Exam 2 STUDY GUIDE

Fluid & Electrolytes
Advanced Concepts in Fluid and Electrolyte Disturbances

The Kidney: Balancing Internal Environment
Major controller of fluid & electrolyte homeostasis
Acid-base balance
Metabolic & endocrine functions:
o BP regulation
o EPO production
o insulin degradation
o prostaglandin synthesis
o Ca2+/Phosphorous regulation
o Vitamin D metabolism
Kidneys
Receive ~25% of cardiac output

Filtration of plasma (~160170L/ 24hr.)
o Liver=other filtration system
Proximal tubules:
o Reabsorb Na, K, Cl, HCO3, Ca, Mg, Glu, AAs, proteins, vitamins + water
Distal tubules secrete:
o H+, K, UA & excrete urea and Cr
**Major controller of fluid & electrolyte homeostasis

BP regulation: Renin, Angiotensin, Aldosterone
EPO production: Regulation of RBC production
Insulin degradation:
o ~25% of insulin produced by pancreas is degraded by kidneys daily
Prostaglandin synthesis:
o The kidney increases prostaglandin synthesis to modulate renal vascular resistance d/t
ischemia, vasoconstriction, or angiotensin II
Ca2+/Phosphorous Regulation:
o Via Vitamin D absorption from food and promoting resorption of calcium in kidneys
Vitamin D metabolism:
o Facilitates conversion of Vitamin D to its active form
Acute Renal Failure
Abrupt of kidney function
~10% of kidney functioning
Sudden BUN and Creatinine (norm ratio 1:10)
o BUN: protein intake, muscle, hydration & bleeding affect BUN
o Cr: less factors that affect so more indicative of kidney function
Urine output < 40ml/hr
Occurs in 530% of hospitalized patients
One of leading causes for inpatient mortality
o Not excreting waste -> metabolic acidosis
o In acute phase pt may still be creating urine
S3, S4, weight gain , edema d/t fluid overload
Decline in GFR
o Anuria: < 100 ml/24 hrs.
o Oliguria: < 400 ml/24 hrs (50% cases with ~80% mortality rate)
o Azotemia: BUN
Symptoms: S3, S4; crackles, DOE, weight gain, edema
Types of ARF
Prerenal: stems from heart d/t ed perfusion

Intrarenal (Kidney): anything damaging kidney within the kidney
ex: ABX processed through kidney

Postrenal: after the kidneys there is an obstruction; BPH, spinal cord injury
Glomerulonephritis
Inflammation of glomeruli ESRD (possibly leading to transplant)
Initial stage:
o Nephrotic syndrome (decreased Albumin, proteinuria >3.5g/day decreased
plasma volume increased aldosterone fluid & sodium retention, edema)
o Hypertension
o Hematuria
Damaged kidney attempts to filter through, sloughs off tissue and causes
blood in the urine
Little blood can cause it to look like more blood loss than actually
occurred
Late stage: Azotemia, N/V, pruritus (inability to excrete toxins -> lack of blood flow),
dyspnea, malaise, fatigue, anemia, severe HTN (cardiac hypertrophy, heart failure)
Lab Tests:
o Urine: Proteinuria, hematuria, RBCs
o Serum: Increased BUN & creatinine
Acute Tubular Necrosis
Damage to renal tubular epithelium due to:

o Ischemic Injury
Decreased perfusion: decreased CO, intravascular volume loss (hemorrhage,
dehydration), severe prolonged hypotension
Shock: Hypovolemic, cardiogenic, septic
Sepsis & anaphylaxis
o Nephrotoxic injury
Endogenous: Rhabdomyolysis (seen in athletes, immigrants, crushing
injuries), TLS
Rhabdo: breakdoen of muscle, release myoglobin and it cannot be
filteres
Antimicrobials: Aminoglycosides, cephalosporins, antifungals, antivirals
Immunosupressants: Cyclosporin, tacrolimus
Chemotherapy
NSAIDS
Street drugs: Heroin, amphetamines, PCP
Collaborative Treatment of ARF
Prerenal: crystalloid, colloid, pRBCs

fluid volume increase in vasculature to increase perfusion to kidneys
Intrarenal: fluid restriction depends on pt and function of kidneys
ABX: monitor peak and trough of vanco before and after tx

Phases of ATN
1. Onset: (initial phase)
Pathophysiology: Integrity of renal tubular epithelium disrupted

Duration: Hours to days (longer with toxic factors)
o Reversible by early intervention
2. Oliguric/Anuric: Occurs within 1 day of onset; lasts 5 days to 16 days.
Pathophysiology: Accumulation of necrotic cellular debris blocks urine flow & damages
tubular wall & basement membranes
o Inability to excrete fluid, electrolytes, and waste
Oliguiria: <400ml/ 24hr. (<30mL/hr)
o Older adult: 600 700ml/24hr
o Anuria <100ml/ 24hr
Decreased GFR increased BUN, Creatinine; Increased K+ & Phosphorous; Decreased
Ca2+; metabolic acidosis
3. Diuretic (7-14 days)
Patho: Tubular obstruction has corrected but edema & scaring prevent solute filtration
o BUN
o Increased GFR
o Large amounts (up to 45L/day) fluid lost
4. Recovery: Normalizing of fluid & electrolyte balance

Patho: Renal function returns to near normal
o GFR ~70 80% of normal within 1-2 years
o ~33% with long term renal insufficiency
ARF: Inability to Excrete Waste & Maintain Homeostasis (Electrolytes, acid/base, heme)
Increasing BUN (up to 30mg/ dL/ day)
Increasing Creatinine (> 1.2)
o BUN/Creatinine ratio = 11:1 40:1
Normal BUN/Creatinine ratio = 10:1
Hyperkalemia (> 5.5 mEq/L)
o Damaged distal convoluted tubule unable to exchange K+ for Na+ or H+
Hyponatremia (< 130 mEq/L)
o Due to overhydration leading to dilution of serum
Metabolic Acidosis
o H+ ion secretion and bicarbonate ion production diminish
o Lungs cant fully compensate
Hyperphosphatemia/hypocalcemia
Anemia
ARF: Select Nursing Diagnoses
Fluid volume deficit versus Fluid volume excess
Imbalanced nutrition: < body requirements
Risk for impaired skin integrity
Risk for infection
Anxiety
Goals of Care:
o Restore & preserve renal function
o Prevent complications from renal failure
ARF: Collaborative Treatment
Prevention:
o Avoid nephrotoxic drugs:
NSAIDS & ACE inhibitors
ACE: important but also toxic to kidneys

o IV contrast dye in high risk patients
Must look @ BUN & Cr cause its filtered through kidneys
Monitor for effects of altered protein binding sites, altered absorption, distribution, and
metabolism: drug toxicity concerns
Hypovolemia: Use of hypotonic solutions
Hypovolemia d/t blood loss: PRBCs and isotonic NS
Inflammation: Glucocorticosteroids
Maintain nutritional status: High calorie, low protein
Renal Failure: Dietary Management
Protein restriction (~0.5g/kg/day)
o If pt is predialysis: you want to restrict protein
o If ON dialysis, pt requires more high protein diet to supplement
Na+ restriction
o Cause it will increase fluid
K+ restriction
o d/t inability to excrete
Phosphorous restriction
o Give Ca+ phosphate binders to try to bring down phosphate then build up Ca+
Vitamin supplements (iron, folate, B 12)
o Helps to RBC production
Kidneys produce EPO
Fluid restriction (1000ml 1500ml/ d)
Chronic Renal Failure
Kidney damage is progressive and irreversible:
o Decreased renal reserve: 4075% nephron functional loss
o Renal Insufficiency: 7580% nephron functional loss
o End Stage Renal Disease (ESRD): <15% of nephron function
Causes:
o Urinary tract obstruction, PKD
o Chronic illness: Diabetes (32%), long-term HTN (28%), recurrent infections
o Glomerulonephritis (1%)
Peak incidence: 2064 years old
Clinical Manifestations
Hematopoietic: Anemia
Cardiovascular: CHF, HTN, dysrhythmias (d/t ed K+), percarditis, edema
Respiratory: Pulmonary edema, infection
Endocrine: Altered glucose control, hypothyroidism
Gastrointestinal: N/V, altered taste
Neurological: LOC, numbness & tingling, hyperreflexia, seizures (d/t Ca++ & toxins)
Skeletal: Calcifications, aches (d/t bone spurs)
Skin: Pruritis, delayed wound healing
o Appear grayish
GU/ Reproductive: ovulation & spermatogenesis
Other: Metabolic acidosis
Renal Failure: Treatment-Dialysis
Waste products in serum are filtered through a semi-permeable membrane
Principles of Dialysis:
o Osmosis
o Diffusion
o Ultrafiltration
In pt. with fistula: check for Circulation, thrill (pulsation), bruit (hear with steth)
o No ore than a gallon of milk
o Perform hand exercises
Hemodialysis (HD)
Access: Dialysis catheter (short term); AV fistula (long term)

Indications:
o BUN >90 & Cr >9
o K > 6.0
o Drug toxicity
o FVE (fluid volume excess)
o Metabolic acidosis
Contraindications: Hemodynamic instability; inability to coagulate, no access
Tx: about 3 hours 3x/week
Continuous Renal Replacement Therapy (CRRT)
Gradual over 8-24 hrs.
Patients hydrostatic pressure (MAP >70) drives blood through the filter
Arterial-venous
Veno-venous
Indications:
o Hemodynamic instability with FVE unresponsive to diuretics, MODS
o Inability to coagulate
o BUN >60
Changes in BUN & Cr seen quicker in CRRT then hemo; doesnt mean
kidneys working better, just indicates better filtering
Short term use for BP management
o Main reason why CRRT used rather than dialysis
Dialysis es fluid & BP
Dialysis: Nursing Management
Monitor VS (hypotension)
Monitor fluid balance
Monitor electrolytes
o Hyperkalemia: Kayaxelate
o Metabolic acidosis: Bicarbonate

o Hypocalcemia: Calcium supplements
o Hyperphosphatemia: Phosphate binders
Administer medications at appropriate times
Fatigue management (EPO, iron, Vitamin B complex)
GI disturbance symptom control: antiemetics, laxatives
Psychological care
Teaching
Pre Dialysis Question
A patient with ESRD is admitted for cellulitus of the right leg. The nurse is preparing a
patient for hemodialysis. The patients VS are: T=99 F, HR= 100, BP= 148/98, RR=20.
Which of the following medications should not be given before hemodialysis.
o Vancomycin (IV)
Will get filtered out
o Morphine sulfate IV
Give morphine; it will act quick & cellulitis painful
o Diltiazem (PO)
Will drop BP
o Atenolol (PO)
BP will drop anyway
o Heparin (SQ)
Will be getting heparin during HD
o MVI (PO)
o Aspirin (PO)
o Senna PO
o Calcium PO
Post Dialysis Question
A patient with ESRD is admitted for cellulitus of the right leg. The nurse is receiving the
patient from the hemodialysis unit. The patients VS are: T=99 F, HR= 112, BP= 98/66,
RR=20. Which of the following medications should not be given be given after
hemodialysis.
o Vancomycin (IV) [Give after each Rx]
o Morphine sulfate (IV)? [Give low dose PRN]

HR goes up with temp & pain
o Diltiazem (PO)
o Atenolol (PO)?
Affects HR (Beta-blocker); possibly give for HR
Call doc & ask
o Heparin subQ
o Calcium PO
o Nephrocap PO
o Aspirin PO
o Senna PO
Delicate Balance of Fluids & Electrolytes in Complex Client Care
Mrs. Black Case Study
87yo admitted to the intermediate care unit with

pneumonia, CHF, and renal insufficiency.
PMHx: MI x2, Afib, HTN, Diabetes-type 2
x10yrs, osteoarthritis, osteoporosis, s/p right hip
replacement 2mths ago
VS: T= 38.6C, HR= 106 with S3 present, EKG=
Atrial fibrillation irregular with peaked T waves
& widened QRS, BP= 158/90, RR= 20 at rest ,
pOx=90% on 30% VentiMask.
Weight/Height:185lbs/ 5ft 2in.
I/O: 2400/ 1200 via Foley catheter
Labs: Na= 130, Cl= 95, K= 5.5, CO2= 20, BUN=
10, Cr= 2.1, Glu= 302, Mg =1.5, Ca= 8, PO4=
5.5, Alb= 1.9
Current patient complaints: palpitations and
SOB and being fuzzy in the head, right hip
pain, diarrhea
Questions? Concerns?
What is the patient experiencing? Priorities?
Medications
Azithromycin 500mg IV daily
Digoxin .25mg po daily
Vancomycin 500mg IV every 12 hrs
Lisinopril 10mg po daily
Methylprednisolone 20mg IV every 12
hrs
Losartan 50mg po daily
Insulin continuous infusion (conc:
100Units/ 100ml) sliding scale Regular
Diltiazem 60mg po daily
IV Fluids: D5 1/2NS + 20mEq @
125ml/hr
Furosemide 40mg IVP twice a day
KCl 40mEq po daily - discontinued
Other Orders:
Activity: OOB to chair x3/ day
Diet: Low sodium, low carbohydrate +
high protein snacks BID
What is the patient experiencing?
Priorities?
Diabetes Insipidus:
Water diabetes
Occurs when secretion or action of ADH is abnormal
o Hypothalamus produces insufficient ADH
o Posterior pituitary fails to release ADH
o Nephron does not respond to ADH
Results:
o Severe dehydration, thirst, hypernatremia
o Uncommon; 1 case in 25,000 people
Diabetes Insipidus: Causes
1. Central (decreased ADH)

