Pccn Review Part 2

““Education is a progressive Education is a progressive

discovery of our own ignorance”discovery of our own ignorance” Will DurantWill Durant

PCCN REVIEW PART 2PCCN REVIEW PART 2

Sherry L. Knowles, RN, CCRN, CRNISherry L. Knowles, RN, CCRN, CRNI

TOPICSTOPICS Renal Alterations Renal Alterations

– Acute Renal FailureAcute Renal Failure

– ElectrolytesElectrolytes

– IV Fluid TherapyIV Fluid Therapy Neurological Alterations Neurological Alterations

– AVM’s & Cerebral AVM’s & Cerebral AneurysmsAneurysms

– Intracranial HemorrhageIntracranial Hemorrhage

– Stroke Stroke

PCCNPCCN REVIEW PART 2REVIEW PART 2

Metabolic Alterations Metabolic Alterations

– DKA & HNNKDKA & HNNK

– DI & SIADHDI & SIADH

– DICDIC

– Shock StatesShock States

– SepsisSepsis

OBJECTIVESOBJECTIVES1.1. 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 of List 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 cellular Describe the different treatments for intravascular depletion verses cellular dehydration.dehydration.

10.10. Identify the risk factors and signs & symptoms of brain aneurysms and Identify 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 associated Describe the different types of intracranial hemorrhage and their associated signs & symptoms. signs & symptoms.

PCCNPCCN REVIEW PART 2REVIEW PART 2

OBJECTIVESOBJECTIVES13.13. 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.

PCCNPCCN REVIEWREVIEW

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 Calcitriol Calcitriol

TheThe KidneyKidney

TheThe NephronNephron

GlomerulusGlomerulus– Network of capillariesNetwork of capillaries

Bowman’sBowman’s capsulecapsule– Membrane that surrounds Membrane that surrounds

the glomerulusthe glomerulus

Renal TubulesRenal Tubules– Travel from cortex to Travel 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 of Controls the activity of the nephronthe nephron

Plays major role in the Plays major role in the renin-angiontension-renin-angiontension-aldosterone systemaldosterone system

The Juxtaglomerular ApparatusThe Juxtaglomerular Apparatus

UrineUrine FormationFormation


DEFINITIONSDEFINITIONS

– Sudden interruption of kidney function resulting Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of from 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 levels elevated BUN and Creatinine levels decreased urine output (usually but not always)decreased urine output (usually but not always)

AcuteAcute RenalRenal FailureFailure 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

– Elderly Elderly

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Azotemia Azotemia – HyperkalemiaHyperkalemia– Electrolyte DisturbancesElectrolyte Disturbances

K+ K+ phosphate phosphate

Na+ Na+ calcium calcium

Cr Cr BUN BUN– Metabolic acidosisMetabolic acidosis– Nausea/VomitingNausea/Vomiting

– Oliguria - anuriaOliguria - anuria– HTNHTN– Hypovolemia Hypovolemia – Pulmonary edemaPulmonary edema– AscitesAscites– Metabolic acidosisMetabolic acidosis– AsterixisAsterixis– EncephalopathyEncephalopathy



COMPLICATIONSCOMPLICATIONS

– Results in retention of toxins, fluids, and end Results 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


AcuteAcute RenalRenal FailureFailure PHASESPHASES

– OnsetOnset 1-3 days with 1-3 days with BUN and BUN and creatinine and creatinine and

possible decreased UOPpossible decreased UOP– Oliguric Oliguric

UOP < 400/day, UOP < 400/day, BUN, BUN, Cr, Cr, P04, P04, K, may K, may last up to 14 dayslast up to 14 days

– DiureticDiuretic UOP UOP to as much as 4000 mL/day but without to as much as 4000 mL/day but without

waste products, may begin to see improvement at waste products, may begin to see improvement at end of this stageend of this stage

– Recovery Recovery things go back to normal or may remain things 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

