CCRN Review part 2

““Education is a progressiveEducation is a progressive
discovery of our own ignorance”discovery of our own ignorance”
-- Will Durant -Will Durant -
CCRN REVIEW PART 2CCRN REVIEW PART 2
Sherry L. Knowles, RN, CCRN, CRNISherry L. Knowles, RN, CCRN, CRNI


TOPICSTOPICS

Renal AlterationsRenal Alterations
– Acute Renal FailureAcute Renal Failure
– ElectrolytesElectrolytes
– IV Fluid TherapyIV Fluid Therapy

Neurological AlterationsNeurological Alterations
– AVM’s & CerebralAVM’s & Cerebral
AneurysmsAneurysms
– Intracranial HemorrhageIntracranial Hemorrhage
– StrokeStroke

Metabolic AlterationsMetabolic Alterations
– DKA & HNNKDKA & HNNK
– DI & SIADHDI & SIADH
– DICDIC
– Shock StatesShock States
– SepsisSepsis


OBJECTIVESOBJECTIVES
1.1. List the main functions of the kidney.List the main functions of the kidney.
2.2. List the common diagnostic tests associated with renal function.List the common diagnostic tests associated with renal function.
3.3. List the complications associated with acute renal failure.List the complications associated with acute renal failure.
4.4. Describe the common treatments of acute renal failure.Describe the common treatments of acute renal failure.
5.5. List the major signs & symptoms associated with electrolyte disturbances ofList the major signs & symptoms associated with electrolyte disturbances of
sodium, potassium magnesium and calcium and phosphorus.sodium, potassium magnesium and calcium and phosphorus.
6.6. Define serum osmolality.Define serum osmolality.
7.7. List the intracellular & extracellular fluid compartments of the body.List the intracellular & extracellular fluid compartments of the body.
8.8. Describe the effects of hypotonic, isotonic and hypertonic IV fluids.Describe the effects of hypotonic, isotonic and hypertonic IV fluids.
9.9. Describe the different treatments for intravascular depletion verses cellularDescribe the different treatments for intravascular depletion verses cellular
dehydration.dehydration.
10.10. Identify the risk factors and signs & symptoms of brain aneurysms andIdentify the risk factors and signs & symptoms of brain aneurysms and
AVM’s.AVM’s.
11.11. Explain the current treatments available for brain aneurysms and AVM’s.Explain the current treatments available for brain aneurysms and AVM’s.
12.12. Describe the different types of intracranial hemorrhage and their associatedDescribe the different types of intracranial hemorrhage and their associated
signs & symptoms.signs & symptoms.


OBJECTIVESOBJECTIVES
13.13. List the potential complications of associated with intracranial hemorrhages,List the potential complications of associated with intracranial hemorrhages,
brain aneurysms and AVM repairs.brain aneurysms and AVM repairs.
14.14. List the types of CVA’s, their risk factors and related pathophysiology.List the types of CVA’s, their risk factors and related pathophysiology.
15.15. Identify the recommended treatments for CVA’s.Identify the recommended treatments for CVA’s.
16.16. Differentiate between the signs and symptoms of DKA and HHNK.Differentiate between the signs and symptoms of DKA and HHNK.
17.17. Describe the treatment of DKA and HHNK.Describe the treatment of DKA and HHNK.
18.18. Differentiate between the signs and symptoms of DI and SIADH.Differentiate between the signs and symptoms of DI and SIADH.
19.19. Describe the treatment of DI and SIADH.Describe the treatment of DI and SIADH.
20.20. List the signs & symptoms of Disseminated Intravascular Coagulation.List the signs & symptoms of Disseminated Intravascular Coagulation.
21.21. Explain the treatments for disseminated intravascular coagulation.Explain the treatments for disseminated intravascular coagulation.
22.22. Understand the different stages of shock.Understand the different stages of shock.
23.23. Differentiate between different types of shock.Differentiate between different types of shock.
24.24. Identify the different treatments used for the different types of shock.Identify the different treatments used for the different types of shock.
25.25. Describe the stages of the sepsis syndrome.Describe the stages of the sepsis syndrome.
26.26. Explain the treatment of septic shock.Explain the treatment of septic shock.


Acute Renal FailureAcute Renal Failure

ElectrolytesElectrolytes

IV Fluid TherapyIV Fluid Therapy
RenalRenal AlterationsAlterations

AcuteAcute RenalRenal FailureFailure

WHAT DO THE KIDNEYS DO?WHAT DO THE KIDNEYS DO?
– Filter bloodFilter blood

Regulates electrolytesRegulates electrolytes
– Regulate blood pressureRegulate blood pressure

Renin-angiotensin system (RAS)Renin-angiotensin system (RAS)
– Maintain acid/base balanceMaintain acid/base balance

Removes wastes, detoxifies bloodRemoves wastes, detoxifies blood


WHAT ELSE DO THE KIDNEYS DO?WHAT ELSE DO THE KIDNEYS DO?
– Stimulate RBC productionStimulate RBC production

Make erythopoietinMake erythopoietin
– Make corticosteroidsMake corticosteroids

Regulate kidney functionRegulate kidney function
– Increase calcium absorptionIncrease calcium absorption

Convert Vitamin D to its active formConvert Vitamin D to its active form CalcitriolCalcitriol


GlomerulusGlomerulus
– Network of capillariesNetwork of capillaries

Bowman’sBowman’s capsulecapsule
– Membrane that surroundsMembrane that surrounds
the glomerulusthe glomerulus

Renal TubulesRenal Tubules
– Travel from cortex toTravel from cortex to
medulla and back to cortexmedulla and back to cortex

Collecting ductCollecting duct
– Within the medullaWithin the medulla
TheThe NephronNephron

TheThe KidneyKidney

The Renal Cortex ContainsThe Renal Cortex Contains
– Bowman's CapsulesBowman's Capsules
– GlomerulusGlomerulus
– Proximal TubulesProximal Tubules
– Distal Convoluted TubulesDistal Convoluted Tubules

The Renal Medulla ContainsThe Renal Medulla Contains
– The PyramidsThe Pyramids

Loop of HenleLoop of Henle

Collecting DuctCollecting Duct

Blood VesselsBlood Vessels


Lies within CortexLies within Cortex

Controls the activity ofControls the activity of
the nephronthe nephron

Plays major role in thePlays major role in the
renin-angiontension-renin-angiontension-
aldosterone systemaldosterone system
The Juxtaglomerular ApparatusThe Juxtaglomerular Apparatus


DEFINITIONSDEFINITIONS
– Sudden interruption of kidney function resultingSudden interruption of kidney function resulting
from obstruction, reduced circulation, or disease offrom obstruction, reduced circulation, or disease of
the renal tissuethe renal tissue
– Rapid deterioration of renal functionRapid deterioration of renal function

increase of creatinine of >0.5 mg/dl in <72hrsincrease of creatinine of >0.5 mg/dl in <72hrs

““azotemia” (accumulation of nitrogenous wastes)azotemia” (accumulation of nitrogenous wastes)

elevated BUN and Creatinine levelselevated BUN and Creatinine levels

decreased urine output (usually but not always)decreased urine output (usually but not always)


TERMINOLOGYTERMINOLOGY
– Anuria:Anuria: No UOP (or <100mL/24hrs)No UOP (or <100mL/24hrs)
– OliguriaOliguria:: UOP<400-500 mL/24hrsUOP<400-500 mL/24hrs
– AzotemiaAzotemia:: (Increased BUN, Cr, Urea)(Increased BUN, Cr, Urea)

May be prerenal, renal, postrenalMay be prerenal, renal, postrenal

Does not require any clinical findingsDoes not require any clinical findings
– Chronic Renal InsufficiencyChronic Renal Insufficiency