o CNS tumors
o Cerebrovascular disease
o Traumatic brain injury
o CNS infections
o Pregnancy: vasopressinase destroys vasopressin
2. Nephrogenic (kidney resistance to ADH)
o Chronic tubulo-interstitial disease (such as ATN, PKD, MM, Lupus)
o Medications: lithium, ampho B, phenytoin, steroids, aminoglycosides
o Electrolyte problems: hypercalcemia, hypokalemia
DiabetesInsipidus:Symptoms
Labs(diagnosticcriteria):
o SerumOsmo>300
o SerumNa>145
o Urineosmo<300
o SG<1.005
o IVF>5liters/24hours
Symptoms:Onset=510daysafterinitialinjury
o Polyuria:u/o34liters/day(>200ml/hr)
o Polydipsia:intensivethirst
Hypernatremia
Causes:Renallosses,severeGLU,thirst,fluidlossfromskin/lungs,hypertonicfeedings,
sodiumintake,hyperaldosteronism,increasedcortisol,diabetesinsipidus
Symptoms:Dryflushedskin/mucousmembranes,thirst,fever,neuromuscularirritability,
HR,BP,CO,oliguria
Treatment:
o DecreaseNalevel
o Fluidresuscitationwithhypotonicsolution
DiabetesInsipidus:CollaborativeManagement
Monitorintake&outputhourly
Monitorelectrolytes(esp.sodium&chloride)
Replacefluidshourlywithhypotonicfluids(0.45%NaCl)
ml/mlhourlyreplacement
Hormonalreplacement
o DDVAP,Vasopressin
HormonalReplacementTherapy
SyndromeofInappropriateADH
IncreasedproductionofADH
Increasedwaterreabsorptioninrenaltubules
Increasedwaterretention&dilutionalhyponatremia
Causes:
Smallcelllungcancer
Pulmonarydisease:COPD,TB,bacterialpneumonia
GImalignancies
Medications
Chlorpropamide
Carbamazepine
Thiazidediuretics
Tricyclicantidepressants;SSRI
Nicotine
SIADH:
Pathophysiology
Increasedwaterreabsorption
o Increasedextracellular<intracellularfluid
o Decreasedsodiumconcentration(dilutional)
o Hypoosmolalitycellularswelling
IntracranialincludesincreasedICP
WaterIntoxication
Symptoms
Labvalues:
o SerumNa+:<130mEq/L
o SerumOsmolarity:<280mOsm/kg
o UrineOsmolarity:>500mOsm/kg
o UrineNa+:>20mEq/L
Symptoms:
o Weakness,fatigue
o AlteredLOC(IncreasedICP);seizures
o NormalCVstatus
o N,V,D
o Oliguria(<400ml/24hr)
o Increasedweight
o Hypoactivereflexes
Hyponatremia
Causes:Diuretics,vomiting,diarrhea,diaphoresis,renalfailure,hypervolemia,SIADH
Symptoms:N/V/D,hyperactiveBS,DBP,tachycardia,neuroSx,dryskin,pallor,dry
mucousmembranes
Treatment:
o IncreasesodiumtowaterratioinECF
o Hypertonicsalinereplacement
HyponatremiaTreatment:
1.Assessplasmaosmolality
2.Assessvolumestatusofpatient
o Hypervolemic,Euvolemic,Hypovolemic
3.AssessUrineSodiumConcentration
o Neededfordefinitivediagnosis,notneededfortreatmentpurposes
4.CalculateNa+Deficit
o 0.6xweight(kg)x(130plasma[Na+])
5.Correctatnomorethan0.5mEq/Lperhouror12mEq/Lper24hours
SIADH:CollaborativeInterventions
Waterrestriction(~1L/day)
Seizureprecautions
Diet:highsodium
NSIVorhypertonicsaline(3%)
Demeclocycline(derivativeoftetracycline)
o InhibitseffectofADHonrenaltubules
o Allowsdiuresisofwater
ComparisionofDI&SIADH
DI(InadequateADH)
o Hypernatremia>150
o Dehydration
o Increasedserumosmolality
o Decreasedurineosmolality
o DecreasedurineNa+
CellularDestruction:Rhabdomyolysis
Definition:
o Rapidreleaseofcellularcontentsfromdamagedskeletalmusclecells
Athighestrisk:
o Crushinginjury/musculoskeletaltrauma
o Strenuousexercise
Etiology:
o Releaseofmusclecellcontents(myoglobin,potassium,phosphorus,nucleicacids>
uricacid)
CellularDestruction:Rhabdomyolysis
Signs&Symptoms:
o Myoglobulinuriabrownurine
o Hyperkalemia
o Hyperphosphatemia
o Hyperuricemia
o Hypocalcemia cardiacarrhythmias
o Acuterenalfailure,MODS
SIADH(ExcessADH)
o Hyponatremia<130
o Overhydration
o Decreasedserumosm
o Increasedurineosm
o IncreasedurineNa+
CollaborativeManagement:
o Alkalinizationofurine(preventmetabolicacidosis)withNS&NaHCO3
o Correctelectrolyteimbalances
o Hydrationanddiuresis
o Dialysis
CellularDestruction:TumorLysisSyndrome
intracellularcontents
Athighestrisk:
o Largetumorburden(leukemia,lymphoma,SCLC,breast,neuroblastoma)ontherapy,
o Comorbidities(renalorcardiac)
Etiology:Releaseofcellularcontents(potassium,phosphorus,nucleicacids>uricacid)
Signs&symptoms:
o Hyperkalemiacardiacarrhythmias
o Hyperphosphatemia,
o Hyperuricemiametabolicacidosis
o Hypocalcemiacardiacarrhythmias
o Acuterenalfailure(increasedBUN&Cr),MODS
o Alkalinizationofurine(preventmetabolicacidosis)withNS&NaHCO3
o Urateoxidase;xanthineoxidaseinhibitors
o Correctelectrolyteimbalances
o Hydrationanddiuresis
o Dialysis
HepaticRelatedAscites
Definition:Abnormalcollectionoffluidinabdominalcavityd/tadvancedstagehepatic
Definition:Rapidtumorcellkillresultingfromcancertherapywhichcausesrapidreleaseof
dysfunction
Causes:
o colloidosmoticpressured/talbumin
o Inabilityoflivertometabolizeprotein
o CirrhosisPatiens:IncreasedNaretentionbykidneyexpansionofintravascular
volumefluidshiftingtotissuesdecreasedNaClandwaterexcretionr/t
decreasedalbumen(colloidal),increasedaldosterone(Naconservation),and
increasedADH(H2Oconservation)
HepaticRelated:HepatorenalSyndrome
Definition:ComplicationofESLDARFwithoutunderlyingkidneypathology
Athighestrisk:
o Hepaticdysfunction
o Cirrhosis
Etiology:
o TypeIdecreasedBP(s/paggressivediuresis,largevolumeparacentesis,GIbleed,
majorsurgicalprocedure)ORacuteviralhepatitisincirrhosispt.
o TypeIIsevereascites,refractorytodiuresis
Signs&Symptoms:
o TypeI:Rapid,progressive(doublingserumCrover2wks;>2.5mg/dL)
o TypeII:Chronic,slowlyprogressive(slowincreaseofserumCr;>1.5mg/dL)
o General:LiverfailurewithincreasedLFTs
Oliguria(<400ml/24hrs)
DecreasedserumandurineNa
IncreasedBUN&Cr;decreasedGFR
CollaborativeManagement:Focusedonsupportivecareforliverdisease
o Fluidresuscitation
o CRRT
o Pharmacologic
Midodrine(peripheralconstriction)
Octreotide(splanchnicvasoconstriction)
Albumin(oncoticagent)
o Surgical
Livertransplantation
TIPS(transjugularintrahepaticportosystemic)shunt
DiabeticKetoacidosis
Description:Suddenonset(hours)
Athighestrisk:Type1diabetes
Etiology:
o Infection,surgery,trauma
o Undiagnoseddiabetestype1(20%)
o Changesindiabeticmanagement
o Lifechangeswhichincreasesinsulindemand
o Acutepancreatitis
o Starvation;increasedalcoholintake
Signs&Symptoms:
o Glucose>250mg/dLbut<600mg/dL
o ArterialpH<7.3
o Serumbicarbonate<18mEq/L
o Moderateketonemiaorketouria
Manifestations:Polys(dypsia,uria,phagia);dehydration,drymouth;tachycardia;changes
inLOC;Resp(airhunger,acetonebreath,increasedRR);N/V
o Dehydration:0.9%NS@1L/hr,then250500ml/hr;whenglucose=200mg/dL
then5%dextrose+.45%NS@150200ml/hr
o Correcthyperglycemia:Regularinsulin@.1units/kg/hrcontinuousinfusion
o Correcthypokalemia:IfK<3.3mEq/L,thengive2030mEq/Lperhruntil3.3;
checkKlevelevery2hrswhileoninsulindrip
o CorrectpHIVNaHCO3
HyperglycemicHyperosmolarState
Description:Slow,insidious(days,weeks)
o Athighestrisk:
Type2diabetes
Older,obesepatientswithunderlyingcardiovascularconditions
Etiology:
o Infection(pneumonia,UTI)
o Stroke/MI
o Trauma
o Burns
o Stressofillness
o Medications(corticosteroids,phytoin,thiazidediuretics,betablockers,dobutamine,
antipsychotics)
Signs&Symptoms:
o Glucose>600mg/dL
o ArterialpH>7.3
o Serumbicarbonate>15mEq/L
o Minimalketonemiaorketouria
o IncreasedHct
Manifestations:
o Resp(rapid&shallow)
o GI(nausea/vomiting)
o Electrolyteimbalance:decreasedK&phosphorus
o Metabolicacidosisd/tdehydration,decreasedtissueperfusion,accumulationoflactic
acid
o Dehydration:0.9%NS@1L/hr;whenglucose=200mg/dLthen5%dextrose+.
45%NS@150250ml/hr(mayneed610Lwithin1st10hrsBP&CVPneedto
beWNL)
o Correcthyperglycemia:Regularinsulin@.1units/kg/hrcontinuousinfusionAND
hourlyglucosemonitoring
**Glucoseshoulddecreaseby5070mg/dLperhour
o Correcthypokalemia:IfK<3.3mEq/L,thengive2030mEq/Lperhruntil3.3;
checkKlevelevery2hrswhileoninsulindrip
MaintainingFluid&ElectrolyteImbalancesinHighAcuityPatientsREVIEW
Question1:ApatientdiagnosedwithSIADHisadmittedwiththefollowingsymptoms:
headache,nausea,vomiting,confusion,decreasedurineoutput,decreasedDTRs,and
HR=114.
o Thenurseshouldanticipatewhichofthefollowinglabresults?
1.Serumcreatinineof0.9(symptomsofdehydration)
2.Serumsodiumof120mEq/L(dilutionald/texcessivewaterretention)
3Serumpotassiumof5.4mEq/L(generallylowKd/tdilution)
4.Serumosmolalityof270mOsm/kg(serumosmolality<280indicateswater
excess)
Question2:Apatientdiagnosedwithdiabetesinsipidusisexperiencingthefollowing
symptoms:increasedurineoutput,excessivethirst,weakness,severeitching,dryskin,
fatigue,HR=116,andBP=88/58.
o Thenurseshouldanticipatewhichofthefollowinglabresults?(ADHinsufficiency)
1.Decreasedchloride(fluctuateswithsodium)
2.Decreasedcalcium(calciumnotgenerallyeffected)
3.Increasedsodium(lackofADHallowsforexcessivediuresis&sodium
retention)
4.Increasedpotassium(generally,potassiumexcreted)
Question3:ApatientappearsintheEDafterrunninghisfirstmarathonwiththefollowing
symptoms:colacoloredurine,myalgias,muscletenderness,andweakness.
o Thenurseshouldanticipatewhichofthefollowinglabresults?(Rhabdomyolysis)
1.NormalCPK(CPKiselevatedwithmuscledamage)
2.Negativeserummyoglobin(myoglobiniselevated)
3.Serumsodiumof151mEq/L(sodiummaydecreased/tinsensibleloss)
4.Serumpotassiumof5.6mEq/L(cellulardamagereleasespotassium)
Question4:ApatientwithWBCcount=52,000with70%blastsreceivedchemotherapy
oneweekagoforacuteleukemia.Symptomsinclude:EKGchanges,musclecramps,
decreasedurineoutput,N/V/D,anddecreasedBP.Labresultsareasfollows:sodium=
132mEq/L,potassium=5.7mEq/L,phosphorus=5.0mg/dL,increaseduricacid&LDH.
o Thenursesuspectswhichofthefollowing:
1.SIADH(generallyNa<130&H2Oimbalance)
2.DI(sodium>150)
3.TLS(TumorLysisSyndrome);increasedK,PO4,UA,LDH,BUN,Cr;
decreasedCa2+
4.CRF(ARFislikelyinthiscaseunlesspthascomorbiditiessuchasDMor
HTN)
Advanced Concepts in Fluid & Electrolyte Management

Kidneys
Receive ~25% of cardiac output

Filtration of plasma (~160-170L/ 24hr.)
Proximal tubules:
o Reabsorb Na, K, Cl, HCO3, Ca, Mg, Glu, AAs, proteins, vitamins + water
Distal tubules secrete:
o H+, K, UA & excrete urea and Creatinine
*Major controller of fluid & electrolyte homeostasis
o BP regulation, EPO production, insulin degradation, prostaglandin synthesis, Ca2+/
Phosphorous regulation, Vitamin D metabolism
Nephron
Glomerulus: Filter of capillaries

Bowmans capsule: Contains glomerulus & filters for urine
Proximal convoluted tubule: Resorption of Glu, amino acids, metabolites, electrolytes from
filtrate
Loop of Henle: Further concentration of urine
Distal convoluted tubule
Collecting tubule: Releases urine
kidney stones: can be formed from too much calcium and can block up the collecting duct
(which collects urine)
Fluid and Electrolyte Regulation Hormones
SIADH occurs when ADH goes wrong

Fluid Regulation
Parathyroid: Regulates calcium & phosphorus
o Thyroid: Also regulates calcium
GIT absorbs & excretes: Sodium, chloride, potassium & water
o If pt on NG tube, it is best to flush with NS to maintain osmolality
SW (hypotonic): will draw electrolytes to it, therefore diminishing electrolytes
in the system
o ostomies: ascending colostomy presents the greatest risk for F&E imbalances
Albumin: Holds water in the right spaces (water follows)
o ed albumin could affect BP, ing it d/t fluid loss
Fluid Regulation Hormones
Angiotensin I: converted to A-2 in pulmonary tract

Adrenal cortex: secrete cortisone (glucocorticoids)
If pt severely dehydrated, obtaining IV access is difficult cause veins flat and small
o AC area would provide best access
Age-Related Changes: Renal

Age 30yo, kidney at max. size = 150 300gm
o Gradual decrease in size & volume over decades; by 90yo by 30 40% (By age
70yo, 30 50% glomeruli lost)
Decrease renal perfusion ( GFR)
Decreased vascular compliance
ACE inhibitors: renal perfusion pressure
NSAIDS: inhibit prostaglandin potentiate vasoconstriction
o Prostaglandins dilate
Serum Creatinine stable with age
Decreased muscle mass & increased fat
o Less Creatinine produced; less Creatinine excreted
Decreased ability to conserve water & sodium Dehydration & Hyponatremia
Decrease GFR; 1mL/min after age 40
o Decreased filtration efficiency
Decreased rate of drug excretion
Assess for toxicity: anti-infectives, digoxin, diuretics, beat-blockers, statin
lipid-lowering agents, ACE inhibitors, oral antidiabetic agents
o Therefore ABX could cause renal failure
Increased permeability: Increased loss of protein & electrolytes (Na)
Nocturia
o Suggested that GFR & electrolyte clearance enhanced with horizontal positioning
Best time to take diuretic is in the morning & diminish intake 2-3 hr before
bedtime
Physically vulnerable: Effects of extreme temperatures
Taste alteration decreases fluid and nutritional intake
o May get full quicker and eat less
Cellular Fluids
Intracellular (2/3) [inside cell]
o About 20% of fluid
Extracellular (1/3 mostly for lubricant [for joints and to keep cells working]): about 40%
of fluid
o Intravascular
BP influence
o Interstitial [surrounding cell]
Transcellular
o CSF, pericardial, pleural, intraocular, joints
Maintaining Fluid Balance
Daily weights: most accurate because it allows for monitoring of fluid that removed via
lungs (norm loss=300 mL), skin, etc. (insensible loss)
o Insensible loss through lungs includes water, sodium (follows water), and chloride
(follows NA+)
Osmolality
Measure of number of particles in a fluid (mOsm)
Normal: 275 - 295 mOsm/kg
o If a pt has ascites, then they dont necessarily have a lot of fluid; rather it is in the
wrong places so they may have a significant in BP
Starling Forces: Movement of Body Fluids
**Body fluids move between interstitial & intravascular compartments
Capillary hydrostatic pressure:
o Fluid moving through capillary (A>V)
BP
Capillary colloidal osmotic pressure = Oncotic Pressure: keeps fluid in the right places
o Exerted by plasma protein as flow through capillary
Interstitial fluid pressure:
o Pushes against capillary to prevent fluid leaking
Tissue hydrostatic pressure:
o Exerted by proteins located in interstitial space
Fluid Movement: Capillary Bed
Normal Fluid Balance

1L ~ 1kg
Intake: ~2500ml/d
o Oral: ~1300ml
o GI [food]: ~1000ml
o Metabolic: ~300ml
Output: ~2500ml/d
o Urine: ~1500ml [~1ml/kg/hr]
o Stool: ~350ml
Insensible loss:
o Sweat: ~500ml
o Breathing: ~350ml
POC:
o -K+ correction (arrhythmias & cardiac issues)
Furosemide (works best with renal insufficiency/kidney failure) & Lasixs would be
important to give
o Work in about 5 min
o Although resp is questionable, its probably okay for now; RR=20
Address high glucose with regular insulin
o Insulin drip (regular) adjusted q1h
o WATCH for K+
Insulin drip drives K+ into the cell (other go with it, but K most important)
After furosemide & insulin drip, K+ could greatly
Feeding tube d/t low albumin, resp probs & ed nutrition
o But not too much, cause protein could affect kidneys and BUN
Protein broken down in gut to ammonia & travels to liver, creating urea (a
byproduct of ammonia), and then excreted in kidneys
w/ kidney failure, urea cannot be excreted ad builds up
methylprednisone (Ms. Blacks med): affects sodium & glucose

Fluid Imbalances
**Fix dehydration/overhydration first if they are not overly symptomatic, because the numbers
are false
Assessing Fluids & Electrolytes
Intake & output

o Extrarenal fluid loss: Insensible loss (fever, hyperventilation, ambient
temperatures), GI losses (V/D, NG drainage, fistulas), distributive loss (3rd spacing
pleural, peritoneal, capillary leak, evaporative/ transudative)
Urine volume
o ARF or CRF
o FVD or FVE
o Redistribution: Ascites, pancreatitis, burns, CHF
o Diuresis
Urine concentration (measure specific gravity)
o <1.003: hyponatremia, FVE, RF, FVD
o >1.035: hypernatremia, FVD, clearance of solutes
Skin turgor
o Tenting versus edema
Tongue turgor & mucous membranes
o Dry tongue with fissures, dry mucosa, viscous mucous, cracked/ chapped lips
Body weight (gain versus loss)
Thirst
o Alterations may be due to neurological disorders; hypothalamus damage; decreased
function of osmoreceptors
Tearing & salivation
Edema
o Edema pitting edema, pulmonary edema
Neck veins & CVP:
Nl = 3-4cm above sternal angle: flattened versus elevated

Neuromuscular irritability
o Tetany & hyperreflexia (+Chvosteks & Trousseaus signs): resp. alk., hypocalcemia
& hyperphosphatemia, hyponatremia & chloremia, hypomagnesemia
o Weakness & hyporeflexia (DTRs): Hypercalcemia & hypophosphatemia,
hypokalemia, hypermagnesemia
When checking or pronator drift, can identify tremor: may be a sing of
electrolyte imbalance
Chvosteks: Can tap of zygomatic process; twitching indicates hyperactivity?
Trousseaus signs: Put BP cuff on, pump it up, and diminished flow will cause
arm to come up
If you dont replace Ca & Mg fast, they can experience seizures
ed causes weakness
Evaluation of Edema:
Pitting edema:
o Accumulation of fluid greater than what can be absorbed by interstitial tissue gel
If pitting edema in feet, you could raise feet

Must consider: hip replacement; when elevating feet, you can potentially exacerbate right
sided CHF (ing workload of heart)
o TEDs, SCDs (to compress and push fluid)
Assessing Fluids & Electrolytes
Vital signs
o Skin & body temperature
ed body temp indicative of dehydration
o Pulse:
Bounding: FVE
Tachy: FVD, resp. acidosis, hypernatremia
Brady: hypokalemia, hypermagnesemia
Thready: severe FVD, hyper kalemia & phosphatemia, hypocalcemia
o Blood pressure: HTN versus hypotension
o Respiration: Hyperventilation (Cl, resp. alk.); hypoventilation (K, Mg, met.
Acidosis, resp. alk.)
Fluid Resuscitation (Crystalloids)

