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ªExtracellular Fluid (ECF)
ª Intracellular Fluid (ICF)
ª Interstitial Fluid
ª Transcellular Fluids
Homeostasis: Proper functioning of all body systems requires
F&E balance
ªICF & ECF solute concentration are similar, but the concentration
of the specific electrolytes differs between compartments
Body Fluid Composition
Body Fluid Distribution: Intracellular fluid (ICF)
ª This visual shows the distribution of three major types of fluid
in the body. ICF comprises approximately 40% of the total body
weight. ECF (intravascular & interstitial) comprises about 20% of
total body weight. Solids comprise the remaining 40% of body
weight
ªFound within cells: About two thirds of the body water is located
within cells & is termed intracellular fluid (ICF).
ª Essential for normal cell function
Body Fluid Distribution: Extracellular fluid (ECF)
ªLocated outside cells & is the other third of above
ª Futher classification by location
ª Intravascular- fluid refers to the liquid part of blood, or plasma
ª Interstitial- fluid refers to fluid located in the spaces between the
cells & lymph
ª Transcellular- fluids include cerebrospinal fluid; fluid in the gastrointestinal (GI) tract & joint spaces; & pleural, peritoneal, intraocular, & pericardial fluid.
ª About one third of ECF is in the intravascular space as plasma (3
L in a 70-kg man), & two thirds is in the interstitial space (10 L in
a 70-kg man). The fluid in the transcellular spaces totals about 1
L at any given time.
Calculation of Fluid Gain or Loss
ª 1L of water weighs 2.2 pounds (1 kg)
ª Body weight change is an excellent indicator of overall fluid
volume loss or gain
ª If a patient drinks 240 mL (8 oz) of fluid, weight gain will be 0.5 lb
(0.23 kg).
ª A patient receiving diuretic therapy who loses 4.4 lb (2 kg) in 24
hours has experienced a fluid loss of about 2 L.
ªOsmoreceptors in hypothalamus sense fluid deficit or increase
ª Deficit stimulates thirst & antidiuretic hormone (ADH) release
Regulation of Water Balance: Hypothalamic-Pituitary Regulation
ª Decreased plasma osmolality (water excess) suppresses ADH
release
Regulation of Water Balance: Renal Regulation
ªPrimary organs for regulating fluid & electrolyte balance
ª Adjusting urine volume
ª Selective reabsorption of water & electrolytes
ª Renal tubules are sites of action of ADH & aldosterone
Regulation of Water Balance: Adrenal Cortical Regulation
ªReleases hormones to regulate water & electrolytes
ª Glucocorticoids: Cortisol
ª Mineralocorticoids: Aldosterone
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Regulation of Water Balance: Cardiac Regulation
ªNatriuretic peptides are antagonists to the RAAS
ª Hormones made by cardiomyocytes in response to increased
atrial pressure
ª They suppress secretion of aldosterone, renin, & ADH to decrease blood volume & pressure
Regulation of Water Balance: GI Regulation
ªOral intake accounts for most water
ª Small amounts of water are eliminated by GI tract in feces
ª Diarrhea & vomiting can lead to significant fluid & electrolyte loss
Gerontologic Considerations
ªStructural changes in kidneys decrease ability to conserve water
ª Hormonal changes include a decrease in renin & aldosterone &
increase in ADH & ANP
ª Subcutaneous tissue loss leads to increased moisture lost
Electrolyte Composition: ICF
ªPrevalent cation is K+
ª Prevalent anion is PO43
Electrolyte Composition: ECF
ªPrevalent cation is Na+
ª Prevalent anion is Cl
Electrolytes
ªSubstances whose molecules dissociate into ions when placed
in water
ª Cations: positively charged
ª Anions: negatively charged
ª Concentration of electrolytes is expressed in milliequivalents
(mEq)/L
Concentrations of Cations & Anions in ICF & Plasma
Fluid Shifts
ªPlasma-to-interstitial fluid shift results in edema
ª Interstitial fluid drawn into plasma decreases edema
ª Edema, an accumulation of fluid in the interstitial space, occurs
if venous hydrostatic pressure rises, plasma oncotic pressure
decreases, or interstitial oncotic pressure rises. Edema may also
develop if an obstruction of lymphatic outflow causes decreased
removal of interstitial fluid.
ª An increase in the plasma osmotic or oncotic pressure draws
fluid into the plasma from the interstitial space. This can occur with
administration of colloids, dextran, mannitol, or hypertonic solutions. Additionally, an increase in tissue hydrostatic pressure can
cause a shift of fluid into the plasma. Wearing elastic compression
gradient stockings to decrease peripheral edema is a therapeutic
application of this effect.
Fluid Spacing
ªThe distribution of body water
First Spacing
ªNormal distribution
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Second Spacing
ªAbnormal (Edema)
Third Spacing
ªFluid is trapped where it is difficult or impossible for it to move
back into cells or blood vessels
Fluid & Electrolyte Balance: Dependent on
ªFiltration
ª Diffusion
ª Osmosis
Fluid & Electrolyte Balance: Filtration
ªMovement of fluid through cell of blood vessel membrane because of differences in water pressure (hydrostatic pressure)
ª This is related to water volume pressing against confining walls
ª Hydrostatic Pressure- "water-pushing pressure" Force that pushes water outward from a confined space through a membrane
ª Amount of water in any body fluid space determines pressure
ª Example: Blood Pressure
ª Moving whole blood from the heart to capillaries where filtration
occurs to exchange water, nutrients, & waste products between
the blood & tissues
ª Clinical significance is EDEMA this develops with changes in
normal hydrostatic pressure differences
ªFluid balance between the intravascular & interstitial spaces is
maintained in the capillary beds by a balance of filtration at the
arterial end & osmotic draw at the venous end.
Fluid & Electrolyte Balance: Filtration
Fluid & Electrolyte Balance: Filtration
Fluid & Electrolyte Balance: Diffusion
ªDynamics of fluid exchange between a capillary & tissue. An
equilibrium exists between forces filtering
ª Fluid out of the capillary & forces absorbing fluid back into the
capillary. Note that the hydrostatic pressure is
ª Greater at the arterial end of the capillary than at the venous end.
The net effect of pressures at the arterial end of
ª The capillary causes a movement of fluid into the tissue. At the
venous end of the capillary, there is net movement
ª Of fluid back into the capillary.
ªFree movement of particles (solute) across the permeable membrane from an area of higher to lower concentration
ª Important in transport of most electrolytes; other particles diffuse
through cell membranes
ª Sodium pumps
ª Glucose cannot enter most cell membranes without the help of
insulin
ªThis visual demonstrates diffusion—the movement of molecules
from an area of higher concentration to an area of lower concentration.
ª Movement stops when the concentration equalizes
Diffusion
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Facilitated Diffusion
ªMovement of molecules from high to low concentration without
energy
ª Uses specific carrier molecules to accelerate diffusion
ª Facilitated diffusion is passive & requires no energy other than
that of the concentration gradient
ª Facilitated diffusion involves use of protein carrier in the cell
membrane to move molecules that cannot otherwise pass through
the membrane
ª Example: Glucose transport- a carrier molecule on most cells
increases or facilitated the rate of diffusion of glucose into these
cells
ªOsmosis is the process of water movement through a semi-permeable membrane from an area of lowsolute concentration to an
area of high solute concentration
ª Note the movement of water from one side to another until the
concentration is equal
Osmosis
Hormonal Regulation of Fluid Balance
ªAldosterone
ª Antidiuretic hormone
ª Natriuretic Peptides
Hormonal Regulation of Fluid Balance: Aldosterone
ªSecreted by the adrenal cortex when Na levels in extracellular
fluid are low
ª Aldosterone prevents water & sodium loss
ª When secreted acts on kidney nephrons triggering them to absorb sodium & water from the urine back into the blood
ªReleased from posterior pituitary gland in response to change in
blood osmolality
ª Hypothalamus is sensitive to changes in osmolality
ª Acts on kidney nephrons making them more permeable to water
Hormonal Regulation of Fluid Balance: Antidiuretic Hormone (Va- so water is reabsorbed & returned to the blood decreasing blood
sopressin)
osmolality because it is more dilute
ª When blood osmolality decreases with low sodium levels less
water is reabsorbed the osmoreceptors swell & inhibit release of
ADH- less water reabsorbed & more excreted in the urine bringing
ECF osmolality up to normal
ªAntidiuretic hormone (ADH) release & effect. Increased serum
osmolality or a fall in blood volume stimulates the release of ADH
from the posterior pituitary. ADH increases the permeability of
distal tubules, promoting water reabsorption
Antidiuretic Hormone (ADH)
ªHormones secreted by special cells that line the atria (atrial
natriuretic peptide- ANP) & the ventricles of the heart
ª Peptide secreted by the heart ventricular cells is brain natriuretic
peptide (BNP)
ª These peptides are secreted in response to increased blood
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Hormonal Regulation of Fluid Balance: Natriuretic Peptides
volume & pressure which stretch heart tissue
ª NP binds to receptors in the nephrons creating opposing effects
of aldosterone
ª Kidney reabsorption of sodium inhibited while urine output is
increased resulting in decreased circulating blood volume & decreased blood osmolarity
Significance of Fluid Balance: Renin-Angiotensin II Pathway
ªBlood (plasma) volume & intracellular fluid most important to keep
in balance
ª Kidneys are major regulator of water & sodium balance; maintain
blood & perfusion pressure to all organs & tissues
ª When kidneys sense a low parameter, they secrete renin
ª Renin-angiotension II pathway is greatly stimulated with shock, or
shen stress response is stimulated
ACE (Angiotensin-Converting Enzyme) Inhibitors
ªDisrupt renin-angiotensin II pathway by reducing amount of ACE
produced
ª With less angiotensin II, less vasoconstriction & reduced peripheral resistance
ª Greater excretion of water & sodium in urine
ª By locking angiotensin II receptors, blood pressure lowers
ª Patients with hypertension often take ACE-inhibitor medications
Normal Physiology
ªMaintenance of homeostasis
ª Composition & volume of fluids & electrolytes kept within narrow
limits
ª Water content varies with age, gender, & fat content
Homeostasis
ªState of equilibrium in body
ª Naturally maintained by adaptive responses
ª Body fluids & electrolytes are maintained within narrow limits
ª Body fluids & electrolytes play an important role maintaining
homeostasis- the body's internal environment
ª Body fluids are in constant motion transporting nutrients, electrolytes, & oxygen to cells also carrying waste products away from
cells
ª Body uses adaptive responses to maintain composition of fluids
& electrolytes within narrow limits to maintain homeostasis
ª Various disease processes can effect F&E balance. Important for
nurses to carefully monitor for changes
ª The more fat present in the body, less total water content. Women
generally have a lower % of body water as they tend to have less
lean body mass than men
ª 50%to 60% of body weight in adult
ª 45% to 55% in older adults
ª 70% to 80% in infants: Varies with gender, body mass, & age
ª Need 2500mL of water over a 24 hour period
ª Average daily output is 1200-1500mL in adults
ª Body content over the lifespan
Water Content in the Body
ªAlthough osmolality & osmolality are often used interchangeably,
they are different measurements.
ª Osmolality measures the total milliosmoles per liter of solution
ª Osmolality measures the number of milliosmoles per kilogram of
water
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Osmolality & Osmolality
ª Means concentration of a solution- as number of solutes per
kilogram of water
ª Reported in milliosmoles per kilogram (mOsm/kg)
ª Osmolality of ECF depends on Na concentration
ª Glucose & Urea contribute of osmolality of ECF but effect is
smaller than Na concentration
Osmotic Movement of Fluids
ªThe osmolality of the fluid surrounding cells affects them
Isotonic
ªFluids with the same osmolarity, or tonicity, as the cell interior:
There is no fluid movement between isotonic fluids
Hypotonic
ªSolutions in which the solutes are less concentrated than the cells
Hypertonic
ªSolutions in which the solutes are more concentrated than the
cells
Fluid Balance
ªClosely linked to/affected by electrolyte concentrations
Fluid Intake
ªRegulated through thirst drive
ª Fluid enters the body as liquids & solid foods which contain up to
85% water
ª Rising blood osmolarity or decreased blood volume initiates thirst
ª Adult takes 2300mL of fluid a day
Fluid Loss
ªMinimum urine amount needed to excrete toxic waste products
is 400 to 600 mL/day
ª Insensible water loss—through skin, lungs, stool
Routes of Fluid Ingestion & Excretion
Fluid & Electrolyte: Dehydration
ªFluid intake/retention does not meet body's fluid needs; results in
fluid volume deficit
ª May be an actual decrease in total body water caused by either
too little intake of fluid or too great a loss of fluid
ª Relative dehydration: no actual loss of total body water- water just
shifts from the plasma into the interstitial space
Fluid & Electrolyte Exemplar: Isotonic Dehydration
ªMost common type of fluid loss
ª Fluid lost only from ECF space
ª No shift of fluids between spaces so ICF remains normal
Fluid & Electrolyte Exemplar: Hypovolemia
ªCirculating blood volume is decreased
ª Leads to reduced perfusion
ª Body compensates to keep perfusion to vital organsª Increases vasoconstriction & peripheral resistance to maintain
blood pressure
Common Causes of Fluid Imbalances: Dehydration
ªExcessive fluid replacement
ª Kidney failure- late
ª Heart Failure
ª Long-term corticosteroid therapy
ª Syndrome of inappropriate antidiuretic hormones (SIADH)
Common Causes of Fluid Imbalances: Fluid Overload
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ª Psychiatric disorders with polydipsia
ª Water Intoxication
Facts to Remember
ª 1L of water weighs 2.2 lbs, equal to 1 kg
ª Weight change of 1 lb=fluid volume change of about 500 mL
Assessment/Noticing: Dehydration - Cardiovascular
ªGood indicators of hydration
ª Heart rate increases
ª Weak peripheral pulses
ª Blood pressure decreases- greater decrease in diastolic
ª Hypotension more sever in standing position
ª Distended neck veins are flattened even when moved into sitting
position (neck veins normally distended in supine position, & hand
veins distended when lower than the heart)
Assessment/Noticing: Dehydration - Respiratory
ªIncreased rate- a compensatory mechanism to maintain oxygen
delivery with decreased perfusion
Assessment/Noticing: Dehydration - Skin Changes
ªOral mucous membranes may be dry, covered with sticky thick
coating & may have cracks or fissures
ª Poor skin turgor
Assessment/Noticing: Dehydration - Neurologic Changes
ªChanges in mental status
ª Changes in temperature-low grade fever: For every degree (Celsius) increase in body temp is above normal a minimum of additional 500 mL of body fluid lost
Assessment/Noticing: Dehydration - Kidney Changes
ªConcentrated urine
ª Specific gravity greater than 1.030
ª Dark amber urine
ª Strong odor
ª Output below 500mL/day for patient without kidney disease is
cause of concern
Analysis/Nursing Diagnosis: Interpreting
ªDehydration as a result of excess fluid loss or inadequate fluid
intake
ª Potential for injury as a result of blood pressure changes & muscle
weakness
ª Fluid imbalance
ª Impaired cardiac output
ª Acute confusion
ª Potential complication: Hypovolemic shock
Planning & Prioritizing/Responding: Dehydration - Planning
ªBlood pressure normal range
ª Urine output within 500 mL of total intake or 30 mL per hour
ª Moist mucous membranes
ª Normal skin turgor
ªDehydration may result of excess fluid loss or inadequate fluid
intake
Planning & Prioritizing/Responding: Dehydration - Interpretation
ª Potential injury as a result of blood pressure changes & muscle
weakness
Planning & Prioritizing/Responding: Dehydration - Electrolyte Imbalance
ªCan occur in healthy people as result of changes in fluid I&)
ª Can be life threatening if severe; can occur in any setting
Planning & Prioritizing/Responding: Dehydration - Priorities
ªFluid replacement
ª Drug therapy
ª Patient safety
ªMild to moderate=oral therapy
ª Fluids patient likes
ª Time to take the fluids
ª Divide the total fluids needed by nursing shifts
Implementation/Responding: Dehydration - Fluid Replacement ª 60-120mL of fluid per hour for those dehydrated & risk for severe
dehydration
ª Rehydration solutions oral (ORS)
ª IV therapy for sever not tolerating ORS: Need to monitor pulse
rate & quality & urine output
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Implementation/Responding: Dehydration - Drug Therapy
ªAntidiarrheal drugs if cause
ª Antimicrobial if bacterial diarrhea
ª Antiemetic's when vomiting
ª Antipyretics for fever
Implementation/Responding: Dehydration - Prevention of Injury
ªGet up slowly
ª Sit if light headed
ª Ask for assistance
ª Fall protocol
QSEN: Patient with Dehydration
ªOral fluids that meet dietary restrictions
ª Collaborate to determine amount of fluid needed
ª Give fluids on an even schedule & at least every 2 hours over 24
hours
ª UAP understands not to hold fluids
ª Infuse IV fluids at rate consistent with hydration needs & cardiac,
or pulmonary problems
ª Assess IV line hourly
ª Give meds as ordered
QSEN: Patient with Dehydration - Monitor Patient response to
Fluid Therapy
ªPulse quality
ª Urine output
ª Pulse pressure
ª Weight every 8 hours
QSEN: Patient with Dehydration - Monitor & report fluid overload
ªBounding pulse
ª Difficulty breathing
ª Neck vein distention in upright position
ª Presence of dependent edema
Fluid Overload: Over Hydration
ªExcess of body fluid
ª Fluid intake or retention is greater than body fluid needs
ª Hypovolemia most common type
ª Problems from this related to excessive fluid in vascular spaces
or dilution of electrolytes & blood components
ª Causes: Excessive fluid replacement, kidney failure, heart failure,
steroid therapy, water intoxication, psychiatric disorders with polydipsia, Syndrome of inappropriate antidiuretic hormone (SIADH)
ªAdaptive changes & mechanisms to prevent cardiac & pulmonary
complications during fluid overload.
