentration to one of lower
concentration; does not require expenditure of energy
• Filtration
• Hydrostatic pressure in the capillaries tends to filter out of the vascular compartment into the
interstitial fluid.
• Filtration allows the kidney to filter 180 L of plasma per day
• Sodium-Potassium Pump
• This tendency is offset by the sodium-Potassium Pump, which is located in the cell membrane and
actively moves sodium from the cell into the ECF. The high intracellular K+ concentration is
maintained.

Routes of Gains and Losses


• Kidney
• Skin
• Continuous water loss by evaporation is approx. 600 mL/day (insensible perspiration); fever and
burns
• Sensible perspiration
• Lungs
• Insensible loss of approx. 400 mL/day
• GI Tract
• Usual loss is 100 – 200 mL/day
• Diarrhrea and fistulas v
• Can cause large losses

Average Daily Intake and Output in an Adult:


INTAKE
• Oral liquids 1,300
• Water in food 1,000
• Water produced by metabolism 300

Total Gain 2,600

OUTPUT
• Urine 1,500
• Stool 200
• Insensible
lungs 300
skin 600

Total Loss 2,600

Laboratory Tests for Evaluating Fluid Status:


• Osmolality
• Reflects the concentration of fluid that affects the movement of water between fluid compartments
by osmosis.
• Measures the solute concentration per Kg in blood and urine
• Serum Osmolality : Reflects the concentration of sodium ; 280 –300 mOsm/kg
• Urine Osmolality : is determined by urea, creatinine and uric acid ; most reliale indicator of urine
concentration; 250 – 900 mOsm/kg
• Osmolarity
• Another term that describes the concentration of solutions
• Measured in milliosmoles per liter (mOsm/L)
• Urine Specific Gravity
• Measures the kidneys’ ability to excrete or conserve water
• 1.010 to 1.025
• Less reliable indicator of urine osmolality
• Creatinine
• It is the end product of muscle metabolism
• It is a better indicator of renal function than BUN.
• It is increased when renal function decreases
• 0.7 to 1.5 mg/dL
• Hematocrit
• Measures the volume percentage of red blood cells in whole blood.
• Increased in dehydration and polycythemia
• Decreased in anemia and overhydration
• Urine Sodium
• It changes with Na+ intake and the status of fluid volume
• 50 to 220 mEq/24h ; 50-220 mmol/24h
• Used to assess volume status and useful In diagnosis of hyponatremia and ARF
• Blood Urea Nitrogen
• BUN is made up of urea, an end product of metabolism of protein by the liver.
• 10 – 20 mg/dL ; 3.5 – 7 mmol/L
• Factors that increase BUN: Factors that decrease BUN
• Decreased renal function * End-stage liver disease
• GI bleeding * Low protein diet
• Dehydration * Starvation
• Increased protein intake
• Fever and sepsis

HOMEOSTATIC MECHANISMS:
Keep the composition and volume of body fluid within narrow limits of normal.

Kidney Functions
• Regulation of ECF volume and osmolality by selective retention and excretion of body fluids
• Regulation of electrolyte levels in the ECF by selective retention of needed substances and
excretion of unneeded substances
• Regulation of pH of the ECF by rention of hydrogen ions
• Excretion of metabolic wastes and toxic substances
Heart and Blood Vessel Functions
• Pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow
for urine formation
Lung functions
• Through exhalation, the lungs remove approx. 300 ml of water daily
• Has a major role in acid-base balance
Pituitary Functions
• ADH maintain the osmotic pressure of the cells by controlling the retention or excretion of water by
the kidneys and by regulating blood volume.
Adrenal Functions
• Aldosterone and cortisol
Parathyroid Function
• Regulate calcium and phosphate balance by means of parathyroid hormone (PTH)
• PTH influences bone resorption, calcium absorption from the intestines, and calcium reabsorption
from the renal tubules

Other Mechanisms:
Baroreceptors
• Are small nerve receptors that detect changes in pressure within blood vessels and transmit this
information to the central nervous system.
Renin-Angiotensin-Aldosterone System
• Renin is an enzyme that converts angiotensin
• ACE
• Aldosterone is a volume regulator and is also released as serum K+ increases, serum sodium
decreases
ADH and Thirst
• Oral intake is controlled by hypothalamus
• Water excretion is controlled by ADH, Aldosterone and baroreceptors
• ADH determines whether the urine that is excreted is concentrated or dilute
Osmoreceptors
• Sense changes in Na+ concentration
Release Of Atrial Natriuretic peptide
• ANP is released by cardiac cells in the atria in response to increased atrial pressure.

