Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
215 Cards in this Set
- Front
- Back
|
parietal lobe
|
lets you know who you are and ties all other lobes together
|
|
|
occipital lobe
|
visual perception is affected
|
|
|
cerebellum
|
coordination is affected
|
|
|
temporal
|
hearing perceptionmen aggression
|
|
|
brain stem
|
lifeforce
|
|
|
Traumatic Brain Injury
|
mild moderate severeGCStemporary or permanent damage
|
|
|
non TBI
|
factors other than external forceinfection, tumors, anoxia, toxic exposureanoxia - stroke, near drowningtoxic exposure - drugs!
|
|
|
concussion
|
temporary - only one that is solely temporarytransient in nature until you hit 5 concussions
|
|
|
Contusion
|
Bruise on the brainthin later of blood - bruise on the braindamage depends on how big the bruising is
|
|
|
skull fractures
|
hai
|
|
|
hematoma
|
collection of blood outside of a vessel
|
|
|
hairline skull fractures
|
small - not a problem - heal fine
|
|
|
periorbital edema and ecchymosis
|
raccoon eyes - immediately look behind ear for postauricular ecchymosis (battle sign)basilar skull fracture
|
|
|
ear and nasal drainage from Skull Fractures
|
red is blood and clear is CSF
|
|
|
halo sign
|
csf on the outside with blood in the insidesuspect basilar skull fracture
|
|
|
epidural hemorrhages
|
emergent - patient hit in head, goes unconsciouswakes back up and is ANOx4decline very rapidly
|
|
|
subdural hematomas
|
sneaky - 12-24 hours later - near dead because someone found them on floorbleed slower because spacing is tightercan come up negative at firstmost important is education
|
|
|
subarachnoid hematoma
|
usually emergent usually a result of aneurysm rupture
|
|
|
intracerebral rupture
|
in the brain tissue - caused by leaking or ruptured blood vessel. usually emergeny
|
|
|
ICP
|
inracranial pressure - normal pressure exerted7-15 mm/Hgconstant flux in response to activities like exercising, coughing, breathing, arterial pulsationwhen the components of the cranium are balanced the result is normal intracranial pressure
|
|
|
increased ICP
|
when the pressure in the cranium increased the body tries to compensate via cerebral auto regulation, if this fails then compensation and decompensation occur in response to the pressure change
|
|
|
Cerebral Auto Regulation
|
cerebral blood vessels dilate and constrict in response to CO2 and O2 levels in blood to maintain a healthy intracranial pressure
|
|
|
compensation
|
cerebral spinal fuil regulationdeceased production CSFincreased reabsorption CSFif the pressure continues to increase and the CSF can no longer compensate, decompensation begins with compromise of the cerebral blood flowno blood to brain equals death
|
|
|
decompensation = herniation = death
|
displacement or herniation of tissuesportion of the brain shifts and interferes with blood perfusion and will result in brain death
|
|
|
Cushings Response
|
seen with decreased cerebral blood flow. The brain in attempt to restore blood flow increases arterial pressure to overcome inreased ICP
|
|
|
Cushings Triad
|
the S&S that cushings response is occurring and death is imminentincreased BP (widening systolic pressure)Decreased PulseDecreased respirations (raspy and slow)expected Tx of Cushings..Mechanical VentilationOsmotic Diuretic - mannitolcorticosteroids - dethimethazoneICP Bolt - measures ICP never leave your patienthead of the bed down
|
|
|
complications of increased ICP
|
Diabetes Insipidus - most common type of DI and is called Central DI - caused by a decrease in production of ADH, resulting in a fluid volume imbalanceUrine SG < 1.015SIADH - increased secretion of ADH, resulting in a fluid volume imbalanceurine SG > 1.030
|
|
|
Medical Management of ICP
|