Fluid Overload
ªChanges in fluid compartment volumes with fluid overload
Hypovolemia
ªIncreased & bounding pulse
ª Elevated B/P
ª Decreased pulse pressure
ª Elevated central venous pressure
ª Distended neck & hand veins
ª Weight gain
ª Engorged varicose vein
Assessment/Noticing: Fluid Overload - Cardiovascular
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Assessment/Noticing: Fluid Overload - Respiratory
ªIncreased rate
ª Shallow respirations
ª SOB
ª Crackles
Assessment/Noticing: Fluid Overload - Skin & Mucous
ªPitting edema in dependent areas
ª Skin pale, cool to touch
Assessment/Noticing: Fluid Overload - Neuromuscular
ªAltered LOC
ª Headache
ª Visual Disturbances
ª Skeletal Muscle Weakness
ª Paresthesia's
Assessment/Noticing: Fluid Overload - Gastrointestinal
ªIncreased motility
ª Enlarged Liver
Priorities: Fluid Overload
ªSafety
ª Restore normal fluid balance
ª Supportive Care until restored
ª Prevent future overload
Analysis/Nursing Diagnosis: Fluid Overload
ªFluid imbalance
ª Impaired gas exchange
ª Impaired tissue integrity
ª Activity intolerance
ª Disturbed body image
ª Potential complications: Pulmonary edema, ascites
Priorities/Interventions/Responding: Fluid Overload - Safety
ªAssess every two hours at least to recognize pulmonary edema
ª Worsening fluid overload= increasing symptoms
ª Prevention of getting worse
ª Edema: Risk of skin breakdown - Change position every two
hours or more
Priorities/Interventions/Responding: Fluid Overload - Drug Therapy
ªDiuretics
ª Monitor response to drugs especially weight loss & increased
output
ª Observe F&E imbalances- monitor labs
Priorities/Interventions/Responding: Fluid Overload - Nutrition
Therapy
ªMay be fluid & Na restrictions
ª For sever overload= 2-4 g/day of sodium
ª Teach how to monitor & check for sodium in foods
ª Explain need of restriction
Priorities/Interventions: Fluid Overload - Monitoring
ªI&O
ª Schedule fluids over 24 hours
ª Monitor urine characteristics
ª Monitor IV
ª Fluid retention may not be visible- rapid weight fain is best
indicator or fluid retention & overload
ª Metabolism can account for only ½ lb of weight per day
ª Each pound equates to about 500 mL fluid retained
ª Weigh same time each day, with same scale & clothing
Serum Electrolyte Concentrations & Significance of Abnormal
Values
Sodium
ªNormal level 136-145 mEq/L
ª Major cation (positively charged particle) in extracellular fluid that
maintains ECF osmolality
ª Vital for muscle contractions, cardiac contraction & nerve impulse
transmission
ª Where sodium goes, water follows
ª Changes in Na levels change fluid volume & distribution of electrolytes
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ª Enters body through food & fluids
ª Hyponatremia
ª Hypernatremia
Sodium- Hyponatremia
ªSodium levels below 136 mEq/L
ª Sodium imbalances often occur with fluid imbalance because
same hormones regulate sodium & water balance
Causes of Hyponatremia: Actual Sodium Deficits
ªExcessive diaphoresis
ª Diuretics
ª Wound drainage
ª Decreased secretion of aldosterone
ª Hyperlipidemia
ª Kidney disease
ª NPO
ª Low-salt diet
ª Cerebral salt-wasting syndrome
ª Hyperglycemia
Causes of Hyponatremia: Relative Sodium Deficits (Dilution)
ªExcessive ingestion of hypotonic fluids
ª Psychogenic polydipsia
ª Freshwater submersion accident
ª Kidney failure
ª Irrigation with hypotonic fluids
ª Syndrome of inappropriate antidiuretic hormone secretion
ª Heart Failure
Assessment/Noticing: Hyponatremia - Cerebral Most Obvious
Changes
ªBehavioral changes from cerebral edema & ICP- monitor behavior & LOC, seizures & death can occur when very low
Assessment/Noticing: Hyponatremia - Neuromuscular
ªMuscle weakness worse in legs & arms
ª Deep tendon reflexes decrease
ª Assess for respiratory status as muscle weakness can effect this
Assessment/Noticing: Hyponatremia - Intestinal
ªIncreased motility with nausea, diarrhea & cramping
ª Bowel sounds hyperactive
Assessment/Noticing: Hyponatremia - Cardiovascular
ªRapid, weak, thread pulse, peripheral pulses difficult to palpate
ª B/P decreased
Interventions/Responding: Hyponatremia - Priorities
ªMonitor response to therapy to prevent hypernatremia & fluid
overload
Interventions/Responding: Hyponatremia - Drug Therapy
ªReduce those that cause sodium loss
ª IV's
Interventions/Responding: Hyponatremia - Nutrition Therapy
ªIncreasing oral sodium intake & restricting oral fluid intake
ª Teach about foods
ª Fluid restriction may be long-term with kidney impairment
ª Skin protection
Sodium: Hypernatremia
ªSerum sodium over 145 mEq/L
ª As level rises larger differences in ECF & ICF
ª More sodium present means movement rapidly across cell membranes that makes excitable tissues more excitable or Irritability
ª When levels high severe cellular dehydration with cellular shrinkage occurs
Causes of Hypernatremia - Actual Sodium Excesses
ªHyperaldosteronism
ª Kidney failure
ª Corticosteroids
ª Cushing Syndrome
ª Excessive oral intake
ª Excessive administration of sodium containing IV fluids
Causes of Hypernatremia - Relative Sodium Excesses
ªNPO
ª Increased rate of metabolism
ª Fever
ª Hyperventilation
ª Infection
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ª Excessive diaphoresis
ª Watery diarrhea
ª Dehydration
Assessment/Noticing: Hypernatremia - Nervous System
ªAltered function
ª Short attention span
ª Agitated
ª Confusion
Assessment/Noticing: Hypernatremia - Skeletal Muscle
ªMuscle twitching & irregular muscular contractions
ª As worsens progressive weakening
ª Late- reduced or absent reflexes
Assessment/Noticing: Hypernatremia - Cardiovascular
ªPulse increased
ª Peripheral pulsed difficult to palpate
ª Hypotension
ª Hypernatremia with hypovolemia: slow to normal bounding pulses, peripheral pulse full, B/P & diastolic pressure in increased
Interventions/Responding: Sodium - Drug Therapy
ªIsotonic saline (0.9%) & dextrose 5% in 0.45% NaCl
ª Other drug therapy
Interventions/Responding: Sodium - Nutrition Therapy
ªAdequate water intake
ª Dietary sodium restriction
ª Education
ª Patient safety- skin
Potassium
ªNormal level 3.5-5.0 mEq/L
ª Major cation of intracellular fluid
ª Need a large difference between ICF & ECF is critical for excitable
tissues to generate action
ª Because levels in interstitial fluid is low any change can seriously
affect physiology
ª Found in almost all foods
ª Main controller of ECF K+ is sodium potassium pump in all body
cells
ª 80% of K+ is removed from the body from the kidney
ª Regulate protein synthesis, glucose use, & storage
ª Hypokalemia
ª Hyperkalemia
Hypokalemia
ªSerum K+ below 3.5 mEq/L
ª It can be life threatening because every body system is effected
ª Reduction in excitability of the cells results- so nerve & muscle
are less responsive to normal stimuli
Causes of Hypokalemia: Actual Potassium Deficits
ªDrug abuse
ª Diuretics
ª Digitalis like drugs
ª Steroids
ª Increased aldosterone secretion
ª Cushing's syndrome
ª V&D
ª Wound drainage
ª NG suctioning
ª Excessive diaphoresis
ª Kidney disease
ª NPO
Causes of Hypokalemia: Relative Potassium Deficits
ªAlkalosis
ª Hyperinsulinism
ª Hyperalimination
ª TPN
ª Water intoxication
ª IV therapy
Assessment/Noticing: Hypokalemia
ªAge: Older more likely because urine concentration decreases
ª Drugs: Diuretics, steroids, digoxin, supplements
ª Disease: Chronic disorders, recent illnesses, nutrition hx
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Assessment/Noticing: Hypokalemia - Respiratory
ªShallow respirations
ª Breath sounds
ª Effort
ª Oxygenation: Nail beds, mucous membranes, rate & depth of
Assessment/Noticing: Hypokalemia - Musculoskeletal
ªWeakness
ª Sever causes flaccid paralysis
Assessment/Noticing: Hypokalemia - Cardiovascular
ªThready pulse, palpation difficult
ª Pulse ranges from very slow to very rapid
ª Irregular- dysrhythmia
ª B/P changes
Assessment/Noticing: Hypokalemia - Neurologic
ªAltered mental status
ª Short term irritability followed by lethargy
ª Progresses to acute confusion & coma
Assessment/Noticing: Hypokalemia - Intestinal
ªHypoactive bowel sounds
ª N&V
ª Constipation
ª Distention
Assessment/Noticing: Hypokalemia - Lab
ªMonitor values
ª ECG changes
ªThe effects of changes in potassium levels on the electrocardiogram (ECG). A, Normal ECG; B, ECG in hypokalemia; C, ECG in
hyperkalemia.
ECG Effects Potassium Levels
Interventions/Responding: Hypokalemia - Drug Therapy
ªAdditional K+ drugs to prevent loss
ª Route of administration depend on the degree of loss
ª IV is available in different concentrations with high alert therapyconcentrated dosed must be diluted & added to solutions in the
pharmacy & not available on the units
ª Severe tissue irritant & never given by injection- tissue damage
can be necrotic- assess site hourly
ª Oral doses - unpleasant taste & can cause N& V
Interventions/Responding: Hypokalemia - Nutrition
ªTeach how to increase dietary intake
ª Supplementation
Interventions/Responding: Hypokalemia - Safety
ªFall precautions due to muscle weakness
Interventions/Responding: Hypokalemia - Respiratory
ªMonitor hourly
ª O2 sats
ª Ability to cough to check for weakness
QSEN Safety Hypokalemia
ªAssessment drug use
ª Give oral supplements with a meal or snack
ª Check & re-check IV K+ to be sure max dose is no greater than
1 mEq/10mL of solution
ª IV access with large vein- avoid the hand
ª Infusion rate not faster than 5-10mEq/hr
ª Assess IV site hourly
ª Stop immediately if burning, or infiltration
ª Monitor ECG if possible
ª Keep on bedrest until hypokalemia resolves or provide assistance
when OOB
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Hyperkalemia
ªK+ levels >5.0mEq/L
ª Small increases can effect excitable tissues including the heart
ª Increases cell excitability causing tissues to decrease response
to stimuli
ª Heart very sensitive to changes
ª Interferes with electrical conduction of the heart leading to hearlt
block & ventricular fibrillation
ª Rare in people with normal kidney function
Causes of Hyperkalemia
Assessment/Noticing: Hyperkalemia - Cardiovascular
ªMost sever problems & most common cause of death
ª Bradycardia
ª Hypotension
ª ECG changes
ª Asystole
ª Ventricular Fibrillation
Assessment/Noticing: Hyperkalemia - Neuromuscular
ªParesthesia- tingling, burning then numbness of hands, feet &
around mouth
ª Flaccid paralysis as worsens
ª Resp muscles NOT effected
Assessment/Noticing: Hyperkalemia - Intestinal
ªIncreased motility with diarrhea, hyperactive bowel sounds
Assessment/Noticing: Hyperkalemia - Lab
ªMonitor values
ª If caused by dehydration follow other labs- H&H, BUN
ECG Effects of Hyperkalemia
Interventions/Responding: Hyperkalemia
ªDrug Therapy
ª Cardiac monitoring
ª Teaching: Foods
Patient Teaching: Hyperkalemia - Foods to Avoid
ªMeats- esp organ meats
ª Dairy products
ª Dried fruit
ª High K+ Fruits: Bananas, cantaloupe, Kiwi, oranges
ª High K+ Vegetables: Avocados, broccoli, dried beans or peas,
lima beans, mushrooms, potatoes, soybeans, spinach, seaweed
Patient Teaching: Hyperkalemia - Food to Eat
ªEggs
ª Breads
ª Butter
ª Cereals
ª Sugar
ª Low K+ Fruits: Apples, apricots, berries, cherries, cranberries,
grapefruit, peaches, pineapple
ª Low K+ Vegetables: Cabbage, carrots, cauliflower, celery, eggplant, green beans, lettuce, onions, peas, peppers, squash
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Calcium
ªNormal 9.0-10.5 mg/dL
ª Absorption requires active form of vitamin D
ª Stored in bones
ª When needed parathyroid hormone released in increases levels
ª Releases free calcium from bone storage
ª Stimulating vitamin D activation for absorption of Ca
ª Inhibiting kidney calcium excretion
ª Stimulating kidney calcium reabsorption
Hypocalcemia
ªCalcium < 9.0 mg/dL
ª Any change in calcium levels has major effects on functions
Causes of Hypocalcemia
Assessment/Noticing: Hypocalcemia
ªFrequent painful muscle spasms (charley horses) in calf or foot
ª Food history
ª Neuromuscular: Paresthesia if worsens muscle twitching,
spasms, painful cramps. Trousseaus & Chvosteks signs
ª Cardiovascular: May be slower or faster than normal with weak
thread pulse, ECG changes
ª Intestinal: Hyperactive bowel sounds, cramping, diarrhea
ª Skeletal: Loss of bone density, brittle bones, fragile, may break
easily
Assessment/Noticing: Hypocalcemia - Trousseau's
ªB/P cuff on arm, inflate greater than systolic, keep on 1-4 min
ECG Effects of Hypokalemia
Interventions/Responding: Hypocalcemia - Drug Therapy
ªSupplementation
Interventions/Responding: Hypocalcemia - Nutrition Therapy
ªCalcium rich diets
Interventions/Responding: Hypocalcemia - Safety
ªEnvironmental concerns due to excitable membranes of nervous
system & skeletal
ª Reduce stim in room
ª Limit visitors
ª Lighting
ª Soft voice
ª Careful lifting & positioning
Hypercalcemia
ªSerum Calcium > 10.5 mg/dL
ª Small increases have severer effects on body
ª Causes excitable tissues to be less sensitive to stimuli & need
stronger stimuli to respond
ª Heart, skeletal muscles, nerves & intestinal smooth muscle affected
Causes of Hypercalcemia
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Assessment/Noticing: Hypercalcemia - Cardiovascular
ªMost serious & life threatening conditions
ª Mild- causes increased HR & B/P
ª Severe- depresses electrical conduction, slowing the heart rate
ª Poor perfusion- cyanosis & pallor
ª ECG tracings
ª Clots
Assessment/Noticing: Hypercalcemia - Neuromuscular
ªSevere muscle weakness
ª Deep tendon reflexes decreased
ª Confusion & lethargy
Assessment/Noticing: Hypercalcemia - Intestinal
ªDecreased peristalsis
ª Constipation
ª Anorexia
ª N&V
ª Distention/pain
Interventions/Responding: Hypercalcemia
ªReducing serum calcium levels
Interventions/Responding: Cardiac Monitoring Important
ªIdentify dysrhythmias & decreased cardiac output
ª Compare with baseline
ª Look for T wave changes & QT interval changes (shortened) in
rate & rhythm
ª Pulse rate, B/P, perfusion changes
ª Monitor for clots- & interventions
Interventions/Responding: Drug Therapy
ªMedications & Fluid volume
Phosphorus
ªNormal 3.0-4.5 mg/dL
ª Found in bones
ª Activates vitamins & enzymes
ª Assists in cell growth & metabolism
ª Plasma levels of calcium & phosphorus exist in a balanced
relationship
ª Serum levels controlled by parathyroid hormone
ª Maintenance requires adequate renal functioning
ª Reciprocal relationship with calcium
ª Hypophosphatemia
ª Hyperphosphatemia
Hyperphosphatemia: High serum PO43 caused by