Fluid Volume & Electrolyte Disturbance


Fluid Volume Deficit (Hypovolemia)
• Occurs when loss of extracellular fluid volume exceeds the intake of fluid
• Occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids
• It may occurs alone or in combination with other imbalances
• Dehydration, loss of water alone with increased serum Na+ levels

Causes of FVD:
• Vomiting
• Diarrhea
• GI suctioning
• Sweating
• Decreased intake (inability to gain access to fluids)

Additional Risk Factors:


• Diabetes insipidus
• Adrenal insufficiency
• Osmotic diuresis
• Hemorrhage
• Movement of of fluid from the vascular system to the body spaces (ascites, edema)

Clinical Characteristics
• Acute weight loss
• Decreased skin turgor
• Oliguria
• Concentrated urine
• Postural hypotension
• Weak rapid pulse
• Flattened neck veins
• Increased temperature
• Decreased CVP
• Cool clammy skin
• Thirst
• Anorexia
• Muscle weakness and cramps

Assessment & Diagnostic Findings


• Health history
• Physical exam
• BUN : increased
• Hematocrit level: increased
• Urine Specific gravity: increased
• Urine Osmolality: greater than 450 mOsm/kg
• Electrolyte changes:
• Hypokalemia: GI and renal losses
• Hyperkalemia: adrenal insufficiency
• Hyponatremia: increased thirst and ADH release
• Hypernatremia: increased insensible losses and diabetes insipidus

Gerontologic Considerations:
• Fluid balance in the elderly client is often marginal because of physiologic changes
• Decrease muscle mass
• Decreased cardiorespiratory functions
• Hormonal regulatory functions
• Assessment should be modified from that of younger adults
• Perform functional assessment
• Some elderly clients deliberately restrict their fluid intake to avoid embarrassing episodes of
incontinence

Medical Management of FVD:


Mild
• Oral route
Acute or Severe
• IV route: LR or .9% Sodium Chloride, 0.45% sodium chloride
• Assess I & O, weight, V/S, CVP, LOC, and breath sounds
• Fluid challenge

Nursing Management of FVD:


• Monitor and measure I & O as ordered
• Weigh client daily
• Monitor vital signs
• Assess skin turgor
• Assess urine concentration; urine specific gravity
• Assess mental function; decreased cerebral perfusion
• Preventing FVD
• Identify patients at risk
• Correcting FVD
• Considers likes and dislikes of patient
• Administer fluid by an alternative route as directed

Fluid Volume Excess (Hypervolemia)


• Refers to an isotonic expansion of the ECF caused by abnormal water retention and Na+ in approximately
the same proportions in which they normally exist in the ECF.
• Contributing factors:
• Heart failure
• Renal failure
• Liver cirrhosis
• Consumption of excessive amount of table salt
• Excessive administration of Na+ containing fluids

Clinical Manifestations:
• Edema
• Distended neck veins
• Crackles
• Tachycardia
• Increased blood pressure
• Pulse pressure
• Central venous pressure
• Increased weight
• Increased urine output
• Shortness of breath

Assessment & Diagnostic Findings:


• BUN and Hematocrit levels
• Decreased because of plasma dilution
• Serum Osmolality & Na+ levels
• Decreased in CRF due to excessive water retention
• Chest x-ray
• Pulmonary congestion

Medical Management of FVE:


• Pharmacologic Therapy
• Diuretics
• Thiazide diuretics: blocks Na+ reabsorption in the distal tubule
• Loop Diuretics : Block Na+ in the ascending limb of the loop of Henle
: furosemide (lasix) bumetanide (bumex)
*Azotemia – increased nitrogen levels in the blood
*Hyperurecemia – high uric acid levels
• Hemodialysis
• Pharmacologic can not anymore act efficiently
• Remove nitrogenous wastes and control K+ and acid-base balance
• Nutritional Therapy
• Dietary restriction of Na+

Nursing Management of FVE:


• Measure I & O
• Weigh daily
• Assess breath sounds
• Assess the degree of edema
• Preventing, detecting and controlling FVE:
 Health teachings

IMPORTANCE OF SODIUM
• It is the most abundant electrolyte in the ECF (135 to 145 mEq/L)
 Primary determinant of ECF osmolality
 Primary regulator of ECF volume
• Control water distribution throughout the body
• Also function in establishing the electrochemical state necessary for muscle contraction and transmission of
nerve impulses.