Deterioration over months-yearsDeterioration over months-years

GFR 10-20 mL/min, or 20-50% of normalGFR 10-20 mL/min, or 20-50% of normal
– ESRD:ESRD: GFR <5% of mL/minGFR <5% of mL/min


PERSONS AT RISKPERSONS AT RISK
– Major surgeryMajor surgery
– Major traumaMajor trauma
– Receiving nephrotoxic medicationsReceiving nephrotoxic medications
– Hypovolemia > 40 minutesHypovolemia > 40 minutes
– ElderlyElderly


SIGNS & SYMPTOMSSIGNS & SYMPTOMS
– AzotemiaAzotemia
– HyperkalemiaHyperkalemia
– Electrolyte DisturbancesElectrolyte Disturbances
⇑⇑ K+K+ ⇑⇑ phosphatephosphate
⇓⇓ Na+Na+ ⇓⇓ calciumcalcium
⇑⇑ CrCr ⇑⇑ BUNBUN
– Metabolic acidosisMetabolic acidosis
– Nausea/VomitingNausea/Vomiting
– Oliguria - anuriaOliguria - anuria
– HTNHTN
– HypovolemiaHypovolemia
– Pulmonary edemaPulmonary edema
– AscitesAscites
– Metabolic acidosisMetabolic acidosis
– AsterixisAsterixis
– EncephalopathyEncephalopathy


COMPLICATIONSCOMPLICATIONS
– Results in retention of toxins, fluids, and endResults in retention of toxins, fluids, and end
products of metabolismproducts of metabolism
– May be reversible with medical treatmentMay be reversible with medical treatment


DIAGNOSTIC TESTSDIAGNOSTIC TESTS
– H&PH&P
– BUN, creatinine, sodium, potassium, pH,BUN, creatinine, sodium, potassium, pH,
bicarb, Hgb and Hctbicarb, Hgb and Hct
– Urine studiesUrine studies
– US of kidneysUS of kidneys
– 24 hour urine for protein and creatinine24 hour urine for protein and creatinine
– Urine eosinophilsUrine eosinophils


OTHER DIAGNOSTIC TESTSOTHER DIAGNOSTIC TESTS
– Albumin, glucose, prealbuminAlbumin, glucose, prealbumin
– KUBKUB
– Abd and Renal CT/MRIAbd and Renal CT/MRI
– Retrograde pyloegramRetrograde pyloegram
– Renal biopsyRenal biopsy
– Post-void residual or catheterizationPost-void residual or catheterization


PHASESPHASES
– OnsetOnset

1-3 days with1-3 days with ⇑⇑ BUN andBUN and ⇑⇑ creatinine andcreatinine and
possible decreased UOPpossible decreased UOP
– OliguricOliguric

UOP < 400/day,UOP < 400/day, ⇑⇑ BUN,BUN, ⇑⇑ Cr,Cr, ⇑⇑ P04,P04, ⇑⇑ K, mayK, may
last up to 14 dayslast up to 14 days
– DiureticDiuretic

UOPUOP ⇑⇑ to as much as 4000 mL/day but withoutto as much as 4000 mL/day but without
waste products, may begin to see improvement atwaste products, may begin to see improvement at
end of this stageend of this stage
– RecoveryRecovery

Things go back to normal or may remainThings go back to normal or may remain
insufficient and become chronicinsufficient and become chronic


CAUSESCAUSES
– Pre-renalPre-renal (hypoperfusion)(hypoperfusion)
– RenalRenal (intrinsic)(intrinsic)
– Post-renalPost-renal (obstructive)(obstructive)


SPECIFIC CAUSESSPECIFIC CAUSES
– PrerenalPrerenal

Hypovolemia, shock, blood loss, embolism,Hypovolemia, shock, blood loss, embolism,
pooling of fluid due to ascites or burns,pooling of fluid due to ascites or burns,
cardiovascular disorders, sepsiscardiovascular disorders, sepsis
– IntrarenalIntrarenal

ATN, nephrotoxic agents, infections, ischemiaATN, nephrotoxic agents, infections, ischemia
acute tubular necrosis, acute nephritis, polycysticacute tubular necrosis, acute nephritis, polycystic
kidney diseasekidney disease
– PostrenalPostrenal

Stones, blood clots, BPH, urethral edema fromStones, blood clots, BPH, urethral edema from
invasive procedures, renal calculiinvasive procedures, renal calculi

Pre-Renal or Intra-Renal?Pre-Renal or Intra-Renal?
Pre-renal Intra-renal
BUN/Cr > 20 < 20
Urine Na
(mEq/L)
< 20 > 40
Urine
Specific Gravity
High Low
BUN/CR Ratio > 20:1 < 10-15:1


TREATMENTTREATMENT
– Make/consider the diagnosisMake/consider the diagnosis
– Treat life threatening conditionsTreat life threatening conditions
– Identify the cause if possibleIdentify the cause if possible

HypovolemiaHypovolemia

Toxic agents (drugs, myoglobin)Toxic agents (drugs, myoglobin)

ObstructionObstruction
– Treat reversible elementsTreat reversible elements

HydrateHydrate

Remove drugRemove drug

Relieve obstructionRelieve obstruction


NURSING CARENURSING CARE
– Fluid and dietary restrictionsFluid and dietary restrictions

Protein, potassium & phosphate restrictionProtein, potassium & phosphate restriction
– Maintain electrolytesMaintain electrolytes
– D/C or reduce causative agentD/C or reduce causative agent
– Adjust medication dosesAdjust medication doses
– May need dialysis to jump start renal functionMay need dialysis to jump start renal function
– May need to stimulate production of urine withMay need to stimulate production of urine with
IV fluids, Dopamine, diuretics, etc.IV fluids, Dopamine, diuretics, etc.


DIALYSISDIALYSIS
– HemodialysisHemodialysis
– Peritoneal DialysisPeritoneal Dialysis
– Continuous Renal Replacement Therapy (CRRT)Continuous Renal Replacement Therapy (CRRT)


TREATMENTTREATMENT
– Strict I&OStrict I&O
– Daily weightsDaily weights
– Watch for heart failureWatch for heart failure
– Monitor lab resultsMonitor lab results
– Watch for hyperkalemiaWatch for hyperkalemia
– Watch forWatch for
hyper/hypoglycemiahyper/hypoglycemia
– Maintain nutritionMaintain nutrition
– Mouth careMouth care
– Monitor skinMonitor skin
– S & S of Hyperkalemia: Malaise, anorexia,S & S of Hyperkalemia: Malaise, anorexia,
parenthesia, muscle weakness, EKG changesparenthesia, muscle weakness, EKG changes
Chronic RenalChronic Renal FailureFailure
S & S

BREAKBREAK

ElectrolyteElectrolyte
DisturbancesDisturbances
Na+
Ca++
Cl-
Mg+
K+
PO4
NH3
Cu
HCO3-
NaCl


Dominant intracellular electrolyteDominant intracellular electrolyte

Primary buffer in the cellPrimary buffer in the cell
K+K+
Potassium (KPotassium (K++))
Normal serum K+ level: 3.5-5.5 mEq/LNormal serum K+ level: 3.5-5.5 mEq/L


INVOLVED ININVOLVED IN
– Muscle contractionMuscle contraction
– Nerve impulsesNerve impulses
– Cell membrane functionCell membrane function
– Attracting water into the ICFAttracting water into the ICF
– Imbalances interfere with neuromuscular functionImbalances interfere with neuromuscular function
and may cause cardiac rhythm disturbancesand may cause cardiac rhythm disturbances
Potassium (KPotassium (K++))

HyperkalemiaHyperkalemia

– Weakness, malaise, lethargyWeakness, malaise, lethargy
– AnorexiaAnorexia
– Muscle crampsMuscle cramps
– ParesthesiasParesthesias
– DysrhythmiasDysrhythmias