Decreasing cerebral edema-osmotic diuretics - mannitol, glycerol, isosorbide-corticosteroids - dexamaethasonekeep head of bed upmaintain CO2 levelsincrease COs - vasodilation - increase blood flow - increase ICPdecresed CO2 - vasoconstriction - decrease blood flow - decrease ICPIdeal CO2 levels for patients with increased ICP is 27-30 (non COPD pts) normal CO2 is 35-45) monitos pHMonitor Lab ValuesABGsGlucose - steroidsElectrolytesCBC, CoagsMaintain Cerebral perfusionincreased cardiac outputICP monitoringto identify increased pressure before cerebral damage occursto quantigy the degree of elevationinitiate appropriate treatmentto provide access to CSF for sampling and drainageto evaluate effectiveness of treatmentRegulation of body temperaturefever increases cerebral metabolismincreasing edemareduction of metabolic needsreduction of CSF-drains-LPOther ways to decrease ICP-head of bed >30 degress-Decrease Stimuli- Calm Environment! (consider migraine headache patients)
|
|
|
Neuro Assessment
|
Evaluation of Consciousness
|
|
|
Conscious
|
Fully Alert and Oriented, Follows CommandsLethargy - Drowsy but awakensObtunded - difficult to arouse, needs constant stimulation to stay awake or follow a simple commandStupor - needs vigorous stimulation, often painful stimuli to arouse. will often to moan or withdraw from the painComa - patient does not respond to continuous or painful stimuli
|
|
|
Mentation
|
ANO to person, place, time, and situation
|
|
|
pupils -
|
size, shape, reactivity - change can indicate increase in ICP
|
|
|
assess for motor dysfunction
|
conscious patientstrength and ROM bilaterallyPronation or drift present in limbs
|
|
|
Unconscious Patient
|
central or peripheral stimulation ****peripheral to avoid patient swinging
|
|
|
reflexesSensory
|
if patient is awake and can cooperate
|
|
|
Pain
|
Headache
|
|
|
Vital Signts
|
Often late indicator - cushings triad - increase bp, decrease pulse
|
|
|
Vomiting
|
Not GI related - projectile when related to head
|
|
|
Cardiovascular
|
Volume Status
|
|
|
Sympathetic Storming
|
en exaggerated stress response that occurs in 15-30% of severely brain injured patientsGCS 3-8Imbalance between sympathetic and parasympatheticS/SX - posturing, dystonia, HTN, hyperthermia, tachycardia, tachypnea, diaphoresis, agitationTx - treat symptoms
|
|
|
Collaborative Problems
|
Resp failurepneumoniaaspirationinfectionDISIADH
|
|
|
PHARM
|
mannitolglyceroldecadrondobutaminetylenolvasopressin
|
|
|
Rotation
|
Risk of Severance
|
|
|
Flexion
|
Lateral, Forward
|
|
|
Extension/ hyperextension
|
whiplash
|
|
|
Vertical/compression
|
risks fx
|
|
|
Penetraating
|
foreign body
|
|
|
SCI can be sustained through different mechanisms with the following common 3 abnormalities leading to tissue damage
|
DestructionCompressionIschemia/Swelling
|
|
|
Complete Spinal Cor dInjury
|
Result in complete loss of sensation and muscle control below the injury
|
|
|
Incomplete Spinal Cord Injury
|
Results in partial loss of sensation and muscle control below the injury
|
|
|
Paraplegia
|
T-1 and below
|
|
|
Quadriplegia
|
C8 and above
|
|
|
Incomplete Injuries
|
Spinal tracts are three groups of pathways; all tracts cross and travel to opposite side of brain
|
|
|
posterior tract conducts sensation
|
touch, pressure, vibration, position, passive motion
|
|
|
spinothalmic
|
transmits pain and temperature impulses
|
|
|
lateral
|
conducts motor impulses
|
|
|
Medical Management of SCI
|
ET tubeVentilatorInotropic drugs (dopamine)SteroidsO2Immobilization/ Stabilization-halo-TLSO-Traction-Cervical CollarImmobilization and stabilization
|
|
|
Complication of SCI
|
Resp-Decrase in Vital capacity-retention of Secretions-Decreased Cough reflex-Increased PO2-Decreased PO2Pulmonary EdemaInfectionResp failureCV-orthostatc hypotensionneurogenic shocknervous systemspinal shockhyperthermia secondary to lack of perspiration in the affcted areaautonomic - dysreflecia - hyperreflexiaGI and RenalReflexes for the bowel and bladder are affectedretention occurs paralytic ileusUTIsIntegumentary systemDVTPressure UlcersInfection/ CellulitisMusculoskeletal systemspasmscontractions