Sodium Deficit (Hyponatremia)


• Dilutional Hyponatremia
• Serum Na+ level is diluted by an increase in the ratio of water to Na+
• SIADH
• Excessive ADH activity
• Result of either sustained secretion of ADH by the hypothalamus or production of an ADH-like
substance from a tumor
• Head injuries
• Endocrine and pulmonary disorders
• Physiologic and Psychological stress
• Use of medications such as oxytocin, cyclophosphamide

Clinical Manifestations of Hyponatremia:


• Depends on the cause, magnitude and speed with which the deficit occurs
• Poor skin turgor
• Dry mucosa
• Decreased saliva production
• Orthostatic fall in blood pressure
• Nausea
• Altered mental status

Assessment and Diagnostic Findings


• Serum Na+ level
• Serum osmolality : decreased
Medical Management:
• Sodium replacement
• Water restriction

Nursing Management:
• Identify clients at risks for hyponatremia
• Monitor fluid intake and output
• Monitor body weights
• Alert for CNS changes, neurologic signs

Sodium Excesss (Hypernatremia)


• Serum sodium level exceeding 145mEq/L
• Caused by a gain of sodium in excess of water or by a loss of water in excess of sodium.

Causes:
• Unconscious patients
• Very old
• Very young
• Cognitively impaired
• Diabetes insipidus
• Heat-stroke
• Near-drowning in sea water 500mEq/L
• IV administration of hypertonic saline or excessive use of Na+ bicarbonate

Clinical Manifestations:
• Restlessness & weakness
• Disorientation & delusions
• Thirst
• Dry, swollen tongue
• Sticky mucous membranes
• Postural hypotension

Assessment & Diagnostic Findings:


• Serum sodium level
• Serum osmolality: exceeds 295mOsm/kg
• Urine specific gravity: increased

Medical Management:
• Administration of hypotonic solution (.3%NaCl) or isotonic nonsaline solution (D5water
• General Rule: serum Na+ level is reduced at a rate no faster than 0.5 to 1 mEq/L

Nursing Management:
• Obtain history of the client
• Monitor changes in behavior
• Monitor temperature and thirst
• Prevention and correcting hypernatremia

SIGNIFICANCE OF POTASSIUM
• It is the major intracellular electrolyte
• 98% of the body’s K+ is inside the cells
• Influences skeletal and cardiac muscle activity
• Primary regulator of K+ balance is the KIDNEY (80%, 20% bowel and sweat)
Potassium Deficit (Hypokalemia)
Causes:
• Vomiting
• Frequent gastric suction
• Diarrhea
• Alterations in Acid-base balance
• Hyperaldosteronism
• Medications: K+ lossing diuretics
• Patients with persistent insulin hypersecretion
• Unable and unwilling to eat normal diet

Clinical Manifestations:
• Fatigue
• Anorexia
• Nausea and vomiting
• Muscle weakness
• Leg cramps
• Paresthesias
• Decreased bowel motility
• Cardiac or respiratory arrest
• Death

Assessment & Diagnostic Findings:


• Serum K+ Concentration
• Electrocardiogram

Medical Management:
• Increased K+ intake in daily diet (59 to 100 mEq/day)
• Oral or IV replacement therapy

Nursing Management:
• Monitor for its early presence in client’s at risk
• Monitor and assess for dysrhythmias
• Monitor intake and output (40mEq K+/L of urine output)
• Refer if urine output is less than 20mL/Hr for 2 consecutive hours: STOP!

Nursing Alert !!!


• Potassium is never administerd IV push or IM.
• It should not be administered faster than 20 mEq/L unless hypokalemia is severe
• For IV solutions, fluid should be agitated well to prevent bolus doses

Potassium Excess (Hyperkalemia)


• Seldom occurs in clients with normal renal function
• Often due to iatrogenic or treatment induced.
• Cause: decreased renal excretion of K+ , medications and high K+ intake
• Causes of pseudohyperkalemia:
• Hemolysis of the blood sample
• Drawing blood above the site

Clinical Manifestations:
• Cardiac effects
• Peaked,narrow T waves
• ST-segment depression
• Short QT-interval
• Prolonged PR-interval followed by disappearance of P waves
• Prolongation of QRS complex
• Ventricular dysrhythmias and cardiac arrest
• Skeletal muscle weakness and paralysis
• Quadriplegia
• Paralysis of the respiratory and speech muscles
Assessment and Diagnostic Findings:
• Serum potassium levels
• Electrocardiogram
• Arterial Blood Gas Analysis: Metabolic Acidosis

Medical Management:
• ECG and repeat serum K+ should be obtained
• Restriction of dietary potassium and K= containing medications
• Administer Calcium gluconate(antagonizes K+)
• IV administration of insulin and a hypertonic dextrose solution (30 min. onset)
• Cation exchange: Hemodialysis or peritoneal dialysis

Nursing Management:
• Identify clients at risks
• Physical assessment
• Check serum K+ levels
• Blood sample should be delivered to laboratory ASAP

SIGNIFICANCE OF CALCIUM
• It is the major component of bones and teeth
• More than 99% of the body’s Ca is located in the skeletal system
• Transmit nerve impulse
• Regulate muscle contraction and relaxation
• Plays a role in blood coagulation
• 8.5 to 10.5 mg/dL ; 2.1 to 2.6 mmol/L