– Intrarenal Intrarenal ATN, nephrotoxic agents, infections, ischemia ATN, nephrotoxic agents, infections, ischemia

acute tubular necrosis, acute nephritis, polycystic acute tubular necrosis, acute nephritis, polycystic kidney diseasekidney disease

– Postrenal Postrenal Stones, blood clots, BPH, urethral edema from Stones, 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

UNa (mEq/L) < 20 > 40

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

HypovolemiaHypovolemiaToxic agents (drugs, myoglobin)Toxic agents (drugs, myoglobin)ObstructionObstruction

– Treat reversible elementsTreat reversible elementsHydrateHydrateRemove drugRemove drugRelieve obstructionRelieve obstruction


NURSING CARENURSING CARE– Fluid and dietary restrictionsFluid and dietary restrictions

Protein, potassium & phosphate restrictionProtein, potassium & phosphate restriction

– Maintain electrolytes Maintain 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 with May 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 for Watch for hyper/hypoglycemia hyper/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 changes parenthesia, muscle weakness,EKG changes

Chronic RenalChronic Renal FailureFailure

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 contraction Muscle contraction – Nerve impulses Nerve impulses – Cell membrane function Cell membrane function – Attracting water into the ICFAttracting water into the ICF– Imbalances interfere with neuromuscular function Imbalances interfere with neuromuscular function

and may cause cardiac rhythm disturbancesand may cause cardiac rhythm disturbances

Potassium (KPotassium (K++))

HyperkalemiaHyperkalemia

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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 wave QRS-T wave

merge = “sine wave”merge = “sine wave”



CAUSESCAUSES– Chronic or acute renal failure Chronic or acute renal failure

– Burns Burns

– Crush injuries Crush 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

– Lasix Lasix

– AlbuterolAlbuterol

– HemodialysisHemodialysis


SIGNS & SYMPTOMSSIGNS & SYMPTOMS

–Malaise Malaise –Skeletal muscle weakness Skeletal muscle weakness –Decreased reflexes Decreased reflexes –Hypotension Hypotension –Vomiting Vomiting –Excessive thirstExcessive thirst–Cardiac arrhythmias and cardiac arrestCardiac arrhythmias and cardiac arrest–Flattened T waveFlattened T wave–U waveU wave

HypokalemiaHypokalemia

Sine WaveSine Wave

HypokalemiaHypokalemia

CAUSESCAUSES– Reduced dietary intake Reduced dietary intake

– Poor absorption by the body Poor absorption by the body

– Vomiting and/or diarrhea Vomiting and/or diarrhea

– Renal disease Renal disease

– Medications (typically diuretics)Medications (typically diuretics)

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Cold, clammy, pale skinCold, clammy, pale skin– NervousnessNervousness– Shakiness, lack of coordination, staggering gait Shakiness, 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

HypoglycemiHypoglycemiaa

SIGNS & SYMPTOMSSIGNS & SYMPTOMSCardiovascular 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

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– ThirstThirst– PolyuriaPolyuria– DehydrationDehydration– Nausea, vomitingNausea, vomiting– DKADKA– HNNKHNNK

HyperglycemiaHyperglycemia

Normal serum Glu level: Normal serum Glu level: 70 - 110 mg/dL 70 - 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

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Deficiency of sodium in the bloodDeficiency of sodium in the blood

– HypotensionHypotension

– TachycardiaTachycardia

– Muscle weaknessMuscle weakness

– Mental ConfusionMental Confusion

HyponatremiHyponatremiaa

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Excess sodium in the bloodExcess sodium in the blood– HypertensionHypertension– Muscle twitchingMuscle twitching– Mental confusionMental confusion– ComaComa

HypernatremiaHypernatremia

Activates many enzymes Activates many enzymes

50% is insoluble in bone 50% is insoluble in bone

45% is intracellular 45% is intracellular

5% is extracellular5% is extracellular

Mg+Mg+

Magnesium (MgMagnesium (Mg++))