|
|
|
Reflex Arc
|
neural pathway that controls an action reflex
|
|
|
Spinal Shock
|
Transient physiological reflex depression below level of injuryneurological in naturelasts from minutes after injury up to weeks unril reflx arc returnsinitial hypertension secondary to catecholamine release, followed by hypotensionconcussion of cord
|
|
|
Neurogenic Shock
|
usually ocurs in injuries of T-6 and aboveloss of sympathetic stimulation of the blood vesselscaused by the triad of hypotension, bradycardia, and hypothermiavessels are relaxed and pooling of blood can occurorgans dysfunctions can occurcan cause death if not treated.treat with fluids, dopamine, atropine, and vasopressincirculatory in nature
|
|
|
Resp status
|
high injuries - c4 and up = resp failureintercstal, diaphragm, and abdominal muscles are paralyzed, ventilator is most likely neededinjuries from c-6 through t-6 can be compromised - intercostal muscles may be weak or paralyzed -- ability to cough or deep breathe may be affectedassess - lung soundsstrength of coughbreathing patternso2 sats
|
|
|
cardio assessment for Neuro
|
BP, HR, Lower extremity edema, temperature and color of extremities
|
|
|
Nervous system for Neuro
|
assesss neurological leveltempsensory functionreflexes
|
|
|
mucsuloskeletal system for neuro
|
motor functionmuscle tone
|
|
|
Nursing intervetions for resp for neuro
|
Suctioning/ HOB elevatedQuad coughBreathing ExercisesHumidificationo2 sats
|
|
|
CV interventions for neuro
|
TEDs, SCDs, circulationDVT
|
|
|
Nervous system interventions for neuro
|
management of shockAutonomic Dysreflexiabladder/bowel distentionskin pressure or temp controlled
|
|
|
neurogenic shock triad!
|
hypotension, bradycardia, hypothermia!Fluids, Atropine, Dopamine
|
|
|
Skin function for fluid balance
|
Diaphoresis, Prevention of loss
|
|
|
Lungs function for fluid balance
|
Exhalation
|
|
|
Kidneys function for fluid balance
|
reabsorption, excretion
|
|
|
GI Tract function for fluid balance
|
Reabsorption, Excretion
|
|
|
what is 24 hour average urine ouput?
|
1500 mL or 62.5 mL/hour
|
|
|
what is 24 hour output that would concern the nurse?
|
720 mL or 30 mL / hour
|
|
|
What is the definition of Oliguria in mls/24 hours?
|
500 mL or 20.8 mL/ hr
|
|
|
What is the definition of anuria in mls/ 24 hours?
|
less than 50 mL or 2mL/hour
|
|
|
Serum Osmolality
|
275-310 mOsm
|
|
|
Urine Osmolality
|
200-800
|
|
|
Osmolarity
|
Concentration of solutes per liter of solution - outside the body
|
|
|
Osmolality
|
Concentration of solutes per kilogram of solution-inside the body
|
|
|
how to calculate serum osmolality?
|
(2 x (Na + K) + (BUN/ 2.8) + (glucose/18)
|
|
|
Hydrostatic Pressure
|
Forces fluid and solutes out through capillary walls into interstitial fluid
|
|
|
Colloid Osmotic Pressure
|
causes reabsorption - prevents too much fluid from leaving the capillaries - vacuum cleaner - maintains pressure lack of COP = edema, third space shifting, i.e ascites
|
|
|
Prealbumin
|
Range - 17-40precursor of Albuminused for nutrition assessmentmore sensitive than albumindecreased in malnutrition, protein wasting, diseases, inflammation, malignancy, cirrhosiselevated in - hodgkins disease, steroid/ NSAID use
|
|
|
Albumin
|
Normal Range 3.5-5Increases COPDecreased in - cirrhosis, liver failure, severe burns, malnutrition, preeclampsia, renal disordersincreased in - Dehydration, Severe Vomiting, Severe diarrhea
|
|
|
during FVD the Renin-angiotensin Cascade kicks in
|
Renin secreted by the kidneysrenin causes peripheral vasoconstrictionStimulates Angiotensin productionCauses release of aldosterone by the adrenal cortexaldosterone causes water and sodium retention
|
|
|
Diabetes Insipidus
|
Decreased ADHIncreased Urine Excretion=Fluid Volume Deficitdry patient
|
|
|
SIADH
|
Increased ADHDecreased Urine excretion=Fluid Volume Excesslow sodium, wet patient
|
|
|
what do renin, ADH, and aldosterone help to improve?