Isotonic solutions: Normal Saline, Lactated Ringers, Ringers
o No fluid shift; vascular expansion; electrolyte replacement
o *Lactated Ringers: Liver converts lactate to bicarbonate to buffer against metabolic
acidosis or plain Ringers
Hypotonic solutions: 1/4 NS, 1/2 NS, D5W
o Shifts fluid out of vessels into cells; hydrates cells
o *Used to hydrate patient fast
Hypertonic solutions: D5 1/2NS (very low end hypertonic; more like isotonic), D5 NS,
o 3%NS, 5%NS (may cause cellular dehydration)
o Shifts fluid back into circulation; vascular expansion
Increased blood volume, ing BP
*You will see it first in brain w/ major confusion
fluid pulled out of brain cells causing brain cells to shrink
*May cause fluid overload & electrolyte imbalances
Uses:
Mobilizing 3rd spaced fluids, BP, expanding intravascular volume
Types:
Albumin (5% or 25%)
o Not used very often; expensive
Maintains volume
Dextran (polysaccharide)
Shifts fluid into vessels; vascular expansion
Mannitol (alcohol sugar)
o cerebral edema
Oliguric diuresis; reduces cerebral edema
Blood Products
o Colloid
o Could cause ed urine output
Transfusing RBCs leads to pulling of fluid into vasculature space, ing
outflow
o POC: fluid overload
Nursing considerations: Fluid overload leading to CHF, pulmonary edema
*Whole blood causes biggest osmotic pull
Albumin
Available as 5% or 25% in glass bottles
Blood tranfusion sets not required
5% is osmoticaly similar to plasma
25% is >5x osmotic than that of plasma

Nonhemorrhagic shock, burns, ascites, hepatic failure
No compatibility testing (no ABO antigens, antibodies)
Give 5% 2-4 ml/min; 25% in I ml/min
Fluid & Electrolyte Distrubances with Transfusions
Hyperkalemia
o Destruction of RBCs when blood is stored
o Hemolyzed blood (mismatched)
Cell lysis -> release of K+
Hypocalcemia
o Citrate preservative combines with ionized Ca in patients blood
o 5-8 units PRBC in < 4 hours, give Calcium gluconate
o Clinical manifestations: twitches, tremors in face, tingling lips
Acid-Base Changes
o Banked blood 2-3 wks old, pH 6.9
Overview of Electrolytes
Conduct electricity across cell membranes
Maintain osmolality of body fluid compartments
Regulate acid/ base balance
Aid in neurological/ neuromuscular functioning
Electrolyte Composition of Body Fluid
Electrolyte Excretion
Excessive elimination of body fluids
Renal excretion after diuretics
GI elimination: Vomiting and diarrhea
LGI: Bicarbonate lost
UGI: Hydrogen, sodium and potassium lost
Excessive diaphoresis: Sodium and chloride loss
Surgical drains
Renal Function by Numbers
**BUN, Cr, important to memorize

Electrolyte Regulation
Main regulators: Kidneys and endocrine system
Kidneys: Glomerular filtration, tubular reabsorption, and secretion
Endocrine: Pituitary adrenocorticotropic hormone -->release of aldosterone -->sodium
reabsorption-->K+ excretion
Endocrine: Cortisol sodium & water retention
o Excess cortisol (Cushings) would negatively affect ability to control CHF
Endocrine: parathormone & calcitonin -> calcium/ phosphorus balance
GI: Fluid & electrolyte absorption
Cardio/ Pulmonary
Electrolyte Documentation
Sodium Imbalance: (shifting Na+ should be done slowly to give cells time to adjust & prevent
cell lysis)
Neuro changes occur when shifting occurs too quickly
Hyponatremia [<135mEq/L]
Causes: Diuretics, vomiting, diarrhea, diaphoresis, burns, renal failure, hypervolemia,

adrenal insufficiency, SIADH (dilutional)
Symptoms: N/V/D, hyperactive BS, DBP, tachycardia, dry skin, dry mucous membranes
Neuro Sx: Muscle cramps/ twitching, H/A, confusion & dizziness
Treatment:
o Increase sodium to water ratio in ECF; give NS
o Give hypertonic saline with caution (3%NS)
o Free water restriction
o Patient safety
Hyponatremia Treatment (contd)
o 1. Assess plasma osmolality
o 2. Assess volume status of patient
Hypervolemic, Euvolemic, Hypovolemic
o 3. Assess Urine Sodium Concentration
Needed for definitive diagnosis, not needed for treatment purposes
o 4. Calculate Na+ Deficit
0.6 x weight (kg) x (130 plasma [Na+])

o 5. Correct at no more than 0.5mEq/L per hour or 12 mEq/L per 24 hours
Hypernatremia [>145mEq/L]
Causes: Renal losses, severe GLU, thirst, fluid loss from skin/ lungs, hypertonic
feedings, sodium intake, osmotic diuresis
Symptoms: Dry flushed skin/ mucous membranes, thirst, fever,
o Neuromuscular irritability: Hyperactive reflexes, lethargy, HR, oliguria
Treatment:
o Decrease Na level using hypotonic solutions (except for D5W)
Potassium Imbalance:
Hypokalemia [<3.5mEq/L]
Causes: GI losses, metabolic alkalosis, medications, ARF, severe diaphoresis, dialysis, high
doses of IV insulin
excessive corticosteroids (exogenous & Cushings Dx),
Symptoms: Anorexia, N/V/D, digitalis toxicity
musculoskeletal alterations (weakness, arrhythmias, decreased ST segment on EKG, DTRs,
lethargy/ fatigue, drowsiness, decreased bowel motility)
Treatment: Prevent cardiac symptoms
o Potassium replacement: 10mEq/50ml over 1hr IV OR PO
KCl overdose cardiac arrest
K level = 3 3.4mEq/L needs ~100-200 mEq of IV potassium for increase of
1mEq/L serum K
**ABX therapy causes ed levels of K= & Mg
Hyperkalemia
Causes: Renal failure, adrenal insufficiency (Addisons), metabolic acidosis (H+ ion enters
cell; K+ exits), hyponatremia (K+ retention), excessive release of K, TPN
Symptoms: Muscle paralysis, parathesias of face, feet & hands, GI peristalsis, oliguria,
ventricular arrhythmias (widened QRS), EKG (prolonged PR, tented T wave)
Treatment: Decrease K+ to normal as quickly as possible; prevent cardiac symptom
o Cardiac monitor (prolonged, widened EKG tracing)
o Oxygen therapy
o Assess for metabolic acidosis
o Insulin IV (facilitates moving K+ into cell)
o Kayexalate (promotes K+ excretion via GI route)
K+ of 6= Bad for heart
Insulin drives K+, phos & Ca into cell
Kayexalate (promote K+ excretion via GI route)
Calcium Imbalance
Hypocalcemia [< 8.0mg/dL]

Causes: Diet, medications, metabolic acidosis, renal failure, hypothyroidism (decreased
calcitonin), hypoparathyroidism (decreased calcium absorption), Vitamin D deficiency
Symptoms: Dyspnea, laryngeal spasm, diarrhea, arrhythmias (prolonged QT interval, long
ST segment), pathological fractures
neuroexcitability (+Chvosteks sign; +Trousseaus sign; seizures; hyperactive DTRs; muscle
spasms)
o laryngealpasm is most concerning cause airway can close
Treatment:
o Calcium replacement (oral with Vitamin D OR IV calcium gluconate)
Vit D helps with conversion of straight Ca to Ca used more efficiently
**Low Ca High Phos
o treating Ca usually treats phos; unless pt in renal failure
Hypercalcemia [>10.0mg/dL]
Levels:
o Mild: 10.5 11.9 mg/ dL
o Moderate: 12 13.9 mg/ dL
o Hypercalcemic crisis: 14 16mg/ dL
Causes: Metastatic malignancy, hyperparathyroidism, hypophosphatemia, thiazide diuretics,
immobility
Symptoms:
o Anorexia, dehydration, constipation, kidney failure, digoxin toxicity, bone pain and
fractures
o mental acuity, arrhythmias, muscle weakness
Treament: Normalize calcium levels
o IV NS @ high hourly rate
o Loop diuretics
o Calcitonin (decreases osteoclastic activity)
o IV bisphosphonates
*High Ca Low Phos
Albumin [3.5-5g/dL]
Produced in liver
Fluid connection: Assists in maintaining oncotic pressure
Relationship to total protein: 60% TP is albumin
Calcium connection (50% albumin bound)
Calculation for corrected Ca2+ =
(4.0g/dL pts albumin) (0.8) + patients serum Ca level
Protein binding of Ca2+ influenced by pH
o Increased ionized Ca in metabolic acidosis

o Decreased ionized Ca in metabolic alkalosis
Phosphorus Imbalance
Hypophosphatemia [<2.5mEq/L]
Causes: Hypercalcemia, diabetic ketoacidosis treatment, hyperparathyroidism, malnutrition,
TPN, alkalosis (increased pH > phosphate shifts into cell)
Symptoms: Similar to hypercalcemia
o Muscle weakness, fatigue, confusion) tachycardia
Treatment:
o Prevention by monitoring po intake and TPN
o Phosphorus supplements
Hyperphosphatemia [>4.5mEq/L]
Causes: Hypocalcemia, hypoparathyroidism, poor nutrition, adrenal insufficiency, vitamin D
toxicity, bone breakdown, cell lysis (rhabdomyolysis, TLS), acidosis (decrease pH >
phosphate driven out of cell to buffer)
o Many phos issues are corrected when Ca corrected or underlying cause of Phos
imbalance is corrected
Symptoms: Similar to hypocalcemia, pruritus, renal failure
Treatment:
o Normalize phosphorus levels
o Calcium supplements
o Phosphate binders
o Dialysis (renal failure patients)
Regulation of Calcium & Phosphorus Balance
80% phosphorus is bound to Calcium in bone
Kidneys:
o Filter & reabsorb ~ unbound serum Ca2+
o Activate vitamin D3 promotes intestinal Ca2+ absorption & regulates phosphate
excretion
Endocrine:
o Parathyroid: PTH (acts on bone to release Ca2+, works with Vitamin D in GIT to
increase Ca2+ absorption, kidneys respond by decreasing Ca2+ excretion)
o Increased Ca2+ and decreased PO4
o Thyroid: calcitonin (decrease Ca2+release from bones)
Albumin:
o Albumin 3.5 + Ca2+ level = Ca2+ corrected
Magnesium Imbalance
Hypomagnesemia [<1.3mEq/L]
Causes: Chronic malnutrition/ malabsorption, GI losses (diarrhea, NGT sxn, N/V), loop
diuretics, ARF, burns, antibiotics & chemotherapy
o Excessive calcium (hyperparathyroidism)
o Excessive sodium (Cushings, hyperaldosteronism)
Symptoms: Cardiac arrhythmias, digoxin toxicity, potassium, calcium
o Neuroexcitability (tetany, seizures, confusion, hyperactive DTRs, +Chvosteks &
Trousseaus signs, laryngeal stridor)
Treatment: Prevent cardiac symptoms
o 1-2g IV magnesium sulfate in 100ml of NS over 1hr
o PO magnesium oxide
Hypermagnesemia [>2.1mEq/L]
Causes: Dehydration, renal failure, hypothyroidism, Addisons disease
Symptoms: Similar to hyperkalemia mental acuity, BP, HR, RR, EKG changes, N/V,
thirst, hypoactive DTRs
Treatment: Normalize magnesium levels
o Diuretic therapy
o Calcium gluconate (decrease cardiac effects of Increased Mg)
Relationships: Ca2+ ,PO4, Mg, K+
Hypocalcemia may respond to Mg
Mg increases intestinal absorption of Ca
Mg , Ca, & K fluctuate together
Ca and PO4 fluctuate inversely
Insulin drives potassium, magnesium, & phosphate into cell
Chloride Imbalance
Hypochloremia [<95mEq/L]
If Cl drops, then bicarbonate increases proportionally metabolic alkalosis
Causes: Excessive vomiting, sweating, NGT to suction, diuretics, fluid overload
Symptoms: Metabolic alkalosis d/t bicarb retention (muscle hyperexcitability, resp.
depression, hypotension)
Treatment:
o Prevention
o IV fluids NS
Hyperchloremia [>110mEq/L]
Causes: Excessive diarrhea, dehydration, cortisone/ corticosteroids d/t Na+ retention
Symptoms: Metabolic acidosis d/t bicarb depletion (weakness, lethargy, tachypnea)
Treatment: Prevention
Bicarbonate
Ratio of HCO3 to H2CO3 (carbonic acid) is 20 to 1
Reabsorption: In proximal tubule; used in chemical buffering system

Formation: Produced by kidneys in response to hydrogen ion level
Hydrogen ion excretion: Maintains acid/ base balance
What is the difference between BICARBONATE & pCO2?
Blood Urea Nitrogen: 10 20mg/dL

Directly related to metabolic function of liver & excretory function of kidney
Protein amino acids catabolized ammonia urea formed by combined ammonia
molecules
Creatinine: 0.5-1.2mg/dL
Description: Product of skeletal muscle metabolism
Exclusively excreted by kidneys
Directly proportional to GFR
CrCl decreases 6.5ml/min with each decade of age
BUN/ Cr ratio: 10:1
Increased: Decreased renal blood flow, ATN, glomerulonephritis; rhabdomyolysis,
acromegaly (increased muscle mass)
Decreased: decreased muscle mass
Glucose Imbalance
Hypoglycemia
Causes: Starvation, Insulin overdose, Addisons disease, malignant disease
Symptoms: Headache, irritability, dizziness, weakness, lightheaded
Treatment: Carbohydrates, 5% Dextrose/ 50% Dextrose

Hyperglycemia
Causes:
o Endocrine= DM, Cushings disease, acute stress, pituitary dysfunction, pancreatitis,
o Organ= chronic liver or renal disease
Symptoms: Classic polys (thirst, hunger, diuresis)
Treatment: Oral hypoglycemics, insulin
High Risk for Fluid & Electrolyte Imbalances
Cardiac disease: CHF
Diabetes: Dehydration with increased glucose
Renal disease: Overhydration & electrolyte imbalance
GI dysfunction: Upper vs lower
Respiratory dysfunction: Insensible fluid loss with related sodium loss
Burns: General fluid & electrolyte loss
IV therapy: Fluid overload, altered electrolytes
Enteral feedings/ PPN/ TPN: Altered electrolytes
Endocrine
o Addisons Disease or abrupt discontinuing of systemic long-term glucocorticoids
Weakness, fatigue, nausea/ vomiting, lethargy,
Decreased concentration,
Hypotension, dehydration,
Hyperpigmentation,
Decreased urine output
Burns
23/02/2015 18:15:00
Burn units in AZ
St Marys Hospital Burn Unit closed 2008
UAMC beginning burn unit now
2 burn units in Phoenix Arizona Burn Center at Maricopa Hospital and Grossman Burn
Center at St Lukes Hospital
Burn Teams
Burns are complex systemic injuries. The interdisciplinary burn team consists of many
experts with specialized knowledge:
Social Workers
Surgeons
Anesthesiologists
Nurses
CNAs/PCTs
PT/OTs
Housekeepers
Psychologists
Dieticians (burn patients require high cal high protein diet)
Child Life Specialists
Rehabilitation specialists (Scar management)
Major vs. Minor Burns
Major burns may involve:
o > 20% TBSA
Inhalation injury
o Chemical injury
Electrical injury
o Lg Full Thickness
Large fluid loss
Minor burns may involve:
o 1-10% TBSA
Minimal fluid loss
o Superficial burns
NO inhalation
o Some small chemical injury
Skin Anatomy
Zone of coagulation is the area of necrosis; the deepest part of the burn; it will not heal. The
zone of stasis is characterized by decreased tissue perfusion; it has the potential to recover
with adequate fluid resuscitation and oxygenation. The zone of stasis may convert to
necrosis 24-48 hours after the initial burn. The zone of hyperemia (erythema-sunburn like) is
the outermost zone that is noted by hyper-perfusion; this area is not lost and will return to
normal
Faschia: does not stretch
o Can create compartment syndrome
Burn Depth
1st Degree = Superficial
2nd Degree = Superficial Partial Thickness

and Deep Partial Thickness
3rd Degree = Full Thickness
4th Degree = Subdermal
Superficial=1st degree (involves epidermis only)
Pink or Red
Painful
No blisters
Sensitive to air
Immediate capillary refill
Usually not admitted: mainly only if dehydrated & need hydration
Superficial {atrial Thickness=2nd degree (damage extends into dermis)
Very Painful
o Epidermis opened up & nerve endings in dermis are opened up
Edema
Blisters
Sensitive to air
Rapid capillary refill
o Nerves, sweat glands, hair follicles intact
Deep Partial Thickness = 2nd Degree (damage deep into dermis)
Painful
Pale or mottled
Edema
Delayed capillary refill
Nerves, sweat glands, hair follicles damaged
May convert to a 3rd degree burn over next 24 hours
Full Thickness = 3rd Degree (All of dermal layer destroyed)

Painless to pinprick or light touch
o Cause pain is deeper inside of tissues
o Consistency of tennis show leather
Edema
White, gray, charred
o Cells need absolute excision
o Does not stretch
Leathery
No capillary refill
Subdermal = 4th degree

Damage extends through subcutaneous layer to deep tissues - fascia, muscle or bone
Measuring Total Body Surface Area (TBSA)
The Rule of Nines

o Adult:
o Head 9%
o Each arm 9%
o Ant. Trunk 18%
o Post. Trunk 18%
o Each leg 18%
o Perineum 1%
Child 2 years and under:

o Head 18%
o Each Arm 9%
o Ant. Trunk 18%
o Post. Trunk 18%
o Each leg 14%
Measuring TBSA
Lund and Browder
Palm Rule
Pts. Palm and fingers = 1% of THEIR total body surface area
o Does not work in very obese patient
Palm = 0.5%
Calculate TBSA Burned and Determine Depth
1st pic: 28-29%; 2nd degree burn that will probably turn to 3rd degree in 24 hours
2nd pic: ~1%; 2nd (red) & 3rd (where it is white)
gasoline burn
3rd pic: ~9%; 3rd degree burn
palm rule to count cause you cant see chest
4th pic: ~5%; 3rd degree with little 2nd degree