K > 5.5 -6K > 5.5 -6

Tall, peaked T’sTall, peaked T’s

Wide QRSWide QRS

Prolong PRProlong PR

Diminished PDiminished P

Prolonged QTProlonged QT

QRS-T waveQRS-T wave
merge = “sine wave”merge = “sine wave”

Sine (Off) WaveSine (Off) Wave


CAUSESCAUSES
– Chronic or acute renal failureChronic or acute renal failure
– BurnsBurns
– Crush injuriesCrush injuries
– Excessive use of Potassium saltsExcessive use of Potassium salts


TREATMENTTREATMENT
– Calcium Gluconate (carbonate)Calcium Gluconate (carbonate)
– Calcium ChlorideCalcium Chloride
– Sodium BicarbonateSodium Bicarbonate
– Insulin/glucoseInsulin/glucose
– KayexalateKayexalate
– LasixLasix
– AlbuterolAlbuterol
– HemodialysisHemodialysis


–MalaiseMalaise
–Skeletal muscle weaknessSkeletal muscle weakness
–Decreased reflexesDecreased reflexes
–HypotensionHypotension
–VomitingVomiting
–Excessive thirstExcessive thirst
–Cardiac arrhythmias and cardiac arrestCardiac arrhythmias and cardiac arrest
–Flattened T waveFlattened T wave
–U waveU wave
HypokalemiaHypokalemia

HypokalemiaHypokalemia

CAUSESCAUSES
– Reduced dietary intakeReduced dietary intake
– Poor absorption by the bodyPoor absorption by the body
– Vomiting and/or diarrheaVomiting and/or diarrhea
– Renal diseaseRenal disease
– Medications (typically diuretics)Medications (typically diuretics)

Hypo Verses Hyper PotassiumHypo Verses Hyper Potassium

 SIGNS & SYMPTOMSSIGNS & SYMPTOMS
– Cold, clammy, pale skinCold, clammy, pale skin
– NervousnessNervousness
– Shakiness, lack of coordination, staggering gaitShakiness, lack of coordination, staggering gait
– Irritability, hostility, and strange behaviorIrritability, hostility, and strange behavior
– Difficulty concentratingDifficulty concentrating
– FatigueFatigue
– Excessive hungerExcessive hunger
– HeadacheHeadache
– Blurred vision and dizzinessBlurred vision and dizziness
– Abdominal pain or nauseaAbdominal pain or nausea
– Fainting and unconsciousnessFainting and unconsciousness
HypoglycemiaHypoglycemia

Cardiovascular SignsCardiovascular Signs
PalpitationsPalpitations
TachycardiaTachycardia
AnxietyAnxiety
IrritabilityIrritability
DiaphoresisDiaphoresis
Pale, cool skinPale, cool skin
TachypneaTachypnea
Neurological SignsNeurological Signs
AgitationAgitation
ConfusionConfusion
Slurred SpeechSlurred Speech
Staggering GaitStaggering Gait
ParaplegiaParaplegia
SeizuresSeizures
ComaComa
Acute HypoglycemiaAcute Hypoglycemia


– ThirstThirst
– PolyuriaPolyuria
– DehydrationDehydration
– Nausea, vomitingNausea, vomiting
– DKADKA
– HNNKHNNK
HyperglycemiaHyperglycemia
Normal serum Glu level:Normal serum Glu level: 70 - 110 mg/dL70 - 110 mg/dL


Dominant extracellur electrolyteDominant extracellur electrolyte

Chief determinant of osmolalityChief determinant of osmolality
NaClNaCl
Sodium (NaSodium (Na++))
Normal serum Na+ level: 135-145 mEq/LNormal serum Na+ level: 135-145 mEq/L


– Deficiency of sodium in the bloodDeficiency of sodium in the blood
– HypotensionHypotension
– TachycardiaTachycardia
– Muscle weaknessMuscle weakness
– Mental ConfusionMental Confusion
HyponatremiaHyponatremia


– Excess sodium in the bloodExcess sodium in the blood
– HypertensionHypertension
– Muscle twitchingMuscle twitching
– Mental confusionMental confusion
– ComaComa
HypernatremiaHypernatremia


Activates many enzymesActivates many enzymes

50% is insoluble in bone50% is insoluble in bone

45% is intracellular45% is intracellular

5% is extracellular5% is extracellular
Mg+Mg+
Magnesium (MgMagnesium (Mg++))
Normal serum Mg+ level: 1.5 - 2.5 mg/dLNormal serum Mg+ level: 1.5 - 2.5 mg/dL


– TremorsTremors
– Positive Chvostek & TrousseauPositive Chvostek & Trousseau
– NystagmusNystagmus
– Confusion/HallucinationsConfusion/Hallucinations
– DiarrheaDiarrhea
– Hyperactive deep reflexesHyperactive deep reflexes
– SeizuresSeizures
HypomagnesemiaHypomagnesemia
– DysrhythmiasDysrhythmias
– ECG ChangesECG Changes

Flat T waveFlat T wave

ST interval depressionST interval depression

Prolonged QT intervalProlonged QT interval
– May lead toMay lead to
Torsade deTorsade de
PointesPointes


CAUSESCAUSES
–AlcoholismAlcoholism
–MalabsorptionMalabsorption
–StarvationStarvation
–DiarrheaDiarrhea
–DiuresisDiuresis
HypomagnesemiaHypomagnesemia


– Peaked T wavePeaked T wave
– BradycardiaBradycardia
– CNS DepressionCNS Depression
– AreflexiaAreflexia
– SedationSedation
– Respiratory paralysisRespiratory paralysis
HypermagnesemiaHypermagnesemia


CAUSESCAUSES
– Not commonNot common
– Occurs with chronic renal insufficiencyOccurs with chronic renal insufficiency
– Treatment is hemodialysisTreatment is hemodialysis
HypermagnesemiaHypermagnesemia

– ESSENTIAL FORESSENTIAL FOR
– Neuromuscular transmissionNeuromuscular transmission
– Growth and ossification of bonesGrowth and ossification of bones
Ca++Ca++
Calcium (CaCalcium (Ca++++))
Normal serum Ca++ level: 8 - 11 mg/dLNormal serum Ca++ level: 8 - 11 mg/dL

– INVOLVED ININVOLVED IN
– Blood clottingBlood clotting
– Nerve impulseNerve impulse
Ca++Ca++
Calcium (CaCalcium (Ca++++))
Excreted through urine, feces, and perspirationExcreted through urine, feces, and perspiration


– TetanyTetany (cramps/convulsions in wrists and ankles)(cramps/convulsions in wrists and ankles)
– Weak heart muscleWeak heart muscle
– Increased clotting timeIncreased clotting time
– Prolonged QT intervalProlonged QT interval

May lead to Torsade de PointesMay lead to Torsade de Pointes
– Abnormal behaviorAbnormal behavior
– Chvostek's sign (facial twitching)Chvostek's sign (facial twitching)
– Trousseau”s Sign (carpopedal spasm)Trousseau”s Sign (carpopedal spasm)
– ParesthesiaParesthesia
HypocalcemiaHypocalcemia


CAUSESCAUSES
– Renal insufficiencyRenal insufficiency
– Decreased intake or malabsorption of CalciumDecreased intake or malabsorption of Calcium
– Deficiency in or inability to activate Vitamin DDeficiency in or inability to activate Vitamin D
HypocalcemiaHypocalcemia


– Kidney stonesKidney stones
– Bone painBone pain
– Hypotonicity of musclesHypotonicity of muscles (decreased tone)(decreased tone)
– Altered mental statusAltered mental status
– Cardiac arrhythmiasCardiac arrhythmias
– Shortened QT intervalShortened QT interval
HypercalcemiaHypercalcemia