ªAcute kidney injury or chronic kidney disease
ª Excess intake of phosphate or vitamin D
ª Hypoparathyroidism
Hyperphosphatemia: Manifestations
ªTetany, muscle cramps, paresthesias, hypotension, dysrhythmias, seizures (hypocalcemia)
ª Calcified deposition in soft tissue such as joints, arteries, skin,
kidneys, & corneas (cause organ dysfunction)
Hyperphosphatemia: Management
ªIdentify & treat underlying cause
ª Restrict intake of foods & fluids containing phosphorus
ª Oral phosphate-binding agents
ª Hemodialysis
ª Volume expansion & forced diuresis
ª Correct any hypocalcemia
Hypophosphatemia: Low serum PO43 caused by
ªMalnourishment/malabsorption
ª Diarrhea
ª Use of phosphate-binding antacids
ª Inadequate replacement during parenteral nutrition
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Hypophosphatemia: Manifestations
ªCNS depression
ª Muscle weakness & pain
ª Respiratory & heart failure
ª Rickets & osteomalacia
Hypophosphatemia: Management
ªOral supplementation
ª Ingestion of foods high in phosphorus
ª IV administration of sodium or potassium phosphate: Monitor
serum calcium & phosphorus levels every 6 to 12 hours
Magnesium
ªNormal 1.3-2.1 mg/dL
ª Critical for skeletal muscle contraction, carbohydrate metabolism,
vitamin activation, cell growth
ª Hypomagnesemia
ª Hypomagnesemia
Hypomagnesemia
ªLevel < 1.8 mEq/L
ª Most often caused by decreased absorption of dietary magnesium or increased kidney magnesium excretion
ª Major causes loop or thiazide diuretics
Hypomagnesemia: Assessment - Cardiovascular
ªHypertension, atherosclerosis, dysrhythmias
Hypomagnesemia: Assessment - Neuromuscular
ªHyperactive deep tendon reflexes, numbness, tingling, painful
muscle contractions
ª Positive Chvesteks & Trousseau's due to calcium connection
(hypo)
Hypomagnesemia: Assessment - Intestinal
ªReduced motility
ª Anorexia
ª Nausea
ª Constipation, distention, crampling
Hypomagnesemia: Intervention
ªCorrect imbalance
ª Drugs
Hypomagnesemia
ªLevels > 2.6 mEq/L
ª Symptoms usually not apparent until above 4.0 mEq/L because is
a membrane stabilizer so needs membranes to destabilize before
symptoms
Hypomagnesemia: Assessment - Cardiac
ªBradycardia
ª Peripheral vasodilation
ª Hypotension
Hypomagnesemia: Assessment - Nervous System
ªDrowsy or lethargic
Hypomagnesemia: Assessment - Neuromuscular
ªReduced or absent reflexes
Hypomagnesemia: Interventions
ªFix the level or underlying problem
ª Drugs- oral or IV
Common Causes of Magnesium Imbalance
Chloride
ªNormal 98-106 mEq/L
ª Imbalance occurs as a result of other electrolyte imbalance
ª Treat underlying electrolyte imbalance of acid-base problem
IV Fluid & Electrolyte Replacement
ªPurposes
ª Maintenance: When oral intake is not adequate
ª Replacement: When losses have occurred
ª Types of fluids categorized by tonicity
IV Fluids: Hypotonic
ªLower osmolality when compared to plasma: Dilutes ECF
ª Water moves from ECF to ICF by osmosis
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ª Usually maintenance fluids
ª Monitor for changes in mentation
D5W
ªTechnically isotonic: Dextrose quickly metabolizes. Net result free
water
ª Provides 170 cal/L
ª Used to replace water losses, helps prevent ketosis
IV Fluids: Isotonic
ªSimilar osmolality to ECF: Expands only ECF
ª No net loss or gain from ICF
ª Ideal to replace ECF volume deficit
Normal Saline
ªNS, 0.9% saline, NSS
ª Isotonic
ª Slightly more NaCl than ECF
ª Used when both fluid & sodium lost
ª Only solution used with blood
Lactated Ringer's Solution
ªIsotonic
ª Contains sodium, potassium, chloride, calcium & lactate
ª Expands ECF—treat burns & GI losses
ª Contraindicated with liver dysfunction, hyperkalemia, & severe
hypovolemia
IV Fluids: Hypertonic
ªHigher osmolality compared with plasma
ª Draws water out of cells into ECF
ª Require frequent monitoring of: Blood pressure, Lung sounds,
Serum sodium levels
D5 ½ NS
ªHypertonic
ª Common maintenance fluid
ª Replaces fluid loss
ª KCl added for maintenance or replacement
D10W
ªHypertonic
ª Provides 340 kcal/L
ª Provides free water but no electrolytes
ª Limit of dextrose concentration that may be infused peripherally
Colloids
ªStay in vascular space & increase oncotic pressure
ª Include:
ª Human plasma products (albumin, fresh frozen plasma, blood)
ª Semisynthetics (dextran & starches, [Hespan])
ªSeparates dermis & epidermis
Skin Basics: Dermal-Epidermal Junction
ªTop layer of skin
Skin Basics: Epidermis
Skin Basics: Dermis
ªInner layer of skin
ª Collagen
Wound Classification: Acute
ªA Wound that passes through the routine process of repair &
restoration
ª Caused by trauma or surgical incisions
ª Easily cleaned & repaired, wound edges intact
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ªWound that does not go through the routine process of repair &
restoration
ª Caused by vascular compromise, chronic inflammation or repeated tissue damage
ª Difficult to heal because continued exposure slows healing
Wound Classification: Chronic
ªEdges brought together with skin lined up in correct anatomical
position
ª Wound is closed
ª Heals quickly with minimal scarring
Phases of Wound Healing: First Intention or Primary Intention
ªRequires gradual filling in of dead space with connective tissue
ª Edges not approximated
ª Pressure ulcers, surgical wounds with tissue loss
ª Heal by granulation tissue & wound contraction
Phases of Wound Healing: Second Intention
ªDelayed closure; high risk for infection with resulting scar
ª Wound left over for several days, then edges approximated
ª Wounds that are contaminated & need watched for infection
Phases of Wound Healing: Third Intention or Tertiary Intention
Mechanisms of Wound Healing: Partial Thickness Wounds
ªDamage to epidermis, upper layers of dermis
ª Superficial wounds with minimal loss of tissue integrity from
damage to the epidermis & upper dermal layers
ª Heal by re-epthelialization which is the production of new skin
cells by undamaged epidermal cells in the basal layer of the
dermis
ª Fibrin clot is formed & release of growth factor that stimulate
epidermal cell division, new skin cells & re growth (resurfacing)
ª Heal by re-epithelialization within 5 to 7 days
ªPartial- thickness wound repair
ª Inflammatory phase- redness, swelling, edema, first 24 hours,
Mechanisms of Wound Healing: Partial Thickness Wounds Repair
epithelial proliferation & migration- starts at wound edges & cells
migrate across the wound bed. Moisture helps healing
ªThe image at the right details the process of re-epithelialization.
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Re-Epithelialization
ªHemostasis: Injured blood vessels constrict & clot formation
occurs
ª Inflammatory Phase: Redness, swelling, edema- & inflammatory
response begins
ª Proliferative Phase: 3-24 days- granulation tissue & contraction
of the wound
ª Remodeling: Collagen scar formation
Mechanisms of Wound Healing: Full Thickness Repair - Four
Phases
Complications of Wound Healing: Hemorrhage
ªBleeding from a wound site- normal during & immediately after
initial trauma
Complications of Wound Healing: Hematoma
ªLocalized collection of blood underneath the tissues
Complications of Wound Healing: Infection
ªSecond most common health care associated infections. Edges
of wound inflamed, may have odorous & purulent drainage (yellow, green, brown color depending on the organism)
Complications of Wound Healing: Dehiscence
ªPartial or total separation of wound layers.
Complications of Wound Healing: Evisceration
ªTotal separation of wound layers & protrusion or organs through
the wound. Emergency needs surgical repair
Cleaning Skin: Interventions for Wounds
1. Clean in a direction from the least contaminated area such as
from the wound or incision to the surrounding skin or from an
isolated drain site to the surrounding skin.
2. Use gentle friction when applying solutions locally to the skin.
3. When irrigating, allow the solution to flow from the least to the
most contaminated area.
Methods for Cleaning a Wound Site: Interventions for Wounds
Drainage Evacuators: Interventions for Wounds
Staples & Remover: Interventions for Wounds
Removal of Intermittent Suture: Interventions for Wounds
Approximated Wounds: Interventions for Wounds
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Approximated Wounds: Interventions for Wounds
Bandages & Binders: Interventions for Wounds
ªFunctions: Create pressure, immobilize &/or support a wound,
reduce or prevent edema, secure a splint, secure dressings
ª Bandages: Rolled gauze, elasticized knit, elastic webbing, flannel,
& muslin
ª Binder application: Breast, abdominal, sling
ª Assessment of: After applying a bandage, the nurse assesses,
documents, & immediately reports changes in circulation, skin
integrity, comfort level, & body function. Neurovascular checks
(pain, pallor, pulse, paresthesia, paralysis)
Heat & Cold Therapy: Interventions for Wounds
ªAssessment for temperature tolerance
ª Assess the skin & skin integrity.
ª Assess the patient's response to stimuli.
ª Assess the equipment being used.
ª Identify any contraindications.
ª Bodily responses to heat & cold- neurovascular checks
ª Local effects of heat & cold
ª Factors influencing heat & cold tolerance
ª Application of heat & cold therapies- usually ordered 15-20 minutes on & off
Contraindications to Cold & Heat: Interventions for Wounds - Cold
is Contraindicated
ªIn the presence of neuropathy
ª If the patient is shivering
ª If the patient has impaired circulation
Contraindications to Cold & Heat: Interventions for Wounds - Heat
is Contraindicated
ªFor areas of active bleeding
ª For an acute localized inflammation
ª Over a large area if a patient has cardiovascular problems
Evaluation
ªWas the etiology of the skin impairment addressed? Were the
pressure, friction, shear, & moisture components identified; &
did the plan of care decrease the contribution of each of these
components?
ª Was wound healing supported by providing the wound base with
a moist protected environment?
ª Were issues such as nutrition assessed & a plan of care developed that provided the patient with the calories to support
healing?
QSEN Best Practice for Wound Monitoring: Wounds Without Tissue Loss (EX Surgical incisions, Clean lacerations that are closed
with sutures)
ªLoss of tissue integrity caused when skin & underlying soft tissue
are compressed between a bony prominence & external surface
ª Can occur on any body surface
Tissue Integrity Concept Exemplar: Pressure Injuries - Pathophysiology Overview
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Pressure Injuries: Etiology & Genetic Risk
ªDependent upon mechanism & timing
ª Friction
ª Shearing force
Pressure Injuries: Incidence & Prevalence
ª 3million adults affected annually
ª 0.6% - medical device-related pressure injuries
Pressure Injuries: Health Promotion & Maintenance
ªRecognize risk & implement interventions to prevent injury
ª Begin interventions early for any existing injury
ª Key health team members can assist
Health Promotion & Maintenance
ªNeed to recognize the risk- they can be prevented
ª Prevention program: Early identification of high-risk patients. Implementation of aggressive intervention for prevention
ª Pressure Mapping: A computerized tool that measures pressure
distribution during sitting & lying to identify areas for breakdown.
Map displayed in colors- red area=greater heat production &
increased pressure. Blue=risk assessment with lower pressure
Pressure Injuries: Assessment: Recognize Cues - History
ªConduct with risk factors in mind
ª Identify cause for any existing injury
ª Contributing factors
ª Bedrest, immobility
ª Incontinence
ª Diabetes mellitus &/or peripheral vascular disease
ª Malnutrition
ª Decreased sensory perception or cognitive problems
Assessment: Physical & Signs & Symptoms
ªOverweight patient = Higher Risk
ª Inspect entire body
ª Special attention to bony prominences & areas with moisture
ª Tubing & devices not under patients
ª Proportion of height & weight
ª Overall cleanliness of skin, hair, nails
ª Any loss of mobility
ªNeeds positive nitrogen balance (associated with periods of
growth & tissue repair) ( intake of nitrogen in the body is greater
than the loss) & adequate serum protein level
ª Needs 1500kcal/day Vitamins A & C & protein to heal
ª Assessment: labs, weight & changes, ability to consume adequate diet, need for supplementation (Vit & Min)
ª Serum pre-albumin used to monitor nutrition status (low malnutrition)
Pressure Injuries: Assessment: Recognize Cues - Risk Factors - ª Nitrogen balance (dietary protein requirements- protein)
Nutrition
ª Positive intake 30-35 calories per kilogram of weight
ª Protein intake 1.25 to 1.5 g/kg/day
ª Up to 2 g/kg/day of protein may be needed to heal if has a deficit
ª Inadequate blood levels
ª Prealbumin < 15 g/dL (normal 15-36 mg/dL) ( measurement of
short term impairment- 2-4 days)
ª Albumin < 3.5 g/dL (normal 3.5-5.5 g/dL) (longer term measurement- 20-22 days)
ª Lymphocyte < 1800/mm3 (normal 1,000-4,800 mm3)
Pressure Injuries: Assessment: Recognize Cues - Risk Factors Incontinence
ªExcessive moisture macerates skin & leads to breakdown
ª Daily inspection needed for redness, maceration or skin loss
needed
ª Maintenance of clean, dry, intact skin needed for prevention
Patient at Risk for Pressure Injuries Assessment
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ªCardiovascular Disease, Diabetes
ª Braden Scale- risk assessment tool. Categories: mental status,
activity level, mobility, nutritional status, incontinence
ª Mental Status Changes & Decreased Sensation. Stoke, head inPressure Injuries: Assessment: Recognize Cues - Risk Factors jury, organic brain disease, Alzheimer's, sedation, other cognitive
changes
ª Impaired Mobility: Anyone who requires assistance with turning
& positioning, or unable to verbalize discomfort
ª Nutrition & incontinence
Braden Scale
Stage 1: Pressure Injury
ªIntact skin with localized area of non-blanchable erythema (may
appear differently in skin with darker pigmentation).
ª May be preceded by changes in sensation, temperature or firmness.
ª Color changes are not purple or maroon.
ªPartial-thickness loss of skin with exposed dermis.
ª Wound bed is viable, pink or red, & moist.
ª May look like intact or ruptured serum-filled blister.
Stage 2: Pressure Injury
Stage 3: Pressure Injury
ªFull-thickness skin loss with adipose (fat) visible in the ulcer.