**ONLY count what you can see
Physiologic Response
Coagulation of cellular proteins causing cell death
Release of complement, cytokines, histamine, and oxygen free radicals Increased capillary
permeability Fluid shift from intravascular to interstitial space Edema
o ed cap permeability causes more fluid to shift
Hemoconcentration Increased hematocrit (simply d/t leaking of fluid) Increased blood
viscosity Increased risk of emboli formation
Decreased intravascular volume Decreased cardiac output Vasoconstriction
Increased systemic vascular resistance Decreased blood flow to the skin, kidneys, and GI
tract in order to spare the vital organs (brain and heart)
Inflammatory mediators lead to bronchoconstriction which may lead to acute respiratory
distress syndrome (ARDS)
Hypermetabolism: increased oxygen consumption, negative nitrogen and potassium balance
lead to muscle wasting and catabolism
Immunological down regulation of cell mediated and humoral immune pathways creates
vulnerability to infection
If the responses go uncorrected, the results will be:
o Hypovolemic shock (burn shock)
o Metabolic Acidosis
o Hyperkalemia/Hypokalemia
Hyper when burn 1st happens
Hypokalemic after getting hydrated (D/t dilution)
o Pulmonary Hypertension
o Compartment Syndrome
o Multiple organ failure and death
o Renal failure
Primary Survey
Airway
o S/S of Inhalation Injury:
Facial burns
Singed facial hair
Absence of nasal hair
Carbon deposits
Edema/erythema of oro/nasopharynx
Hoarse voice/Brassy cough
Anxiety/Agitation
SOB/Tachypnia
Stridor (late sign of airway closure)
Hypoxia
Breathing
o Assess Breathing
o Carbon deposits in mouth or on face?
o Hoarse voice or Brassy Cough?
o Auscultate each lung field
POSTERIORLY: base then go up
Listen for crackles (Sounds indicating overhydration)
o Look for circumferential chest/neck burns
o Assess rate and depth of respiration
o Obtain oxygen saturation (not reliable in carbon monoxide poisoning)
Airway & Breathing
o Deliver 100% Oxygen to ALL pts with 20% TBSA or more
o Maintain patent airway
o Be prepared to intubate
o Avoid succinylcholine it exaggerates hyperkalemia poss. Cardiac arrest
o (Usually a problem in thermal burns 6-8hrs old. Immediate danger in electrical
injuries)
o Intense edema to soft tissues of lower face 24 hrs after a 21% TBSA flame burn
o Same pt. 72hrs post burn. Elevation of all affected areas is essential to prevent
complications of edema
o **intubate early & with largest tube you can find (7 preferably; 8)
need to bronchoscope pt (can only be done with #7)
Breathing
o Circumferential trunk/neck burns:
o Loss of chest wall compliance
Difficult to oxygenate
o Difficult oxygenation
o Escharotomy
Cut from healthy to healthy tissue if possible to release rib cage for expansion
Other considerations
o Carbon Monoxide poisoning:
CO has affinity to hemoglobin that is 200-500 times that of oxygen
Give 100% oxygen until carboxyhemoglobin levels are less than 15%
Pulse oximetery is of no value in CO poisoning since it is not specific to
oxygen
Hyperbaric oxygen is of unproven value in burn patients
Circulation
o Assess Circulation hourly:
Skin Color
Sensation
Peripheral pulses
Call doctor/burn squad EARLY when you feel the pulse weakening
Capillary refill
Circumferential burns
Disability, Neurologic Deficits
o Burn patients are typically alert and oriented
o Consider hypoxia, assoc. injury, substance abuse, pre-existing medical conditions
o Assess level of consciousness: AVPU
o
A = Alert
If not why? -> head injury? Drugs? Diabetic coma? Etc.
o V = Verbal Stimuli
o P = Painful stimuli
o U = Unresponsive
Expose and Examine
o Remove all clothing adherent clothing may be left undisturbed

Clothes act as tourniquet
o Remove all jewelry including piercings
o Examine for deformities, foreign or protruding objects, or other injuries
o Log roll to examine posterior surfaces
Fluid Resuscitation
o IV access 2 Large bore IVs
o May place IV in burned areas if necessary
o Begin fluid resuscitation for 20% or greater TBSA burns
o Lactated Ringers
o Weigh patient as soon a possible (estimate if necessary)
Fluid resuscitation is based on weight
o Why Lactated Ringers for resuscitation?
Large amounts of NS can lead to hyperchloremic metabolic acidosis
As chloride levels rise, bicarbonate levels decline in a 1:1 ratio to maintain
electroneutrality
As bicarbonate drops, metabolic acidosis results
Lactate in LR is converted by the liver to bicarbonate, so it makes up for the
bicarbonate that is lost with the addition of chloride that is in the LR
o Consensus Formula:
Lactated Ringers 2-4ml x pt wt. in kg x TBSA Burn = Amount to be
infused in 1st 24 hours post burn.
Start @ 4ml
Dont convert TBA to decimal
Give of total amount in 1st 8 hours from the time the injury occurred
Give the remaining over the next 16 hours
*Note: Children need 3-4ml/kg/TBSA LR burn replacement plus maintenance
fluids of 100ml/kg for up to 10kg in wt., 50ml/kg for additional 11-20kg,
20ml/kg for additional 21-30kg.
o Fluid Resuscitation ex: Adult
A 68 y/o woman sustained 2nd and 3rd degree burns to her anterior chest,
abdomen and the front of both legs in a fire in her office building
TBSA = 36%
1kg = 2.2lbs
154lbs 2.2 = 70kg
4ml x 36 x 70 = 10,080 over 24 hours
Give 5040ml in first 8 hours at 630ml/hr (5040ml 8hrs = 630ml/hr)
Give 5040ml over next 16 hours at 315ml/hr (5040 16hrs = 315ml/hr)
Fluid Resuscitation
o Place Foley catheter with urimeter (temp probe)

o Monitor urine output hourly
amount of fluids given if even a drop <30cc/hr
o Titrate fluids to keep urine output at a minimum of 30-50cc/hr
o (75-100cc/hr for electrical burns)
o Monitor vital signs hourly
o Assess for signs of pulmonary edema
o Unreliable indicators:
Blood pressures taken in the burned limb can be misleading due to edema
Heart rates of 100-120 bpm are common in adequately resuscitated patients
Hemoglobin/Hematocrit is an unreliable guide for fluid resuscitation in the
first 24 hours
Hct will be ed @ first cause fluid escaped from intravascular space
Hct will then be ed once fluid resuscitation has began d/t
hemodilution
o Patients requiring more fluid than formula predicts:
Electrical injury
Inhalation injury
Delayed fluid resuscitation
Prior dehydration
Pediatrics
o Volume Sensitive Patients:
o Pre-existing cardiopulmonary disease
o Extreme age (young or old)
Second Survey
o History
Circumstances of injury
Cause
Open or closed space
A lot more chance of inhalation injury in closed space
Possibility of smoke inhalation?
Chemicals involved?
Related trauma?
o Medical History
Pre-existing medical conditions
Medications/alcohol/drugs
Allergies
Last tetanus immunization within last 5 years for burns
If unknown, shot will be given

More important to know in dirty burn (stop drop roll)
AMPLE
A = Allergies
M = Medications
P = Previous illness, past medical Hx
L = Last meal or drink
E = Events preceding injury
Relieve Pain
Morphine is drug of choice
IV only IM and SQ routes are unpredictable due to changes is tissue blood
flow to skin & extremities
Consider Anxiolysis
Warm Patient (cannot control body temp w/out skin)
Avoid shivering
Close door
Pre-warm room
Warm blankets
Portable warmer
Warm fluids
Burn pts prefer ambient temperature of 90F
NG/Orogastric Tube
Place NG/OG tube in burns of 20% or greater
Prone to gastric dilatation (bloat or twisted stomach) and ileus (blockage of
intestine)
Begin tube feeding early (usually w/in 24 hours, prefer 1st few hours)
Stimulates gut to stay more alive
Other Considerations:
Lab tests:
ABGs
CBC
Electrolytes
BUN, Creatinine
Glucose
Urinalysis
Toxicology screen
Urine myoglobin (muscle damage 2nd to electrical injuries)
Carboxyhemoglobin
Chest X-ray
Bronchoscopy
Injury below glottis needs for more fluids, to be on vent longer,
pulmonary toileting
o Wound Management
Always treat life threatening injuries first (ABC)
Stop the burning process Usually done in field
Never use ice cool water acceptable on small TBSA burns
Ice causes vasoconstriction
Ice may feel good at first, but when taken away it will feel bad again
Protect from hypothermia
Assess for circumferential burns and need for escharotomy
Elevate burned extremities above the heart
Cover with clean dry blanket, sheet or towel
Contact burn M.D. for specific dressings
Tar Burns
Heated to 450-500F
Thick and slow to cool
Cool immediately in cold water
Results in deep burn, often full thickness/3rd degree
Remove with mineral oil or adhesive remover (Medi-Sol)
Tar Burn 2-4days post STSG (slit thickness skin grafting) follow same as above
o STSG: Shave healthy skin off (typically thigh; take part of dermis), put through
mesher (take make a big a piece as possible)
Electric Injury
AC = Alternating Current, households
DC = Direct Current, industrial, car battery, electrosurgical devices
Tissue injury results as electric energy is converted into heat.
The greatest heat is at contact points
Common contact sites are hands, wrists, and head
An arc may form with flash of flames causing flame burn

The heated tissue acts as a volume radiator with the superficial tissues cooling more rapidly
than deep tissue bone does not conduct electricity, it acts as an insulator and holds heat
Tissue destruction may extend to bone
Exit wound may be larger than entrance = Blow out
Difficult to assess extent of damage
Tip of the Iceberg effect
o May appear minor/tiny on outside but severe/deeper
Assess for Fractures and dislocations
Vfib, Vtach, cardiac arrest possible
Monitor continuously for at least 24 hrs
o Foley used for this
o Goal: 75-100cc/hr
Myoglobin and Hemoglobin are released when muscles are damaged
Myoglobin/Hemoglobin are proteins that obstruct renal tubules causing Acute Renal Failure
Alkalinize the urine with 1 amp Sodium Bicarbonate per liter of LR
Use Mannitol 12.5gm/liter if myoglobin and UO do not respond to adequate fluid volume
and sodium bicarbonate
Large fluid volumes needed for resuscitation
Titrate fluid volume to keep urine output between 75-100 cc/hr
Chemical Injury
Severity of injury is related to:
o Chemical agent
o Concentration
o Volume
o Duration of contact
A delay in treatment = continued tissue damage
IRRIGATE, IRRIGATE, IRRIGATE!
o For 30 min minimum
Alkalis commonly found in oven cleaners, drain cleaners, fertilizers, and heavy industrial
cleaners. Form the structural bond in concrete
Bond to proteins and require prolonged irrigation
Acids commonly found in many bathroom cleaners, rust removers, pool products
Organic phenol, creosote, disinfectants, gasoline, and petroleum
Protect yourself
Remove contaminated clothing
Brush off powders before irrigating
o DONT add water; it will activate powder
Irrigate with water x 30 minutes
Do not neutralize
Hydroflouric Acid: MUST be neutralized
o Used in refrigerants and metal industry to clean chrome
o Flouride ion penetrates and binds to tissues
o The activity ceases when it combines with calcium or magnesium to produce an
insoluble salt
o Activity is ceased when pain is stopped
Irrigate with copious water or benzalkonium chloride (Zephiran) solution
Topical calcium gluconate should be applied to neutralize
If pain persists, a solution of 10% calcium gluconate should be injected subcutaneously
directly to the burn site
***Severe injury to neurovascular bundles and tissues and ischemia may result from
inappropriate injection of calcium gluconate, especially fingers and toes. This should be
done only after consultation with the burn surgeon***
Gasoline and diesel fuel
may cause tissue injury
Prolonged contact and absorption of hydrocarbons can cause liver and renal failure and
death
Assess and Treat
*Look at week 8 Burn lecture for specific examples
Endocrine
23/02/2015 18:15:00
The endocrine system includes the organs of the body that secrete hormones directly into body
fluids such as blood

Regulates chemical reaction in cells and therefore control functions of the organs, tissues,
and other cells
Hormones
Endocrine glands
o Ductless
o Release hormones
Directly into target tissues
Into bloodstream to be carried to target tissues
Hormones chemicals secreted by a cell that affect the functions of other cells
Many are derived from steroids that easily cross the cell membrane
Steroids also cause rapid weight gain and edema
o Steroids affect metabolism & production of glucose
Examples of steroid hormones
o Estrogen
o Progesterone
o Testosterone
o Cortisol
Nonsteroidal hormones
o Made of amino acids or proteins and cannot cross the cell membrane easily
o Bind to receptors on the surface of the cells (do not travel through cell membrane)
o G-protein activated by the hormone-receptor complex (2-step process)
Activates enzymes inside cell
Prostaglandins (crosses tissue)
o Local, or tissue, hormones
o Derived from lipid molecules
o Do not travel in the bloodstream (travel directly though tissues)
o Target tissues are located close by
o Produced by organs such as

Kidneys
Heart
Stomach
Uterus
Brain
Negative & Positive Feedback Loops
Control hormone levels
Negative feedback loop
o Hormone release stops in response to decrease in stimulus
Stimulus (eating) raises blood glucose levels
Pancreas releases insulin in response to elevated blood glucose
Blood glucose decreases as it is used by the body or stored in the liver
Insulin release stops as blood glucose levels normalize
Positive feedback loop

o As long as stimulus is present, action of hormone continues
Infant nursing at mothers breast stimulates hypothalamus stimulates
posterior pituitary
Oxytocin released stimulates milk production and ejection from mammary
glands
Milk release continues as long as infant continues to nurse
Hypothalamus (controls pituitary)

o Hormones
Oxytocin
Antidiuretic hormone (ADH)
o Hormones transported to the posterior pituitary for storage
o Directs posterior pituitary to release hormones
Pituitary gland
o Controlled by the hypothalamus
o Located at the base of the brain
Protected by a bony structure called the sella turcica
The optic chiasm is located just above the pituitary gland
Carries visual information to the brain for interpretation
o Two lobes
Anterior lobe
Posterior lobe
**Know the function of glands & secreting hormones function

Adrenal glands
o Located on top of each kidney
o Divided into the adrenal medulla and adrenal cortex
o Adrenal medulla
Central portion
Hormones
Epinephrine
Norepinephrine
Same effects as sympathetic nervous system
o Adrenal cortex
Outermost portion
Secretes many hormones, but main ones are
Aldosterone
Stimulates body to retain sodium and water
Important in maintaining BP
Cortisol
Released when stressed
Decreases protein synthesis, resulting in slowed tissue repair
Decreases inflammation
Pancreas
o Located behind the stomach
o Both exocrine gland and endocrine gland
Exocrine secretes digestive enzymes into a duct leading to the small
intestine
Endocrine secretes hormones into bloodstream
o Islets of Langerhans secrete hormones into bloodstream
Alpha cells secrete glucagon
Beta cells secrete insulin
Other Hormone Producing organs

o Pineal body
Small gland
Located between cerebral hemispheres
Melatonin
Regulates circadian rhythms
May play a role in onset of puberty
o Thymus gland
Located between lungs
Thymosin
Promotes production of
T lymphocytes
o The gonads
Ovaries
Estrogen
Progesterone
Testes
Testosterone
o Stomach
Gastrin
o Small intestine
Secretin
Cholecystokinin
o Heart
Atrial natriuretic peptide regulates BP
o Kidneys
Erythropoietin stimulates blood cell production
Thyroid disorders: Goiter

There are a number of causes. For example:
o Inadequate dietary iodine intake leads to an inability to synthesize TH
TSH stimulation continues, resulting in an enlarged thyroid gland
o Hereditary factors - some people inherit a tendency for a thyroid to swell
o Thyroiditis (inflammation of the thyroid)

Assessment
o TSH and T4 levels are measured to determine if goiter is associated with
hyperthyroidism
hypothyroidism
normal thyroid function
o Normal levels
TSH .5 to 5.0 mIU/L
T4
4.5 to 11.2 mcg/dL
o Ultrasound scan of thyroid
o Biopsy (d/t cancerous tumor possibility)
o Radioactive iodine scan
Management
o Iodine deficiency/suppression of T4
Diet higher in iodine (at least 50 mg/day). Use iodized salt.
Preparations of iodine
Reduces size and vascularity
Thyroid hormones
Levothyroxine (Levothroid, Levoxyl, Synthroid)
Typical dose 100 mcg to 125 mcg/day
Surgical management discussed with hyperthyroidism
Breathing problems
Hypothyroidism
o Under activity of thyroid gland resulting from:
o Primary thyroid dysfunction
TSH levels are elevated (thyroid is not responding)
Most common form of primary
Hashimotos Disease
Autoimmune
o Secondary to anterior pituitary dysfunction
Insufficient stimulation of a normal thyroid gland
Malfunction of pituitary gland or hypothalamus
o Decreased level of TH leads to
overall slowing of metabolic rate
decreased secretion of hydrochloric acid in stomach (achlorhydria)
decreased GI tract motility
bradycardia
slowed neurologic functioning
decrease heat production resulting in decrease body temperature

inadequate stimulation of RBC development in the bone marrow
anemia with possible vitamin B12 and folate deficiency
reduction in lipid metabolism, results in
increased serum cholesterol and triglycerides
increased arteriosclerosis and CAD
Clinical manifestations:
Mild (most common)
May be asymptomatic or vague manifestations
Cold
Lethargy
Dry skin
Forgetfulness
Depression
Weight gain
Constipation
Development of small goiter
Diagnostics
Labs
TSH
T4
Radioactive iodine uptake
History
Physical Exam
Severe (myxedema)
Develops in undiagnosed or undertreated clients that experience stress
Exposure to cold
Infection
Respiratory failure
Heart failure
Trauma
Drug use
an accumulation of hydrophilic mucopolysaccharides in dermis and other
tissues
Puffiness
Periorbital edema
Masklike affect : classic sign
Complicated (myxedema coma): MEDICAL EMERGENCY
Triggered by stress or noncompliance with thyroid treatment