|
Fluid Volume Deficit States
|
|
|
BNP
|
located in the atrial heart musclesuppress renin, aldosterone, ADHkicks in when patients are retaining waternormal BNP is less than 1005lbs = 1L of retention
|
|
|
Dehydration
|
Loss of water from the bodywater moves to vascular space and shrinks cellblood becomes more concentrated
|
|
|
Causes of Dehydration
|
decreased or inadequate intakeNG tubesVomitingDiarrheaWound DrainageBurnsDiureticsFeverThird Space shifing
|
|
|
Hypovolemia
|
loss of water and solutes into vascular spacevessels constrict maintaining a low BPeventually BP and cardiac output drophypoxemia occurs
|
|
|
Causes of Hypovolemia
|
hemorrhageshocksevere malnutritionburns third space shifting
|
|
|
Nursing assessments for FVD
|
increased tempdecreased bpincreased pulse, weak and threadyincreased respirationsdecreased weightdry skin and mucous membranesdecreased urine outputdark concentrated urinealtered mental status
|
|
|
Nursing Interventions for FVD
|
I&OVSweightsskin careIV therapyEnteral or Parenteral feeding
|
|
|
hypervolmia
|
retain water and solutes in the same proportionincreased in fluid and solutes
|
|
|
causes of hypervolemia
|
overhydration ( PO or IV)decreased renal functionheart failurehormonal (increased aldosterone or ADH)Obstructed lymph vesselsLong-term Steroid Use
|
|
|
Water intoxication
|
more water than solutecell is full of fluidexcess water can cause cell to burstMannitol treates water intoxication
|
|
|
Causes of water intoxication
|
Hormonal (increased aldosterone or ADH)Decreased renal outputOver Hydration
|
|
|
Fluid Volume Excess nursing assessments
|
Increased BPJVDEdemaincreased pulse, boundingincreased respirationss3 heart soundscrackles in the lungsincreased weightstretched, shiny skinincreased urine outputdilute urinepossible altered mental status
|
|
|
Nursing interventions for FVE
|
I&OFluid restrictionSodium restrictionVSweightsSkin CareDiuretics
|
|
|
BUN
|
10-20
|
|
|
Creatinine
|
0.6-1.5
|
|
|
hematocrit
|
37-54%
|
|
|
urine sodium
|
50-130
|
|
|
urine SG
|
1.010-1.025
|
|
|
PTH function with electrolytes
|
regulates calcium
|
|
|
Kidneys function with electrolytes
|
regulate potassium, sodium, phosphorous
|
|
|
External components for Electrolyte balance maintenance
|
DiureticsIV fluidsPO replacementHormonesBinders
|
|
|
calcium and phosphorous
|
opposites
|
|
|
what medication can bring magnesium down?
|
calcium gluconate
|
|
|
Sodium (NA+)
|
135-145
|
|
|
Causes of Hypernatremia
|
excessive intake, decreased excretion, water loss, inadequate water intake
|
|
|
s/sx of hypernatremia
|
Thirst, swollen dry tongue, restlessness, tachycardia
|
|
|
Tx of hypernatremia
|
restrict sodium intake, HCTZ, increased water intake
|
|
|
Hyponatremia causes
|
inadequate intake, excessive loss, water gain
|
|
|
hyponatremia s/sx
|
nausea, headache, muscle cramps/weaknessALTERED MENTAL STATUS
|
|
|
Tx for hyponatremia
|
replacement IVF, increase dietary intake, restrict water intake
|
|
|
Potassium
|
3.5-5
|
|
|
hyperkalemia causes
|
excessive intake, decreased excretion, water loss, shift from intracellular to extracellular, metabolic acidosis
|
|
|
s/sx of hyperkalemia
|
Acidosis, irregular pulse rates/ rhythmsEKG changes - tall tented T waves, widened QRS
|
|
|
Tx of hyperkalemia
|
restriction of intake, loop diuretics ( furosemide), increased water intake, kayexalate (sodium polystyrene sulfonate), regular insulin
|
|
|
hypokalemia causes
|
inadequate intake, excessive loss, water gain, shift from extracellular to intracellular
|
|
|
s/sx of hypokalemia
|
alkalosis, anorexia, vomiting, decreased bowel motility, leg crampsEKG changes (u waves, ST depression)