ª Granulation tissue & rolled wound edges are often present.
ª Slough &/or eschar may be present.
ª Undermining & tunneling may be present.
ª Subcutaneous tissues may be damaged or necrotic.
Stage 4: Pressure Injury
ªFull-thickness skin loss with exposed or palpable fascia, muscle,
tendon, ligament, cartilage, or bone.
ª May have slough or eschar.
ª Rolled edges, undermining, or tunneling may be present.
Unstageable Deep Tissue Injury: DTI
Pressure Injuries: Assessment: Recognize Cues
ªDocument location, size, color, extent of tissue involvement, cell
types in wound base & margin, exudate, condition of surrounding
tissue, presence of foreign bodies
ª Record by length, width, depth (using mm or cm)
ª "Clock concept"
Wound Assessment: Location & Size
ªLength, width & depth using millimeters or centimeters
ª Face of the clock with 12:00 position of the head & 6:00 the
patients feet
ª Length is 12 to 6
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ª Width 9-3
ª Depth- deepest portion
Wound Assessment
ªColor
ª Extent of involvement
ª Cell types in wound base & margins- wound bed & perimeter
ª Exudate
ª Condition of surrounding tissue
ª Presence of foreign bodies
ª Eschar - Necrotic Tissue: Early stage of healing: eschar is dry
leathery, & firmly attached to the wound
ª Granulation tissue- early pale pink, beefy red as improves
ª Dressing- compare now to what was documented
ª Blanching
ª Tunneling
Wound Assessment: Documentation
ªLocation, size of wound
ª Location & length of tunnel if present
ª Photographs if permitted by facility policy & informed consent
Wound Assessment: Psychological
ªBody image
ª Refer to social service or case worker if financial barrier is noted
ª Refer to home care nurse if patient or caregiver can't safely carry
out plan of care
ª Family & patient knowledge of treatment & outcomes
ª Skills with care for caring for the wound
ª Stress
Wound Assessment: Labs
ªWound culturing is not routinely performed
ª If performed, tissue culture is done (not just wound swab)
ª Exposed chronic wound always colonized with microorganisms
but not always infected
ª Colonization is the presence of one or more communities of
organisms that attach to the wound surface in the form a wound
biofilm.
ª Wound infection is a state of critical colonization with pathogenic
organisms to the degree that organism growth & spread cannot
be controlled by the bodies immune system
ª Wounds that are red, with moderate to heavy exudate & odor
should be cultured for infection
ª Purulent exudate alone does not indicate infection because pus
forms where necrotic tissue liquefies & separates
ª If blood supply to the wound is decreased bacterial growth quickens
Wound Assessment: Labs - Clinical Indicators of Infection
ªCellulitis, progressive increase in ulcer size or depth, changes in
the quantity & quality of exudate, systemic signs of bacteremia
(fever, increased WBC)
Wound Assessment: Labs - Cultures
ªSwabs- help to identify the type of bacteria on the ulcer surface
& may not show what is deeper in the wound
Wound Assessment: Labs - Biopsies
ªAllow numbers of bacteria to be analyzed- tests are expensive
Wound Assessment: Other Diagnostic
ªArterial blood flow studies if arterial occlusion is suspected
ª Duplex ultrasound imaging
ª Blood tests for nutritional deficiencies
ª Prealbumin< 15 g/dL (normal 15-36 mg/dL)( shorter duration 2-4
days)
ª Albumin < 3.5 g/dL (normal 3.5-5.5 g/dL) ( 20-22 days)
ªCompromised tissue integrity due to vascular insufficiency &
trauma as evidenced by _______________
Pressure Injuries: Analysis: Analyze Cues & Prioritize Hypotheses
ª Potential or risk for for infection due to insufficient wound management
ªPad contact surfaces with foam, silicone, air pads or other devices
ª Do not keep the head of bed elevated above 30 degrees to
prevent shearing
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QSEN: Preventing Pressure Injuries - Positioning
ª Use lift sheet to move in bed
ª When positioning on side use a 30 degree angle
ª Re-position immobile patient as needed
ª Do not place rubber ring or donut in sacral area
ª Use lubricated slide board or mechanical lift
ª Keep heels off bed, using pillow under ankles
QSEN: Preventing Pressure Injuries - Nutrition
ªFluid intake 2000-3000 mL/day
ª Adequate intake of protein & calories
QSEN: Preventing Pressure Injuries - Skin Care
ªDaily inspection of skin
ª Document & report any manifestations
ª Use moisturizers daily on dry skin & apply to damp skin
ª Keep moisture from prolonged contact with skin
ª Dry areas where skin touches
ª Place absorbent pads under areas of perspiration
ª Moisture barriers on skin for wound drainage of incontinence
QSEN: Preventing Pressure Injuries - Skin Cleaning
ªClean as soon as possible with soiling & routine intervals
ª Use mild, heavily fatted soap, or gentle commercial cleanser for
incontinence
ª Tepid water- not hot
ª Perineal area- use disposable cleaning cloth that has skin barrier
ª Minimum scrubbing force necessary
ª Pat dry skin
ª No powders or talk directly on perineum
ª After cleaning apply commercial skin
Pressure Injury: Implementation - Improving Tissue Integrity
ªNonsurgical Management
ª Dressings
ª Physical therapy
ª Drug therapy
ª Nutrition therapy
ª Adjuvant therapies
ª Surgical management
Pressure Injury: Implementation - Preventing Infection
ªMonitor for signs & symptoms of infection
ª Report changes to primary health care provider
ª Maintain safe environment
Pressure Relieving Techniques: Support Surfaces & Devices
ªMost important is management of adequate pressure distribution
over bony prominences & maintain capillary closing pressure
(pressure needed to occlude skin capillary blood flow)
ª Capillary blood flow normal ranges 12-32 mmHg
ª Should have re-distribution below capillary closing pressure to
promote perfusion
ª Most support surfaces have a pressure-distribution reading but
they do not ensure capillary blood flow for any patient is adequate
ª Need to assess & observe skin color, cap refill, tissue integrity, &
temp
Pressure Relieving Techniques: Support Surfaces & Devices
ªFactors to consider when selecting
ª Number & severity of existing injuries
ª Risk for developing new pressure injuries
ª Patient ability to reposition self to relieve pressure
ª Need for microclimate control to help manage skin temperature
for moisture
ª Need to reduce shearing forces
ª Compatibility of produce with the care setting
Pressure Relieving Techniques: Positioning
ª 30-degree-rule- ensures a patient is positioned & propped so
whatever part of the body is tilted back no more than 30 degree
angle to the mattress
ª If you need more than that for breathing should be 30 degrees
with pillows behind the back to keep off coccyx & sacrum
ª While sitting- assess for chair cushioning, PT
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ª Many facilities require every 2 hour positioning- pressure injury
can occur sooner than this so needs to be individualized
QSEN Implementation Nonsurgical Management
ªIf covered, change dressing according to manufacturer's instructions, when dressing seal is compromised or drainage is visible,
or wet
ª Measure wound size at greatest length & width using disposable
paper tape measure, at least weekly or more if deterioration (face
of a clock with 12:00 at the head & 6:00 feet. Length is 12-6, width
9-3)
ª Compare all subsequent measurements against initial
ª Assess injury for necrotic tissue & exudate
ª Assess & document condition of the skin surrounding the pressure injury in terms of color, temp, moisture & appearance
ª Remove or trim loose bits of tissue- done by appropriate personnel
ª Cleanse the injury with saline, non-toxic wound cleaner or prescribed solution
ª Rinse & dry injury surface
ª Collaborate & select correct dressing
ª Avoid positioning on the site- if possible
ª Re-position frequently
ª Use pressure reduction devices & techniques
Implementation Nonsurgical Management
ªDressings: Help healing by removing the surface debris, protecting exposed healthy tissue, & creating a barrier until the ulcer is
healed.
ª For a draining necrotic ulcer the dressing must also remove
excess exudate & loose debris without damaging health cells or
granulation tissue.
ª Mechanical debridement (wet to dry dressings): Mechanical entrapment & detachment of dead tissue
ª Topical Chemical Debridement: Topical enzyme preparations to
loosen necrotic tissue
ª Natural Chemical Debridement: Promoting self-digestion of dead
tissue by naturally occurring bacterial enzymes (autolysis)
Common Dressing Techniques for Wound Debridement
Dressings: Hydrocolloid
ªHydrocolloid: Protects the wound from surface contamination,
they are adhesive & occlusive-The wound contact layer of this
dressing forms a gel as fluid is absorbed & maintains a moist
healing environment. Hydrocolloids support healing in clean granulating wounds & autolytically debride necrotic wounds; they are
available in a variety of sizes & shapes. This type of dressing has
the following functions:
ª Absorbs drainage through the use of exudate absorbers in the
dressing
ª Maintains wound moisture
ª Slowly liquefies necrotic debris
ª Is impermeable to bacteria & other contaminants
ª Is self-adhesive & molds well
ª Acts as a preventive dressing for high-risk friction areas
ª May be left in place for 3 to 5 days, minimizing skin trauma &
disruption of healing
Dressings: Hydrogel
ªHydrogel—maintains a moist surface to support healing; dressings are gauze or sheet dressings impregnated with water- or
glycerin-based amorphous gel. Hydrogel has the following advantages:
ª Is soothing & can reduce wound pain
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ª Provides a moist environment
ª Debrides necrotic tissue (by softening necrotic tissue)
ª Does not adhere to the wound base & is easy to remove
Nonsurgical Management Pressure Injury: Dressings - Hydrophobic
ªNonabsorbent waterproof material is used when the wound has
little drainage & needs to be protected from external contamination
Nonsurgical Management Pressure Injury: Dressings - Hydrophilic
ªAbsorbent material draws excessive drainage away from the
injury surface, preventing maceration
ªChanged when outer layer is saturated with exudate
Nonsurgical Management Pressure Injury: Dressings - Dry Gauze
ª Gauze drainage for debridement of a wet wound are changed
Dressings
often enough to take off debris- usually 4-6 hours
Nonsurgical Management: Physical Therapy
ªConsult & implement strategies to off-load pressure & increase
cardiovascular status
Nonsurgical Management: Physical Therapy - Ultrasound
ªLow frequency energy sound waves to cleanse & debride necrotic
tissueª Administered with disposable applicator moved over the wound
without touching
Nonsurgical Management: Physical Therapy - Electrical Stim
ªTo promote healing if appropriate
ª Low-voltage current to a wound to increase blood vessel growth
& promote granulation
ª Voltage delivered in pulses that may cause a "tingling" sensation
ª Usually 1 hour 5-7 days
ª Do not use with pacemaker, wound over the heart, or skin cancer
involving the wound or periwound skin
ª Restores natural electric impulses shown to promote healing
Nonsurgical Management Pressure Ulcers: Drugs
ªAntibiotics if necrotic or infection
ª Topical antibiotics/ topical antibiotic dressings
Drug Therapy
ªAdequate calories, protein, vitamins, minerals, & water
ª Protein deficiency inhibits healing
ª Consult with dietician
Interventions: Pressure Ulcers - Nutrition
ªRemoval of fluids or infections found in the wound & enhances
granulation tissue
ª Suction tube covered by specific sponge & sealed in place
Interventions: Pressure Ulcers - Negative Pressure Wound Ther- ª Usually changed every 48-72 hours
apy (NPWT)
ª Continuous low-level negative pressure applied
ª Duration of treatment depends on response
ª Should monitor every 2 hours for bleeding
ª Failure of therapy is usually inadequate seal
ªThe vacuum-assisted closure (V.A.C.) is a device that assists in
wound closure by applying localized negative pressure to draw
the edges of a wound together.
ª Modifications have been made to the V.A.C. The V.A.C. Instill
allows intermittent instillation of fluids into the wound, especially
those wounds not responding to traditional (negative-pressure
wound therapy (NPWT). NPWT is used in treating acute & chronic
wounds.
ª The schedule for changing NPWT dressings varies, depending
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on the type of wound & the amount of drainage. Wear time for the
dressing is anywhere from 24 hours to 5 days.
ª As the wound heals, granulation tissue lines its surface. The
wound has a stippled or granulated appearance. The surface area
Interventions: Pressure Ulcers - Negative Pressure Wound Ther- sometimes increases or decreases, depending on wound location
apy (NPWT)
& the amount of drainage removed by the NPWT system. NPWT
is also used to enhance the take of split-thickness skin grafts. It is
placed over the graft intraoperatively, decreasing the ability of the
graft to shift & evacuating fluids that build up under it. An airtight
seal must be maintained.
Interventions: Pressure Ulcers - Negative Pressure Wound Therapy (NPWT)
ªOxygen administered under high pressure that raises tissue
oxygen levels
ª Used in life-threatening wounds- burns, necrotizing infections,
limb-threatening wounds, recluse spider bites, osteomyelitis &
diabetic ulcers
ª Patient in large chamber with 100% oxygen at pressures greater
than atmospheric pressure
ª Systemic oxygen enhances ability of WBC to kill bacteria
ª Smaller oxygen delivery systems are also available
Interventions: Hyperbaric Oxygen Therapy (HBOT)
QSEN Best Practice for Monitoring Wounds with Tissue Loss (Full
or partial thickness caused by pressure, vascular disease, trauma
& allowed to heal by secondary intention)
Interventions: Pressure Ulcers - Self Management/Education
ªPrior to discharge:
ª Demonstrate competence with removing dressing, cleaning of
wound, applying dressing
ª Caregiver ability of above
ª Finances to cover above
ª Diet & nutrition needs
ª Incontinence care if applicable
Pressure Injuries: Evaluation: Evaluate Outcomes
ªExperience progress toward wound healing by second intention
as evidenced by granulation, epithelialization, contraction, & reduction or resolution of wound size
ª Re-establish skin tissue integrity & restore skin barrier function
ª Remain free from local or systemic infections
Priorities & Interrelated Concepts: Priority is Glucose Regulation
ªOther concerns
ª Nutrition
ª Tissue Integrity
ª Sensory Perception
ª Immobility
ª Fluid & electrolyte imbalance
ª Acid-base imbalance
Diabetes Mellitus
ªHyperglycemia resulting from problems with glucose regulation
that include reduced insulin secretion or reduced insulin action or
both
ªCommon, chronic complex disorder of impaired nutrient metabolism (especially glucose)
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Diabetes Mellitus: Pathophysiology Overview
ª Types - our focus is on Type 1 & Type 2
ª Glucose regulation & homeostasis
ª Absence of insulin
ª Acute & chronic complications
Diabetes Mellitus Overview
ªA chronic multisystem disease characterized by hyperglycemia
related to abnormal insulin production, impaired insulin use, or
both
ª Affects 29.1 million people in United States: 8.1 million unaware.
86 million have prediabetes
ª Seventh leading cause of death
Diabetes Mellitus: Leading Cause Of
ªAdult blindness
ª End-stage renal disease
ª Nontraumatic lower limb amputations
Diabetes Mellitus: Major Contributing Factor
ªHeart disease & stroke (2 to 4 times higher): Many have HTN &
high cholesterol
Diabetes Mellitus: Etiology & Pathophysiology
ªTheory of cause: single or combination of factor(s):
ª Genetic
ª Autoimmune
ª Environmental
ª Disorder of glucose metabolism related to absent/insufficient
insulin &/or poor utilization of insulin
The American Diabetes Association (ADA) recognizes four different classes of diabetes
ªType I
ª Type 2
ª Gestational
ª Other
The Pancreas: Exocrine Function
ªDigestion
The Pancreas: Endocrine Function
ªEnsure blood glucose regulation
ªAlpha cells that secrete glucagon
Pancreas Endocrine Function: Pathophysiology - Islets of Langer- ª Beta cells which produce insulin & amylin (a peptide hormone
hans Contain
that is secreted with insulin- function is to slow digestion & block
glucagon secretion, & enhances the feeling of fullness)
Pancreas Endocrine Function: Pathophysiology - Glucagon
ªCounterregulatory hormone that's actions oppose insulin
ª Prevents hypoglycemia by triggering release of glucose from the
liver storage & in skeletal muscle
Glucose Regulation
ªProcess of maintaining glucose regulation
ª When stomach is empty glucose is maintained between 60-150
mg/dL
ª Glucose main fuel for CNS- BRAIN CANNOT STORE MUCH
GLUCOSE
ª Other organs use glucose & fatty acids for energy
ª Insulin is the key that opens membranes to glucose- this allows
the cells to generate energy
Etiology & Pathophysiology : Normal Glucose & Insulin Metabolism
ªInsulin—hormone produced by -cells in islets of Langerhans
ª Released continuously into bloodstream in small increments
with larger amounts released after food Daily amount of insulin
secreted by adult = 40 to 50 U
ª Stabilizes glucose level in range of 74 to 106 mg/dL
Insulin Physiology
ªProinsulin, secreted by & stored in the beta cells of the islets
of Langerhans in the pancreas, is transformed by the liver into
active insulin. Insulin attaches to receptors on target cells, where
it promotes glucose transport into the cells through the cell membranes.