Normal serum Mg+ level: 1.5 - 2.5 mg/dL Normal serum Mg+ level: 1.5 - 2.5 mg/dL

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Tremors Tremors

– Positive Chvostek & Trousseau Positive Chvostek & Trousseau

– Nystagmus Nystagmus

– Confusion/Hallucinations Confusion/Hallucinations

– Diarrhea Diarrhea – Hyperactive deep reflexes Hyperactive deep reflexes – Seizures Seizures

HypomagnesemiaHypomagnesemia

– Dysrhythmias Dysrhythmias – ECG ChangesECG Changes

Flat T waveFlat T wave ST interval depressionST interval depression Prolonged QT interval Prolonged QT interval

– May lead to May lead to Torsade de Torsade de PointesPointes

CAUSESCAUSES–Alcoholism Alcoholism

–Malabsorption Malabsorption

–Starvation Starvation

–Diarrhea Diarrhea

–DiuresisDiuresis

HypomagnesemiaHypomagnesemia

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Peaked T wavePeaked T wave– BradycardiaBradycardia– CNS Depression CNS Depression – Areflexia Areflexia – Sedation Sedation – Respiratory paralysisRespiratory paralysis

HypermagnesemiaHypermagnesemia

CAUSESCAUSES– Not commonNot common

– Occurs with chronic renal insufficiencyOccurs with chronic renal insufficiency

– Treatment is hemodialysis Treatment is hemodialysis

HypermagnesemiaHypermagnesemia

– ESSENTIAL FORESSENTIAL FOR – Neuromuscular transmission Neuromuscular transmission

– Growth and ossification of bones Growth and ossification of bones

– Muscle contraction Muscle contraction

Ca++Ca++

Calcium (CaCalcium (Ca++++))

Normal serum Ca++ level: 8 - 11 mg/dL Normal serum Ca++ level: 8 - 11 mg/dL

– INVOLVED IN INVOLVED IN – Blood clottingBlood clotting– Nerve impulseNerve impulse– Muscle contractionMuscle contraction

Ca++Ca++

Calcium (CaCalcium (Ca++++))

Excreted through urine, feces, and perspirationExcreted through urine, feces, and perspiration

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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)

– ParesthesiaParesthesia

HypocalcemiaHypocalcemia

CAUSESCAUSES

– Renal insufficiency Renal 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

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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 and Usually aimed at underlying disease and

hydration hydration – Severe hypercalcemia may be treated with Severe hypercalcemia may be treated with

forced diuresisforced diuresis

INVOLVED IN INVOLVED 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

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Respiratory difficultyRespiratory difficulty

– ConfusionConfusion

– IrritabilityIrritability

– ComaComa

HypophosphatemiaHypophosphatemia

CAUSESCAUSES– Severe infectionsSevere infections

– Kidney failureKidney failure

– Thyroid failureThyroid failure

– Parathyroid FailureParathyroid Failure

– Often associated with hypercalcemia or Often associated with hypercalcemia or hypomagnesemia or too much Vitamin Dhypomagnesemia or too much Vitamin D

– Cell destruction - from chemotherapy, when the Cell destruction - from chemotherapy, when the tumor cells die at a fast rate tumor 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

HyperphosphatemiHyperphosphatemiaa

TREATMENTTREATMENT

– Calcium Carbonate tabletsCalcium Carbonate tablets

– Aluminum hydroxide Aluminum hydroxide

Can cause aluminum toxicityCan cause aluminum toxicity

HyperphosphatemiHyperphosphatemiaa


OSMOLALITYOSMOLALITY– Concentration of a solution Concentration of a solution

– The higher the osmolality the greater The higher the osmolality the greater its pulling power for waterits pulling power for water

Normal serum osmolality is Normal serum osmolality is 275 to 295275 to 295 mOsm/L mOsm/L

Serum OsmolalitySerum Osmolality

Sodium = major solute in plasmaSodium = major solute in plasma – Estimated serum osmolality = 2 X serum Na Estimated serum osmolality = 2 X serum Na