Drastic decrease in metabolic rate
Hypoventilation lead to respiratory acidosis
Hypothermia
Hypotension
Hyponatremia
Hypercalcemia
Hypoglycemia
Water intoxication
o Management
Vital functions are supported
Airway
IV fluids
Warmth
Vasopressors (to keep BP stable)
IV Levothyroxine
IV Glucose
IV corticosteroids
Correct TH deficiency
Reverse manifestations
Most improve in 2-3 weeks with TH therapy
o Patient/Family Education
Imperative!
Diet
Iodized Salt
High fiber
Recognizing signs and symptoms of medical emergency
Monitor weight
Lifelong drug therapy is stressed
Levothyroxine Sodium (Synthroid) is the drug of choice
MONITOR DRUG LEVELS TO ENSURE ADEQUATE
DOSAGE!
o Its not the dose youre receiving, its the level you are
maintaining
Hyperthyroidism
o Excessive secretion of TH due to
over functioning of entire gland
tumors (thyroid cancer)
o Most common form is Graves Disease

Autoimmune
Three principal hallmarks
Hyperthyroidism
Goiter
Bulging eyes
Autoimmunity against orbital tissues-> causing eyes to

protrude out (eyes never go back to normal completely)
Does not regress with therapy
o Decrease edema with diuretics and glucocorticoids
(prednisone)
o Clinical Manifestations
Extreme agitation/irritability
Hand tremors at rest
Thin
Loose BM
Heat intolerance
Profuse diaphoresis
Skin is warm
Hair is thin
Mood swings
Extreme fatigue
Depression
o Diagnostics
Confirmed on physical exam/clinical manifestations
Labs
Serum TH levels elevated
Serum cholesterol levels are depressed
o Management
Reduce excessive secretion of TH
Prevent and treat complications
Removal of thyroid tumors (surgery)
Administration of adrenergic blocking agents (control SNS activity)
Propranolol
Administration of antithyroid medications
Propylthiouracil (PTU)
Tapazole
Radio iodine therapy (potassium iodide)
To treat thyroid storm
Because radioiodine destroys thyroid cells, hypothyroidism is a
complication.
Exophthalmos (Bulging eyes)
Wear dark eyeglasses to reduce discomfort and reduce risk of getting
dirt/dust in eyes
Use sleeping mask or lightly tape eyes shut with paper/non-allergic
tape
Elevate HOB at night
o Diet
Restrict salt intake
High calorie/high protein
Supplemental vitamins
Weigh daily
Thyroidectomy
o Total
Secondary to cancer
Clients must take thyroid hormones permanently
o Partial
To correct hyperthyroidism and extreme cases of goiter
5/6th the gland is removed. Since 1/6th of the functioning gland is left, hormone
replacement therapy may not be necessary
many times med control still needed
o Preoperative
TH suppression a must! May take 2-3 months.
Antithyroid meds/iodine preparations
Diminishing chance of hemorrhage
o Postoperative, at risk for

Infection/hemorrhage
Thyroid storm
Secondary to infection, thyroid surgery, stopping antithyroid meds
o Hypoparathyroidism
Inadvertent removal of parathyroid glands
o Respiratory obstruction
Secondary to swelling
Observe for hypoxia
o Laryngeal edema
o Vocal cord injury
Secondary to nerve damage
Thyroid storm (thyrotoxicosis)
o All hyperthyroid manifestations
are heightened
High fever
Severe tachycardia
Increased B/P
Increased RR
Atrial fibrillation
Delirium
Dehydration
Extreme irritability
o Potentially fatal acute episode
o Clinical diagnosis
KNOW YOUR PATIENTS
No lab tests differentiate hyperthyroidism from thyroid storm
o Management
Hypothermia blankets
IV fluids
Suppressing hormone release
Inhibiting hormone synthesis
Blocking conversion of T4 to T3
Amiodarone (antiarrythmic drug)
K+ channel blocker
Inhibiting effects of TH on body tissues
Beta blockers
Treat cause (if known)
Thyroiditis
o Appears in three basic forms:
Acute/sub-acute (painful)
Uncommon
Bacterial/viral invasion
Following respiratory tract infection
Most have pre-existing thyroid disorder
o Lymphocytic (silent/painless)
Genetic predisposition
o Chronic (Hashimotos disease)
Most common form of thyroiditis
Long-term inflammatory disorder
Auto immune destruction of thyroid gland
Genetic predisposition
o Clinical Manifestations:
Abrupt unilateral anterior neck pain which radiates to ear (acute/sub-acute)
Fever
Diaphoresis
Sore throat
About 50% present with thyroid storm
Painless goiter in lymphocytic/chronic form
o Diagnostics
TH levels
Thyroid antibodies
o Management
Antibiotics
Pain management
Prednisone
Outpatient incision and drainage of thyroid glad (acute)
Fine needle biopsy to rule out malignancy (chronic)
Parathyroid & Parathyroid hormones
Embedded in the posterior surfaces of thyroid gland
Monitor calcium levels
When calcium concentration falls below normal, cells secrete parathyroid hormone (PTH)
o PTH stimulates osteoclasts (to break down bone)
o Inhibits bone-building
o Reduces urinary excretion of calcium
Hyperparathyroidism
o Over activity of parathyroid glands
Excessive PTH leads to bone damage, hypercalcemia, and kidney damage
o Classified as primary, secondary, & tertiary
Primary (hyperactivity of glands themselves)
Secondary
Secondary to another condition that lowers calcium levels
Therefore, your parathyroid glands overwork to compensate for

the loss of calcium
Tertiary
Persistent secondary hyperparathyroidism after successful renal
transplantation
Idiopathic hypersecretion of parathyroid hormone
Skeletal disease
joint pain, Fractures, Deformity
Renal involvement
Polyuria (excessive urine)
Calculi in urine
Hypertension
GI disorders (secondary to hypercalcemia)
Polydipsia (excessive thirst)
Psychiatric abnormalities
o Diagnostics
Lab
Serum calcium levels are elevated
Serum phosphate are depressed
X-ray findings
o Management
Short-term
Lowering severely elevated calcium levels
Hydration (Lasix to flush out kidneys)
o NOT thiazides (which promote calcium reabsorption
through kidneys)
Promote calciuria (urinating out excess calcium)
o Lasix - AFTER rehydration
NO Thiazides! They promote calcium retention
in kidneys
Diet - Low in calcium and Vitamin D

Long-term
Increase bone resorption (medications)
Phosphates
Calcitonin
Encourage fluids
Monitor urine for stones and blood
Hypoparathyroidism
o Hyposecretion of parathyroid glands
due to accidental removal of parathyroid glands or damage to these glands
thyroidectomy
genetics
o Low Serum calcium levels
o High Serum phosphate levels
o Tetany (painful muscular spasms/tremors) may develop
Painful muscle spasms
Numbness, tingling on fingers/toes
Dysrhythmias
Chvosteks Sign
Unilateral spasm of the oris muscle is initiated by a slight tap over the
facial nerve
Trousseaus Sign
Carpal spasm occurs when the upper arm is compressed, as by a
tourniquet
o Diagnostics
Physical Exam
Labs
Low calcium levels
Low PTH level

High phosphorus level
o Emergency Management
Restore serum calcium levels to normal quickly (ONLY time youd give
Calcium chloride is when coding cause very hard on body)
10% calcium gluconate IV (takes longer for body to convert to calcium
chloride but less harsh)
Prevent and treat seizures
Control laryngeal spasms and respiratory obstruction which may lead to
distress
o Long-term
Oral calcium salts
Vitamin D
PTH replacement
Diet high in calcium, but low in phosphorous
Life long medications
Visit health care provider regularly
Monitor serum calcium levels
Dietary modifications
Omit cheese and milk
The adrenal glands
Two parts:
o Outer cortex
Produces steroid hormones:
Corticosteroids/glucocorticoids
Cortisol
Mineralocorticoids Aldosterone
Androgens - Male sex hormones
o Inner medulla
Produce:
epinephrine
norepinephrine
Adrenal insufficiency
o Hypofunction of adrenal glands
Primary Type (cause probs within organ itself)
Addisons Disease (rare)
Idiopathic destruction of adrenal glands
(AIDS & metastasis from lung, breast, or GI)
All steroids hormones are reduced
Risk factors:
History of other endocrine disorders
Not tapering off glucocorticoids
Adrenalectomy
TB (infection can destroy glands)
Usually insidious
Anorexia
Mild fatigue
Irritability
Weight loss
Nausea and vomiting
Postural hypotension
o Diagnostics
Low cortisol production rate
High plasma ACTH concentration
Serum electrolyte levels
Blood glucose level

CT/MRI of adrenal glands and pituitary
Medication importance/tapering
Maintain a normal electrolyte balance
Follow-up visits with health care provider
Monitor steroid levels
Medic-Alert Band
IM self-injection
Dexamethasone
Addisonian Crisis
o Emergent condition
Acute adrenal insufficiency
o Causes
Stress
Pregnancy
Surgery
Infection
Dehydration
Anorexia
Fever
Emotional upheaval
Lack/insufficient hormone replacement
Penetrating pain in back
Depressed or changed mentation
Volume depletion
Hypotension
Loss of consciousness
Shock
Hyponatremia & hyperkalemia
o Management
Correct fluid and electrolyte imbalances
Rapid rehydration with .9% NS
Replace steroids
Hydrocortisone 100 mg IV, followed by 100mg q 8 hours x 24-hours,
then PO hydrocortisone
Correct hypoglycemia
5% Dextrose IV
Vasopressors
Kayexalate
Treatment of hyperkalemia
Adrenal Insufficiency
o Secondary type, causes
o Hypofunction of adrenal glands
o hypofunction of the pituitary-hypothalamic unit (lack of ACTH - Adrenocorticotropic
hormone )
o chronic treatment with glucocorticoids for non-endocrine uses
Circulating levels of corticosteroids remain high. Patients do not experience
manifestations of adrenocortical insufficiency unless therapy is stopped
o Pituitary tumor
o Radiation
Adrenocortical Hyperfunction
o Hyperfunction of adrenal cortex
o Result in excessive production of glucocorticoids, mineralocorticoids, and androgens
o Major conditions
Hypercortisolism (glucocorticoid excess)
Primary Aldosteronism (aldosterone excess)

Hypercortisolism
o Cushings Syndrome
o Over activity of adrenal gland, with consequent hypersecretion of glucocorticoids
o Causes
Medical interventions account for most cases
Adrenal tumor
Excessive ACTH secretion
Pituitary hypersecretion secondary to pituitary tumor
o Rare
Normal function of the glucocorticoids become exaggerated
Poor wound healing
Masculine characteristics in women
Memory loss, poor concentration
Persistent hyperglycemia (steroid diabetes)
Potassium depletion
Sodium and water retention
HTN
Abnormal fat distribution
Moon shaped face
Fat pad on back of neck (buffalo hump)
Obesity with slender limbs
Purple striae on breasts and abdomen
o Diagnostics
Physical exam
Clinical manifestations
ACTH levels
24 hour urine collection for free cortisol
High dose dexamethasone suppression test
checks to see how taking a corticosteroid medicine (dexamethasone)
changes the levels of cortisol in the blood
CT (pituitary and adrenal glands)
MRI
o Management
Reducing corticosteroid use over time while still managing condition
(example: asthma/arthritis)
Medications that interfere with ACTH production or adrenal hormone
synthesis
Mitotane (Lysodren)
Surgical (adrenalectomy)
Adrenal tumor
Lifelong glucocorticoid mineralocorticoid replacement
Surgical (resection of pituitary tumors)
Transsphenoidal adenomectomy (through nose)
Surgical removal of a small, well-defined pituitary adenoma
Patients on glucocorticoids are at risk for Cushings
Recognizing manifestations
Don't reduce dose of corticosteroid drugs or stop taking them on your own.
Hyperalosteronism
o Aldosterone conserves sodium and promotes potassium excretion
o Primary
Hypersecretion of aldosterone secondary to adrenal lesion (usually benign)
Produces secondary HTN, hypernatremia, & hypokalemia
o Secondary, results from
Renal disease
Laxative or diuretic abuse

Dehydration
Cirrhosis with ascites
Heart failure
Primary
May be asymptomatic
HTN
Hypernatremia
Hypokalemia
Excessive urinary excretion
o Muscle weakness
o Cardiac dysrhythmias
o Diagnosis
Serum potassium levels
Alkalosis
Elevated urine or plasma aldosterone levels
o Management
Primary
Spironolactone (Aldactone) drug of choice
To increase sodium excretion
Treat HTN
Improves hypokalemia
Surgery
Unilateral or bilateral adrenalectomy
Temporary/permanent replacement therapy
Secondary
Manage causative disease

Comply with treatment of disease
Comply with treatment and maintain control of the causative disease process
(secondary)
Pheochromocytoma
o A rare condition characterized by an adrenal medulla tumor that produces excessive
catecholamines
o The tumor is benign in most cases.
o The secretion of excessive catecholamines results in severe hypertension.
o If undiagnosed and untreated may lead to
diabetes mellitus
cardiomyopathy
death
o Manifestations
Severe, episodic hypertension accompanied by classic triad of
severe, pounding headache
tachycardia with palpitations and profuse sweating, and
unexplained abdominal or chest pain.
Attacks may be provoked by many medications, including
Antihypertensives
Opioids
Radiologic contrast media
Tricyclic antidepressants.
The treatment consists of surgical removal of tumor (tumors can be very hard
to find & small)
Acromegaly
o Results from excess secretion of growth hormone (GH)
o It is a rare condition of bone and soft tissue overgrowth
o Bones increase in thickness and width but not length
o Clinical manifestations
enlargement of hands and feet
thickening and enlargement of face and head bony and soft tissue
sleep apnea (d/t excessive soft tissue)
signs of diabetes mellitus
cardiomegaly
hypertension (extreme)
o Diagnostic Studies
History
Physical Assessment
CT
MRI
Oral glucose challenge
Definitive test
GH concentration falls during oral glucose tolerance test.
In acromegaly, GH levels do not fall below 1ng/ml3
o Treatment
Focuses on returning GH levels to normal through surgery, radiation, and drug
therapy
Octreotide Acetate (Sandostatin)
Transsphenoidal Hypophysectomy (surgical removal of pituitary
gland)
Treatment of choice
o Nursing Care
Postoperatively includes
Avoidance of vigorous coughing, sneezing & straining at stool (could
cause CSF leaks)
to prevent cerebrospinal fluid leakage from where the sella
turcica (sphenoid bone) was entered
Hypopituitarism
o Rare and involves a decrease in one or more of the pituitary hormones
o The anterior pituitary gland secretes

adrenocorticotrophic hormone (ACTH)
thyroid-stimulating hormone (TSH)
follicle-stimulating hormone (FSH)
luteinizing hormone (LH)
growth hormone (GH)
prolactin (PRL)
Melanocyte-stimulating hormone (MSL)
o Posterior pituitary gland secretes
ADH
Oxytocin
Normal changes in endocrine function d/t aging
Endocrine system functions well in most older people
Some changes do occur because of normal damage to cells during the aging process
o hormone production and secretion
o hormone metabolism (how quickly excess hormones are broken down and leave the
body, for example, through urination)
o hormone levels circulating in blood
o target cell or target tissue response to hormones
o rhythms in the body, such as the menstrual cycle
Alterations in Immune Heme systems

18:15:00
23/02/2015
Hematopoiesis: Bone marrow manufactures all blood cells

Blast cells are immature blood cells
Bone marrow produced in long bones of the body & the sternum
o Iliac crest produces the most followed by the femur
Epo stimulates bone marrow to produce RBCs
Marrow starts to decline at age 7
Stem cells: basic cell that everythings made from
o Plant in body -> migrates to bone marrow -> generates to platelets & RBCs
Aging Hematologic System
At ~ age 70yo, amount of bone marrow in long bones begins to decline
Decreased # stem cells in marrow
Decreased effectiveness of EPO
Decreased platelet adhesiveness
o & therefore they bruise easily
Average H & H decreases slightly to low normal
No changes: RBC life span, Blood volume, total WBC count, platelet structure & function
CBC w/ differential & platelets
WBCs (5,000-10,000/cu mm)
o Differential: segs + bands (50 70%)
Determines individuals ability to fight off infection
o lymphs (20 40%)
rise in lymphs with in neuts
o monos (2 8%)
o eos (1 4%)
w/ allergic reaction
o basos
o blasts
RBCs
o Hct (men: 42-52%; women: 37-47%)
o Hgb (men: 14-18g/dl;women: 12-16g/dl)
* Hgb x3 ~ Hct
Plts (150,000-400,000/ cu mm)
o Spontaneous bleeding @ <20,000
o 200: when pt can go home
Anemia: decreased RBCs, Hgb, Hct
Neutropenia: decreased neutrophils
Thrombocytopenia: decreased plts
Pancytopenia: decrease in all cellular components of the bone marrow; caused by bone marrow
supression
Immune response
Neutrophils -> Colony Stimulating Factors (CSF): GM-CSF, G-CSF, IL-3 act on bone
marrow
Immune response
o 24-48H when 1st exposed & for antigen to start the reaction
o 2nd time: could start in just minutes
o antigen will get picked up by neutrophils (1st line of defense)
o macrophages are next
o B-lymph is 3rd line of defense
These specialized cells manufacture antibodies against antigen
B-cell can hold memory to start response faster
o T-cells:
Cytotoxic: directly kill
Have memory
Helper T-cells: help B cells develop into plasma cells that secrete antibody
Suppressor T cells: Turn off the whole immune system

o IL/IFN: chemotactic (call next cells in & also fever causing antigen)
Immunoglobulins
IgG: what we give to patients