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Etiology & Pathophysiology
ªInsulin is synthesized from proinsulin (precursor)
ª Enzymes split proinsulin into insulin & C-peptide in equal
amounts: Serum & urine C-peptide measurements is a good
clinical indicator of -cell function & insulin levels
Insulin
ªProtein made up of amino acids
ª Secreted daily into liver circulation by:
ª At low levels during fasting
ª Two phase release after eating (prandial- during or relating to
food)
ª Early burst within 10 minutes of eating
ª Then increasing release that lasts until blood glucose is back to
normal
Glucose Regulation: Insulin Effects
ªMetabolic Effects of Insulin- Overall keeps blood glucose from
being to high
ª Stimulate glucose uptake in skeletal & heart muscle
ª To suppress liver production of glucose & very low density
lipoprotein
ª In Fat Cells Insulin
ª Promotes triglyceride storage
ª In muscle Insulin
ª Promotes protein & glycogen synthesis
ª In the liver Insulin
ª Glucose promotes production & storage of glycogen(glycogenesis)
ª Inhibits glycogen breakdown into glucose (glycogenolysis)
ª Increases protein & lipid synthesis
ª Inhibits ketogenesis (conversion of fats to acids)
ª Conversion of proteins to glucose (gluconeogeneisis)
Insulin
ªPromotes glucose transport from bloodstream across cell membrane to cytoplasm of cell: Decreases glucose in the bloodstream
ª ‘ insulin after a meal
ª Stimulates storage of glucose as glycogen in liver & muscle
ª Inhibits gluconeogenesis
ª Enhances fat deposition
ª ‘ protein synthesis
ª The fall in insulin level during normal overnight fasting facilitates
the release of stored glucose from the liver, protein from muscle,
& fat from adipose tissue.
Glucose Regulation: Insulin Effects - Fasting State
ªNot eating for 8 hours
ª Insulin secretion is suppressed
ª Leads to gluconeogenesis (conversion of proteins to glucose) in
liver & kidney
ª Increased glucose by breakdown of liver glycogen
Normal Glucose & Insulin Metabolism
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Normal Glucose Ranges
Normal Insulin Secretion
Etiology & Pathophysiology
ªSkeletal muscle & adipose tissue: Have receptors for insulin;
insulin-dependent
ª Insulin "unlocks" receptors so glucose can move into the cell to
be used for energy
ª Other tissues don't require insulin for glucose transport but still
require glucose to function
ª Liver Cells: Not insulin-dependent but have receptor sites to
facilitate uptake of glucose & convert it to glycogen
Etiology & Pathophysiology - Counterregulatory Hormones
ªGlucagon, epinephrine, growth hormone, cortisol
ª Oppose effects of insulin
ª Stimulate glucose production & release by the liver
ª Decrease movement of glucose into cell
ª Help maintain normal blood glucose levels
Glucose Regulation: Counterregulatory Hormones
ªIncrease blood glucose by having opposite actions of insulin when
energy is needed
ª Increase blood glucose levels
ª Provide regulated release of glucose for energy
ª Help maintain normal blood glucose levels
ª Glucagon-main one
ª Epinephrine
ª Norepinephrine
ª Growth hormone
ª Cortisol
Physiologic Response to Insufficient Insulin
ªDecreased glycogeneisis (conversion of glucose to glycogen)
ª Increased glycogenolysis (conversion of glycogen to glucose)
ª Increased gluconeogenesis (formation of glucose from noncarbohydrate sources such as amino acids & lactate)
ª Increased lipolysis (breakdown of triglycerides to glycerol & free
fatty acids)
ª Increased ketogenesis (formation of ketones from free fatty acids)
ª Proteolyisis (breakdown of protein with amino acid release in
muscles)
ªHyperglycemia: Blood glucose too high
ª Polyuria: Excessive urination
ª Polydipsia: Excessive thirst
ª Polyphagia: Excessive eating
ª Ketone bodies: Abnormal breakdown products that collect in
blood leading to metabolic acidosis
ª Hemoconcentration: Increased blood concentration
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ª Hypovolemia: Decreased blood volume
ª Hypoxia: Poor tissue perfusion
ª Potassium Changes: Depletion: Due to increase fluid loss. Increased: depending on hydration
ª Kussmaul Respiration: Triggered from acidosis in attempt to
"blows off" carbon dioxide & acid. Increase rate & depth of respirations. Acetone is exhaled= fruity breath. Blood pH drops & metabolic acidosis occurs along with respiratory alkalosis (decreased
partial pressure of arterial carbon dioxide)
Absence of Insulin
Classifications Overview
Type 1 Diabetes
ªFormerly known as juvenile-onset or insulin-dependent diabetes
ª Accounts for about 5% to 10% of all people with diabetes
ª Generally affects people under age 40: Can occur at any age
Type 1 Diabetes Mellitus: End result of long-standing process
ªProgressive destruction of pancreatic
cells by body's own T cells
ª Autoantibodies cause a reduction of 80% to 90% in normal -cell
function before manifestations occur.
ª Idiopathic diabetes is a form of type 1 diabetes that is not related
to autoimmunity but is strongly inherited. This occurs only in a
small number of people with type 1 diabetes & is most often in
those of African or Asian ancestry.
Type 1 Diabetes Mellitus: Causes
Type 1 Diabetes Mellitus
ªGenetic predisposition: Related to human leukocyte antigens
(HLAs)
ª Exposure to a virus
ªLong preclinical period
ª Antibodies present for months to years before symptoms occur
ªRapid onset of symptoms
ª Present at ED with ketoacidosis
ª Occurs in absence of exogenous insulin
Type 1 Diabetes Mellitus - Manifestations develop when pancreas ª Life-threatening condition
can no longer produce insulin.
ª Results in metabolic acidosis
ª Body breaks down fat too fast- liver processes the fat into ketones
which causes the blood to be acidotic
ª All patients with DM experience hyperglycemia.
Type 1 Diabetes Mellitus - The Signs & Symptoms of Hyperglycemia
ªPolyuria
ª Polydipsia
ª Polyphagia.
ª Weight loss
ª Malaise
ª Fatigue
ª Blurred vision
ª Blood glucose above 180mg.dL (above renal threshold)
Type 1 Diabetes: Onset of Disease
ªIslet cell autoantibodies are present for months to years before
symptoms occur
ª Manifestations develop when pancreas can no longer produce
insulin—then rapid onset with ketoacidosis. Recent history of
sudden weight loss & polydipsia, polyuria, & polyphagia
ª Requires exogenous insulin
ª Patient may have temporary (3 to 12 months) remission after
initial treatment
Type 2 Diabetes
ªFormerly known as adult-onset diabetes (AODM) or non-insulin-dependent diabetes (NIDDM)
ª Most prevalent type (90% to 95%)
ª Many risk factors: overweight or obese, advanced age, family
history. prevalence in children due to obesity
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Type 2 Diabetes Mellitus
ªMost prevalent type of diabetes
ª More than 90% of patients with diabetes
ª Usually occurs in people over 35 years of age
ª 80% to 90% of patients are overweight
ª Prevalence of type 2 diabetes increases with age, with about half
of those diagnosed being older than 55.
ª Prevalence increases with age.
ª Genetic basis
ª Greater in some ethnic populations
ª Increased rate in African Americans, Asian Americans, Hispanic
Americans, & Native Americans
ª Native Americans & Alaskan Natives: Highest rates of diabetes
in the world
Type 2 Diabetes Mellitus: Etiology & Pathophysiology
1. Insulin resistance: Body tissues do not respond to insulin.
Insulin receptors are either unresponsive or insufficient in number.
Results in hyperglycemia
2. Pancreas “ ability to produce insulin.²cells fatigued from compensating. ²-cell mass lost.
3. Inappropriate glucose production from liver. Liver's response
of regulating release of glucose is haphazard. Not considered a
primary factor in development of type 2
4. Alteration in production of hormones. Play a role in glucose &
fat metabolism. Contribute to pathophysiology of type 2 diabetes
Type 2 Diabetes: Etiology & Pathophysiology
ªPancreas continues to produce some endogenous insulin but
Not enough insulin is produced &/or Body does not use insulin
effectively
ª Major distinction: In type 1 diabetes, there is an absence of
endogenous insulin
Type 2 Diabetes: Genetic Link - Multiple Genes & Metabolic
Abnormalities
1. Insulin resistance
2. Decreased insulin production by pancreas
3. Inappropriate hepatic glucose production
4. Altered production of hormones & cytokines by adipose tissue
(adipokines)
5. Research continues on role of brain, kidneys, & gut in type 2
diabetes
Type 2 Diabetes: Metabolic Syndrome increases risk for: Type 2
Diabetes
ªIncreased glucose levels
ª Abdominal obesity
ª High BP
ª High level of triglycerides
ª Decreased levels of HDLs: 3 of 5 components = metabolic syndrome
ªCluster of abnormalities that increase risk for cardiovascular disease & diabetes ( high blood pressure, high glucose, excess body
weight around the waist, abnormal cholesterol & triglycerides)
Type 2 Diabetes Mellitus: Individuals with Metabolic Syndrome at ª Characterized by insulin resistance
increased risk for
ª Elevated insulin levels, ‘ triglycerides, LDLs, “ HDLs, hypertension
Type 2 Diabetes
ª Hyperinsulinemia- dark, thick, velvety skin folds & creases behind
the neck & under the arms.
ª Risk Factors: Central obesity, sedentary lifestyle, urbanization,
certain ethnicities
Type 2 Diabetes: Onset of Disease
ªGradual onset
ª Hyperglycemia may go many years without being detected
ª Often discovered with routine glucose testing or hemoglobin A1C
ª At time of diagnosis: About 50% to 80% of²cells are no longer
secreting insulin. Average person has had diabetes for 6.5 years
ªBMI > 25
ª Relative with DM
ª Physically inactive
ª Ethnicity- African American, Hispanic, Indian
ª Baby over 9 Lbs or had GDM
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Indications for Testing People for Type 2 Diabetes Mellitus
ª Hypertensive
ª HDL less than 35 mg/dL
ª Triglyceride > 250 mg/dL
ª Polycystic ovary syndrome
ª A1C > 5.7%
ª History of vascular disease
Prediabetes
ªIncreased risk for developing type 2 diabetes
ª Impaired glucose tolerance (IGT). OGTT—140 to 199 mg/dL
ª Impaired fasting glucose (IFG). Fasting glucose of 100 to 125
mg/dL
ª May have both IGT & IFG
ª Intermediate stage between normal glucose homeostasis & diabetes
Prediabetes: Patient Teaching Important
ªAsymptomatic but long-term damage already occurring
ª Undergo screening; glucose & A1C
ª Learn & manage risk factors
ª Monitor for symptoms of diabetes
ª Maintain healthy weight, exercise, make healthy food choices
Other Specific Types of Diabetes
ªResults from injury to, interference with, or destruction of ²-cell
function in the pancreas
ª From medical conditions &/or drugs
ª Resolves when underlying condition is treated or drug is discontinued
Health Promotion & Maintenance
ªControl of diabetes & its complications is major focus for health
promotion activities
ª Low-calorie diet
ª Increase activity
Assessment/Recognize Cues: Type 1 Diabetes Mellitus
ªClassic symptoms
ª Polyuria (frequent urination)
ª Polydipsia (excessive thirst)
ª Polyphagia (excessive hunger)
ª Weight loss
ª Weakness
ª Fatigue
ª Ketoacidosis
Assessment/Recognize Cues: Type 2 Diabetes Mellitus
ªNonspecific symptoms: Classic symptoms of type 1 may manifest
ª Fatigue
ª Recurrent infection
ª Recurrent vaginal yeast or candida infection
ª Prolonged wound healing
ª Visual problems
Diabetes & the Older Adult
ªMost develop Type 2
ª People over 65 may not experience polyuria & thirst
ª These conditions indicate patient diabetic screening
ª Hypertension
ª Periodontal disease
ª Frequent infections
ª Central arterial disease
ª Peripheral Artery disease
ª Slow gastric emptying
Assessment
ªRisk Factors
ª Symptoms
ª Weight & changes
ª Fatigue
ª Polyuria
ª Polydipsia
ª Polyphagia
ª Infections- vaginal, skin
ª Vision changes
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ª Kussmaul Respirations
ª Poor healing
ª Past health history
Nursing Assessment: Subjective Data
ªFunctional health patterns. Health-perception-health management. Positive family history, malaise
ª Nutrition: Metabolic. Obesity, weight loss or gain, thirst, hunger,
nausea/vomiting, poor healing, dietary compliance
ª Elimination: Constipation/diarrhea, frequent urination, bladder
infections, nocturia, urinary incontinence
Functional Health Patterns
ªActivity-exercise. Muscle weakness, fatigue
ª Cognitive-perceptual. Abdominal pain, headache, blurred vision,
numbness/tingling, pruritus
ª Sexual-reproductive, Impotence, frequent vaginal infections, decreased libido
ª Coping-stress. Depression, irritability, apathy
ª Value-belief. Commitment to lifestyle changes
Nursing Assessment: Objective Data
ªEyes. Soft, sunken eyeballs, history of vitreal hemorrhages,
cataracts
ª Integumentary. Dry, warm, inelastic skin, pigmented skin lesions,
ulcers, loss of hair on toes, acanthosis nigricans
ª Respiratory. Kussmaul respirations
ª Cardiovascular. Hypotension, weak, rapid pulse
ª Gastrointestinal. Dry mouth, vomiting, fruity breath
ª Neurologic. Altered reflexes, restlessness, confusion, stupor,
coma
ª Musculoskeletal. Muscle wasting
ª Possible diagnostic findings
ª Serum electrolyte abnormalities
ª Fasting blood glucose level of 126 mg/dL or higher
ª Oral glucose tolerance test &/or random glucose level exceeding
200 mg/dL
ª Leukocytosis
ª Blood urea nitrogen, creatinine
ª Increased triglycerides, cholesterol, LDL, VLDL
ª Decreased HDL
ª Hemoglobin A1C value > 6.0%
ª Glycosuria
ª Ketonuria
ª Albuminuria
ª Acidosis
Diagnostic Studies
1. A1C level: 6.5% or higher
2. Fasting plasma glucose (FPG) level > 126 mg/dL
3. 2-hour plasma glucose level during OGTT greater than 200
mg/dL (with glucose load of 75 g). Repeat criteria 1 to 3 on another
visit to confirm. Be attentive to influencing factors
4. Classic symptoms of hyperglycemia or hyperglycemic crisis or
a random plasma glucose level greater than 200 mg/dL
Diagnostic Studies: A1C
ªGlycosylated hemoglobin: reflects glucose levels over past 2 to
3 months. Glucose attaches to hemoglobin molecule; higher the
glucose levels = higher the A1C
ª Used to diagnose, monitor response to therapy, & screen patients
with prediabetes
ª Goal: Less than 6.5% to 7% (reduces complications). Estimated
average glucose = 28.7 × A1C 46.7
Diagnostic Studies: Fructosamine
ªCompound formed when glucose combines with protein
ª Reflects glycemia in previous 1 to 3 weeks. May show change
before A1C
ª Used for hemoglobinopathies or short-term measurement of
glucose levels
ª Islet cell autoantibody testing
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Diagnostic Studies: Other
ªLipids, BUN, creatinine, electrolytes
ª Albuminuria & urine acetone
ª BP, ECG, eye exam, dental exam, foot exam, neurologic exam,
ABI, weight
Criteria for Diagnosis: Four Methods of Diagnosis
1. AIC e 6.5%- 8%-9% Levels of 5.7% to 6.49% indicate diabetes
& cardiovascular disease
1. Fair diabetic control 8%-9%
2. Poor diabetic control >9%
2. Fasting plasma glucose level >126 mg/dL (normal 100mg/dL)
1. Confirmed by repeating on another day
3. Random or casual plasma glucose measurement e200 mg/dL
plus symptoms
4. Two-hour OGTT level e200 mg/dL
1. Eat balanced diet for three days, no vigorous exercise 8 hour
prior to test- may take a few hours to do the test. Several blood
tests taken- drink sweet drink loaded with glucose.