CAUSESCAUSES
– Neoplasms (tumors)Neoplasms (tumors)
– Excessive administration of Vitamin DExcessive administration of Vitamin D
HypercalcemiaHypercalcemia

TREATMENTTREATMENT
– Usually aimed at underlying disease andUsually aimed at underlying disease and
hydrationhydration
– Severe hypercalcemia may be treated withSevere hypercalcemia may be treated with
forced diuresisforced diuresis


INVOLVED ININVOLVED IN
–Energy metabolismEnergy metabolism
–Genetic codingGenetic coding
–Cell functionCell function
–Bone formationBone formation
POPO44
Phosphorus (P, POPhosphorus (P, PO44))
Normal serum PO4 level: 2.5-4.5 mg/dLNormal serum PO4 level: 2.5-4.5 mg/dL


– Respiratory difficultyRespiratory difficulty
– ConfusionConfusion
– IrritabilityIrritability
– ComaComa
HypophosphatemiaHypophosphatemia


CAUSESCAUSES
– Severe infectionsSevere infections
– Kidney failureKidney failure
– Thyroid failureThyroid failure
– Parathyroid FailureParathyroid Failure
– Often associated with hypercalcemia orOften associated with hypercalcemia or
hypomagnesemia or too much Vitamin Dhypomagnesemia or too much Vitamin D
– Cell destruction - from chemotherapy, when theCell destruction - from chemotherapy, when the
tumor cells die at a fast ratetumor cells die at a fast rate

Can cause tumor lysis syndromeCan cause tumor lysis syndrome
HypophosphatemiaHypophosphatemia


– Elevated blood phosphate levelElevated blood phosphate level
– There are no symptoms of hyperphosphatemiaThere are no symptoms of hyperphosphatemia
HyperphosphatemiaHyperphosphatemia


TREATMENTTREATMENT
– Calcium Carbonate tabletsCalcium Carbonate tablets
– Aluminum hydroxideAluminum hydroxide

Can cause aluminum toxicityCan cause aluminum toxicity
HyperphosphatemiaHyperphosphatemia


OSMOLALITYOSMOLALITY
– Concentration of a solutionConcentration of a solution
– Concentration of solutes per kilogramConcentration of solutes per kilogram
– The higher the osmolality the greaterThe higher the osmolality the greater
its pulling power for waterits pulling power for water
Normal serum osmolality isNormal serum osmolality is 275 to 295275 to 295 mOsm/LmOsm/L

Serum OsmolalitySerum Osmolality

Sodium = major solute in plasmaSodium = major solute in plasma
– Estimated serum osmolality = 2 X serum NaEstimated serum osmolality = 2 X serum Na

Urea (BUN) and Glucose are large moleculesUrea (BUN) and Glucose are large molecules
thatthat ↑↑ serum osmolalityserum osmolality
– When either or both are elevated, the serum osmolalityWhen either or both are elevated, the serum osmolality
will be higher than 2 times the sodium level, so thewill be higher than 2 times the sodium level, so the
following formula is more accurate:following formula is more accurate:
Serum osmolality = 2 X serum Na +Serum osmolality = 2 X serum Na + BUNBUN ++ glucoseglucose
3 183 18

Major Mediators ofMajor Mediators of
Sodium and Water BalanceSodium and Water Balance

Angiotensin IIAngiotensin II

AldosteroneAldosterone

Antidiuretic hormone (ADH)Antidiuretic hormone (ADH)

Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone
Angiotensin IIAngiotensin II  1. Stimulates production of aldosterone1. Stimulates production of aldosterone
2. Acts directly on arterioles to cause vasoconstriction2. Acts directly on arterioles to cause vasoconstriction
3. Stimulates Na3. Stimulates Na++
/H/H++
exchange in the proximal tubuleexchange in the proximal tubule
AldosteroneAldosterone  1. Stimulates reabsorption of Na1. Stimulates reabsorption of Na++
and excretion of Kand excretion of K++
inin
the late distal tubulethe late distal tubule
2. Stimulates activity of H2. Stimulates activity of H++
ATPase pumps in the lateATPase pumps in the late
distal tubuledistal tubule

Antidiuretic Hormone (ADH)Antidiuretic Hormone (ADH)

Synthesized in the hypothalamus and stored in theSynthesized in the hypothalamus and stored in the
posterior pituitaryposterior pituitary

Released in response to plasma hyperosmolalityReleased in response to plasma hyperosmolality
and decreased circulating volumeand decreased circulating volume

Actions of ADHActions of ADH
– Increases the water permeability of the collecting tubuleIncreases the water permeability of the collecting tubule
(makes kidneys reabsorb more water)(makes kidneys reabsorb more water)
– Mildly increases vascular resistanceMildly increases vascular resistance

IsotonicIsotonic – same osmolality as serum– same osmolality as serum
HypotonicHypotonic – lower osmolality than serum– lower osmolality than serum
HypertonicHypertonic – higher osmolality than serum– higher osmolality than serum

Effect on CellsEffect on Cells

IV SolutionsIV Solutions
D5WD5W Hypotonic in the bodyHypotonic in the body
HypotonicHypotonic
SolutionsSolutions
Used for cellular dehydrationUsed for cellular dehydration
Not used with head injuriesNot used with head injuries
IsotonicIsotonic
SolutionsSolutions
Hydrates extracellular compartmentHydrates extracellular compartment
HypertonicHypertonic
SolutionsSolutions
Pulls fluid into vascular spacePulls fluid into vascular space

IV SolutionsIV Solutions
D5WD5W
D10WD10W
D50WD50W
½ NS½ NS
NSNS
D51/2 NSD51/2 NS
D5NSD5NS
D5WD5W Hypotonic in the bodyHypotonic in the body
IsotonicIsotonic
HypotonicHypotonic
IsotonicIsotonic
IsotonicIsotonic
3% NaCl3% NaCl
LRLR
D5LRD5LR
AlbuminAlbumin
DextranDextran
HetastarchHetastarch
PRBC’sPRBC’s

Daily Fluid BalanceDaily Fluid Balance
Intake:Intake:
1-1.5 L1-1.5 L
Insensible LossInsensible Loss
- Lungs 0.3 L- Lungs 0.3 L
- Sweat 0.1 L- Sweat 0.1 L
Urine: 1.0 to 1.5 LUrine: 1.0 to 1.5 L

IntracellularIntracellular
(2/3)(2/3)
ExtracellularExtracellular
(1/3)(1/3)
Solids 40% of WtSolids 40% of Wt
HH22OO HH22OO
NaNa

Intra-Intra-
vascularvascular
((1/4)1/4)
E.CE.C..FF.. COMPARTMENTSCOMPARTMENTS
Interstitial (3/4)Interstitial (3/4)
HH22OO HH22OO
NaNaNaNa
ColloidsColloids
& RBC’s& RBC’s

““Third Space”Third Space”

Third space refers to collection of fluids (usuallyThird space refers to collection of fluids (usually
isotonic) that is sequestered in potential spaces.isotonic) that is sequestered in potential spaces.

This situation is not normal and the fluid is derivedThis situation is not normal and the fluid is derived
from extracellular fluid.from extracellular fluid.