Calcium Deficit ( Hypocalcemia)


Causes:
• Hypoparathyroidism
• Parathyroid surgery
• Massive administration of citrated blood
• Renal failure
• Inadequate vitamin D consumption
• Low intake of calcium
Clinical Manifestations:
• Tetany
• Tingling sensations of the :
• Fingers
• Around the mouth
• Feet
• Spasms of the muscles of the extremities and face
• Trousseau’s sign
• Carpopedal spasm
• Chvostek’s sign
• seizure
Assessment and Diagnostic Findings:
• Evaluate serum Ca+ level
Nursing Management:
• Seizure precaution
• Clarify physicians orders on calcium
• Iv site must be observed often

Medical Management:
• Administer parenteral calcium salts:Ca gluconate,Ca chloride, Ca gluceptate
• IV calcium should be diluted with D5W and given as IV bolus or slow IV infusion
Calcium Excess (Hypercalcemia)
Causes:
• Malignancies
• Hyperparathyroidism
• Immobilization
• Thiazide diuretics
Clinical Manifestations:
• Muscle weakness
• Incoordination
• Anorexia
• Nausea
• vomiting
• Constipation
• Abdominal
• & bone pain
• Polyuria
• Lethargy & confusion
Assessment and Diagnostic Findings:
• Serum Calcium level
• Electrocardiogram
• Double-antibody PTH test
• X-rays

Medical Management:
• Treat underlying cause
• Administer fluids to dilute serum Ca+
• Restrict dietary intake of calcium
• Administer furosemide
• Administer IV phospahate(reciprocal drop of Ca+)
• Adminster Calcitonin
• Lowers serum Ca+ level
• Reduces bone resorption
• Increase s deposit of Ca+ & phosphorus in the bones
• Increases urinary excretion of Ca+ & phosphorus
Nursing Management:
• Increase patients mobility
• Encourage oral fluids
• Watch out for ECG changes
• Health teachings

SIGNIFICANCE OF MAGNESIUM
• Plays a role both in carbohydrate and protein metabolism
• Mg balance is important in neuromuscular function,irritability and contractility
• It has sedative effect at the neuromuscular junction
• Has effect on the cardiovascular system
• Have a direct effect on the peripheral arteries and arterioles

Magnesium Deficit (Hypomagnesemia)


Normal Magnesium serum level=
1.5 to 2.5 mEq/L
1.8 to 3.0 mg/dL
1/3 is bound to protein and 2/3 exists as free cations like Ca+
Causes:
 diarrhrea
 fistulas
 Nasogastric suctioning
 alcoholism
 burns
Clinical Manifestations:
• neuromuscular changes are hyperexcitability with muscle weakness
• Tremors
• Involuntary twisting
• Tetany
• Generalized tonic-clonic seizures
• ECG changes: prolonged QRS,depressed ST-segment and PVC
• Mood alterations: apathy, depression, agitation and delirium
Assessment and Diagnostic Findings:
• Serum Mg+ level : decreased
• Frequently assoc. with Hypok+, Hypo Ca+
• Mg is CHON bound esp. to albumin
• ECG changes: PVC, prolonged PR intervals,and torsades de pointes
Medical Management:
• Can be corrected by diet alone
• Mg salts or carefully administer MgSO4
• Cagluconate should be readily available

Magnesium Excess: Hypermagnesemia


• Is greater than normal serum magnesium concentration
• Results affected by manner of extraction and hemolyzed blood sample
Causes:
• Advanced Renal Failure
• Untreated diabetic ketoacidosis
• Excessive use of antacids and laxatives
Clinical Manifestations:
• At higher concentration level:
• Lethargy and drowsiness
• Difficulty speaking
• Deep tendon reflexes are lost
• At mildly elevated levels
• Low BP because of peripheral vasodilation
• Facial flushing
• Nausea and vomiting
• Sensation of warmth
Assessment and Diagnostic Findings:
• Serum magnesium level
• ECG changes:
• prolonged PR interval
• tall T waves
• widened QRS
Medical Management:
• Can be prevented if administration of Mg is avoided
• Carefully monitor clients with Mg Salts
• Calcium IV should be readily available for use
• Administration of loop diuretics
Nursing Management:
• Monitor vital signs
• Note for changes of LOC
• Check medications esp. Mg

SIGNIFICANCE OF PHOSPHORUS
• It is essential to function of muscle and red blood cells, the formation od adenosine triphosphate (ATP) and
2,3- diphosphoglycerate
• Normal values: 2.5 to 4.5 mg/dL
• 0.8 to 1.5 mmol/L
• 85% is located in the bones & teeth
• 14% tissue
• Less than 1% in the ECF
• It decreases with age