Blood Glucose Values
Analysis: Analyze Cues
ªPotential for injury
ª Potential for poor wound healing
ª Potential for injury
ª Potential for kidney disease
ª Potential for complications
Planning & Implementation: Generate Solutions & Take Action
ªPotential for injury due to hyperglycemia
ª Potential for impaired wound healing due to endocrine & vascular
effects of diabetes
ª Potential for injury due to diabetic neuropathy
ª Potential for injury due to reduced vision
ª Potential for kidney disease due to impaired circulation
ª Potential for hypoglycemia
ª Potential for ketoacidosis
ª Potential of hyperglycemic-hyperosmolar state & coma
Planning: Outcomes
ªManage Diabetes Mellitus & prevent disease progression by
maintain blood glucose levels
ª Performs treatment regimen
ª Follows recommended diet
ª Monitors blood glucose levels
ª Notify HCP with glucose fluctuations outside parameters
ª Meets activity levels
ª Follows drug regimen
ª Reaches/obtains optimum body weight
ª Problem solves barriers to self-management
Care Coordination & Transition Management
ªSelf-management education
ª Home care management
Interventions
ªHealth Promotion
ª Nutrition
ª Blood Glucose Monitoring
ª Exercise program
ª Medications
ª Surgery- Pancreas Transplantation
Treatment Goals: American Diabetes Association
ªA1C levels maintained 7.0% or below
1. Fair diabetic control 8%-9%
2. Poor diabetic control >9%
ª Lower goal may be recommended for individuals
ª Less stringent may also be necessary for those prone to hypoglycemia
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ª Premeal blood glucose levels are 70-130 mg/dL
ª Peak-after-meal blood glucose levels less than 180 mg/dL
Implementation: Health Promotion
ªIdentify those at risk.
ª Provide routine screening for overweight adults over age 45. FPG
is preferred method in clinical settings.
ª Obesity is the number one predictor of type 2 diabetes mellitus.
The Diabetes Prevention Program found that a modest weight loss
of 5% to 7% of body weight & regular exercise of 30 minutes 5
times a week lowered the risk of developing type 2 diabetes by up
to 58%.
Implementation: Drug Therapy Oral
ªWork to improve mechanisms by which insulin & glucose are
produced & used by the body.
ª Work on three defects of type 2 diabetes
ª Insulin resistance
ª Decreased insulin production
ª Increased hepatic glucose production
Implementation: Drug Therapy Oral
ªSulfonylures: (Glucotrol, Glucotrol XL), glyburide (Micronase,
DiaBeta, Glynase), & glimepiride (Amaryl).
ª Meglitinides: Repaglinide (Prandin) & nateglinide (Starlix)
ª Biguanides: Metformin (Glucophage)
ª Incretin Mimetic: Byetta
ª±glucosidase inhibitors: Acarbose (Precose) & miglitol (Glyset)
ª Thiazolidinediones: Include pioglitazone (Actos) & rosiglitazone
(Avandia).
ª Dipeptidyl Peptidase-4: Sitaglipton(Januvia), Saxagliptin (onglyza)
ª Amylin Analog: Pramlintide (Symlin)
Implementation: Insulin
ªManufactured using DNA technology to produce pure human
insulin.
ª Insulin analogs are synthetic human insulins where the structure
of insulin molecule is altered to change the rate of absorption &
duration of action within the body
ª Insulins differ with regard to onset, peak action, & duration
ª Types include- rapid acting, short acting, & intermediate acting,
long acting insulin
ª Various combinations of above can be used to tailor treatment for
blood levels
ª By adding zinc, acetate buffers, & protamine to insulin, onset of
activity, peak, & durations times can be manipulated
ª Genetically engineered in laboratories from E. coli or yeast cells
ª Insulins differ by onset, peak action, & duration. They are categorized as:
ª Rapid-acting: Lispro (Humalog), Aspart (Novolog), & glulisine
(Apidra)
ª Short-acting: Regular
ª Intermediate-acting: NPH
ª Long-acting: Glargine (Lantus), detemir (Levemir)
Insulin Preparations
ªTry to replicate normal insulin pattern from the pancreas
ª Pancreas produces a constant (basal) amount of insulin that
balances liver glucose production with use to maintain normal
glucose levels
ª Pancreas produces mealtime (prandial) insulin to prevent elevated glucose levels with meals
ª Insulin dose needed to maintain levels varies between individuals
ª Usual starting dose
ª 0.5 & 1 unit/kg of body weight per day
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Implementation: Insulin Regimens
ª Multidose regimens or continuous
ª Basal insulin makes up 40% -50% of the total daily dosage with
the remainder divided into premeal doses of rapid acting insulin
analogs or regular insulin
ª Basal: Intermediate or long acting insulins- keep levels stable
during fasting
ª Basal insulin coverage is provided by intermediate-acting insulin
or long acting insulin- with dosages adjusted on blood glucose
levels
ª Basal-bolus: combination of long or long acting & rapid acting
insulin
Insulin Plans: Basal-Bolus Regimen
ªIntensive or physiologic insulin therapy—most closely mimics
endogenous insulin production
ª Administer multiple daily injections (or insulin pump) with frequent
self-monitoring of blood glucose (or continuous glucose monitoring system)
ª Bolus—rapid- or short-acting insulin before meals
ª Basal—intermediate- or long-acting (background) insulin once or
twice a day
ª Goal: achieve glucose level as close to normal as possible as
much of the time as possible
Mealtime Insulin (Bolus)
ªManage postprandial glucose levels
ª Insulin preparations
ª Rapid-acting synthetic (bolus)—mimic natural insulin in response
to meals
ª Aspart, glulisine, & lispro
ª Onset of action 15 minutes
ª Injected within 15 minutes of mealtime
ª Short-acting regular (bolus)
ª Onset of action 30 to 60 minutes
ª Injected 30 to 45 minutes before meal
ª More likely to cause hypoglycemia
Long or Intermediate-Acting (Basal) Background Insulin
ªUsed with mealtime insulin to manage glucose levels in between
meals & overnight (Type 1 diabetics; some Type 2)
ª Long-acting (basal)
ª Degludec (Tresiba), detemir (Levemir), & glargine (Lantus, Toujeo, Basaglar)
ª Released steadily & continuously with no peak action for many
people; onset varies
ª Administered once or twice a day
ª Do not mix or dilute with any other insulin or solution
ª Intermediate-acting insulin (NPH)
ª Duration 12 to 18 hours
ª Peak 4 to 12 hours
ª Can mix with short- & rapid-acting insulins
ª Cloudy; must agitate to mix. Lispro protamine & aspart protamine
are also cloudy.
Combination Insulin Therapy
ªCan mix short- or rapid-acting insulin with intermediate-acting
insulin in same syringe
ª Provides mealtime & basal coverage in one injection
ª Commercially premixed formula or pen; flexible dosing limited
ª May self-mix from two vials. Consider visual, manual, or cognitive
skills
Implementation: Single Daily Injection
ªIncludes one injection of intermediate or long acting insulin or
ª A combination of short & intermediate acting insulin
ª Many type 2 Diabetics combine once daily insulin with oral agents
Implementation: Multiple-Component Insulin
ªCombines short & intermediate acting insulin injected twice a day
ª Two thirds daily dose at breakfast
ª One third before dinner
ª Ratios determined by blood glucose levels
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Implementation: Intensified Insulin Regimens
ªBasal dose of intermediate or long acting & mealtime dose of
short or rapid acting designed to bring the next blood glucose level
to target range
ª Elevated glucose are treated with correction dose of short or rapid
acting insulin (sliding scale)
ª Usually Blood glucose testing 1-2 hours after meals or within 10
minutes of next meal helps determine the needed bolus
Implementation: Insulin Absorption
ªInjection site
ª Absorption rate
ª Injection depth
ª Timing of injection
ª Mixing insulins
Implementation: Insulin Absorption Injection Site
ªArea affects speed of absorption
ª Fastest in abdomen except for a 2-inch radius around the naval
is the preferred injection site
ª Rotating injection site allows healing
ª Rotation within one site is preferred to rotation form one area to
another to prevent day to day variations
Implementation: Insulin Absorption Rate
ªDetermined by the properties of insulin itself
ª The longer the duration of action the more unpredictable the
absorption
ª Larger doses prolong absorption
ª Scarred sites are less sensitive to the injection but increase
absorption
ª Increased blood flow to area increase rate of absorption
ª Application of heat
ª Massage of the area
ª Exercise of the injected area
Implementation: Insulin Injection Depth
ªChanges absorption
ª Usually SQ injection
ª IM is faster but is not routinely used
ª 90 degree angle is used by most
ª 45 may also be used for thin frail older adults
ª No aspiration for blood is needed
ª Those with high BMI can use a 4-mm or 5-mm needed without
pinching of skin
Implementation: Timing of Insulin
ªLag- time is the interval between premeal injections & eating
affects blood glucose levels after meals
ª When blood glucose levels are above target range the lag time
is increased to permit insulin to begin to have a glucose lowering
effect before food
ª When blood glucose levels are below target range injection of the
regular insulin should be delayed until immediately before eating
ª Injection of rapid actin insulin should be delayed until sometime
after eating a meal
Implementation: Mixing Insulins
ªCan change the time of peak action
ª Mixtures of short & intermediate acting insulins produce more
normal blood glucose response than single dose
ª Patient response may be different in individuals
ª Patients may mix the two types of insulin themselves or use a
premixed formula
ª Regular insulin clear- NPH cloudy
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Insulin Pump
ªMajor advantage—keeps blood glucose in a tighter range; avoid
highs & lows
ª Careful programming & constant monitoring makes it possible
because delivery is similar to physiologic patterns
ª More flexibility with meals & activities
ª Potential concerns of insulin pump
ª Infection at insertion site
ª Risk for DKA
ª Cost of pump & supplies
ª Attached to a device
Implementation: Alternatives of Insulin Administration
ªContinuous Subcutaneous Infusion of basal dose of insulin
ª Allows if meal is skipped the additional mealtime dose of insulin
is not given
ª Externally worn
ª Reservoir of rapid acting insulin
ª Site changed 2-3 days
ª Skin infections may occur if not clean site
ª Need to test for ketones when glucose >300
Implementation: Alternatives of Insulin Injection - Needless System
ªNeedle replaced by a ultrathin liquid stream of insulin forced
through the skin under high pressure
ª Absorbed at a much faster rate
ª Shorter duration of action
Implementation: Alternatives of Insulin Injection - Insulin Pen
ªPortable & compact
ª More discrete
ª Consistent accurate dosing
ª Audible clicks for vision impaired
ª Could be mis-read if held upside: Down with lefties so may give
52 U instead, Of 25
Subcutaneous Administration with Pen
ªWash hands
ª Check drug label
ª Remove cap
ª Look at insulin to be sure evenly mixed if has NPH
ª Wipe the tip of the pen where needle will attach with ETOH swab
ª Remove pull tab from the needle & screw it onto the pen
ª Remove plastic outer cap & inner needle cap
ª Look at dose window & turn needle & screw it onto the pen until
snug
ª Hold pen with needle pointing upward, press the button until a
drop appears
ª Dial the number needed
ª Hold pen perpendicular the site
ª Press know slowly all the way
ª Hold pen 6-10 seconds
ª Withdrawal from skin
ª Replace outer needle cap, unscrew until needle is removed &
dispose of needle
ª Replace cap on the insulin pen
Implementation: Insulin Education - Storage
ªRefrigerate insulin not in use- to maintain potency
ª Prevent exposure to sunlight- to inhibit bacterial growth
ª Kept at room temperature for up to 28 days to reduce injection
site irritation
ª Should have a spare supply of insulin at all times
ª Prefilled syringes stable for 30 days when refrigerated
ª Store in the upright position
ª Needle pointing upward or flat so insulin does not clog needle
ª Roll between hands before use
ªInspect vial before each dose for clumps, frosting, precipitation
ª NPH is cloudy after rolling in hands
ª Other insulins should be clear
ª Syringes:
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Implementation: Education Dose Preparation
ª 1-mL (100-U)
ª ½-mL (50-U)
ª 3/10-mL (30-U)
ª Measured in 28, 29, 30, 31 gauge
ª Lengths, 6mm, 8mm, 12.7mm
ª Disposable needles used only once
Problems With Insulin Therapy: Assessing patient treated with
glucose-lowering agents
ªNewly diagnosed or reevaluation of regimen
ª Cognitive
ª Psychomotor
ª Affective
ª Follow-up
ª Effectiveness of therapy
ª Side effects of therapy
ª Self-management behaviors
ª Hypoglycemia
ª Allergic reactions: Local or systemic (rare). Other: preservative or
latex or rubber stopper
ª Lipodystrophy—loss of fatty tissue: Atrophy—wasting of fatty
tissue; indentations
ª Hypertrophy—thickening of subcutaneous tissue: Overuse of site;
alters absorption of insulin
Problems With Insulin Therapy: Somogyi Effect
ªHigh dose of insulin causes glucose during the night
ª Release of counterregulatory hormones causes rebound hyperglycemia
ª Concern when glucose checked in the morning & insulin is given
ª Determine if Somogyi effect by checking glucose between 2 to 4
a.m. Assess patient for headache, night sweats, or nightmares
Problems With Insulin Therapy: Dawn Phenomenon
ªMorning hyperglycemia present on awakening
ª May be due to release of counterregulatory hormones in predawn
hours
ª Growth hormone & cortisol
ª More severe in adolescence & young adulthood—peak time for
growth hormone
Implementation: Complication of Insulin
ªRapid-acting inhaled insulin
ª Administered at beginning of each meal or within 20 minutes after
starting a meal
ª Used in combination with long-acting insulin
ª Common adverse reactions: hypoglycemia, cough, throat pain or
irritation
ª Not recommended for: treatment of DKA, smokers; patients with
asthma or COPD due to risk of bronchospasm
Inhaled Insulin: Afrezza
ªWork to improve the mechanisms by which the body makes &
uses insulin & glucose
ª Work on three defects of type 2 diabetes
ª Insulin resistance
ª Decreased insulin production
ª Increased hepatic glucose production
ª Can be used in combination
Drug Therapy: Oral & Noninsulin Injectable Agents
Implementation: Education Blood Glucose Monitoring - Assessment of Symptoms
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ªAs done in lab
ª Hypo/hyperglycemia
ª Hypoglycemic unawareness
ª Periods of illness
ª Gastroparesis (stomach paralysis- nerves stop working)
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ª Adjustment of antidiabetic drugs
ª Preconception planning
ª Pregnancy
Monitoring of Blood Glucose: Self-Monitoring of Blood Glucose
(SMBG)
ªEnables decisions regarding food intake, activity patterns, &
medication dosages
ª Accurate record of glucose fluctuations & trends
ª Recommended for all diabetics who use insulin & others to help
achieve & maintain glycemic goals
Monitoring Blood Glucose: Frequency of Testing Varies According
To
ªGoals
ª Medication plan
ª Ability to independently check glucose
ª Access to supplies & equipment
ª Willingness & ability
ª Multiple insulin injections or insulin pumps check 4 to 8x/day
ª Other therapies—as needed to meet goals
Monitoring Blood Glucose: Portable Blood Glucose Monitors for
SMBG
ªMany products available
ª Lancet for small drop of blood (finger-stick)
ª Blood on reagent strip
ª Monitor displays digital reading of blood glucose
ª Technology changes with newer & more convenient systems
Monitoring of Blood Glucose
ªAlternative blood sampling sites
ª Forearm or palm
ª Not recommended for rapidly changing readings; during pregnancy, or hypoglycemia
ª Data uploaded to computer
ª Continuous Glucose Monitoring (CGM)
ª Type 1 or 2
ª Insurance coverage & costs limit use
ª Some pumps have CGM integrated
Monitoring Blood Glucose
ªFlash glucose monitoring—wave reader over sensor & get reading
ª Subcutaneous sensor displays glucose values on pump or
pager-like device or smart phone; updates every 1 to 5 minutes
ª Reads interstitial versus blood glucose; lags behind 5-10 minutes
ª Helps identify trends & patterns
ª Goal: "time in range" with fewer &
ª Alerts to hypoglycemia or hyperglycemia
ª No need to check finger-stick first before making insulin dosing
decisions (FDA, 2016)
Self-Monitoring of Blood Glucose (SMBG)
ªPatient & caregiver teaching
ª Initial & follow-up. Instructions how to test, use & calibrate meter
Self-Monitoring of Blood Glucose (SMBG) - When to Test
ªBefore meals
ª Two hours after first bite
ª When hypoglycemia is suspected
ª Every 4 hours during illness
ª Before & after exercise
ª Consider impaired vision, cognition, or dexterity; use adaptive
devices
Implementation: Nutrition Therapy - Individualized plan for diabetic & prediabetic patients includes:
ªCounseling
ª Education
ª Ongoing monitoring
ª Considers behavioral, cognitive, socioeconomic, cultural, religious backgrounds & preferences
Implementation: Nutrition Therapy - Interprofessional Team
ªRegistered dietitian with expertise in diabetes management
ª Others: nurses, CDEs, CNS, social worker, HCPs
ªRecommended for all adults
ª Overweight adults with type 2 can see results with mild weight
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ª Dietician develops the meal plan on patients food choices, ex41 / 52
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Implementation: Nutrition Therapy Principles
pectations & labs
ª Consistency in meals help control glucose
ª Coordinate with insulin
ª Individualized % of carbs, protein & fat
ª Plan based on glucose levels, lipids, A1C
Nutrition Therapy: Food Composition
ªHealthy balance of nutrients is essential to maintain blood glucose
levels & overall health
ª Energy from food intake can be balanced with energy output
ª Individualized to lifestyle & health goals
Nutrition Therapy: ADA Guidelines
ªDiabetic eat the same foods as nondiabetics. Nutrition Guidelines
related to carbohydrates, protein, fat, & alcohol
ª Goals: Achieve & maintain safe & healthy blood glucose levels &
prevent or reduce the risk of complications
ª Normal lipid profiles & blood pressure
ª Prevent or slow complications
ª Individual needs; personal, cultural preferences
ª Maintain pleasure of eating with healthy choices
Implementation: Nutrition Carbohydrates
ªFocus on vegetables, fruits, whole grains, legumes (fruit or seed
of a plant), dairy products
ª Recommended 25 g of fiber daily ( helps to slow down & regulate
carbohydrate & absorption of sugar)
ª Avoid sugary sweet beverages
ª Important source of energy, fiber, vitamins, & minerals; intake is
individualized
ª Includes sugars, starches, & fiber. Fruits, vegetables, whole
grains, low-fat dairy
ª All benefit from including dietary fiber. 25 to 30 g/day
ª Nutritive & nonnutritive sweeteners may be used in moderation
Implementation: Nutrition Fat & Cholesterol
ªFocus on quality over quantity of fat
ª Fat
ª Provides energy, transport of fat-soluble vitamins, & essential
fatty acids
ª Saturated fat intake is individualized. Limit cholesterol to less than
200 mg/day & minimize trans fat decreases risk of CVD
ª Healthy fats come from plants. Olives, nuts, avocados
ª Nonsaturated fatty acids beneficial to lower cardiac complication
risk such as avocados, nuts, seeds, olives & dark chocolate
ª Omega 3 fatty acids from fish oil to decrease heart disease
ª Limit trans fats, saturated fats & cholesterol not different than
others
Nutritional Therapy: Food Composition - Protein
ªDaily protein intake individualized
ª Same as nondiabetics & people with normal renal function. Lean
protein recommended
Implementation: Nutrition ETOH
ªAlcohol effects blood glucose levels
ª Levels not affected by moderate use of ETOH if DM well controlled
ª Two beverages for men one for women with good diet
ª One beverage = 12 ounces beer, 1 ½ ounces others, 5 ounces
of wine
ª Alcohol consumption increases risk of delayed hypoglycemia.