Case study:
o Mrs. Brown is a 78yo with a history of hypertension, Type II diabetes, and chronic
reactive airway disease. She is POD #2 for a hip replacement.
o Patient-related data
o VS: 100.8F, 100/65, HR=110, RR=20 with pOx = 90% on 2L O2 nasal canula
pOx @ 90%: sit pt up a little more; have her take DEEP breaths
o Heart: S1, S2 normal; stable Afib
o Lungs: Course crackles in mid lobes & bases
o GI: hypoactive BS; minimal appetite
o Lab Values: WBC = 15,000 (15% segs, 10% bands, 50% lymphs); Hct = 32% ; Plts =
450,000
WBC: normal inflammatory response for post op patient
Expected to rise a little bit
Lungs are #1 place for infection; if WBC ed greatly, this would be the 1st
place to look besides surgical site
Monitor lung sounds, TCDB, ISqh
o Questions? Concerns?
o What is the patient experiencing? Priorities?
Risk for infection
Checking skin & mouth
Dry mucous membrane es ability to fight off bacteria
Skin: opportunity for infection
o Discussion Question: What would you expect to see as a normal immune response in
this patient?
Factors affecting immune system
o Aging
o Stress
o Nutrition
o Trauma
es overall immune response cause body is in crisis and cannot attend to
everything at once
Aging Immune system
Decreased cellular immunity (helper & cytotoxic T cells)

Decrease humoral immunity: decreased response to antigen stimulation
Decreased speed, strength & duration of immune response & Immune regulation
*Results: atypical presentation of infections ie UTI, pneumonia (low grade fever & MS
changes)
Mrs. Brown is a 78yo with a history of hypertension, Type II diabetes, and chronic reactive
airway disease. She is POD #3 for a hip replacement.

*Pt. was diagnosed with pneumonia confirmed by CXR and started on azithromycin IV. Pt.
received the 2nd dose about 2hrs ago.

Patient-related data
VS: 101.8F, 90/58, HR=112, RR=24 with pOx = 88% on 2L O2 nasal canula
Heart: S1, S2 normal; stable Afib; c/o lightheadedness
Lungs: Wheezes in all lung fields; c/o chest tightness
GI: hypoactive BS; nausea, cramping
Patient was observed as being anxious and restless with facial flushing , hives on her neck &
itching.
What is the patient experiencing?
Allergic reaction to antibiotic; Watch for anaphylaxis

o Allergic reaction: wheezing
o Progression to get worse -> stridor
Give Benadryl: 25 mg (d/t elderly) IV STAT
Priorities of care? Priority interventions?
Hypersensitivity response
Type I : allergic response

Requires repeated exposures
o Priming (IgE attaches to mast cells)
Secondary or triggered response (rapid degradation of mast cells & release of

mediators
Patho:
o Primed mast cells release: histamine, leukotrienes, platelet activating factors,
prostaglandins, chemotactic factors
o Local: common allergies
o Systemic: severe allergic reaction = anaphylaxis
Anaphylaxis
o Causes: drugs, insect venom, food proteins
o System response
Skin: hives, urticaria (histamine)
Cardiovascular: capillary dilation, increased vascular permeability ->redness,
swelling & hypotension, (histamine, leukotrienes, prostaglandins)
Pulmonary: bronchoconstriction (histamine, leukotrienes)
When you hear stridor
GI: smooth muscle contraction & edema of mucosa ->cramps, nausea,
diarrhea
o Treatment of Anaphylaxis
Epinephrine: stimulates and receptors in SNS (increases HR, BP, CO;
bronchodilation, decreases release of histamine)
Tell pt they will feel like their heart is beating out of chest
Causes smooth muscle relaxation -> bronchodilation
Antihistamines: blocks histamine release
Glucocorticoids: anti-inflammatory & immunosuppressive actions
Push inflammation away to open tube
Beta2-agonists: act on beta2-receptors of smooth muscles ->bronchdilation;

inhibit histamine release from mast cells
Albuterol
Goal: inflammation & open breathing tube
Monitor BP to ensure adequate perfusion
Type II (cytotoxic): transfusion incompatibility; drug-induced hemolytic anemia (PCN,
quinine, sulfonamides)
Type III (Immune Complex-mediated): Involve IgG & Ig M antibody and antigen complexes
commonly seen in transplant rejection, SLE, glomerulonephritis
Type IV (delayed): primarily involves T lymphocytes & involves tissue destruction (GVHD,
HVGD, rheumatoid arthritis, Type 1 diabetes mellitus)
Priorities of care: Hypersensitive reactions
Fluid Volume Deficit
Decreased Cardiac Output
o r/t fluid volume deficit
Impaired Gas Exchange: #1
Risk for Infection
Imbalanced Nutrition: < Body Requirements
Hemostasis
Thrombocytopenia (<150,000 cells/dL)

o Causes
1. Decreased production
Medications (ASA, NSAIDS, chemotherapy)
Bone marrow injury
Megaloblastic anemia
2. Increased destruction
Immune-related: drugs, toxins, bacterial sepsis

3. Increased utilization
Idiopathic thrombocytopenia purpura (autoimmune process- platelet
autoantibodies)
4. Distribution problems
Splenomegaly associated with cirrhosis, leukemia, lymphoma, etc.
Immune-mediated Heparin-Induced Thrombocytopenia (HIT type II)
o ~.5 5% pts treated with heparin
o Risk factors: use of unfractionated heparin, cardiac transplant patient, hemodialysis
patient and patients s/p orthopedic, cardiac, neuro related surgeries
o Type I: transient decrease in platelets in patients on heparin therapy
o Type II: immune-mediated complication of heparin therapy which involves
decreased platelets and thrombi formation
o Onset of HIT: 5 14 days after initiation of heparin therapy; plt count ~50 80,000
o Patho of type II HIT:
Heparin binds with platelet factor 4 forming a foreign complex (antigen)
IgG production response is triggered
IgG binds to heparin-PF4 complex then activates platelets to initiate cellular
activities leading to thrombi formation
o Health complications resulting from HIT: CVA, MI, PE, arterial occlusion, DIC
o Treatment:
Discontinue heparin and initiate alternative anticoagulation
Direct thrombin inhibitors: argatroban, lepirudin (do not trigger heparin-PF4
antibody production)
Not Coumadin; Coumadin can exacerbate problem
Disorder of coagulation: Disseminated intravascular coagulopathy (DIC)
o Imbalance between coagulation and anticoagulation with end result of hemorrhage
and organ failure (any organ)
Always watch for this in septic patient
o Symptoms:
>Bleeding-related: petechiae (seen more on abd & legs), ecchymosis, scleral
bleeding, oozing from IV lines, arterial lines, injured tissues & internal
bleeding
in response to low platelets
>Microthrombosis-related:
*Superficial: cyanosis/ ishchemia fingers, toes, nose, ears
*Organ dysfunction: CNS (altered LOC), Cardiac (tachycardia,

hypotension), Resp (dyspnea, tachypnea, cyanosis, hypoxemia,
ARDS), renal failure
o Labs:
Prolonged: bleeding time, PT, PTT, thrombin time
Increased: fibrin degradation products, d-dimer
Decreased: clotting factors, fibrinogen level, plts.
o Treatment Goal: Maintain fluid and hemodynamic balance (IVFs, RBC, Plt, & FFP
transfusions) and treat the cause

Transfusions: platelet s, FFP (has clotting factors in it), RBCs
Heparin drip
Coagulation inhibitor: antithrombin III
Leukocyte Disorders: Leukemia
o Malignant disease of the blood
Dysfunction of the bone marrow
o Types: Acute (A) vs. Chronic (C)
o Cell type: Myeloid (M)
*myeloblastic, myelocytic
o Cell type: Lymphoid (L)
*lymphoblastic, lymphocytic)
o Nomenclature:
AML, CML, ALL, CLL
Chronic leukemia pt: on low dose chemo daily; live in community
Acute: rapid onset, many manifestations
o Etiologies: genetic, radiation & chemical exposure, drugs, viruses
o Pathophysiology: lack of normal regulatory mechanisms of bone marrow cell
proliferation and maturation
o Primary symptoms: d/t granulocytopenia, anemia, thrombocytopenia
o Secondary symptoms: d/t leukemic cell infiltration of tissue & BMD
o Diagnosis:
Symptom profile (evidence of leukemic infiltrates and pancytopenia)
CBC
WBC range: <1000/mm3 to >200,000/mm3
Differential will define type
Platelets & Hemoglobin low
Bone marrow aspiration: increased # immature cells (blasts)
LP: blast cells in CNS (~5% pts)
MRI & CT: infiltrates and sites of infection
o Therapeutic treatments:
Induction of a remission using chemotherapy
Chemotherapy maintenance
(lower dose over longer time period)
Bone Marrow Transplantation
Syngeneic
Allogeneic (matched)
Case example:
o Ms. Jones is a 26yo newly diagnosed leukemia patient who is admitted to the
inpatient unit with fever and neutropenia five days after her first cycle of
chemotherapy.
o VS: 101.8F, 90/56, 110 (NSR), RR=20
o Lab Data: WBCs=650/mm3
o (5% segs, 7% bands,10% lymphs, 20% monos); Hct=23%, Hgb=6g/dL;
Plts=5,000/mm3
o Interventions:
Blood transfusion; Platelets; O2; iron
Birth control: dont want her to have menses
Brush teeth carefully w soft toothbrush; No flossing
No rigorous nose blowing
es ICP
fall precautions if lightheaded
No drugs to plt aggregation
Ibuprofen, aspirin
Protective isolation
No fresh fruits, veggies, pets, flowers
*Concept of neutropenia
o Abnormal decrease in neutrophils (<1,000/ mm3)
o Determining neutropenia
Absolute Neutrophil Count (ANC) =
(bands
+segs) x WBC count
100
o Normal ANC= 2,500-5,000
o ANC <500 severely increases risk for infection
Priorities of care
o
o
o
o
o
o
o
o
o
Risk for Infection

Risk for Injury: Bleeding
Anemia-related diagnoses (Fatigue)
Pain
Fatigue
Risk for Altered Thought Processes
Risk for Fluid Volume Deficit
Imbalanced Nutrition: < body requirements
Ineffective Individual/ Family Coping
Supportive therapy
o Anti-infectives (gram +/-, antiviral, antifungal)
o Antipyretics (acetominophen; no NSAIDS)
o Transfusions (RBCs, Plts)
o Fluids and electrolytes (NS, K & Mg)
o Symptom Management (pain, N/V, fatigue, etc.)
o Psychological (coping, fear, anxiety, depression)
o Spiritual (hopelessness, spiritual distress)
HIV
Acute infection
Asymptomatic Infection
Persistent Generalized Lymphadenopathy
Other symptoms: constitutional, neurological, secondary infections, secondary malignancies
Management of primary infection
o Monitor HIV status (CD4 count, symptoms)
o Antiviral therapy: HAART(Highly active antiretroviral therapy)
Non-nucleoside Reverse Transcriptase Inhibitors
Nucleoside/ Nucleotide Reverse Transcriptase Inhibitors
Protease Inhibitors
Entry Inhibitors
o Psychological support
Treatment: HAART
o Non-nucleoside Reverse Transcriptase Inhibitors (NNRTI):
prevents conversion of RNA to DNA
o Nucleoside/ Nucleotide Reverse Transcriptase Inhibitors (NRTI):
stops construction of viral DNA
o Protease Inhibitors (PI):
Prevent successful release of new virus particles
o Entry Inhibitors (EI):
Prevent HIV from entering healthy T cells
o *Adherence to therapy is a major issue
*Common Manifestations of Progressive Disease
o Pulmonary: pneumonia, TB
o Gastrointestinal: chronic diarrhea, oral candidiasis, wasting syndrome: proteinenergy malnutrition
o Malignancy: Non-Hodgkins lymphoma, Kaposis sarcoma, Cervical cancer
o Neurological: encephalopathy, meningitis, neuropathies
o Non-biological: Fear, anxiety, depression, social isolation
o Lymphoid system disorder: NHL
Epidemiology: unknown; possibly immunodeficiency, Epstein-Barr virus,
environmental/ occupational exposure
Pathophysiology: most are B cell origin
Symptoms: B symptoms (fever, nights sweats, anorexia + weight loss,
weakness, SOB), enlarged lymph nodes, spleen, & liver, neuro deficits
Treatment: combination chemo & radiation
Case example:
o Mr. White is a 42yo diagnosed with AIDS 1.5yrs ago who is admitted to the inpatient
unit with fever, dehydration and shortness of breath. Pt. was recently diagnosed with
NHL and the admitting diagnosis is PCP pneumonia.
o VS: 101.8F, 90/56, 110(NSR), RR=22, pOx=90% on 2L NC
o Lab Data: WBCs=2000/mm3 (8% segs, 2% bands,5% lymphs, 20% monos, CD 4

count= 200cells/ uL); Hct=27%, Hgb=8.5g/dL; Plts=55,000/mm3
o Questions? Concerns?
o What is the patient experiencing?
o What symptoms would you expect to assess?
o Priorities of care? Priority interventions?
Priorities of care
o Ineffective Breathing Pattern
o Impaired Gas Exchange
o Risk for Infection
o Pain
o Fatigue
o Risk for Altered Thought Processes
o Risk for Fluid Volume Deficit
o Risk for Electrolyte Imbalance
o Imbalanced Nutrition: < body requirements
o Ineffective Individual/ Family Coping
Nursing management
o Immunosuppression-related care
o Anemia-related care
o Fluids and electrolytes
o Nutritional interventions
With difficulty swallowing :avoid fresh fruits/ vegies, spicy, acidic, & salty
foods; alcohol & tobacco; foods at excessive temps; sticky foods; slippery
foods.
Special diet: high protein, high calorie, low-fat in small frequent meals
Hydration: 2 2.5L daily
Nutrient dense foods and beverages
o Safety precautions
o Social support
o Teaching
Questions
A client with leukemia is one week post chemotherapy on 3 anti-infectives and has the
following lab values: WBC= 1200/ mm3 with 20% neutrophils, Hct= 28.5%, platelets=
35,000/mm3, potassium= 3.2, BUN= 23, and creatinine= 2.0.
Which of the following MD orders would the nurse question?
o Morphine 2-4mg IV every 3 hrs. PRN pain
o Acetaminophen 650mg PR every 4 hrs. PRN fever
(rectal route is not recommended in immunocompromised patients)
o Potassium chloride 40mEq IV over 4 hrs.
o Docusate sodium 100mg po bid
A client has the following symptoms: T= 100F, BP= 98/60, HR= 118, RR= 24, WBC= 1800,
Hgb= 9.5mg/dl, platelets= 9000 and complains of headache and has petechiae in the
conjunctiva.
The highest priority nursing diagnosis would be:
o Fatigue
o Risk for Injury (at risk for bleeding d/t low plts)
o Knowledge Deficit
o Impaired Gas Exchange
Exchange (no symptoms to indicate this)
Hgb= 9.5mg/dl, platelets= 9000 and complains of headache and has petechiae in the
conjunctiva.
The priority nursing intervention would be to:
o Institute protective isolation
o Maintain IV fluid infusion
o Elevate the head of the bed (decreases intracranial pressure)
o Prepare for a WBC infusion
A client diagnosed with AIDS has had chronic diarrhea for the past 6 months and has lost 18
pounds during that time. Assessment findings include: tented skin turgor, dry mucous
membranes, and severe fatigue and indifference.
What is the priority nursing diagnosis for this patient?
o Deficient fluid volume
o Imbalanced nutrition: less than body requirements
o Disturbed thought processes
o Risk for infection

The best oral fluid replacement therapy for a client diagnosed with AIDS who has had
chronic nausea, diarrhea, and fatigue for the past 6 months would be a combination of water
and:
o Caffeine free diet soda (can be dehydrating)
o Caffeinated beverages (function as diuretic)
o Sports drinks (provides increased calories and electrolytes)
o Fresh-squeezed citrus juices (high in acid and may cause increase in nausea)
A person with AIDS is admitted to an acute care unit for the treatment of a fungal infection
with amphotericin IV. The nurse should monitor for which of the following electrolyte
disturbances:
o Low potassium (most anti-infectives cause potassium and magnesium wasting)
o Low calcium
o High sodium
o High magnesium
The nurse is admitting a client diagnosed with protein calorie malnutrition secondary to
AIDS. Which intervention would be the nurses first action?
o Assess pt.s body weight & ask what the client has been able to eat.
pt. has malnutrition syndrome; assess first.
o Place in contact isolation and don a mask & gown before entering the room.
standard precautions are used for all patients.
o Check MD orders & determine what lab tests will be done.
assess pt. first
o Teach patient about TPN & monitor the subclavian IV site
this action may be ok but not the first
The pt. diagnosed with AIDS is complaining of a sore mouth and tongue. When the nurse
assess the buccal mucosa, the nurse notes white, patchy lesions covering the hard and soft
palates & right inner cheek.
Which interventions should the nurse implement?
o Teach the pt. to brush the teeth & patchy area with soft-bristle toothbrush
this intervention will not treat oral candidiasis.
o Notify MD for an order for an antifungal swish-and-swallow medication.
o Have the pt. gargle with an antiseptic-based mouthwash several times a day
MW often contains alcohol & burns
o Determine what types of food the client has been eating for the past 24 hours
foods eaten have not connection to this condition
The client on a medical floor is diagnosed with HIV encephalopathy. Which is the priority
nursing diagnosis?
o Altered nutrition, less than body requirements priority for malnutrition
o Anticipatory Grieving requires cognitive abilities
o Knowledge deficit, procedures & prognosis pt. does not have enough cognitive
capacity to understand
o Risk for Injury safety is a primary concern with decreased MS.
The client diagnosed with pneumocystis carinii pneumonia (PCP) is being admitted to ICU.
Which MD order should the nurse implement first?
o Draw serum CD4 level & CBC stat.
o Give oxygen to pt @ 4LPM - ABCs
o Administer trimethoprim sulfa IVPB (antibiotic) 3rd priority
o Obtain sputum for culture & sensitivity 2nd priority
A nurse on a med-surg unit is caring for patients diagnosed with AIDS. Which patient should
be seen first?
o Pt. with flushed warm skin with tented turgor. indicates dehydration (?d/t insensible
loss via respiratory tract; ?AIDS-related diarrhea; malnutrition)
o Pt. states that staff ignores the call light
physical issue a priority
o Pt. with vital signs: T= 99.9F, P= 101, BP = 110/68, RR= 26. VS not critical
o Pt. unable to provide sputum specimen
not a critical priority
Heme application review
23/02/2015 18:15:00
The most common sign of thrombocytopenia is:

Petechaie
Hemostasis (normal blood counts)
Melena (black stool)
Fever (neutropenia)
Which of the following clinical signs and symptoms would suggest an anemia secondary to
vitamin deficiency (ie B12) rather than folic acid deficiency?