Phosphorus Deficit: Hypophosphatemia


• Is a below normal serum concentration of inorganic phosphorus
• Present in:
• malnourished clients
• Alcohol withdrawal
• Poor dietary intake
• Diabetic ketoacidosis
• Major thermal burns

*** Vit. D regulates intestinal ion reabsorption, therefore a deficiency of vit D may cause decreased CA+ ,
phosphorus levels = OSTEOMALACIA

Clinical Manifestations:
• Irritablity
• Fatigue
• Apprehension
• Weakness and numbness
• Paresthesias
• confusion
• Seizures
• Tissue anoxia
• Hypoxia– tachypnea—resp. alkalosis
Assessment and Diagnostic Findings:
• Serum phosphorus level: low
• Insulin affects results of phosphorus= a slight decrease
• PTH : increased in parathyroidism
• X-ray: skeletal changes
• Alkaline Phosphatase: increased
Medical Management:
• Monitor lphosphorus levels
• Administration of adequate amount of phosphorus oral or IV
• Carefully check the infusion site because of tissue sloughing & necrosis

Nursing Management:
• Monitor of phosphorus levels
• Report and document early signs of hypophosphatemia (LOC)
Phosphorus Excess: Hyperphosphatemia
• Is a serum phosphorus level that exceeds normal
Causes:
• Renal failure
• Chemotherapy
• Hypoparathyroidism
• Respiratory acidosis
• Increased phosphorus intake
Clinical Manifestations:
• Has reciprocal relationship bet. Ca+
• Symptoms are similar to Ca+ depletion
• Tetany
• Tingling sensations in fingertips & around mouth
• Muscle weakness
• Nausea and vomiting
• Anorexia
• tachycardia
Assessment and Diagnostic Findings:
• Serum phosphorus level
• X-ray studies : skeletal changes with abnormal bone development
• BUN and CREATININE: assess renal function
• PTH : decreased in hypoparathyroidism
Medical Management:
• Treatment is directed to the underlying disorder
• Dialysis
• Dietary restriction
• Administration of Vit. D preparations
Nursing Management:
• Health teachings on foods high in phosphorus
• Monitor urine output and serum levels of phosphorus.

SIGNIFICANCE OF CHLORIDE
• It is the major anion of the ECF
• More in the interstitial and lymph fluid compartments than in the blood
• It is contained in the gastric & pancreatic juices & sweat
• Direct proportion to sodium
• Bicarbonate has an inverse relationship with Chloride
• Normal level: 96 to 106 mEq/L
Nursing Care of Clients with Burns
I. Background
A. Definition
1. A burn is an injury resulting from heat, chemicals, radiation, electrical current
2. The transfer of energy from source of heat causes physiologic changes and damage to tissues
3. Systemic infection is the leading cause of death in major burn clients

B. Factors associated with burns


1. Age (children and older adults)
2. Careless smoking
3. Alcohol or drug intoxication
4. Physical and/or mental disabilities
5. Certain occupations

C. Types of burns
1. Thermal
a. Results from exposure to dry heat, as with flame; or moist heat, as with steam or hot
fluids
b. Most common type of burn injuries
2. Chemical
a. Direct skin contact with acid or alkaline agents and agent destroys tissue protein
b. Alkali burns are deeper and more severe than acid burns
c. Organic compound burns, as from petroleum distillates, cause cutaneous damage
through fat solvent action; also cause liver and kidney damage
3. Electrical
a. Severity dependent on type and duration of current, and amount of voltage
b. Destructive process from electrical burn is concealed, persists for weeks post
c. Electricity follows path of least resistance: along muscles, bones, blood vessels, nerves
d. Blood coagulation at site of injury leads to impaired blood flow and necrosis of tissue
e. Alternating current from manufactured electricity burns results in sustained muscles
contractions and respiratory arrest
f. Direct current, as with a lightening strike, is high voltage for an instant; have entry and
exit wounds and flash over the skin, which can mean less internal damage
4. Radiation
a. Often from sunburn or radiation treatments as with treatment for cancer
b. Functions of skin are left intact