ETOH blocks production of glucose in the liver
ª Liver has an emergency storage of glucose so if this gets used
up or blocked by ETOH use levels can go dangerously low & even
cause death
ª If drink need to have food & not skip meals, check glucose before,
during & after.
Implementation: Nutrition Carbohydrate Counting
ªUses label information because nutrient has greatest effect on
glucose levels
ª Uses total grams of CHO regardless of food source
ª Can use to determine insulin coverage
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ª 1 unit of rapid acting insulin for 15 g of CHO is basic start
ª Reads labels then covers per formula
Implementation: Nutrition Therapy
ªDiabetes exchange lists: Prescribed meal plan with specific number of servings from a list of exchanges for meals & snacks;
patient chooses foods. Exchanges = starches, fruits, milk, meat,
vegetables, fats, free foods
ª USDA MyPyramid Guide. Appropriate basic teaching tool
ª Plate Method: Helps patient visualize the amounts of vegetable,
starch, & meat that should fill a 9-inch plate. For each meal, one
half of the plate is filled with nonstarchy vegetables, one fourth is
filled with a starch, & one fourth is filled with a protein. A glass of
nonfat milk & a small piece of fresh fruit complete the meal.
Patient Teaching Related to Nutrition Therapy
ªFamily members & caregivers, especially those who do the cooking, should be included in education & counseling.
ª Self-care skills are encouraged; deter reliance on others to make
decisions
ª Consider patient preferences & culturally appropriate foods
Implementation: Exercise Therapy
ªEssential part of DM management
ª Increases insulin receptor sites
ª Lowers blood glucose levels
ª Contributes to weight loss
ª Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia
ª Best done after meals
ª Should be individualized
ª Monitor blood glucose levels before, during, & after exercise
ª Plans should be started. After medical clearance. Slowly with
progression
Exercise
ªRegular, consistent exercise plan essential
ª ADA recommends: At least 150 minutes/week moderate-intensity
aerobic activity. Resistance training 3 times/week
ª Benefits
ª Decreases insulin resistance & blood glucose
ª Weight loss
ª Reduce need for medications (type 2)
ª Decreases triglycerides & LDL , ‘ HDL
ª Decreases BP & increases circulation
Exercise
ªGet medical clearance; start slowly & progress to goal
ª Insulin, sulfonylureas, or meglitinides + physical activity can
cause hypoglycemia if occurs at peak time for drug or didn't eat
enough. May happen if sedentary diabetic is more active
ª Glucose-lowering effect of exercise lasts up to 48 hours. Encourage exercise 1 hour after a meal or have a 10 to 15 g CHO
snack & check glucose before exercise. CHO snack to prevent
hypoglycemia every 30 minutes while exercising
ª Risk for hypoglycemia when exercising. Carry fast-acting source
of carbohydrates. Frequent low glucoses, consult HCP about lowering medications
ª Effect of strenuous activity makes body perceive "stress" causing
release of counterregulatory hormones & temporary increased
glucose. Type 1—delay activity if glucose e 250 mg/dL & ketones
are present in the urine; makes condition worse.
Implementation: Exercise Therapy
ªThe ADA recommends that individuals with diabetes should
perform at least 150 minutes per week of a moderate-intensity
aerobic physical activity. The ADA also encourages those with
type 2 diabetes to perform resistance training 3 times a week in
the absence of contraindications.
Implementation: Exercise with Complication of Diabetes Mellitus
ªDiabetic Retinopathy: Vigorous exercise could cause hemorrhage
ª Peripheral Neuropathy: Decreased pain sensation could mask
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injury so wear proper footwear, examine feet for injury
ª Foot injury/wounds: Should use non-weight bearing activity
Implementation Exercise Safety Education
ªTeach relationship of exercise & glucose
ª Level of exercise recommended for patient- individual
ª Appropriate footwear
ª Examine feet daily & after exercise
ª Stay hydrated
ª No exercise in extreme heat/cold
ª Check blood glucose more frequently on exercise days- may need
more CHO
ª How to prevent hypoglycemia
ª Blood glucose should be between 80 & 250 mg/dL
ª Have CHO snack before exercise if one hour passed since a meal
ª Carry simple sugar during exercise
ª Should have DM ID on while exercising
Implementation: Glucose Control Sick Patients
ªHyperglycemia may occur because of illness or changes in ADL's
ª Hyperglycemia is linked to poorer outcomes
ª Glucose levels >198 associated with higher mortality
ª Hypoglycemia < 40 increased risk of mortality
ª Association of Clinical Endocrinologists & ADA recommend treatment protocols to maintain levels 140 & 180 mg/dL for critically ill
ª Majority of non-critical <140 premeal, random <180 mg/dL
ªIncrease blood glucose level
ª Continue regular meal plan
Implementation: Glucose Control Sick Patients - Stress of Illness ª Increase intake of noncaloric fluids
& Surgery
ª Continue taking oral agents & insulin
ª Frequent monitoring of blood glucose. Ketone testing if glucose
>240 mg/dL
ªPhysical & emotional stress causes increased glucose
ª Stressful situations, for example, acute illness, injury, or surgery,
Nursing Interventions of Diabetes Mellitus During Illness: Acute
may require more intense treatment to maintain glycemic goals
Illness & Surgery
ª Blood glucose levels increase secondary to counterregulatory
hormones
Nursing Interventions of Diabetes Mellitus During Illness
ªDiabetic patients should check their blood glucose every 4 hours
during times of illness
ª If glucose greater than 240 mg/dL, check urine for ketones every
3 to 4 hours
ª Two consecutive glucose levels greater than 300 mg/dL or moderate to high urine ketone levels should be reported to HCP
ª Increase insulin for type 1 diabetes to avoid DKA
ª Increased glucose increases risk of infection & reduces healing
ª Type 2 diabetics may require insulin to treat glucose & avoid a
hyperglycemic emergency
ª Critically ill patients may have a higher target goal of 140 to 180
mg/dL. May get insulin if glucose consistently greater than 180
mg/dL
ªMaintain normal diet if able
ª Increase noncaloric fluids
Nursing Interventions of Diabetes Mellitus During Illness: Acute ª Continue taking diabetic medications
Illness
ª If eating less than normal, supplement with CHO containing fluids
while continuing medications
ª If unable to eat or drink, contact HCP
Implementation: Pancreas Transplantation
ªUsed for patients with type 1 diabetes who also have end-stage
renal disease or had, or plan to have, a kidney transplant
ª Pancreas transplants alone are rare. Usually kidney & pancreas
transplants done together
ª Eliminates need for exogenous insulin
ª Can also eliminate hypoglycemia & hyperglycemia
ª Pancreas transplantation is only partially successful in reversing
the long-term renal & neurologic complications of diabetes.
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ª Pancreatic islet cell transplantation is another potential treatment
measure.
ªPatients with type 2 diabetes or associated co-morbidities
ª When lifestyle & drug therapy management is difficult
ª Need life-long support & monitoring
Bariatric Surgery
ªIV fluids & insulin when NPO. Inform type 2 diabetics that insulin
Nursing Interventions of Diabetes Mellitus During Illness: Intraop- may be temporary & not a sign of worsening diabetes
erative Period
ª Unconscious patient. Frequent monitoring of blood glucose. Monitor for hypoglycemia: sweating, tachycardia, & tremors
Ambulatory Care
ªOverall goal is to enable patient (with caregiver's help) to reach
an optimal level of independence in self-care activities
ª Successful outpatient diabetes management requires ongoing
interaction with interprofessional team, including CDE.
ª Many challenges to face with risks for chronic conditions that
impact self-care activities
Interventions Ambulatory Care: Nurse's Role
ªAssess patient's/caregiver's ability to perform SMBG & insulin
injection. Obtain assistive devices & refer to resources
ª Self-management requires dedication of time & energy to deal
with lifestyle choices; diet, medication, exercise, & preventing or
managing complications
Interventions Ambulatory Care: Patient & Caregiver Education
ªAssess the meaning of having diabetes
ª Determine mutual goals that are based on patient needs &
treatment plan
ª Identify & include support system in planning, teaching, & counseling. Assist patient to meet goals or provide care when patient
is unable. Provide emotional support & encouragement.
Interventions Ambulatory Care: Insulin Therapy - Nurse's Responsibilities
ªProper monitoring, administration, & patient's response
ª Patient/caregiver education
ª Monitoring glucose levels; record for review
ª Interaction of insulin, food, & activity
ª How to prepare & inject insulin; address abilities, fears, beliefs, &
concerns
ª Hypoglycemia & how to treat
Interventions Ambulatory Care: Oral & Noninsulin Injectable
Agents - Nurse's Responsibilities
ªProper monitoring, administration, & patient response
ª Patient & caregiver education. Diabetes management & prevention of complications
ª Determine most appropriate drug for patient. Consider: mental status, eating habits, home environment, leaning ability, resources, attitude, & medications
Interventions Ambulatory Care: Personal Hygiene
ªRegular oral care & dental visits
ª Regular bathing & foot care
ª Inspect daily
ª Avoid going barefoot
ª Proper footwear
ª How to treat & monitor wounds; when to report to HCP
ªCarry medical ID at all times. Medic alert or identification card.
ª Plan ahead for travel
ª Altered activity level
Interventions Ambulatory Care: Personal Medical Identification &
ª Diabetes supplies/equipment & snacks in carry-on
Travel
ª Check TSA guidelines
ª HCP: letter regarding need for supplies; plan for crossing time
zones
Interventions Ambulatory Care: Patient & Caregiver Teaching
ªGoal for self-management of diabetes:
ª Match level of self-management to ability for active participation
for better outcomes
ª "Empowerment approach"—informed decision making
ª Avoids negative & judgmental messages
ª "Partner" in care
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ª Address barriers to effective management
ª Identify resources
Interventions Ambulatory Care: Patient & Caregiver Education
ªAssess knowledge & develop plan
ª Reassess frequently
ª ADA resources for patients & HCP
ª See: Informatics in Practice: Patient Teaching using Smart Phone
Apps
ª See: Complementary & Alternative Therapies: Herbs & Supplements That May Affect Blood Glucose
Evaluation: Evaluate Outcomes
ªAchieve blood glucose control
ª Avoid acute & chronic complications of diabetes
ª Avoid injury
ª Experience relief of pain
ª Maintain optimal vision
ª Maintain a urine output in the expected range
ª Have an optimal level of mental status functioning
ª Have decreased episodes of hypoglycemia
ª Have decreased episodes of hyperglycemia
Nursing Management Evaluation: Expected Outcomes
ªState key elements of the treatment plan
ª Describe self-care measures that may prevent or slow progression of chronic complications
ª Maintain a balance of nutrition, activity, & insulin availability that
results in stable, safe, & healthy blood glucose levels
ª Have no injury from decreased sensation in the feet
ª Implement measures to increase peripheral circulation
Acute Complications
ªHypoglycemia
ª Hyperglycemic
ª Diabetic ketoacidosis (DKA)
ª Hyperosmolar hyperglycemic syndrome (HHS)
Hypoglycemia
ªToo much insulin in proportion to glucose in the blood
ª Blood glucose level < 70 mg/dL
ª Neuroendocrine hormones released
ª Autonomic nervous system activated. Epinephrine released
Hypoglycemia: Signs & Symptoms
ªBlood glucose < 70 mg/dL
ª Cold, clammy skin
ª Numbness fingers, toes, mouth
ª Tachycardia
ª Emotional changes
ª Headache
ª Nervousness, tremors
ª Faintness, dizziness
ª Unsteady gait, slurred speech
ª Hunger
ª Vision changes
ª Seizures, coma
Hypoglycemia: Common Manifestations
ªShakiness
ª Palpitations
ª Nervousness
ª Diaphoresis
ª Anxiety
ª Hunger
ª Pallor
Hypoglycemia
ªAltered mental function—"neuroglycopenia"
ª Difficulty speaking
ª Visual disturbances
ª Stupor
ª Confusion
ª Coma
ª Mimics alcohol intoxication
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ª Untreated hypoglycemia can progress to loss of consciousness,
seizures, coma, & death
Hypoglycemia Unawareness
ªNo warning signs/symptoms until glucose level critically low.