Smooth, sore tongue (Iron deficiency)
Palpitations (general Sx of anemia)
Paresthesias (Vit. B12 deficiency)
Dizziness (general Sx of anemia)
A client has a fever of 101F, BP= 190/102, and CBC reveals a WBC= 5000/mm3, Hgb=12.9g/dl,
and platelet count= 5000/mm3.

Which of the following is the priority nursing intervention?
Oxygen 6L via nasal canula (not efficient oxygen delivery system)

Transfuse with platelets per standing orders (this would be the second priority)
Ibuprofen 200 400mg po every 6hrs. PRN (NSAIDS decrease platelet aggregation)
Nifedipine 10mg po every 6hrs. PRN for SBP>180 (Ca channel blockers are often used to
decrease BP to prevent bleeding)
A client has a fever of 101F, BP= 190/102, and CBC reveals a WBC= 5000/mm3, Hgb=12.9g/dl,
and platelet count= 5000/mm3.

The patient asks why he needs to take a stool softener. The nurses response is based on which of
the following rationale:

Constipation can lead to hemorrhoids.
The Valsalva maneuver can cause increased intracranial pressure. (Increased ICP can lead to
bleeding in pt. with low platelets)
Use of stool softeners lead to minimal GI blood loss.
Constipation increases the risk of perirectal abcess formation.
Client teaching about self management of the fatigue associated with anemia should include
instructions to:
Continue bedrest (increases fatigue)
Participate in all usual ADLs (may increase fatigue)
Follow a progressive ambulatory program (gradually restores energy)
Participate in aerobic exercise training (may increase fatigue)
Which of the following statements would indicate that an anemic patient needs further teaching
about taking iron supplements.

I can take my iron pills with milk to prevent an upset stomach.(Calcium inhibits iron
absorption)
I should take a stool softener when I am taking iron pills.
I can take vitamin C to enhance iron absorption.
It is normal for my stool to be black when I take iron.
A client receiving a unit of packed red blood cells and has baseline vital signs of: Temp= 99F,
HR= 100, BP= 136/72, & RR= 22. Fifteen minutes into the transfusion, the patient complains of flank
pain and has hematuria.
The priority nursing intervention is to:
Continue to monitor the transfusion

Recheck the patient in 15 minutes
Decrease the rate of infusion
Stop the transfusion.
A client receiving a unit of packed red blood cells and has baseline vital signs of: Temp= 99F,
HR= 100, BP= 136/72, & RR= 22. Fifteen minutes into the transfusion, the patient complains of flank
pain and has hematuria.
The patient is most likely experiencing which type of transfusion reaction:
Febrile
Hemolytic
Anaphylactic
Hypervolemic
A client with leukemia is one week post chemotherapy on 3 anti-infectives and has the following
lab values: WBC= 1200/ mm3 with 20% neutrophils, Hct= 28.5%, platelets= 35,000/mm3, potassium=
3.2, BUN= 23, and creatinine= 2.0.
Which of the following MD orders would the nurse question?
Morphine 2-4mg IV every 3 hrs. PRN pain

Acetaminophen 650mg PR every 4 hrs. PRN fever (rectal route is not recommended in
immunocompromised patients)
Potassium chloride 40mEq IV over 4 hrs.
Docusate sodium 100mg po bid
Hgb= 9.5mg/dl, platelets= 9000 and complains of headache and has petechiae in the conjunctiva.
The highest priority nursing diagnosis would be:
Fatigue
Risk for Injury (at risk for bleeding d/t low plts)
Knowledge Deficit
Impaired Gas Exchange (no symptoms to indicate this)
Hgb= 9.5mg/dl, platelets= 9000 and complains of headache and has petechiae in the conjunctiva.
The priority nursing intervention would be to:
Institute protective isolation

Maintain IV fluid infusion
Elevate the head of the bed (decreases intracranial pressure)
Prepare for a WBC infusion
A client diagnosed with AIDS has had chronic diarrhea for the past 6 months and has lost 18
pounds during that time. Assessment findings include: tented skin turgor, dry mucous membranes, and
severe fatigue and indifference.
What is the priority nursing diagnosis for this patient?
Deficient fluid volume

Imbalanced nutrition: less than body requirements
Disturbed thought processes
Risk for infection
The best oral fluid replacement therapy for a client diagnosed with AIDS who has had chronic
nausea, diarrhea, and fatigue for the past 6 months would be a combination of water and:
Caffeine free diet soda (can be dehydrating)
Caffeinated beverages (function as diuretic)
Sports drinks (provides increased calories and electrolytes)
Fresh-squeezed citrus juices (high in acid and may cause increase in nausea)
A person with AIDS is admitted to an acute care unit for the treatment of a fungal infection with
amphotericin IV. The nurse should monitor for which of the following electrolyte disturbances:
Low potassium (most anti-infectives cause potassium and magnesium wasting)
Low calcium
High sodium
High magnesium
The nurse is admitting a client diagnosed with protein calorie malnutrition secondary to AIDS.
Which intervention would be the nurses first action?

Assess pt.s body weight & ask what the client has been able to eat. pt. has malnutrition
syndrome; assess first.
Place in contact isolation and don a mask & gown before entering the room. standard
precautions are used for all patients.
Check MD orders & determine what lab tests will be done. assess pt. first.
Teach patient about TPN & monitor the subclavian IV site. this action may be ok but not
the first.
The pt. diagnosed with AIDS is complaining of a sore mouth and tongue. When the nurse assess
the buccal mucosa, the nurse notes white, patchy lesions covering the hard and soft palates & right inner
cheek.
Teach the pt. to brush the teeth & patchy area with soft-bristle toothbrush. this intervention
will not treat oral candidiasis.
Notify MD for an order for an antifungal swish-and-swallow medication.
Have the pt. gargle with an antiseptic-based mouthwash several times a day. MW often
contains alcohol & burns.
Determine what types of food the client has been eating for the past 24 hours. foods eaten
have not connection to this condition.
The client on a medical floor is diagnosed with HIV encephalopathy. Which is the priority
nursing diagnosis?
Altered nutrition, less than body requirements priority for malnutrition
Anticipatory Grieving requires cognitive abilities
Knowledge deficit, procedures & prognosis pt. does not have enough cognitive capacity to
understand
Risk for Injury safety is a primary concern with decreased MS.
The client diagnosed with pneumocystis carinii pneumonia (PCP) is being admitted to ICU.
Which MD order should the nurse implement first?

Draw serum CD4 level & CBC stat.
Give oxygen to pt @ 4LPM - ABCs
Administer trimethoprim sulfa IVPB (antibiotic) 3rd priority
Obtain sputum for culture & sensitivity 2nd priority
A nurse on a med-surg unit is caring for patients diagnosed with AIDS. Which patient should be
seen first?
Pt. with flushed warm skin with tented turgor. indicates dehydration (?d/t insensible loss
via respiratory tract; ?AIDS-related diarrhea; malnutrition)
Pt. states that staff ignores the call light
o physical issue a priority
Pt. with vital signs: T= 99.9F, P= 101, BP = 110/68, RR= 26. VS not critical
Pt. unable to provide sputum specimen
o not a critical priority
Sepsis/SIRS
23/02/2015 18:15:00
SIRS
Systemic Inflammatory Response Syndrome
A SYSTEMIC response to a variety of insults
No bacterial/viral agent that started SIRS; otherwise, essentially the same as sepsis
Infection
Presence of microorganisms in a normally sterile site
Bacteremia
Cultivatable bacteria in the blood stream
Sepsis
The systemic response to infection. If associated with proven or clinically suspected
infection, SIRS is called sepsis
As soon as bacteria hits the blood, its sepsis
Pt WILL have ARDS
o Can have ARDS without sepsis but cannot have sepsis without ARDS
What is SIRS?
The systemic inflammatory response syndrome is systemic level of acute inflammation, that
may or may not be due to infection, and is generally manifested as a combination of vital
sign abnormalities including fever or hypothermia, tachycardia, and tachypnea.
Risk Factors for SIRS/Sepsis
o Extremes of age
o Oncological chemotherapy and radiation therapy
#1 complication of chemo tx in cancer patients= sepsis (#1) POC= infection
o Immunocompromised states
o Indwelling lines/catheters
o Malnutrition
Immune system drops ->must have nutrition for bone marrow to work
o Alcoholism
Lose all protein/drinking empty cals
o Malignancy
o Diabetes
Blood sugars; perfusion probs; ed immune system; infection; vasculature

issues
o Cirrhosis
Introduction of compromised immune system
o Male sex
o Genetic predisposition?
SIRS
The systemic response to a wide range of stresses
o Temperature >38C (100.4) or <36C (96.8F).
o Heart rate >90 beats/min.
o Respiratory rate >20 breaths/min or PaCO2 <32 mmHg.
o White blood cells > 12,000 cells/ml or < 4,000 cells/ml or >10% immature (band)
forms.
Note
o Two or more of the following must be present
o These changes should be represent acute alterations from baseline in the absence of
other known cause for the abnormalities
Etiology of SIRS
o Mechanical
Trauma
Burns
Can get infected or activate inflammatory response
Surgery
o Chemical
Toxic drugs/fumes
Pancreatitis
o Ischemic
Shock states
Myocardial infarction
Reperfusion injury: anaerobic metabolism occurs d/t cell death and lysed cells
expel K+
Normal inflammatory immune response

o This is a NORMAL response
Injury ->bleeding (attempt to cleanse area) ->clot off ->immune system
activated -> redness (area around wound vasodilates & gets warm d/t blood)->
exudate is being released (protein enriched substance in white cells being
pushed to area) = localized response (think of it body wide)
o Multiple systems are activated to protect the host from insult and limit the extent of
injury & promote rapid healing.
o Insult can be microbial, but also mechanical, chemical, ischemic.
o Mediators involve multiple pathways- from molecular to systemic.
o Patho:
Although inflammation is essential to host response against infection, SIRS
results from a dysregulation of the normal response, with massive,
uncontrolled release of pro-inflammatory mediators.
Triggers caused from bacterial, viral, etc.

o Inflammatory cells
Monocytes/Macrophages
Neutrophils
Mast cells
Endothelial cells
o Plasma protein systems
Complement
Kinin
Coagulation
o Biochemical mediators
C-reactive protein
Interleukins
Tumor necrosis factor (TNF)
Platelet-activating factor (PAF)
Oxygen radicals
Arachidonic acid metabolites
Prostaglandins
Leukotrienes
Thromboxanes
Vasodilation occurs, thereby ing afterload (norm=800-1200)

CVP es -> HR es, BP es, CO es
Microvascular permeability: fluid in 3rd space
It is lost fluid but does NOT harm you
Its lack of fluid in vasculature that causes harm
Hypovolemic
Loss of volume d/t change in permeability (3rd spacing)
Vasodilation: changes size of compartment
* stage of progression: initial, compensatory, progression, refractory
refractory: even with treatment, pt is still hypotensive
o SIRS or sepsis?
SIRS
Inflammation gone WILD!!
Sepsis
Triggered by invading microbes
Clinically SIRS and Sepsis can look the same (early on) except with SIRS,
cultures will be negative

BOTH can lead to shock
Severe sepsis: inability of organs to metabolize O2
Sepsis
Etiology
o Microbial infection
Blood
Bacteria
Gram negative
Gram positive
Fungi
Virus
Abscess
Bacterial translocation in gut
Bacterial translocation when depleted of nutrients
Just 10 cc going in gut will prevent this from happening
Instrumentation/catheterization
o * The definitions for SIRS and sepsis can also be used to describe a disease
continuum with respect to the severity of the illness
o Determining factor of progression: how good/bad immune system works
o * Septic shock is a subset of severe sepsis. Note that current definitions have dropped
the term septicemia that may still be found in older textbooks. Bacteremia is the
term for when organisms are cultured from blood.
Sepsis
o General
Temperature > 38.3 or < 36
Heart rate > 90 beats per minute
Tachypnea
Altered mental status
Significant edema or positive fluid balance (> 20 ml/kg over 24 hours)
o Hemodynamic
Systolic BP <90 mm Hg or >40 decrease in SBP or MAP < 70
Cardiac index > 3.5 L/min
o Tissue perfusion
Decreased capillary refill or mottling
Lactate levels > 2 mmol/L
o Inflammatory
WBC > 12,000 cc/mL, < 4,000, > 10% bands
C-reactive protein levels > 2 times normal
Severe Sepsis
o Sepsis with organ hypoperfusion
1st organ affected: lungs
2nd affected: kidneys
acute tubular necrosis (ATN)

oliguria->anuria
one of the followings :
SBP < 90 mmHg
Acute mental status change
PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250)
Increased lactic acid/acidosis
Oliguria
DIC or Platelet < 80,000 /mm3
Liver enzymes > 2 x normal
Ability to filter impaired d/t hypoperfusion
Organ dysfunction
Arterial hypoxia, P/F ratio (PaO2/FiO2 <300)
PaO2 = 120 and FiO2 = 60% 120/.6 = 200
Hypotension despite fluid resuscitation
Acute oliguria (urine output < 0.5 mL/kg)
Creatinine increase > 0.5 mg/dL
Kidneys hypoperfused
Ileus (absent bowel sounds)
hypoperfused
Total bilirubin > 4 mg/dL
Coagulation abnormalities (INR > 1.5 or a PTT > 60 sec)
Thrombocytopenia (platelet count < 100,000)
Platelets are getting used up quicker than production occurs
Metabolic acidosis (pH < 7.30)
d/t lactic acidosis
kidneys cant compensate
lungs cant compensate cause failing too
Complications
Adult respiratory distress syndrome (ARDS)
Disseminated Intravascular Coagulation (DIC)
Acute Renal failure (ARF)
Intestinal bleeding
Liver failure
Central Nervous System dysfunction
Heart failure
Death
Prognosis
Overall mortality from SIRS/sepsis in the U.S. is approximately 20%.