D. Classification of burns: Determination of Tissue Damage


1. Depth of burn (layers of underlying tissues affected)
a. Superficial: First degree
1. Involvement: only epidermal layer
2. Causes: sunburn, ultraviolet light, minor flash injuries, mild radiation burns
3. Appearance of burn
a. Skin color pink to bright red, slight edema
b. Mildly painful
4. Usual treatment: mild analgesia, application water-soluble lotions
b. Partial-thickness burns: Second degree
1. Involvement: superficial partial-thickness burn or deep partial-thickness burn
depending on the depth of burn throught the layers of the dermis
2. Causes
a. Superficial: Brief exposure to flash flame, dilute chemical agents, hot
surface
b. Deep: Hot liquids, solids; flash or direct flame, radiant energy, chemical
agents
3. Appearance of burn
a. Blisters
1. Superficial: bright red, moist glistening appearance
2. Deep: pale and waxy, moist or dry
b. Severe pain in response to air or heat
4. Usual treatment: analgesia, skin substitutes, grafting may be necessary
c. Full-thickness burns: Third degree
1. Involvement: all layers of skin, may extend into subcutaneous fat, connective
tissue (muscle, bone)
2. Causes: prolonged contact with flames, steam, chemicals, high-voltage electrical
current
3. Appearance of burn
a. Pale, waxy, yellow, brown, mottled, charred, or nonblanching red
b. No sensation of pain or light touch since receptors were destroyed
4. Usual treatment: requires skin grafting
d. Full Thickness / Fourth-degree burn
- Involving injury to muscle and bone.
- Black, edematous lesion, no pain or blisters.
- Spontaneous healing will not occur, grafting required.

Severity
Minor Burns
- Less than 15% TBSA burn in adults less than 40 years old.
- Less than 10% TBSA burn in adults more than 40 years old.
- Less than 10% TBSA burn in children below 10 years old.
With
- Less than 2% TBSA full thickness burn and no cosmetic or functional risk to face, eyes,
ears, hands, feet or perineum.
Moderate Burns
- 15-25% TBSA burn in adults less than 40 years old.
- 10-20% TBSA burn in adults more than 40 years old.
- 10-20% TBSA burn in children less than 10 years old.
With
- Less than 10% TBSA full thickness burn without cosmetic or functional risk to face,
eyes, ears, hands, feet or perineum.

Severe/Major Burns
>25% TBSA burn in adults less than 40 years old.
>20% TBSA burn in adults more than 40 years old.
>20% TBSA burn in children less than 10 years old.
or
- Burns face, eyes, ears, hands, feet, or perineum that will result in cosmetic or
functional disability.
or
- High voltage electrical burn injury.
or
- All burn injuries with concomitant inhalation injury or major trauma.

2. Methods of determining extent of burn (percentage of body surface)


a. Rule of 9’s: involvement of parts of body
b. Lund and Browder: surface area for body parts according to client age
c. American Burn Assn: extent and depth of burn (minor, moderate, major)

E. Process of healing with burn occurs more slowly than with other types of injuries
1. Physiologic events
a. Hemostasis: Platelets aggregate, thrombus formation, wound walled off
b. Inflammation: Local vasodilatation; increased capillary permeability
c. Proliferation: Granulation tissue begins to form to reepithelialization (peak 14 days post
burn)
d. Remodeling: Collagen fibers reorganized, scars contract
2. Two types of excessive scarring, if burn injury extended into dermal layer
a. Hypertrophic scar: overgrowth of dermal tissue but remains within boundaries of wound
b. Keloid: scar extends beyond boundaries of wound
Goals of collaborative management include:
- Maintaining airway breathing, circulation, and fluid balance.
- Preventing infection.
- Supporting nutrition and healing.
- Relieving pain.
- Preventing disability.

Important Nursing Diagnoses (actual or potential) are:


- Complications of burns: shock, infection.
- Ineffective airway clearance, impaired gas exchange.
- Anxiety and Fear.
- Fluid volume deficit.
- Altered body image, altered self-esteem.
- Impaired physical mobility.
- Altered Nutrition.
- Dysfunctional grieving.

II. Prehospital Client Management: First Aid at scene


A. Stop the burning process to limit severity
1. Thermal burns
a. “Stop, drop, and roll” to control fire
b. Remove clothing and lavage area with cool water, no ice
c. Cover to prevent hypothermia
2. Chemical burns
a. Remove clothes and shower or lavage with water
b. Contact poison control center if necessary
3. Electrical burns: disconnect electrical current to protect rescuers
4. Radiation burns: shield, distance, and limit time exposure to radioactive source
B. Support vital functions
1. CPR, if indicated
2. Note any other injuries
3. Initiate fluid replacement
4. Cover client