|
|
|
Tx of hypokalemia
|
replacement PO/IV, increase in dietary intake, restrict water intake
|
|
|
Magnesium
|
1.5-2.5
|
|
|
hypermagnesemia causes
|
Excessive intake, decreased excretion, water loss, renal insufficiecy
|
|
|
hypermagnesemia s/sx
|
hypotension, muscle weakness, decreased DTR's, respiratory paralysis, bradycardia
|
|
|
Tx of hypermagnesemia
|
restriction of intake, promotion of excretion, increased water intake, calcium gluconate
|
|
|
Hypomagnesemia causes
|
inadequate intake, excessive loss, water gain, chronic alcoholism
|
|
|
s/sx of hypomagnesemis
|
positive trousseau's and chvosteks signsmood changeshyperactive DTRs
|
|
|
tx of hypomagnesemia
|
replacement of PO/IM/IV increased dietary intake, restrict water intake
|
|
|
Calcium
|
9-11 total 4.5 - 5.5 ionized
|
|
|
hypercalcemia causes
|
excessive intake, decreased excretion, water loss, bone trauma, hyperparathyroidism, hypophosphatemia
|
|
|
s/sx of hypercalcemia
|
constipation, anorexia, nausea, vomiting, decreased DTR's, lethargy
|
|
|
tx of hypercalcemia
|
restriction of intake, increase water intake, correction of hyperparathyroidism, Etidronate
|
|
|
hypocalcemia causes
|
inadequate intake, excessive loss, water gain, decreased parathyroid functioning, renal failure/ hyperphosphatemia
|
|
|
s/sx hypocalcemia
|
tetany, positive trousseau's and chvosteks signs, increased DTR's, decreased clotting ability and bone density
|
|
|
Tx of hypocelcemia
|
replcement PO/IV increase dietary intake, restrict water intake, correct parathyroid dysfunction, correct hyperphosphatemia
|
|
|
phosphorous
|
2.8-4.5
|
|
|
hyperphosphatemia causes
|
Excessive intake, decreased excretion, water loss, hypocalcemia, renal failure
|
|
|
s/sx of hyperphosphatemia
|
Tetany due to hypocalcemia
|
|
|
Tx of hyperphosphatemia
|
restriction of intake, Phoslo (calcium Acetate) Renagel (Sevelamer) increased water intake (non renal patients)
|
|
|
hypophosphatemia causes
|
inadequate intake, excessive loss, water gain, alcoholism, hypercalcemia
|
|
|
s/sx of hypophosphatemia
|
parathesias, muscle weakness, altered mental status
|
|
|
Tx of hypophopshatemia
|
replacement PO/IV, increase dietary intake, restrict water intake, correction of hypercalcemia
|
|
|
Chloride
|
96-106
|
|
|
hyperchloremia causes
|
excessive intake, decreased excretion, water loss, metabolic acidosis
|
|
|
s/sx of hyperchloremia
|
kussmauls respirationsaltered LOCtachypnea, lethargy, weakness
|
|
|
Tx Hyperchloremia
|
restriction of intake, increased water intake, bicarbonate
|
|
|
hypochloremia causes
|
inadequate intake, excessive loss, water gain, metabolic alkalosis
|
|
|
s/sx of hypochloremia
|
alkalosis, hyperactive DTR's, tetany seizures
|
|
|
Tx of hypochloremia
|
replacement of PO/IV, increase dietary intake, restrict water intake, correct alkalosis
|
|
|
F&E nursing diagnosis
|
FVDFVEKnowledge deficitactivity intolerancealtered body tempaltered thought processaltered tissue integrityaltered tissue perfusionimpaired gas exchangeself care deficit
|
|
|
Crystalloids
|
DextrosesalineRingers
|
|
|
Colloids/plasma
|
plasmaalbumindextran
|
|
|
TPN
|
very hypertonic
|
|
|
Isotonic fluids
|
If the IV fluid has about 1 tsp. ofsolutes (Example: 0.9% Sodium Chloride
|
|
|
hypotonic fluids
|
•Ifthe IV fluid has < 1 tsp. of solutes, (Example: 0.45%Sodium Chloride)
|
|
|
hypertonic fluids
|
•Ifthe IV fluid has > 1 tsp. of solutes, then it is hypertonic (Example: D10W)
|
|
|
what do isotonic fluids cause cells to do
|
neither shrink nor swell
|
|
|
waht to hypotonic solutions cause cells to do
|
swell
|
|
|
what to hypertonic solutions cause the cells to do
|
shrink
|
|
|