Incoherent, combative, loss of consciousness
ª Related to diabetes-related autonomic neuropathy & secretion of
counterregulatory hormones
ª Patients at risk should keep blood glucose levels somewhat
higher
Hypoglycemia: Causes
ªUsually occurs at peak time for meds or with disruption in daily
routine
ª Symptoms can also occur when high glucose level falls too rapidly
ª Alcohol intake without food
ª Too little food
ª Too much diabetes meds
ª Too much exercise without food
ª Diabetes med or food at wrong time
ª Loss of weight without med adjustment
ª Use of -adrenergic blockers interfering with symptoms
ª Too much insulin or oral hypoglycemic agents
ª Too little food
ª Delaying time of eating
ª Too much exercise
Hypoglycemia: Clinical Course
ªMore rapid onset
ª Pattern of manifestations change over time
Nursing & Interprofessional Management: Hypoglycemia
ªQuickly reversible
ª Check blood glucose level
ª If less than 70 mg/dL, begin treatment
ª If greater than 70 mg/dL, investigate further for cause of
signs/symptoms
ª If monitoring equipment not available, treatment should be initiated
Hypoglycemia: Treatment - Rule of 15
ªEat or drink 15 g of rapid-acting carbohydrates
ª Wait 15 minutes, check glucose
ª If less than 70 mg/dL, eat or drink another 15 grams of carbohydrates
ª If stable & meal more than 1 hour away or involved inn activity;
give carbohydrate & protein
ª If glucose remains low after 2 to 3 times; call HCP or EMS
ª Acute care, unresponsive: IV D50 or IM glucagon
Hypoglycemia: Treatment: Rule of 15
ªConsume 15 g of a simple carbohydrate. Fruit juice or regular soft
drink, 4 to 6 oz. Commercial products; gels or tablets
ª Recheck glucose level in 15 minutes. Repeat if still < 70 g/dL; if
remains low after 2 to 3x, contact HCP. If glucose stable; give carb
& protein
ª Avoid foods with fat; slows glucose absorption
ª Avoid overtreatment
Hypoglycemia: Treatment in Acute Care Settings
ª 50%dextrose 20 to 50 mL IV push
ª Patient not alert enough to swallow or no IV access; also teach
family/caregiver
ª Glucagon 1 mg IM or subcutaneously
ª Watch for nausea; prevent aspiration
ª May not be effective with alcohol-related liver disease, starvation
or adrenal insufficiency
ª Explore reason why occurred
Hypoglycemia: Preventions
ªTake meds as prescribed on time
ª Accurately administer insulin, noninsulin injectables or OAs
ª Coordinate eating with meds
ª Eat adequate food as needed with exercise
ª Recognize & treat symptoms & teach family/caregiver too
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ª Carry simple carbohydrates
ª Wear or carry diabetes ID
Hyperglycemia: Signs & Symptoms
ªElevated blood glucose
ª Increased urination
ª Increased appetite followed by lack of appetite
ª Weakness, fatigue
ª Blurred vision
ª Headache
ª Glycosuria
ª Nausea & vomiting
ª Abdominal cramps
ª Progression to DKA or HHS
ª Mood swings
Hyperglycemia: Causes
ªIllness, infection
ª Corticosteroids
ª Too much food
ª Too little or no diabetes meds
ª Inactivity
ª Emotional or physical stress
ª Poor absorption of insulin
Hyperglycemia: Clinical Course
ªMore gradual onset
ª Definition of elevated glucose varies by person, based on personal glucose targets
Hyperglycemia: Treatment
ªGet medical care
ª Continue diabetes med as prescribed
ª Check blood glucose & urine ketones
ª Drink fluids hourly
ª Contact HCP with ketonuria
Hyperglycemia: Prevention
ªTake meds as prescribed on time
ª Accurately administer insulin, noninsulin injectables or OAs
ª Choose healthy foods
ª Follow sick day rules
ª Check blood glucose routinely
ª Wear or carry diabetes ID
Hyper & Hypoglycemia
Long-Term Complications of Diabetes
Chronic Complications Angiopathy
ªDamage to blood vessels secondary to chronic hyperglycemia
ª Leading cause of diabetes-related death. 68% CVD & 16% stroke
age 65 & older
ª Two categories: Macrovascular & Microvascular complications
Chronic Complications: Angiopathy - Theories of how chronic
hyperglycemia damages cells & tissues
ªAccumulation of damaging by-products of glucose metabolism
(e.g. sorbitol) is associated with damage to nerve cells
ª Formation of abnormal glucose molecules in the basement membrane of small blood vessels that circulate to the eyes & kidneys
ª Derangement in RBC function in tissue oxygenation
ªPatients with type 1 diabetes could significantly reduce risk of
microvascular complications by keeping blood glucose levels near
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normal most of the time (tight or intensive therapy)
Chronic Complications: Angiopathy - Diabetes Control & Compli- ª retinopathy & nephropathy
cations Trial (DCCT)
ª Basis for ADA recommendations for near normal blood glucose
levels
ªPatients with type 2 diabetes significantly risk for diabetes-related
Chronic Complications: Angiopathy - United Kingdom Prospective
eye, kidney, & neurologic problems with intensive treatment. 25%
Diabetes Study (UKPDS)
reduction of microvascular disease & 16% reduction of MI
Chronic Complications: Angiopathy - Long-term complications
are devastating; require ongoing monitoring.
ªAnnual exam: Retinopathy, nephropathy, neuropathy (comprehensive foot exam), cardiovascular risk factor assessment
ª As needed or every visit to HCP: Foot & lower extremity exam,
exercise stress testing
ª Daily: Foot exam by patient
Diabetic Foot Assessment: Assess Risk Factors
ªHistory of previous ulcer
ª History of previous amputation
Diabetic Foot Assessment: Assess for Abnormal Skin & Nail
Conditions
ªDry, cracked, fissured skin
ª Ulcers
ª Toenails thickened, ingrown
ª Status of circulation
ª Symptoms of claudication (cramping pain with exercise)
ª Pulses
ª Prolonged cap refill
ª Presence of absence of hair growth
Diabetic Foot Assessment: Assess for Foot Deformity
ªCallous, corns
ª Contractures
ª Bunions
Diabetic Foot Assessment: Assess for Loss of Strength
ªLimited ankle joint range of motion
ª Limited motion of great toe
Diabetic Foot Assessment: Assess Loss of Sensation
ªNumbness, tingling, burning
ª Semmes- Weinstien monofilament testing
Implementation: Foot Care
ªInspect feet daily
ª Wash feet with lukewarm water & soap, dry thoroughly
ª Moisturize after bathing but not between toes
ª Clean cotton socks daily
ª Do not wear the same pair of shoes 2 days in a row
ª Shoes of breathable material only
ª Check shoes for foreign objects, cracks tears
ª Do not go bare foot
ª So not wear sandals or open toes
ª Do not soak your feet
ª Buy shoes later in the day
ª Break in new shoes gradually
ª Wear socks to keep feet warm
ª Trim nails straight across- smooth nails
ª MD if blisters, sores, infections- protect area with dry sterile
dressing- no tape on skin
ª Do not treat blisters, sores, etc with home remedies
ª Do not smoke
ª Check temp of bath water before enter (95- 110 degrees)
ª Do not cross legs or wear constrictive things
Chronic Complications: Macrovascular Angiopathy
ªDiseases of large & medium-sized blood vessels
ª Cerebrovascular disease
ª Cardiovascular disease
ª Peripheral vascular disease
ª Greater frequency & earlier onset in patients with diabetes
ª Women 4 to 6x risk for CVD
ª Men 2 to 3x risk for CVD those nondiabetics
ªObesity: Nutrition & exercise
ª Smoking: Blood vessel disease, stroke & lower extremity amputation; cessation
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ª Hypertension: Optimize BP; CV & renal disease
ª High fat intake/dyslipidemia; statin & lifestyle interventions
ª Sedentary lifestyle: Exercise
Chronic Complications: Macrovascular Angiopathy - Decrease &
Treat CVD Risk Factors
Chronic Complications: Microvascular Complications
ªThickening of vessel membranes in capillaries & arterioles from
chronic hyperglycemia
ª Areas most affected:
ª Eyes: Retinopathy
ª Kidneys: Nephropathy
ª Nerves: Neuropathy
Chronic Complications: Retinopathy
ªMicrovascular damage to retina due to chronic hyperglycemia,
nephropathy, & HTN. Most common cause of new cases of adult
blindness
ª Two classifications:
ª Nonproliferative: More Common
ª Proliferative: More Severe
Chronic Complications: Retinopathy - Nonproliferative
ªPartial occlusion of small blood vessels in retina causes microaneurysms
ª Weakened walls causes fluid leaks resulting in edema & eventually hard exudates or hemorrhages
ª Mild to severe loss of vision. Retina (macula) involvement—severe
Chronic Complications: Retinopathy - Proliferative
ªInvolves retina & vitreous
ª Retinal capillary occlusion results in compensation with new
blood vessels formed (neovascularization): very fragile & bleed
easily. Patient see black or red spots or lines
ª Can cause retinal detachment. Macula involvement causes vision
loss
ª Glaucoma & cataracts can also occur
Retinopathy: Care
ªInitially no changes in vision
ª Annual eye examinations with dilation to monitor
ª Maintain healthy blood glucose levels & manage hypertension
Retinopathy: Treatments
ªLaser photocoagulation. Most common. Laser destroys ischemic
areas of retina
ª Vitrectomy. Aspiration of blood, membrane, & fibers inside the eye
ª Iluvien. Injectable micro-insert that delivers corticosteroids flucinolone acetonide for 36 months
ª Vascular endothelial growth factor (VEGF) blocking drugs - reduce inflammation.
Chronic Complications: Nephropathy
ªDamage to small blood vessels that supply the glomeruli of the
kidney
ª Leading cause of end-stage renal disease in U.S.; 20% to 40%
of people with diabetes have it
Chronic Complications: Nephropathy - Risk Factors
ªHypertension
ª Genetics
ª Smoking
ª Chronic hyperglycemia
ªIf albuminuria present, drugs to delay progression: ACE inhibitors
Chronic Complications: Nephropathy - Annual Screening for Al- or angiotensin II receptor antagonists
buminuria & Albumin-to-Creatinine Ratio
ª Control of hypertension & blood glucose levels in a healthy range:
imperative
Chronic Complications: Neuropathy - Nerve Damage due to
Metabolic Imbalances of Diabetes
ª 60%to 70% of patients with diabetes have some degree of
neuropathy
ª Sensory neuropathy - most common. Loss of protective sensation in lower extremities risk of amputation. 60% of nontraumatic
amputation is related to diabetes
ª Screen: type 2— time of diagnosis type 1— 5 years after diagnosis
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Neuropathy: Etiology & Pathophysiology
ªTheory: persistent hyperglycemia causes accumulation of sorbitol
& fructose that damages nerves. Reduced nerve conduction &
demyelination. Ischemic damage to peripheral nerves
ª May precede, accompany, or follow diagnosis
ª Classifications: sensory or autonomic
Sensory Neuropathy: Distal Symmetric Polyneuropathy
ªMost common form
ª Affects hands &/or feet bilaterally; "stocking-glove neuropathy"
ª Loss of sensation, abnormal sensations, pain, & paresthesias.
Pain—burning, cramping, crushing, tearing; worse or only occurs
at night
Sensory Neuropathy: Paresthesias
ªTingling, burning, itching; "walking on pillows or numb feet;"
ª Very sensitive
ª Complete or partial loss of sensitivity to touch or temperature is
common
ª Foot injury & ulcerations may occur without patient ever having
pain
ª Small muscles of hands & feet may be affected causing deformity
& limited fine movement
Sensory Neuropathy: Treatment
ªManaging blood glucose levels
Sensory Neuropathy: Drug Therapy
ªTopical creams
ª Tricyclic antidepressants
ª Selective serotonin & norepinephrine reuptake inhibitors
ª Antiseizure medications
ª Pregabalin
Autonomic Neuropathy
ªCan affect nearly all body systems & lead to: Hypoglycemic
unawareness, bowel incontinence & diarrhea, & urinary retention
ª Gastroparesis can cause: Delayed gastric emptying resulting in
anorexia, nausea, vomiting, GERD, feeling full, hypoglycemia
ª Cardiovascular Abnormalities: Postural hypotension/falls, resting
tachycardia, painless myocardial infarction
ª Sexual function: Erectile dysfunction—often first manifestation.
Decreased libido. Vaginal infections.
ª Neurogenic bladder can cause urinary retention: Empty frequently, use Credé's maneuver. Cholinergic agonist drugs.
Self-catheterization.
Foot & Lower Extremity Complications: Microvascular &
Macrovascular diseases Increases Risk for Injury & Infection
ªSensory neuropathy & PAD are major risk factors.
ª Other factors: clotting abnormalities, impaired immune function,
autonomic neuropathy
ª Smoking increases risk
Foot & Lower Extremity Complications
ªSensory neuropathy may cause loss of protective sensation
(LOPS) prevents awareness of injury; major risk factor for amputation. Annual monofilament screening
ª Peripheral artery disease (PAD). Decreased blood flow = decreased O2, WBCs, & nutrients causes longer wound healing,
increased risk for infection
Foot & Lower Extremity Complications: Patient Teaching - Foot
Care
ªProper footwear
ª Avoidance of foot injury
ª Skin & nail care
ª Daily inspection of feet
ª Prompt treatment of small problems
ª Diligent wound care for foot ulcers
ª Neuropathic arthropathy (Charcot's foot). Joint dysfunction &
footdrop may cause ulcers
Skin Complications
ªDiabetic dermopathy - most common: Red-brown, round or oval
patches. Scaly then flat & indented; shins
ª Acanthosis nigricans - manifestation of insulin resistance. Velvety
light brown to black skin thickening; flexures, axillae, & neck
ª Necrobiosis lipoidica diabeticorum. Red-yellow lesions; atrophic
skin shiny & transparent uncommon.
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Infection
ªDefect in mobilization of inflammatory cells & impaired phagocytosis. Recurring or persistent infections. C. albicans, boils, &
furuncles; cystitis
ª Antibiotics—prompt & vigorous
Infection: Patient Teaching to Prevent Infection
ªHand hygiene, avoid exposure
ª Flu & pneumococcal vaccine
Psychologic Considerations
ªHigh rates of depression, anxiety, & eating disorders
ª Diminished self-care, helplessness, & poor outcomes
ª Diabetes distress—stress, fear, & burden of living with & managing diabetes
ª Disordered eating behaviors (DEB). Anorexia, bulimia, binge
eating, excessive calorie restriction, & intense exercise. Women,
especially adolescents. Decrease insulin—"diabulimia" causes
weight loss, hyperglycemia, & glycosuria. Many consequences.
ª Open communication is important for early identification; mental
health referral
ªPresent in 25% over age 65 due to -cell function, decreased
insulin sensitivity, & altered carbohydrate metabolism
ª Higher rate of death, functional disability, an coexisting illness
Gerontologic Considerations: Increased Prevalence & Mortality
ª More drugs that interfere with insulin action
ª Many undiagnosed & untreated - signs resemble changes associated with aging
Gerontologic Considerations: Glycemic Control Challenging
ªIncreased hypoglycemic unawareness
ª Functional limitations
ª Coexisting medical problems
ª Cognitive decline
Gerontologic Considerations
ªMeal planning & exercise; response to drugs may be altered
ª Patient teaching must be adapted to needs
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