Principles of TreatmentPrinciples of Treatment

How much volume?How much volume?
– Need to estimate fluid deficitNeed to estimate fluid deficit

Which fluid?Which fluid?
– Which fluid compartment is predominantly affected?Which fluid compartment is predominantly affected?
– Must evaluate other acid/base, electrolyte &Must evaluate other acid/base, electrolyte &
nutrition needsnutrition needs

Fluid Replacement ProductsFluid Replacement Products

CrystalloidsCrystalloids –– able to pass through semi permeable membranesable to pass through semi permeable membranes
–Isotonic solutionsIsotonic solutions
–Hypotonic solutionsHypotonic solutions
–Hypertonic solutionsHypertonic solutions

ColloidsColloids – do not cross the semi permeable membrane and remain– do not cross the semi permeable membrane and remain
in the intravascular space for several days (pulling fluidin the intravascular space for several days (pulling fluid
out of the intracellular and interstitial space)out of the intracellular and interstitial space)
–AlbuminAlbumin
–DextranDextran
–HetastarchHetastarch

1 liter 5% Albumin1 liter 5% Albumin
IntravascularIntravascular
=1 liter=1 liter
Total body waterTotal body water
ECFECF
ICFICF

ECF=1 literECF=1 liter ICF=0ICF=0
=1/4 ECF=250 ml=1/4 ECF=250 ml
1 Liter 0.9% saline1 Liter 0.9% saline
Interstitial=3/4Interstitial=3/4
of ECF=750mlof ECF=750ml

1 liter 5% Dextrose1 liter 5% Dextrose
ECF=1/3 = 300mlECF=1/3 = 300ml ICF=2/3 = 700mlICF=2/3 = 700ml
=1/4 of ECF~75ml=1/4 of ECF~75ml

Ringers LactateRingers Lactate

Infusion of Ringer Lactate solution may lead to metabolicInfusion of Ringer Lactate solution may lead to metabolic
alkalosis because of the presence of lactate ionsalkalosis because of the presence of lactate ions

Lactated Ringer’s should be used with great care withLactated Ringer’s should be used with great care with
patients with hyperkalemia, severe renal failure, andpatients with hyperkalemia, severe renal failure, and
hepatic insufficiencyhepatic insufficiency

Solutions containing lactate are not for use in theSolutions containing lactate are not for use in the
treatment of lactic acidosistreatment of lactic acidosis

NeurologicalNeurological AlterationsAlterations

Brain Aneurysms & AVM’sBrain Aneurysms & AVM’s

Intracranial HemorrhageIntracranial Hemorrhage

StrokeStroke

CerebralCerebral SpinalSpinal FluidFluid
The serum-like fluid that circulates through the ventricles of theThe serum-like fluid that circulates through the ventricles of the
brain, the cavity of the spinal cord, and the subarachnoid spacebrain, the cavity of the spinal cord, and the subarachnoid space

Spinal Cord Nerve TractsSpinal Cord Nerve Tracts
Ascending
Sensory
Tract
Descending
Motor Tract
(Corticospinal Tract)
(Spinothalmic Tract)

Brown-Séquard syndromeBrown-Séquard syndrome
Incomplete
Spinal Cord
Injury
(Hemi-section)

Central Cord SyndromeCentral Cord Syndrome
Walking
Quads

Homonymous HemianopiaHomonymous Hemianopia

 Brain AneurysmBrain Aneurysm
– An intracranial aneurysm is a weak or thin spot on a bloodAn intracranial aneurysm is a weak or thin spot on a blood
vessel in the brain that balloons out and fills with bloodvessel in the brain that balloons out and fills with blood
 AV Malformation (AVM)AV Malformation (AVM)
– Arteriovenous malformation (AVM)Arteriovenous malformation (AVM) of the brain is a "shortof the brain is a "short
circuit“circuit“ between the arteries and veinsbetween the arteries and veins
Brain Aneurysms & AVM’sBrain Aneurysms & AVM’s

Intracranial AneurysmsIntracranial Aneurysms

Usually occur at bifurcations and branches of theUsually occur at bifurcations and branches of the
large arterieslarge arteries located in the Circle of Willislocated in the Circle of Willis

The most common sites include the:The most common sites include the:
– Anterior Communicating artery (30 - 35%)Anterior Communicating artery (30 - 35%)
– Bifurcation of the Internal Carotid and PosteriorBifurcation of the Internal Carotid and Posterior
Communicating artery (30 - 35%)Communicating artery (30 - 35%)
– Bifurcation of Middle cerebral (20%)Bifurcation of Middle cerebral (20%)
– Basilar artery bifurcation (5%)Basilar artery bifurcation (5%)
– Remaining posterior circulation arteries (5%)Remaining posterior circulation arteries (5%)

Types of AneurysmsTypes of Aneurysms
 Saccular aneurysmSaccular aneurysm
– Occurs at bifurcationsOccurs at bifurcations
 Fusiform aneurysmFusiform aneurysm
– Often in basilar arteryOften in basilar artery
 Dissecting aneurysmDissecting aneurysm
 Ruptured aneurysmRuptured aneurysm

Brain CirculationBrain Circulation

Arterial Circulation in the BrainArterial Circulation in the Brain


RISK FACTORSRISK FACTORS
– SmokingSmoking
– Coarctation of the aortaCoarctation of the aorta
– Dissections/traumaDissections/trauma
– Intracranial neoplasmIntracranial neoplasm
– Polycystic kidney diseasePolycystic kidney disease
– Abnormal vessels or High-flow states (eg, vascularAbnormal vessels or High-flow states (eg, vascular
malformations, fistulae)malformations, fistulae)
– HypercholesterolemiaHypercholesterolemia
– Connective tissue disorders (eg, Marfan, Ehlers-Danlos)Connective tissue disorders (eg, Marfan, Ehlers-Danlos)


– Usually asymptomatic until ruptureUsually asymptomatic until rupture

Cranial Nerve PalsyCranial Nerve Palsy

Dilated PupilsDilated Pupils

Double VisionDouble Vision

Pain Above and Behind EyePain Above and Behind Eye

Localized HeadacheLocalized Headache
– Warning signs prior ruptureWarning signs prior rupture

Localized HeadacheLocalized Headache

Nausea & VomitingNausea & Vomiting

Stiff NeckStiff Neck

Blurred or Double VisionBlurred or Double Vision

Sensitivity to Light (photophobia)Sensitivity to Light (photophobia)

Loss of SensationLoss of Sensation

Treatment of Brain AneurysmsTreatment of Brain Aneurysms

SurgerySurgery
–– Craniotomy and clippingCraniotomy and clipping

Endovascular coilingEndovascular coiling

Aneurysm Post-Op RisksAneurysm Post-Op Risks

RebleedingRebleeding
– Most frequently within the first 24 hoursMost frequently within the first 24 hours
– Up to 20% of patients rebleed within 14 daysUp to 20% of patients rebleed within 14 days
– Main preventative measure is control of blood pressureMain preventative measure is control of blood pressure
(preferably beta blockers)(preferably beta blockers)

VasospasmVasospasm
– Usually occurs before 3 days or after 10 days (post bleed)Usually occurs before 3 days or after 10 days (post bleed)
– May require hypervolemic therapyMay require hypervolemic therapy

HydrocephalusHydrocephalus


Fluids / ElectrolytesFluids / Electrolytes

Arterio-Venous MalformationArterio-Venous Malformation

 The arteries and veins have a direct connection,The arteries and veins have a direct connection,
bypassing the capillary networkbypassing the capillary network
 Presents with ongoing headaches, seizures,Presents with ongoing headaches, seizures,
hemorrhage, or progressive neurologicalhemorrhage, or progressive neurological
dysfunctiondysfunction


– HeadachesHeadaches
– ““Whooshing" Sound (Bruit)Whooshing" Sound (Bruit)
– Other SignsOther Signs

Subtle behavioral changesSubtle behavioral changes

Communication or thinking disturbancesCommunication or thinking disturbances

Loss of coordination and balanceLoss of coordination and balance

Paralysis or weakness in one part of the bodyParalysis or weakness in one part of the body

Visual disturbancesVisual disturbances

Abnormal sensationsAbnormal sensations


COMPLICATIONSCOMPLICATIONS
– HemorrhageHemorrhage (into surrounding tissue)(into surrounding tissue)
– IschemiaIschemia
– Brain Cell DeathBrain Cell Death