Urea (BUN) and glucose are large molecules Urea (BUN) and glucose are large molecules that that serum osmolality serum osmolality – When either or both are elevated, the serum osmolality When either or both are elevated, the serum osmolality

will be higher than 2 times the sodium level, so the will 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 of Major Mediators of Sodium and Water Sodium and Water BalanceBalance

Angiotensin IIAngiotensin II

AldosteroneAldosterone

Antidiuretic hormone (ADH)Antidiuretic hormone (ADH)

Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone

Angiotensin II Angiotensin 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 tubule exchange in the proximal tubule

Aldosterone Aldosterone 1. Stimulates reabsorption of Na1. Stimulates reabsorption of Na++ and excretion of K and excretion of K++ in in the late distal tubule the late distal tubule

2. Stimulates activity of H2. Stimulates activity of H++ ATPase pumps in the late ATPase pumps in the late distal tubule distal tubule

Antidiuretic Hormone (ADH)Antidiuretic Hormone (ADH)

Synthesized in the hypothalamus and stored in the Synthesized in the hypothalamus and stored in the posterior pituitaryposterior pituitary

Released in response to plasma hyperosmolality Released in response to plasma hyperosmolality and decreased circulating volumeand decreased circulating volume

Actions of ADHActions of ADH

– Increases the water permeability of the collecting tubule Increases 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

D10WD10W

D50WD50W

½ NS½ NS

NSNS

D51/2 NSD51/2 NS

D5NSD5NS

D5WD5W Hypotonic in the bodyHypotonic in the body

IsotonicIsotonic

HypertonicHypertonic


HypotonicHypotonic

IsotonicIsotonic




IsotonicIsotonic






3% NaCl3% NaCl

LRLR

D5LRD5LR

AlbuminAlbumin

DextranDextran

HetastarchHetastarch

PRBC’sPRBC’s

IV SolutionsIV Solutions

D5WD5W Hypotonic in the bodyHypotonic in the body

HypotonicHypotonicSolutionsSolutions

Used for cellular dehydration Used for cellular dehydration Not used with head injuriesNot used with head injuries

Isotonic Isotonic SolutionsSolutions Hydrates extracellular compartmentHydrates extracellular compartment

HypertonicHypertonicSolutionsSolutions Pulls fluid into vascular spacePulls fluid into vascular space

Daily Fluid BalanceDaily Fluid BalanceIntake: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

Intracellular Intracellular

(2/3)(2/3)

Extracellular Extracellular

(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

NaNa NaNa

Colloids Colloids & RBC’s& RBC’s

““Third Space”Third Space” Third space refers to collection of fluids (usually Third 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 derived This 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 Fluid Replacement ProductsProducts

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 in the intravascular space for several days (pulling fluid 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


ECF=1 literECF=1 liter ICF=0ICF=0

IntravascularIntravascular

=1/4 ECF=250 ml=1/4 ECF=250 ml

1 Liter 0.9% saline1 Liter 0.9% saline

Interstitial=3/4 Interstitial=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

IntravascularIntravascular

=1/4 of ECF~75ml=1/4 of ECF~75ml

Ringers LactateRingers Lactate

Infusion of Ringer Lactate solution may lead to metabolic Infusion 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 with Lactated Ringer’s should be used with great care with patients with hyperkalemia, severe renal failure, and patients with hyperkalemia, severe renal failure, and hepatic insufficiency hepatic insufficiency

Solutions containing lactate are not for use in the Solutions containing lactate are not for use in the treatment of lactic acidosistreatment of lactic acidosis

BREAKBREAK

PCCNPCCN REVIEWREVIEW PARTPART 11

NeurologicalNeurological AlterationsAlterations

Brain Aneurysms & AVM’sBrain Aneurysms & AVM’s

Intracranial HemorrhageIntracranial Hemorrhage

StrokeStroke

TheThe HumanHuman BrainBrain

CerebralCerebral SpinalSpinal FluidFluid

The serum-like fluid that circulates through the ventricles of the The 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

Brain AneurysmBrain Aneurysm

– An intracranial aneurysm is a weak or thin spot on a blood An 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 "short of the brain is a "short circuit“circuit“ between the arteries and veinsbetween the arteries and veins