III. Care of Clients with Burns


A. Minor burns
1. Not extensive, superficial split-thickness <15%, full thickness <2%
2. Not associated with immunosuppression, hypermetabolism, increased susceptibility to infection
3. Pathophysiology
a. Skin remains intact
b. Includes sunburns, minor scald burns
4. Collaborative Care: Treatment
a. Wash with mild soap and water
b. Tetanus toxoid, if needed
c. Prescribed wound care topical agents, dressings
d. Controlling pain: analgesics
e. Range of motion to affected joints
f. Teaching about home care
g. Follow up appointments
B. Major burns
1. Serious injury to underlying layers or skin and cover large body surface area
2. Criteria include
a. > 25% total body surface area if client < 40
b. > 20% total body surface area if client > 40
c. > 10% total body surface area full thickness burn
d. Injuries involving face, eyes, ears, feet, hands, perineum
e. High-voltage electrical burns
f. All burns involving inhalation injury or major trauma
3. Pathophysiology: involves all body systems
a. Integumentary
1. Bull’s eye appearance: most severe burn located centrally, lesser burns at peripheral
edge of wound (like 3 concentric circles)
a. Outer zone of hyperemia: blanches, heals 2 – 7 days
b. Middle zone of stasis: moist, red blisters, blanches on pressure; pale and
necrotic 3 – 7 days post burn
c. Inner zone of coagulation: leathery, coagulated and merges with middle
zone days 3 – 7 days
2. Eschar: hard crust that forms over necrotic skin and tissue
b. Cardiovascular
1. Hypovolemic Shock (Burn Shock)
a. Fluid shift from intracellular and intravascular to interstitial area
b. Occurs due to increased permeability, intracellular edema, and osmosis
c. Initially, hypotension, vasoconcentration reflected in CBC
d. Usually lasts 24 hours, followed by fluid shift back and diuresis
2. Cardiac Rhythm Alterations: burns > 40% total body surface area cause
myocardial dysfunction, cardiac dysrhythmias
3. Peripheral Vascular Compromise: blood vessel damage, compartment syndrome
c. Respiratory: direct inhalation injury or systemic response to injury
1. Inflammation: cilia stop functioning causing bronchial congestion and infection
2. Interstitial Pulmonary Edema: fluid from pulmonary vasculature, sloughed burnt
lung tissue
3. Upper airway thermal injury: soot, charring, blisters, edema in oropharnyx
4. Smoke poisoning: irritant gases, particulate matter direct cytoxic effect
5. Carbon monoxide: impairs oxygen delivery and cellular use
d. Gastrointestinal: dysfunction related to size of burn wound
1. Paralytic ileus (gastric distention, absent bowel sounds)
2. Stress (Curling’s) ulcers: acute ulceration of stomach or duodenum
(hematemesis)
3. Ischemic bowel leads to bacterial translocation and sepsis and multiple organ
dysfunction
e. Urinary
1. Early stages: decreased renal blood flow and glomerular filtration rate
2. Myoglobinuria: dark brown concentrated urine due to damaged erythroctyes
from burn injury
3. May result in renal failure
f. Immune System
1. Cell-medicated and humoral immune system impaired
2. High risk for infection
g. Metabolism
1. Two phases of metabolic response to burn injury
a. Ebb stage (first 3 days) decreased oxygen consumption
b. Flow stage after burn resuscitation accomplished
2. Hypermetabolism: basal metabolic rate significantly increased
3. Protein catabolism, lipolysis, gluconeogenesis
4. Collaborative Care/Burn Team: Three Stages of Treatment
a. Emergent/resuscitative stage
1. Scope: Onset of injury through successful fluid resuscitation
2. Includes
a. Estimate of depth and extent of burn injury
b. First aid measures
1. Limit severity of burns
2. Ventilation maintenance including intubation for all clients with
burns of chest, face, or neck
c. Fluid resuscitation
1. Restore circulating blood volume; counteract burn shock, replace
fluid and electrolyte losses
2. 2 large bore IV’s for venous access
3. Fluid of choice: Crystalloids, i.e. warmed Lactated Ringers
Parkland formula or Modified Brooke formula which
individualize amounts and rates (most in first 8 hours post burn)
4. Enough fluid to maintain urinary output 30 – 50 ml per hour and
pulse rate < 120 (adult)
3. Emergency department staff obtains history of burn injury
a. Time of injury
b. Causative agents
c. Early treatment of burn
d. Client’s past medical history
e. Client age and body weight
4. May include transfer to burn center if client has significant burn
b. Acute stage
1. Scope: Starts at beginning of diuresis and ends with closure of burn
wound
2. Includes
a. Wound care management: hydrotherapy, excision, grafting
b. Nutritional therapies: Enteral and parenteral nutritional interventions
c. Measures to control infections: Topical and systemic antimicrobials
d. Pain management, physical therapy
e. Observation for complications
3.Specific treatment of burn may include surgeries as indicated by client
healing
a. Escharotomy
1. Circumferentially eschar acts as a tourniquet
2. Incision made into eschar to restore circulation
b. Surgical debridement to achieve
1. Excision of wound to level of fascia
2. Removal of thin slices of burn wound to level of viable tissue
c. Autografting: Skin removed from healthy tissue and applied to burn
wound
4. Dressings
a. Biologic and biosynthetic dressings used to promote healing and
prepare wound for skin grafting in future
b. Includes
1. Allograft (human skin)
2. Heterograft/xenograft from animal (usually pig), amniotic
membranes, synthetic materials
c. Rehabilitative stage
1. Scope: Starts with wound closure and ends when client reaches high
level of health restoration; may take years
2. Biopsychosocial adjustment by client
a. Prevention of contractures and scars
b. Client returns to work, family, and social roles
c. May include vocational, occupational, physical and psychosocial
rehabilitation