DIAGNOSISDIAGNOSIS
– MRIMRI (including MR Angiography) as well as(including MR Angiography) as well as CTCT
Angiography help identify AVM’sAngiography help identify AVM’s
– Cerebral AngiographyCerebral Angiography is a prerequisite tois a prerequisite to
treatmenttreatment

To identify the precise anatomy and configurationTo identify the precise anatomy and configuration
of both the lesion and the feeding and drainingof both the lesion and the feeding and draining
vesselsvessels


TREATMENTTREATMENT
– SurgerySurgery

Usually delayedUsually delayed

Open ligation and/or resection of the AVMOpen ligation and/or resection of the AVM
– RadiosurgeryRadiosurgery
– EmbolizationEmbolization

Usually as adjunct to surgeryUsually as adjunct to surgery
– ObservationObservation


RADIOSURGERYRADIOSURGERY
– Believed to "work" by initiating an "inflammatory"Believed to "work" by initiating an "inflammatory"
response in the pathological blood vesselsresponse in the pathological blood vessels
ultimately resulting in their progressive narrowingultimately resulting in their progressive narrowing
and ultimate closureand ultimate closure
– The risk for hemorrhage is not reduced during thisThe risk for hemorrhage is not reduced during this
lag timelag time
– There is the added risk of radiation necrosis ofThere is the added risk of radiation necrosis of
adjacent healthy brain tissue or brain cyst formationadjacent healthy brain tissue or brain cyst formation

Brain RadiosurgeryBrain Radiosurgery

ADVANTAGESADVANTAGES
– NoninvasiveNoninvasive
– Can access all anatomic locations of the brainCan access all anatomic locations of the brain

DISADVANTAGESDISADVANTAGES
– Can only treat smaller lesionsCan only treat smaller lesions
(<3 cm in diameter)(<3 cm in diameter)
– Requires 2 or more years to completeRequires 2 or more years to complete

AVM Post-Op RisksAVM Post-Op Risks

Perfusion-breakthrough bleedingPerfusion-breakthrough bleeding

Endovascular occlusionEndovascular occlusion

Sudden onset of “the worst headache of my life”Sudden onset of “the worst headache of my life”
IntracranialIntracranial HemorrhageHemorrhage


EpiduralEpidural

SubduralSubdural

SubarachnoidSubarachnoid

IntraparencymalIntraparencymal

IntraventricularIntraventricular

CerebellarCerebellar


ICH is a dynamic, not a static processICH is a dynamic, not a static process

Hemorrhage volume can increase over timeHemorrhage volume can increase over time

CT scan is the most important diagnostic toolCT scan is the most important diagnostic tool

Managing blood pressure is extremely importantManaging blood pressure is extremely important

Must aggressively manage fever and seizuresMust aggressively manage fever and seizures

Consider hyperventilation and paralytics in settingConsider hyperventilation and paralytics in setting
of increased ICP and deteriorationof increased ICP and deterioration

Treatment of ICHTreatment of ICH

KEY CONCEPTSKEY CONCEPTS
1)1) Intracranial PressureIntracranial Pressure
– Elevated when ICP >20 mm HgElevated when ICP >20 mm Hg
2)2) Cerebral Perfusion PressureCerebral Perfusion Pressure
– CPP = MAP - ICPCPP = MAP - ICP
– Must maintain CPP > 70 mm HgMust maintain CPP > 70 mm Hg
– Example: MAP = 100, ICP = 20Example: MAP = 100, ICP = 20
CPP = 80 mmHgCPP = 80 mmHg

Subarachnoid Hemorrhage (SAH)Subarachnoid Hemorrhage (SAH)

DEFINITIONDEFINITION
–When a blood vessel just outside the brain ruptures, theWhen a blood vessel just outside the brain ruptures, the
area of the skull surrounding the brain (the subarachnoidarea of the skull surrounding the brain (the subarachnoid
space) rapidly fills with bloodspace) rapidly fills with blood


–Sudden, intense headacheSudden, intense headache
–Neck painNeck pain
–Nausea or vomitingNausea or vomiting
–Neck stiffnessNeck stiffness
–PhotophobiaPhotophobia
Sudden onset of “the worst headache of my life”Sudden onset of “the worst headache of my life”


SAH may be spontaneous or traumaticSAH may be spontaneous or traumatic

Spontaneous SAH causesSpontaneous SAH causes
–Cerebral aneurysmsCerebral aneurysms
–AV malformationsAV malformations
–TraumaTrauma

Uncommon causesUncommon causes
–Neoplasms, venous angiomas, infectionsNeoplasms, venous angiomas, infections


Warning bleeds” are relatively commonWarning bleeds” are relatively common

Sentinel headache 30-50%Sentinel headache 30-50%

Early diagnosis prior to rupture will improve outcomesEarly diagnosis prior to rupture will improve outcomes

50% of patients die within 48 hours irrespective of50% of patients die within 48 hours irrespective of
therapytherapy
Subarachnoid HemorrhageSubarachnoid Hemorrhage


Often accompanied by a period of unconsciousnessOften accompanied by a period of unconsciousness
(50% never wake up)(50% never wake up)

Common signs include neck stiffness, photophobia,Common signs include neck stiffness, photophobia,
headacheheadache

20% have ECG evidence of myocardial ischemia20% have ECG evidence of myocardial ischemia
Subarachnoid HemorrhageSubarachnoid Hemorrhage

Complications of SAHComplications of SAH

HydrocephalusHydrocephalus may develop within the first 24may develop within the first 24
hours because of obstruction of CSF outflow in thehours because of obstruction of CSF outflow in the
ventricular system by clotted bloodventricular system by clotted blood

RebleedingRebleeding of SAH occurs in 20% of patients in theof SAH occurs in 20% of patients in the
first 2 weeks. Peak incidence of rebleeding occurs the dayfirst 2 weeks. Peak incidence of rebleeding occurs the day
after SAH and may be from lysis of the aneurysmal clotafter SAH and may be from lysis of the aneurysmal clot

VasospasmVasospasm from arterial smooth muscle contractionfrom arterial smooth muscle contraction
(symptomatic in 36% of patients)(symptomatic in 36% of patients)

Re-bleeding After SAHRe-bleeding After SAH

Re-bleeding occurs most frequently within the first 24 hrsRe-bleeding occurs most frequently within the first 24 hrs

Up to 20% of patients rebleed within 14 daysUp to 20% of patients rebleed within 14 days

The main preventative measure is to control the bloodThe main preventative measure is to control the blood
pressure – preferably beta blockerspressure – preferably beta blockers

Early clipping of the aneurysm allows hypertensive andEarly clipping of the aneurysm allows hypertensive and
hypervolemic therapy to prevent vasospasmhypervolemic therapy to prevent vasospasm

Vasospasm After SAHVasospasm After SAH

Worst time is day 7 to day 10 (most frequent time forWorst time is day 7 to day 10 (most frequent time for
vasospasms)vasospasms)

Diagnosed by neurologic exam, transcranial doppler andDiagnosed by neurologic exam, transcranial doppler and
angiographyangiography

May use calcium channel blockersMay use calcium channel blockers
– Reduces vasospasm, neurological deficit, cerebral infarctionReduces vasospasm, neurological deficit, cerebral infarction
and mortalityand mortality

May use some antispasmodicsMay use some antispasmodics

Vasospasm & HHH TherapyVasospasm & HHH Therapy

HemodilutionHemodilution
–Hct 30-35%Hct 30-35%

HypertensionHypertension
–Phenylephrine / NorepinephrinePhenylephrine / Norepinephrine
–BP titration to CPP/examBP titration to CPP/exam