Brain Aneurysms & AVM’s Brain Aneurysms & AVM’s

Intracranial AneurysmsIntracranial Aneurysms

Usually occur at bifurcations and branches of the Usually 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 Communicating artery (30 - 35%)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 Circulation Brain Circulation

Arterial Circulation in the Brain Arterial Circulation in the Brain

RISK FACTORSRISK FACTORS– SmokingSmoking– HypertensionHypertension– Coarctation of the aortaCoarctation of the aorta– Dissections/traumaDissections/trauma– Intracranial neoplasm Intracranial neoplasm – Polycystic kidney diseasePolycystic kidney disease– Abnormal vessels or High-flow states (eg, vascular Abnormal 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)


SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Usually asymptomatic until ruptureUsually asymptomatic until rupture

Cranial Nerve PalsyCranial Nerve PalsyDilated PupilsDilated PupilsDouble VisionDouble VisionPain Above and Behind EyePain Above and Behind EyeLocalized Headache Localized Headache

– Warning signs prior ruptureWarning signs prior ruptureLocalized HeadacheLocalized HeadacheNausea & VomitingNausea & VomitingStiff NeckStiff NeckBlurred or Double VisionBlurred or Double VisionSensitivity to Light (photophobia)Sensitivity to Light (photophobia)Loss of Sensation Loss of Sensation


Treatment of Brain Treatment of Brain AneurysmsAneurysms SurgerySurgery

– – Craniotomy and clipping Craniotomy 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 pressure Main 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 HyponatremiaHyponatremia Fluids / ElectrolytesFluids / Electrolytes

Arterio-Venous Arterio-Venous MalformationMalformation

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 neurological hemorrhage, or progressive neurological dysfunctiondysfunction

Arterio-Venous Arterio-Venous MalformationMalformation

Arterio-Venous Arterio-Venous MalformationMalformation SIGNS & SYMPTOMSSIGNS & SYMPTOMS

– Seizures Seizures – Headaches Headaches – ““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 balance Loss of coordination and balance Paralysis or weakness in one part of the bodyParalysis or weakness in one part of the body Visual disturbances Visual disturbances Abnormal sensationsAbnormal sensations

Arterio-Venous Arterio-Venous MalformationMalformation COMPLICATIONSCOMPLICATIONS

– HemorrhageHemorrhage (into surrounding tissue)(into surrounding tissue)

– IschemiaIschemia

– Seizures Seizures

– Brain Cell DeathBrain Cell Death

Arterio-Venous Arterio-Venous MalformationMalformation DIAGNOSISDIAGNOSIS

– MRI MRI (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 to is a prerequisite to treatment treatment

To identify the precise anatomy and configuration To identify the precise anatomy and configuration of both the lesion and the feeding and draining of both the lesion and the feeding and draining vesselsvessels

Arterio-Venous Arterio-Venous MalformationMalformation TREATMENTTREATMENT

– Surgery Surgery 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

Arterio-Venous Arterio-Venous MalformationMalformation RADIOSURGERYRADIOSURGERY

– Believed to "work" by initiating an "inflammatory" Believed to "work" by initiating an "inflammatory" response in the pathological blood vessels response in the pathological blood vessels ultimately resulting in their progressive narrowing ultimately resulting in their progressive narrowing and ultimate closureand ultimate closure

– The risk for hemorrhage is not reduced during this The risk for hemorrhage is not reduced during this lag timelag time

– There is the added risk of radiation necrosis of There 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– Noninvasive Noninvasive

– Can access all anatomic locations of the brainCan access all anatomic locations of the brain

DISADVANTAGESDISADVANTAGES– Can only treat smaller lesions Can 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 setting Consider 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)

DEFINITION DEFINITION –When a blood vessel just outside the brain ruptures, the When a blood vessel just outside the brain ruptures, the

area of the skull surrounding the brain (the area of the skull surrounding the brain (the subarachnoid subarachnoid space) rapidly fills with bloodspace) rapidly fills with blood