isotonic or isoosmolar
|
same as the fluids in the vascular system (stays in the vascular space)
|
|
|
Hypotonic or hypoosmolar
|
shifts from the vascular space into the cell because it is more diulutes than the vascular systemunequal concentration within cell compared to vascular space - cell enlarges and little change to vascular space with fluid movements
|
|
|
hypertonis or hyperosmolar
|
more concentrated than the vascular system so water moves from the cells into the vascular space via osmosisunequal concentration within cell compared to vascular space - cell shrinks and vascular space enlarges with fluid movements
|
|
|
hypotonic solutions
|
.45% sodium chloride (half normal saline)0.22% sodium chloride (1/4 normal saline)
|
|
|
Isotonic Solutions
|
0.9% NS (normal saline)LR (lactated Ringers)5% Dextrose injection (D5W)
|
|
|
Hypertonic Solutions
|
D5NSD5LRD5-1/2NSD5-1/4NS
|
|
|
Indications for Sodium
|
Vascular Fluid LossHyponatremia
|
|
|
Indications for Dextrose
|
Cellular Energy
|
|
|
indications for LR
|
electrolyte Replacement
|
|
|
Osmotic Diuresis?
|
occurs with administration of hypertonic solutions into vascular spaceconcentration of vascular space pulls fluid from interstitial and intracellular spaces, urine ouput increases to large amounts of dilute urine - up to 3000mL per shift
|
|
|
composition of blood
|
55% of blood is plasma - Primarily water (90%)**blood serum is plasma without the clotting factors.Blood cells (45% of blood)
|
|
|
Blood Screening
|
Chagas DiseaseCytomegalovirusHep B VirusHep C VirusHIV types 1 and 2SyphilisWest Nile VirusHuman T-Lymphotropic Virus
|
|
|
Transfusion Reactions
|
80% of ALL reactions involve fever and chillsthe remaining 20 of blood transfusion reactions include allergic, septic, and other non hemolytic reactions
|
|
|
Blood Donation
|
Human DonorsCan donate blood every 2 months or 56 daysprescreening process:-meds-risky behaviors-Travel outside the USmust meet BP, temp (afebrile) , weight, age (16 with parental consent in SC) H&H requiremens at least a 12.5 hgbblood testing for transmittable diseases
|
|
|
ABO typing
|
a test performed to determine an individuals blood type - or antigen which will be A B O or AB groupings
|
|
|
Rh typing
|
a test to determine if an Rh factor is present, (+) or not (-)
|
|
|
Human leukocyte antigen
|
protein-marker-found on most cells in your body and used to match you with a donor for your bone marrow or cord bone marrow blood transplants. located on the surface of platelets and WBC'san HLA reaction may cause destruction of platelets specific donor blood must be matched with the same specific or compatible HLA patient blood. leukocyte poor blood is the preferred blood for transfusions
|
|
|
Whole Blood
|
All components of blood (plasma and blood cells)1 unit = 500mLRaises Hgb by 1g/dL, HCT by 3-4%indicated for acute trauma, hypovolemic shock, burns, 25% or more total blood loss in a single incidence, or massive hemorrhage
|
|
|
PRBC's
|
plasma removed from whole blood1 unit = 250 mLmost commonly seen on Med-surg units1 unit increased Hgb by 1 g/dL, HCT by 3%indicated for anemia or acute blood lossdue to surgery or (hgb <8)improves oxygen carrying capacity, not given for volume expansion or massive hemorrhage (must be infused within 4 hours)
|
|
|
FFP
|
Preparedby separating liquid portion from whole blood Containsclotting factors but no plateletsMustbe kept frozen (thaw before use) 1unit = 200-250mL Mayadminister at a rapid rate Usewithin 2 hours of delivery Usedto treat microvascular bleeding disorders (DIC), liver disease, vitamin K deficiency üMustbe ABO compatible butnot cross matched (no RBC’s in plasma).