HypervolemiaHypervolemia
–Colloids/crystalloidsColloids/crystalloids

Other Vasospasm TherapyOther Vasospasm Therapy

AngioplastyAngioplasty
–BP management during procedureBP management during procedure
–Reperfusion issuesReperfusion issues
–TimingTiming

Papaverine InfusionPapaverine Infusion
–Side effectsSide effects
–Repeated tripsRepeated trips


Neurologic deficitsNeurologic deficits from cerebral ischemia, peaks at days 4-12from cerebral ischemia, peaks at days 4-12

Hypothalamic dysfunctionHypothalamic dysfunction causes excessive sympatheticcauses excessive sympathetic
stimulation, which may lead to myocardial ischemia or labile BPstimulation, which may lead to myocardial ischemia or labile BP

HyponatremiaHyponatremia may result from cerebral salt wasting / SIADHmay result from cerebral salt wasting / SIADH

Nosocomial pneumoniaNosocomial pneumonia and other such complicationsand other such complications

Pulmonary edemaPulmonary edema neurogenic & non-neurogenicneurogenic & non-neurogenic
Other Complications of SAHOther Complications of SAH

1)1) Identify and treat the causative lesionIdentify and treat the causative lesion
– Thus preventing re-bleedingThus preventing re-bleeding
1)1) Treat hydrocephalusTreat hydrocephalus
2)2) Treating and prevent vasospasmTreating and prevent vasospasm
Treatment of SAHTreatment of SAH


Maintain systolic BP >130mmHgMaintain systolic BP >130mmHg
– Use vasopressors if necessary to maintain CPPUse vasopressors if necessary to maintain CPP
and reduce ischemic complications from vasospasmand reduce ischemic complications from vasospasm
– Generally avoid vasodilators (except calciumGenerally avoid vasodilators (except calcium
channel blockers)channel blockers)
Treatment of SAHTreatment of SAH

 RISK FACTORSRISK FACTORS
 TIATIA
 CADCAD
 High Blood PressureHigh Blood Pressure
 High CholesterolHigh Cholesterol
 SmokingSmoking
 Heart DiseaseHeart Disease
 DiabetesDiabetes
 Excessive alcoholExcessive alcohol
 Family HistoryFamily History
 AgeAge
 SexSex
 RaceRace
 ObesityObesity
Annual risk of stroke: Increases with ageAnnual risk of stroke: Increases with age
StrokeStroke


Computed Tomography (CT)Computed Tomography (CT)

Magnetic Resonance Imaging (MRI)Magnetic Resonance Imaging (MRI)

Cerebral Angiography: identify responsible vesselCerebral Angiography: identify responsible vessel

Carotid Ultrasound: carotid artery stenosisCarotid Ultrasound: carotid artery stenosis

Echocardiogram: identify blood clot from heartEchocardiogram: identify blood clot from heart

Electrocardiogram (ECG): underlying heart conditionsElectrocardiogram (ECG): underlying heart conditions

Heart monitors, blood work and more tests!!Heart monitors, blood work and more tests!!
Stroke TestsStroke Tests

CT MRICT MRI
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http://www.strokecenter.org/education/ais_ct_tool/index.htmhttp://www.strokecenter.org/education/ais_ct_tool/index.htm


Tissue plasminogen activator (tPA) can be givenTissue plasminogen activator (tPA) can be given
within three hours from the onset of symptomswithin three hours from the onset of symptoms

HeparinHeparin

Intra-arterial thrombolysisIntra-arterial thrombolysis

HemicraniectomyHemicraniectomy

In addition to being used to treat strokes, theIn addition to being used to treat strokes, the
following can also be used as preventativefollowing can also be used as preventative
measuresmeasures
–Anticoagulants/AntiplateletsAnticoagulants/Antiplatelets
–Carotid EndarterectomyCarotid Endarterectomy
–Angioplasty/StentsAngioplasty/Stents
Treatment of Ischemic CVATreatment of Ischemic CVA


Surgery is often required to remove pooled bloodSurgery is often required to remove pooled blood
from the brain and to repair damaged blood vesselsfrom the brain and to repair damaged blood vessels

Prevention:Prevention:
– An obstruction is introduced to prevent rupture andAn obstruction is introduced to prevent rupture and
bleeding of aneurysms and AVM’sbleeding of aneurysms and AVM’s
– Surgical InterventionSurgical Intervention
– Endovascular ProceduresEndovascular Procedures
Treatment of Hemorrhagic CVATreatment of Hemorrhagic CVA


Control high Blood PressureControl high Blood Pressure

Lower cholesterolLower cholesterol

Quit smokingQuit smoking

Control diabetesControl diabetes

Maintain healthy weightMaintain healthy weight

ExerciseExercise

Manage stressManage stress

Eat a healthy dietEat a healthy diet
Prevention of CVAPrevention of CVA


DKA & HHNKDKA & HHNK

DI & SIADHDI & SIADH

DICDIC

Shock StatesShock States

SepsisSepsis
MetabolicMetabolic AlterationsAlterations

Diabetic KetoacidosisDiabetic Ketoacidosis

What is DKA?What is DKA?
– Diabetic KetoacidosisDiabetic Ketoacidosis
– A life-threatening complication seen withA life-threatening complication seen with
Diabetes Mellitus Type 1Diabetes Mellitus Type 1


– Serum Glucose 300-800Serum Glucose 300-800
– Ketoacidosis PresentKetoacidosis Present
– Large Serum And Urine KetonesLarge Serum And Urine Ketones
– Fruity BreathFruity Breath
– Kussmaul RespirationsKussmaul Respirations
– Serum pH < 7.3Serum pH < 7.3
– DehydrationDehydration
Diabetic KetoacidosisDiabetic Ketoacidosis

HHNKHHNK

What is HHNK?What is HHNK?
– Hyperglycemic Hyperosmolar Nonketonic ComaHyperglycemic Hyperosmolar Nonketonic Coma
– A life threatening complication seen withA life threatening complication seen with
Diabetes Mellitus Type 2Diabetes Mellitus Type 2


– Serum Glucose 600-2000Serum Glucose 600-2000
– Ketoacidosis Not PresentKetoacidosis Not Present
– Absent Or Slight Serum And Urine KetonesAbsent Or Slight Serum And Urine Ketones
– Normal BreathNormal Breath
– Shallow RespirationsShallow Respirations
– Serum pH NormalSerum pH Normal
– Severe DehydrationSevere Dehydration
HHNKHHNK

DKA vs HHNKDKA vs HHNK
DKADKA
 Faster OnsetFaster Onset
 Glucose 300-800Glucose 300-800
 AcidosisAcidosis
 Fruity BreathFruity Breath
 Kussmaul RespirationsKussmaul Respirations
HHNKHHNK
 Slower OnsetSlower Onset
 Glucose 600-2000Glucose 600-2000
 No AcidosisNo Acidosis
 Normal BreathNormal Breath
 Shallow RespirationsShallow Respirations

Treatment of DKA & HHNKTreatment of DKA & HHNK

Reverse DehydrationReverse Dehydration
NS, then ½ NSNS, then ½ NS

Restore Glucose LevelsRestore Glucose Levels
DD55 ½ NS When Glu 250½ NS When Glu 250

Restore ElectrolytesRestore Electrolytes

Diabetes InsipitusDiabetes Insipitus

What is Diabetes Insipitus?What is Diabetes Insipitus?
– A Condition resulting from too little ADHA Condition resulting from too little ADH

Why is it called Diabetes Insipitus?Why is it called Diabetes Insipitus?
– The term Diabetes refers to polyuriaThe term Diabetes refers to polyuria


– PolyuriaPolyuria
– Severe HypovolemiaSevere Hypovolemia
– Severe DehydrationSevere Dehydration
– Elevated Serum OsmolalityElevated Serum Osmolality
– Elevated Serum SodiumElevated Serum Sodium
– ShockShock