SIGNS & SYMPTOMS SIGNS & SYMPTOMS –Sudden, intense headacheSudden, intense headache

–Neck painNeck pain

–Nausea or vomiting Nausea 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 of 50% of patients die within 48 hours irrespective of therapytherapy

Subarachnoid HemorrhageSubarachnoid Hemorrhage

Often accompanied by a period of unconsciousness Often 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 24 may develop within the first 24 hours because of obstruction of CSF outflow in the hours 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 the of SAH occurs in 20% of patients in the first 2 weeks. Peak incidence of rebleeding occurs the day first 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 contraction from 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 blood The main preventative measure is to control the blood pressure – preferably beta blockerspressure – preferably beta blockers

Early clipping of the aneurysm allows hypertensive and Early 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 for Worst time is day 7 to day 10 (most frequent time for vasospasms)vasospasms)

Diagnosed by neurologic exam, transcranial doppler and Diagnosed by neurologic exam, transcranial doppler and angiographyangiography

May use calcium channel blockers May use calcium channel blockers

– Reduces vasospasm, neurological deficit, cerebral infarction Reduces 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 sympathetic causes 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 Other Complications of SAHSAH

1)1) Identify and treat the causative lesionIdentify and treat the causative lesion

– Thus preventing re-bleedingThus preventing re-bleeding

2)2) Treat hydrocephalusTreat hydrocephalus

3)3) 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 CPP Use vasopressors if necessary to maintain CPP and reduce ischemic complications from vasospasmand reduce ischemic complications from vasospasm

– Generally avoid vasodilators (except calcium Generally avoid vasodilators (except calcium channel blockers)channel blockers)

Treatment of SAHTreatment of SAH

StrokeStroke

StrokeStroke

RISK FACTORSRISK FACTORS TIATIA CADCAD High Blood PressureHigh Blood Pressure High CholesterolHigh Cholesterol SmokingSmoking Heart DiseaseHeart Disease DiabetesDiabetes

Excessive alcohol Excessive 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

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 given Tissue 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, the In addition to being used to treat strokes, the following can also be used as preventative following 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 blood Surgery 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 and An 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 Treatment of Hemorrhagic CVACVA

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

BREAKBREAK

PCCN REVIEW PART 1PCCN REVIEW PART 1

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 with A life-threatening complication seen with Diabetes Mellitus Type 1 Diabetes Mellitus Type 1

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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 with A life threatening complication seen with Diabetes Mellitus Type 2Diabetes Mellitus Type 2

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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

DD5 5 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


SIGNS & SYMPTOMSSIGNS & SYMPTOMS– 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– HyponatremiaHyponatremia– Low Serum SodiumLow Serum Sodium

Serum NA < 135Serum NA < 135

– Low Serum Osmolality Low Serum Osmolality – High Urine OsmolalityHigh Urine Osmolality– Elevated Specific GravityElevated Specific Gravity

Urine specific gravity Urine specific gravity

> 1.030> 1.030

– Elevated Urine Osmolality Elevated Urine Osmolality

– Elevated ADH LevelElevated ADH Level

– Weight Gain Without EdemaWeight Gain Without Edema

– Elevated CVP, PAP, PAWPElevated CVP, PAP, PAWP

– HypertensionHypertension

– Concentrated And Concentrated And UOP UOP

– HeadacheHeadache

– Altered LOCAltered LOC

– SeizuresSeizures

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 necessary Replace 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 causes A clotting disorder that ultimately causes bleedingbleeding

Caused by over-activation of the clotting pathways Caused 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 Intravascular Disseminated Intravascular CoagulationCoagulation

Systemic activationSystemic activationof coagulationof coagulation

IntravascularIntravasculardeposition of deposition of

fibrinfibrin

DepletionDepletion of plateletsof plateletsand coagulation and coagulation

factorsfactors

BLEEDINGBLEEDINGThrombosis of smallThrombosis of smalland midsize vesselsand midsize vessels

with organ failurewith organ failure


–BleedingBleeding

–ThrombosisThrombosis

–Organ FailureOrgan Failure

DICDIC

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– Platelets Platelets – Fibrinogen Fibrinogen – Protein C Protein C – Antithrombin Antithrombin