IV. Nursing Care for Clients with Burns


A. Monitoring of vital signs/changes in stability
1. Critical care nursing
2. Cardiac and hemodynamic monitoring
3. Pulse oximetry
B. Diagnostic Tests
1. Urinalysis: adequacy renal perfusion, myoglobinuria
2. Regular monitoring of CBC, electrolytes, serial Arterial Blood Gases
3. Creatine phosphokinase (CPK) for muscle damage with electrical burns
4. Renal function tests (BUN, Creatinine) closely monitored
5. Blood glucose, elevated transiently post burn and with parenteral nutrition
6. Nutritional assessment (most reliable in rehabilitative stage): Total protein, albumin, transferrin,
prealbumin
7. Monitor cardiovascular/respiratory status as needed: chest xrays, electrocardiograms
C. Medications
1. Pain control
a. Intravenous morphine is drug of choice in early stages of care
b. Pain medications are often administered prior to hydrotherapy and physical therapy
c. Alternative therapies added to plan of care for pain control
2. Antimicrobial agents
a. Topical antimicrobial therapy used to eliminate infection of surface of burn wound
b. Most widely used topical agents
1. Mafenide acetate (Sulfamylon) cream
2. Sulfadiazine (Silvadene) cream
3. Silver nitrate 0.5% soaks
c. Systemic antibiotics preoperatively and postoperatively with excisions and autograftings
3. Tetanus prophylaxis: During acute phase to prevent Clostridium tetani infection
4. Control gastric hyperacidity
a. Goal to maintain gastric pH above 5.0
b. Clients have nasogastric tube in place in emergent phase of care
c. Intravenous Histamine H2 blockers, e.g. famotidine (Pepsid), ranitidine (Zantac)
5. Respiratory management: Bronchodilators and mucolytic agents
D. Wound Management
1. Goals
a. Remove nonviable tissues
b. Control microbial colonization
c. Promote reepithelialization
d. Achieve wound coverage as soon as possible
2. Debridement of wounds
a. Process of removing loose tissue, wound debris, eschar from wounds
b. Types of debridement
1. Mechanical: wet to dry or wet to moist dressings; hydrotherapy and/or irrigation;
scissors and tweezers
2. Enzymatic: use of topical enzyme agents to dissolve and remove necrotic tissue,
i.e. collagenase (Santyl), fibrinolysis-deoxyribonuclease (Elase)
3. Surgical (in operating room)
c. Dressing of wounds
1. Open: burn wound open to air with topical agent applied
2. Closed
a. Topical agent applied
b. Burn wound covered with gauze or nonadherent dressing
c. Wrapped with roller gauze bandages
d. Distal to proximal circumferentially, wrap fingers and toes separately
E. Prevention of contractures and scarring/maintain function
1. Physical therapy with correct positioning
a. Use of splints to maintain in flexion except when exercising
b. Early ambulation
c. Range of motion, passive or active every two hours
2. Support garments
a. Uniform pressure reduces hypertrophic scarring
b. Tubular support bandages
c. Later, custom-made elastic pressure garments
F. Nutritional Support
1. Resting energy need increases as much as 100% of normal
2. 4000 – 6000 kcal per day; reverse negative nitrogen balance; adequate protein to build new
tissues
3. Enteral feedings, plus oral feedings if feasible
4. Total Parenteral Nutrition (TPN) via central venous catheter in case of Curling’s ulcer, septic
ileus, bowel obstruction, pancreatitis
G. Psychosocial Support
1. Psychiatric consultation, social worker consultation
2. Support group for burn clients and families
3. Client’s religious support and/or hospital chaplain
H. Nursing Diagnoses
1. Altered skin integrity
2. Altered fluid volume (deficit, then excess)
3. Acute pain
4. Risk for infection
5. Impaired physical mobility
6. Imbalanced nutrition, less than body requirements
7. Powerlessness
I. Health Promotion
A. Primary goals
1. Prevention
2. Reduction in incidence of burns
B. Strategies
1. Smoke alarms, sprinkler systems
2. No smoking in bed
3. Care and observation with lit candle use
4. Teaching regarding control of fire, first aid for burns