|
|
|
platelets
|
Plateletsare separated from whole blood by apheresis1unit= 50-70mL (infuse rapidly)Indicatedfor platelet dysfunction or thrombocytopenia ABOcompatibility is recommended but not required. Febrile and mild allergic reactions are common (may needto premedicate).Can be kept a room temp for up to 5 days.
|
|
|
WBC
|
Indicated for WBC dysfunction, neutropenia or sepsis that does not respond to antimicrobialsAlso called granuloctytes: consists of basophils. eosinophils, and neutrophils (destroy organism invaders through phagocytosis)ABO, Rh, and HLA compatibility is requiredResults are only temporarywatch for: non hemolytic, febrile reactions are common
|
|
|
Cyroprecipitate
|
Source of concentrated factor VIII ( anti-hemophilic factor)prepared from FFPABO compatibility testing is requiredCross-matching is NOT necessaryindicated to correct deficiencies Factor I, VIII, XIII, fibrinogen, and Von Wildebrand'sthaw before giving and infuse rapidly
|
|
|
Colloid Volume Expanders
|
Products for Volumeno screening is requiredindicated for Fluid Volume expansion and to maintain BP (hemophilia, GI bleed)
|
|
|
Examples of Colloid Volume Expanders:
|
Dextran, Hetastarch, Albumin (most used)plasma protein fractionAlbumin and PPF derived from human plasma - Dextran and Hetastarch are synthetic man-madeusually administered in 0.9% normal saline
|
|
|
Albumin
|
Derived from human donor plasmadoes not have to be ABO or Rh compatiblemost common volume expander is albuminalbumin is indicated for shock, hypoproteinemia, ARDS and acute liver failure
|
|
|
Plasma Protein Factor
|
Derived from human donor plasmadoes not have to be ABO or Rh compatibleused to increase plasma volume in hypovolemic shock from surgery or traumacomposed of 83% albumin
|
|
|
Administration of blood products
|
check physicians order for which component to transfusetyping and cross-matching typenex braceletpatient consentprepare equipmentif temps is 100 degrees farenheit or greater (regardless of baseline) notify physician for further instructions
|
|
|
Admin of Whole blood and PRBC's
|
at least a #19 gauge IV catheter or larger bore needleStandard blood tubing with filter (Y-set)Use 0.9% saline infuse within 4 hours or lesstransfusion must be initiated within 30 minutesmay only administer one unit at a timeblood must have a dedicated primary line - no piggybacks
|
|
|
Growth factors
|
stimulate production of blood cells requires normal function of bone marrow.
|
|
|
Eryhtropoietin
|
Medication that stimulates erythropoiesis i.e Procrit, Epogen
|
|
|
Granulocyte Colony-Stimulating Factor ( G-CSF)
|
stimulates proliferation of myeloid stem cells results in an increase of neutrophils in the circulationexample - Neupogen
|
|
|
Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) :
|
Stimulates Myelopoiesisexample - Leukinel
|
|
|
Thrombopoietin
|
Necessary for platelet formationexample - Romiplastin
|
|
|
Autotransfusion - Cell Saver
|
Blood salvage or cell salvagepatients blood is collected and filtered through a machine and returned to the patient during surgerymonitor coagulation studies
|
|
|
Autologous Transfusions
|
Donation of your own bloodcan use a family members blood if compatibledonated every 4-6 weeks before a surgical procedureblood can still become contaminated so observe for s/sx of reaction
|
|
|
Nursing Responsibilities for transfusion reactions
|
if ever in doubt - Stop the TransfusionMeticulous assessment of the patient - watch the temp very carefullyauscultate lungs frequently especially in elderly adults and pediatric patients ( if an overload is suspected - cough, wheezes, crackles, slight dyspnea, distended neck veins, HTN, tachycardia --- SLOW THE IV RATEIf a reaction occurs or is suspected- STOP INFUSION
|
|
|
Actions during a Transfusion Reaction
|
1. prime new IV tubing with normal saline and infuse at KVO rate, unless shock2. Save the used tubing and blood bag to return to blood bank with voided urine for hemoglobinuria ( watch for hematuria, draw a H/H, Type/ Cross, Blood Cultures3. Notify the physician - give meds : vasopressors, Benadryl, Tylenol, Lasix, Epinephrine, calcium gluconate ( facilitates clotting), etc.