Mortality is roughly linearly related to the number of organ failures, with each
additional organ failure raising the mortality rate by 15%.
Hypothermia is one of the worst prognostic signs. Patients presenting with
SIRS and hypothermia have an overall mortality of ~80%
o Surviving sepsis campaign
The SSC aimed to reduce mortality from sepsis via a multi-point strategy,
primarily:
Building awareness of sepsis
Improving diagnosis
Increasing the use of appropriate treatment
Educating healthcare professionals
Improving post-ICU care
Developing guidelines of care
Facilitating data collection for the purposes of audit and feedback
Guidelines for Management of Severe
Sepsis and Septic Shock
Early Goal-Directed Therapy
Sepsis resuscitation bundle
Sepsis management bundle
o Diagnosis
Before the initiation of antimicrobial therapy, at least two blood cultures
should be obtained
At least one drawn percutaneously
At least one drawn through each vascular access device if inserted
longer than 48 hours
Other cultures such as urine, cerebrospinal fluid, wounds, respiratory
secretions or other body fluids should be obtained as the clinical situation
dictates
Lactate has direct correlation to survivability
CBC, ABG, coag panel
Other diagnostic studies such as imaging and sampling should be performed
promptly to determine the source and causative organism of the infection
may be limited by patient stability
o Sepsis resuscitation bundle (must be accomplished within the first 6 hours*)
The Sepsis Resuscitation Bundle describes below, but must be accomplished
within the first 6 hours of presentation for patients with severe sepsis or septic
shock.
Serum lactate measured

Blood cultures obtained before antibiotics administered
Improve time to broad-spectrum antibiotics
within 3 hours of ED admission and within 1 hour of non-ED
In the event of hypotension or lactate > 4 mmol/L (36 mg/dL)
a. Deliver an initial minimum of 20 mL/kg of crystaloid (or colloid
equivalent) For a 85kg patient you would give 1.7 liters of NS/LR
b. apply vasopressors for ongoing hypotension (vasopressors,
inotropes)
blood culture before fluid (or at same time)
give vasopressin to constrict (acts on smooth muscles);
levophed doesnt work in acidotic states
In the event of persistent hypotension despite fluid resuscitation or lactate > 4
mmol/L (36 mg/dL)
a. achieve central venous pressure of > 8 mmHg
fluid will leak out faster than can be put in (must continually
give fluid boluses to maintain CVP)
b. achieve central venous oxygen saturation of > 70%
<70, cells become hypoxic
o Sepsis management bundle
Evidence-based goals that must be completed within 24 hours for patients
with severe sepsis, septic shock and/or lactate > 4 mmol/L (36 mg/dl).
Evaluation for adrenal insufficiency
Stress dose corticosteroid administration
Test for this condition: give pt adrenocorticotropin, draw cortisol level
before and after administration. Should see an in level
Give steroids if levels are decreased (cause cant make their
own and cortisol is essentially a steroid)
Recombinant human activated protein C (xigris) for severe sepsis (Studies
now indicates that Zigris has no effect on outcome on patients with
septicemia)
Low tidal volume mechanical ventilation for ARDS
Tight glucose control
ed glucose impairs tissue healing
bacteria thrive on glucose; prevents healing & impairs
vasculature
o * to lower lactate level, stop anaerobic metabolism
flush out lactate ( urine output)
o Priorities of care
Ineffective tissue perfusion related to progression of septic shock with
decreased cardiac output, hypotension, and massive vasodilatation
Deficient fluid volume related to vomiting, diarrhea, high fever, and shift of
intravascular volume to interstitial spaces
Ineffective breathing pattern related to rapid respirations and progression of
septic shock
Anxiety related to feelings that illness is worsening and is potentially life
threatening, and the transfer to the critical care unit
o Expected outcomes
Regain and maintain stable hemodynamic levels by the end of shift
Maintain adequate circulating blood volume
Regain and maintain blood gas parameters within normal limits by the end of
shift
Verbalize increased ability to cope with stressors by the time of discharge.
*Injury ->bleeding (attempt to cleanse area) ->clot off ->immune system activated -> redness
(area around wound vasodilates & gets warm d/t blood)-> exudate is being released (protein enriched
substance in white cells being pushed to area) ->infection worsens (bacteria in blood)->bacteremia>Sepsis (vasodilation, microvascular permeability, cellular activation {early and late mediators],
coagulation)-> (decreased preload -> decrease in SV -> in CO)
Give norepi (#1) & vasopressin (#2)
ABX!!
o For change in permeability, must treat underlying cause
o Must start w/in 3 hr of arrival at ED & 1 hr on floor
Sepsis case study
43-year-old male
Flu-like symptoms for 1 day
In ER
o Temp 39.5 (ed)
o Pulse 130 (ed HR)
o Blood pressure 70/30 (ed)
o Respirations 32 (ed)
o Petechial rash (D/t DIC; microemboli formation -> microemboli clotting occurs in
capillaries
o Chest, CV, Abdominal exam normal
Case 2
Laboratory
o pH 7.29, Sat 89%, PaO2 72, PaCO2 29 (resp compensation)
o Lactate 6.0 (anything above 2 is ed) ->the higher the lactate the higher the mortality
Start sodium bicarb drip (mix with D5, NEVER NS-> sodium load will be too
high)
3 amps/L
Investigations pending
o Blood, urine cultures
Anything draining out of body
Orally intubated and placed on mechanical ventilation
o Low tidal volumes
o Pressure ventilation if hes bad enough instead of volume
Central venous catheter inserted
o Cefotaxime 2 g IV
o Normal saline 2 litres initially, repeated
Admitted to ICU
Case 3
In ICU:
o Norepinephrine started to support blood pressure
o Additional fluid (NS/ LR)
o Volume expansion with pentastarch {hetastarch}) Albumin based on low CVP
Once permeability has returned to normal limits, thats when you give
albumin
Pentastarch: acts similar to albumin
o Blood products, (PRBC, FFP, cryoprecipitate)
o Pulmonary artery catheter inserted to aid further hemodynamic management
Despite therapy patient remained anuric
o Continuous venovenous hemofiltration initiated
Case 4
Early gram stain on blood revealed gram negative rods
Patient started on:
o Hydrocortisone 100 mg IV q8h
d/t adrenal insufficiency
o Recombinant activated protein C 24g/kg/hour for 96 hours (Studies now indicates
that Zigris has no effect on outcome on patients with septicemia)
o Use of vasopressin vs norepinephrine for BP support
At high doses, stimulates contraction of smooth muscle causing
vasoconstriction when catecholamine's fail (works better than
catecholamines)
o Enteral nutrition via nasojejunal feeding tube
Even without BS
o Prophylaxis for stress ulcers, deep venous thrombosis
DVT: SCDs
Possible heparin
o Final culture: meningococcal septicemia
Anemia
23/02/2015 18:15:00
Hematopoiesis: Bone marrow manufactures all blood cells

Blast cells are immature blood cells
Erythropoiesis: production of RBCs; dependent upon the release of EPO from the kidney in
response to blood cell oxygen demand

CBC w diff & platelets
WBCs (5,000-10,000/cu mm)

o Differential: segs + bands (50 70%), lymphs (20 40%), monos (2 8%), eos (1
4%), basos, blasts
RBCs
o Hct (men: 42-52%; women: 37-47%)
o Hgb (men: 14-18g/dl;women: 12-16g/dl) *most important
* Hgb x3 ~ Hct
o Men have more RBCs than women d/t: bigger bones, lack of menses
Plts (150,000-500,000/ cu mm)
Reticulocyte count: indicator of RBC production rate & EPO response
RBC indices:
o MCV (mean corpuscular [cell] volume): tells us the average size of an RBC
Small RBCs: blood loss, ed #s of immature RBCs, ed iron
Normal size RBCs: normocytic anemia (normal size w ed #s), acute blood
loss
Extra large RBCs: macrocytic anemia, vitamin B12 deficiency/folate
deficiency (B12 & folic are building blocks of nucleic acid; ed #s prevent
cells from dividing properly so they are extra large)
Pernicious anemia: B12 deficiency
May be d/t alcoholism, gastric bypass, anorexia, malnutrition,
long term/untreated hypothyroidism
o MCH (mean corpuscular [cell] hemoglobin): tells us the average (in weight)
amount of Hgb in one RBC
o MCHC (mean corpuscular [cell] hemoglobin concentration): tells us the average
Hgb concentration in one RBC (%)
1 RBC ~ 33% Hgb
other components: enzymes, cytoplasm, etc.
o RDW (RBC distribution with): red cell distribution =avg variance in sizes of RBCs
ed RDW = great diff in sizes
es efficacy of gas exchange in the body
normal size: maximizes gas exchange in the body

o Retic count: young RBC production; tells us how effectively our EPO response from
the kidneys is working
High production of young RBCs d/t anemia, hypoxia, sickle cell anemia*,
altitude*, bleeding, ed RBC destruction (burns)
ed retic count: bone marrow suppression, medication, infection, ed EPO
Heme (iron + oxygen molecule)
o Iron deficiency decreases oxygen carrying capacity
o Globin (protein)
Aging hematologic system
At ~ age 70yo, amount of bone marrow in long bones begins to decline
Decreased # stem cells in marrow
Decreased effectiveness of EPO
Decreased platelet adhesiveness
Average H & H decreases slightly to low normal
No changes: RBC life span, Blood volume, total WBC count, platelet structure & function
Factors effecting the aging immune system
Stress
o SNS stimulation -> hormonal changes -> decrease immune response -> especially
cellular immunity
Cortisol (stress hormones): suppresses immune system & bone marrow
response
Comorbidity
o *Chronic infection/ inflammation decreased EPO, decreased RBC survival,
impaired iron transport
o *Chronic liver disease decreased RBC production & survival, decreased serum iron
and TIBC
o *Renal insufficiency/ renal failure decreased EPO, decreased RBC survival
Exercise
o Exercise: may prevent decrease in cellular immunity
Nutrition
o Vitamins enhance cellular immunity (Vitamins A, B6, C, E, folic acid, iron, copper,
selenium, zinc)
Anemia: decreased RBCs, Hgb, Hct
Mild anemia: 10-12 Hgb

Mod: 7-10 Hgb
Severe: under 7 Hgb
Neutropenia: decreased neutrophils
50-70%: 1st to show up on site

Thrombocytopenia: decreased plts
Less than 150,000

Pancytopenia: decrease in all cellular components of the bone marrow; caused by bone marrow
supression
Types of anemia
Reasons for Anemia

Blood loss: surgery, acute bleeding (hemorrhage, trauma), chronic bleeding (cirrhosis ->
ed vitamin K, colitis [Irritable Bowel Disease], cancer, peptic ulcers/gastric ulcers)
o Confirm: H&H, RBC indices (including retic count), endoscopy (for upper GI bleed),
occult blood sample (for lower GI bleed)
ed RBC production: Vit D deficiency, ed iron, ed B12, folate, bone marrow issues
(BM failure [aplastic anemia], suppression [Rx, Chemo, malignancy], insensitive to EPO
Chronic inflammation/disease: ed WBCs (specifically cytokines [IL-2, IL-6, INF])
o ed cytokines suppress bone marrow encourages cells to uptake iron (ed iron to
uptake RBCs) lysing of cells
Kidney issues
Types of anemia
ed RBC destruction: infections, Rx, blood vessel issues, sickle cell anemia, burns
General symptoms of anemia
S&S of anemia:
Face
o ed pallor (Fe give Hgb its color) skin mucous membranes conjunctiva
(lids of eye)
o ed O2 to brain fatigue HA ed concentration
o sore tongue/bald tongue (smooth & shiny tongue cause papillae not produced
Specific to Fe deficiency anemia (typically chronic)

o Cracking at side of mouth (patients like to chew on mouth) pica (ice [no
nutritional value])
Vitamin deficiencies d/t anemia (common wit other vit deficiencies)
Lungs
o Report feelings of breathlessness ed RR (compensatory mechanism)
Heart
o ed HR (baseline ~110)
Lower extremities
o Cramping, Numbing/tingling (ed B12)
Physiologic Compensatory Mechanisms of Anemia
Increased synthesis of 2,3-DPG: more oxygen released to the tissues

Blood redistribution: decreased urine output, pallor of skin/ mucous membranes
Increased cardiac output: tachycardia, systolic flow murmur, orthostatic hypotension
Increased respiratory rate: DOE, orthopnea
Increased production of erythropoietin: generalized aches and pains, sternal tenderness
Symptoms of compensatory failure: decreased oxygenation to tissues
Angina
Headache
Light-headedness
Nocturnal leg cramps
Irritability
Nursing Diagnoses for Patients with Anemia
Ineffective Tissue Perfusion
Fatigue
Activity Intolerance
Impaired Gas Exchange
Altered Skin Integrity
Altered Nutrition: < body requirements

Altered Mucous Membrane Integrity
Blood transfusion types
Blood transfusion basics

Pretransfusion (history, vital signs, premedication PRN)
Transfuse blood with normal saline only
o 18g for blood products
Older adults at high risk for fluid overload & CHF
One unit RBC ->
o Hct by 3%
o Hgb by 1g/dl
Care of patient with anemia
Questions
Which of the following statements would indicate that an anemic patient needs further
teaching about taking iron supplements.
o I can take my iron pills with milk to prevent an upset stomach.(Calcium

inhibits iron absorption)
o I should take a stool softener when I am taking iron pills.
Fe supplements very constipation
o I can take vitamin C to enhance iron absorption
o It is normal for my stool to be black when I take iron
Client teaching about self management of the fatigue associated with anemia should include
instructions to:
o Continue bedrest (increases fatigue)
o Participate in all usual ADLs (may increase fatigue)
o Follow a progressive ambulatory program (gradually restores energy)
o Participate in aerobic exercise training (may increase fatigue)
Sickle cell anemia
Group of inherited disorders characterized by abnormal hemoglobin: Hb S
Primarily found in African American population frequency 8%
chance if both parents have gene = Hgb S

Autosomal recessive mutation in the hemoglobin chain
o Hgb S (75 95%)
Sickle Cell trait (mixed Hgb A & Hgb S)
o Heterozygous inheritance pattern
o Hgb S (34 45%)
o Carrier which rarely develops clinical manifestations
Pathophysiology
o Hgb S is well oxygenated, then Hgb has normal function
o PaO2 and SaO2 drop, Hgb S forms a fibrous polymer; realignment of polymers
=>sickle shape
Rod shaped cells half moon shape inflexible & very rigid
As these RBCs filter through capillaries they get stuck and cause
issues
ed retic count 5-8x the norm
RBC lasts 12-20 days
o Sickle cell crisis/vaso-occluions
Dehydration
Hypoxic -> ed O2
Cold -> ed perfusion & ed O2 to local areas
Affects all systems
o PE priapism kidney failure* liver spleen (ruptures and dies away)
sepsis pain
If spleen dies it can make pt septic
Sickle Cell Characteristics
o Rigid RBC membrane -> decreased oxygen carrying capacity
o Increased blood viscosity -> slowed blood flow in small capillaries
o Increased adherence of cells to endothelium of vessel walls
o Shortened RBC lifespan to10 20 days (normal RBC lifespan = 120 days)
o Elevated erythropoiesis (5-8x normal)
o Abnormal RBCs destroyed in the spleen -> tissue ischemia & autosplenectomy
Diagnosis:
o Sickle cell screening test
o Hemoglobin electrophoresis
Lab Values:
o Decreased Hgb
o Decreased platelets
o Increased reticulocytes
Clinical manifestations
o Begin to occur at age 6 mths to 1 yr
Chronic hemolytic anemia
Microvascular occlusion which effects all organs
Brain: stroke
Lungs: acute lung injury (~25% deaths)
Spleen: infarction leading to organ loss which predisposes pts. to
infection d/t chronic neutropenia
Renal: ARF (common cause death in adults)
Treatment
o Hydration (D51/2NS @ 150-200ml/hr)
o Oxygenation (O2 2-4L/min via NC)
o Pain management
Morphine sulfate IV continuous with PCA
Ketorolac for bone pain
o Diagnosis and treatment of infections
Prompt anti-infective therapy
o Reverse sickling crisis
Transfusion to increase Hct to >30%

Exam 2 STUDY GUIDE

Uploaded by

Copyright:

Available Formats

Exam 2 STUDY GUIDE

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Exam 2 STUDY GUIDE

Uploaded by

Copyright:

Available Formats

Fluid & Electrolytes

Advanced Concepts in Fluid and Electrolyte Disturbances

Receive ~25% of cardiac output

Metabolic & endocrine functions:

Prerenal: stems from heart d/t ed perfusion

ex: ABX processed through kidney

Damage to renal tubular epithelium due to:

Collaborative Treatment of ARF

Prerenal: crystalloid, colloid, pRBCs

ABX: monitor peak and trough of vanco before and after tx

1. Onset: (initial phase)

Pathophysiology: Integrity of renal tubular epithelium disrupted

4. Recovery: Normalizing of fluid & electrolyte balance

ACE: important but also toxic to kidneys

Access: Dialysis catheter (short term); AV fistula (long term)

o Metabolic acidosis: Bicarbonate

o Morphine sulfate (IV)? [Give low dose PRN]

87yo admitted to the intermediate care unit with

1. Central (decreased ADH)

Advanced Concepts in Fluid & Electrolyte Management

Receive ~25% of cardiac output

Glomerulus: Filter of capillaries

SIADH occurs when ADH goes wrong

Angiotensin I: converted to A-2 in pulmonary tract

Age-Related Changes: Renal

Normal Fluid Balance

methylprednisone (Ms. Blacks med): affects sodium & glucose

Intake & output

Nl = 3-4cm above sternal angle: flattened versus elevated

If pitting edema in feet, you could raise feet

Fluid Resuscitation (Crystalloids)

25% is >5x osmotic than that of plasma

**BUN, Cr, important to memorize

Causes: Diuretics, vomiting, diarrhea, diaphoresis, burns, renal failure, hypervolemia,

0.6 x weight (kg) x (130 plasma [Na+])

Hypocalcemia [< 8.0mg/dL]

o Increased ionized Ca in metabolic acidosis

Reabsorption: In proximal tubule; used in chemical buffering system

Blood Urea Nitrogen: 10 20mg/dL

Treatment: Carbohydrates, 5% Dextrose/ 50% Dextrose

1st Degree = Superficial

2nd Degree = Superficial Partial Thickness

Deep Partial Thickness = 2nd Degree (damage deep into dermis)

Full Thickness = 3rd Degree (All of dermal layer destroyed)

Subdermal = 4th degree

Measuring Total Body Surface Area (TBSA)

The Rule of Nines

Child 2 years and under:

4th pic: ~5%; 3rd degree with little 2nd degree

o Remove all clothing adherent clothing may be left undisturbed

o Place Foley catheter with urimeter (temp probe)

If unknown, shot will be given

An arc may form with flash of flames causing flame burn

fluids such as blood

o Produced by organs such as

Positive feedback loop

Hypothalamus (controls pituitary)

**Know the function of glands & secreting hormones function

Other Hormone Producing organs