CAUSESCAUSES
– Decreased ADHDecreased ADH
– Neurological SurgeryNeurological Surgery
– Head TraumaHead Trauma
– Dilantin or LithiumDilantin or Lithium


TREATMENTTREATMENT
– Fluid ResuscitationFluid Resuscitation
– ADH ReplacementADH Replacement

Vasopressin, Pitressin, DDAVPVasopressin, Pitressin, DDAVP
– Treat The CauseTreat The Cause

SIADHSIADH

What is SIADH?What is SIADH?
– Syndrome of Inappropriate ADHSyndrome of Inappropriate ADH
– Too much ADHToo much ADH

SIADHSIADH
 SIGNS & SYMPTOMSSIGNS & SYMPTOMS
–
–
Low Serum SodiumLow Serum Sodium
 Serum NA < 135Serum NA < 135
– Low Serum OsmolalityLow Serum Osmolality
– High Urine OsmolalityHigh Urine Osmolality
– Elevated Specific GravityElevated Specific Gravity
 Urine specific gravityUrine specific gravity
> 1.030> 1.030
– Elevated Urine OsmolalityElevated Urine Osmolality
– Elevated ADH LevelElevated ADH Level
– Weight Gain Without EdemaWeight Gain Without Edema
– Elevated CVP, PAP, PAWPElevated CVP, PAP, PAWP
– Concentrated AndConcentrated And  UOPUOP
– HeadacheHeadache
– Altered LOCAltered LOC


CAUSESCAUSES
– Head TraumaHead Trauma
– Oat Cell CarcinomaOat Cell Carcinoma
– Other CancersOther Cancers
– Viral PneumoniaViral Pneumonia
SIADHSIADH
– MedicationsMedications
– StressStress
– Mechanical VentilationMechanical Ventilation


TREATMENTTREATMENT
– Monitor Fluid Balance, Monitor I & OMonitor Fluid Balance, Monitor I & O
– Restrict FluidsRestrict Fluids
– Replace Na+ loss when necessaryReplace Na+ loss when necessary
– May Give 3% (Hypertonic) SalineMay Give 3% (Hypertonic) Saline
– May Give Dilantin or LithiumMay Give Dilantin or Lithium
– May require PA Catheter For MonitoringMay require PA Catheter For Monitoring
– May Give DiureticsMay Give Diuretics
SIADHSIADH

DI vs SIADHDI vs SIADH
DIDI

Too Little ADHToo Little ADH

DehydrationDehydration

High Serum SodiumHigh Serum Sodium

High Serum OsmolalityHigh Serum Osmolality

Low Urine OsmolalityLow Urine Osmolality
SIADHSIADH

Too Much ADHToo Much ADH

Water IntoxicationWater Intoxication

Low Serum SodiumLow Serum Sodium

Low Serum OsmolalityLow Serum Osmolality

High Urine OsmolalityHigh Urine Osmolality

DI vs SIADH TreatmentDI vs SIADH Treatment
DIDI

Lots of FluidsLots of Fluids

Hold DilantinHold Dilantin

Hold LithiumHold Lithium

Give ADHGive ADH
SIADHSIADH

Fluid RestrictionFluid Restriction

May Give DilantinMay Give Dilantin

May Give LithiumMay Give Lithium

3% Saline3% Saline

DICDIC

What is DIC?What is DIC?
– Disseminate Intravascular CoagulationDisseminate Intravascular Coagulation
– A clotting disorder that ultimately causesA clotting disorder that ultimately causes
bleedingbleeding


Caused by over-activation of the clotting pathwaysCaused by over-activation of the clotting pathways

Causes widespread fibrin depositsCauses widespread fibrin deposits

Bleeding and renal failure are most common manifestationsBleeding and renal failure are most common manifestations

Treating the underlying disease is the most important stepTreating the underlying disease is the most important step
DICDIC

Disseminated IntravascularDisseminated Intravascular
CoagulationCoagulation
Systemic activationSystemic activation
of coagulationof coagulation
deposition ofdeposition of
fibrinfibrin
DepletionDepletion of plateletsof platelets
and coagulationand coagulation
factorsfactors
BLEEDINGBLEEDING
Thrombosis of smallThrombosis of small
and midsize vesselsand midsize vessels
with organ failurewith organ failure


–BleedingBleeding
–ThrombosisThrombosis
–Organ FailureOrgan Failure
DICDIC


CAUSESCAUSES
– Massive Tissue InjuriesMassive Tissue Injuries
– Obstetric EmergenciesObstetric Emergencies
– SepticemiaSepticemia
– CancersCancers
– Vascular DisordersVascular Disorders
– Systemic DisordersSystemic Disorders
– Many More CausesMany More Causes
DICDIC


CLOTTING FACTORS DEPLETEDCLOTTING FACTORS DEPLETED
– PlateletsPlatelets ↓↓
– FibrinogenFibrinogen ↓↓
– Protein Activated CProtein Activated C ↓↓
– AntithrombinAntithrombin ↓↓
DIC Lab ResultsDIC Lab Results

CLOTTING TESTS ELEVATEDCLOTTING TESTS ELEVATED
– PTPT ↑↑
– aPTTaPTT ↑↑
– Fibrin degradation products (D-dimer)Fibrin degradation products (D-dimer) ↑↑


TREATMENTTREATMENT
–Treat the CauseTreat the Cause
–Replace Clotting FactorsReplace Clotting Factors
–Anticoagulation Therapy (Heparin)Anticoagulation Therapy (Heparin)
DICDIC

THE ENDTHE END
PART 2PART 2
CCRN REVIEWCCRN REVIEW

THANK YOU!THANK YOU!

GOOD LUCK!GOOD LUCK!
CCRNCCRN REVIEWREVIEW

ReferencesReferences
 American Stroke Association. (2007). Acute and Preventative
Treatments. Retrieved March 4, 2007 from
http://www.strokeassociation.org/presenter.jhtml?identifier=2532.
 Block, C., and Manning, H. (2002). Prevention of acute renal failure in
the critically ill. American Journal of Respiratory and Critical Care
Medicine; (165)320-324.
 Brenner, B. M., and Rector, F.C. (2000). The kidney (6th ed), Vol I.
Philadelphia: W.B. Saunders Company; (1)399-416.
 Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN
Clinical Issues; (16)515-525.
 Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial
aneurysms? Lancet; (366)783-785.
 Campbell, D. (2003). How acute renal failure puts the breaks on kidney
function. Nursing 2003; (33)59-63.

References ContinuedReferences Continued
 Campbell, D. (2003). How acute renal failure puts the breaks on kidney
function. Nursing 2003; (33)59-63.
 Carlson, K. (2009) Advanced Critical Care Nursing. Philadelphia, Pa:
Saunders/Elsevier.
 Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. In
A. C. Guyton & J. E. Hall. Textbook of medical physiology (10th ed.).
Philadelphia: W.B. Saunders Company; pg. 264-379.
 Impact of Stroke. (2007). American Stroke Association. Retrieved March 4,
2007 from http://www.strokeassociation.org/presenter.jhtml?identifier=1033.
 Lynn-Mchale Wiegand, D. J. (ed.). (2011). AACN Procedure Manual for
Critical Care. 6th ed. St. Louis, MO: Saunders.
 Pagana, K. D. & Pagana, T. J. (2008). Mosby’s Diagnostic and Laboratory
Test Reference. 9th ed. St. Louis, MO: Mosby/Elsevier.
 Stillwell, S. (2006). Mosby’s Critical Care Nursing Reference. 4th ed. St.
Louis, MO: Mosby/Elsevier.: Diagnosis and Management (5th ed).

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