|
|
|
Early Transfusion Reaction
|
called Mild Reactions) are burningfeeling at the IV site, local itching, facial flushing, chills, fever (not lowgrade), dyspnea, general weakness, back/flank/chest pain, slight hypotension,elevatedheart rate, confusion, macular rash, nausea, vomiting, diarrhea, hives,wheezing, headache, dizziness, skin flushing, anxiety,and red-colored urine.
|
|
|
Middle Stage Transfusion Reaction
|
exacerbation) BP systolic and diastolicmerge together (MAP starts to take a dip), patient may complain of difficultybreathing (typically tachypnea), temp may increase further, skin reddening/rashif present may enlarge very quickly
|
|
|
Late Stage
|
called Severe Reactions) are generalizedbleedingcaused by disseminated intravascular coagulation(DIC), severe hyperthermia (if present), severe tachycardia, life-threateninghypotension, severe onset of ARDS, and possible shock either hypovolemic or allergic ----thisstage usually advances to death.
|
|
|
Acute Hemolytic Reactions
|
An acute hemolytic transfsion reaction is the rapid destruction of red blood cells that occurs during, immediately after, or within 24 hours of a transfusion when a patient is given an incompatible blood type. the recipients body immediately begins to destroy the donated RBC's Kidney damage may result from this reaction up to possible deathmild/severe - usually first 15 minutes of infusionFever, chills, chest pain, dyspnea, facial flushing, hypotension, flank pain, hematuria, burning feeling at the IV site.
|
|
|
Allergic Reactions
|
Anallergic reaction results from an interaction of an allergen in the transfusedblood with preformed antibodies in the person receiving the blood transfusion.In some instances, infusion of antibodies from the donor may be involved. Thereaction may present only with irritation of the skin and/or mucous membranesbut can also involve serious symptoms such as difficulty breathing. Allergicreactionsoccur in about 3 % of all transfusions.These reactions are generally mild and respond to treatment quickly. Benadrylgiven before the transfusion significantly reduces the risk of an allergicreaction.
|
|
|
Delayed Hemolytic Reactions
|
Adelayed hemolytic transfusion reaction occurs when the recipient developsantibodies to red blood cell antigen(s) between 24 hours and 28 days after atransfusion. Symptoms are usually milder than in acute hemolytic transfusionreactions and may even be absent. This reaction isdiagnosed with laboratory testing. Fever, mild jaundice, and decreasedhematocrit are possible.Patienteducation on discharge is critical.
|
|
|
Febrilenon-hemolytic transfusion reactions
|
the most common reaction reported after a transfusion. Usually caused by an interaction between incompatible leukocyte blood. It is characterized by fever and/or chills in the absence of hemolysis (breakdown of red blood cells) occurring in the patient during or up to 4 hours after a transfusion. These reactions are generally mild, occur 20 minutes after administration, and respond quickly to treatment.
|
|
|
Febrilehemolytic reactions
|
are the most deadly of all blood transfusion reactions and require quick interventions. These reactions usually occur within the first 20 minutes of a blood transfusion.
|
|
|
Septic Reactions
|
Atransfusion-transmitted infection occurs when a bacterium, parasite, virus, orother potential pathogen is transmitted in donated blood to the transfusionrecipient.Fever,vomiting, diarrhea, chills and hypotension may be present
|
|
|
Transfusion-related acute lung injury(TRALI)
|
isa serious but rare reaction that occurs when fluid builds up in the lungs, butis not related to excessive volume of blood or bloodproducts transfused. Symptoms include acute respiratory distress with no otherexplanation for lung injury such as pneumonia or trauma occurring within 6hours of transfusion. TRALI is a leading cause of transfusion-related deathreported to the FDA. The mechanism of TRALI is poorlyunderstood,but is thought to be associated with the presence of antibodies in donor blood.The fatality rate is 5% to 14%.
|
|
|
Transfusion-associatedgraft vs. host disease (TAGVHD)
|
Transfusion-associatedgraft vs. host disease is a rare complication of transfusion that occurs whendonor T-lymphocytes (the “graft”) introduced by the blood transfusion rapidlyincrease in number in the recipient (the “host”) and then attack the recipient’sown cells. Mostlikely to occur in the immune compromised patient.Mayoccur weeks to a month after transfusion. Thefatality rate is > 90%.
|
|
|
Other complications of blood transfusions
|
Hyperkalemia, Hypocalcemia
|