DIC Lab ResultsDIC Lab Results

CLOTTING TESTS ELEVATEDCLOTTING TESTS ELEVATED– PT PT – aPTT aPTT – 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

ShockShock

DEFINITIONDEFINITION

–Inadequate perfusion to body tissuesInadequate perfusion to body tissues

ShockShock

COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS –TachycardiaTachycardia

Attempts to deliver more blood to the tissuesAttempts to deliver more blood to the tissues

–VasoconstrictionVasoconstriction Attempts to maintain adequate BP in order to Attempts to maintain adequate BP in order to

adequately perfuse the body tissuesadequately perfuse the body tissues

–Increased ADH SecretionIncreased ADH Secretion ADH makes the body hold onto water in an effort to ADH makes the body hold onto water in an effort to

maintain volume and thus enough blood pressure to maintain volume and thus enough blood pressure to perfuse the body tissuesperfuse the body tissues

Types of ShockTypes of Shock

Hypovolemic ShockHypovolemic Shock– Inadequate perfusion to the tissues due to insufficient intravascular Inadequate perfusion to the tissues due to insufficient intravascular

volumevolume

Cardiogenic ShockCardiogenic Shock– Inadequate perfusion to the tissues due to heart failureInadequate perfusion to the tissues due to heart failure

Distributive ShockDistributive Shock– Inadequate perfusion to the tissues due to blood flow out of the Inadequate perfusion to the tissues due to blood flow out of the

intravascular space causing insufficient intravascular volumeintravascular space causing insufficient intravascular volume

– Anaphylactic, Septic, and Spinal ShockAnaphylactic, Septic, and Spinal Shock Obstructive ShockObstructive Shock

– Inadequate perfusion to the tissues due to obstruction of blood flowInadequate perfusion to the tissues due to obstruction of blood flow

Hypovolemic ShockHypovolemic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardia

Orthostatic Hypotension Orthostatic Hypotension RestlessnessRestlessness

Confusion Confusion Agitation (or Agitation (or listless)listless)

Thirst Thirst PallorPallor

Cool, Clammy SkinCool, Clammy Skin Resp. Rate Resp. Rate

UOPUOP CO CO

PAWPPAWP CVP CVP

SVRSVR Lactate Levels Lactate Levels

Hypovolemic ShockHypovolemic Shock

TREATMENTTREATMENT

–Volume (IVF, Blood)Volume (IVF, Blood)

Cardiogenic ShockCardiogenic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP RestlessnessRestlessness

Agitation (or listless)Agitation (or listless) ConfusionConfusion

TachycardiaTachycardia PallorPallor

UOPUOP CO CO

PAWPPAWP (low with RVF)(low with RVF) CVPCVP

SVR SVR Lactate Levels Lactate Levels

JVDJVD Peripheral EdemaPeripheral Edema

Ventricular Gallop (S3)Ventricular Gallop (S3) DyspneaDyspnea

Pulmonary CracklesPulmonary Crackles

TREATMENTTREATMENTBedrestBedrest O2O2

COCO Positive InotropesPositive Inotropes

Preload & AfterloadPreload & Afterload DiureticsDiuretics

VasodilatorsVasodilators PositioningPositioning

Myocardial DemandMyocardial DemandIABPIABP

Cardiogenic ShockCardiogenic Shock

Anaphylactic ShockAnaphylactic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestlessness Confusion Confusion Agitation (or listless)Agitation (or listless) Thirst Thirst PallorPallor Warm FeelingWarm FeelingPruritusPruritus HivesHivesAngioedemaAngioedema BronchoconstrictionBronchoconstrictionWheezingWheezing LaryngoedemaLaryngoedemaDyspneaDyspnea Cool, Clammy SkinCool, Clammy Skin UOPUOP CO CO PAWPPAWP CVP CVP

SVRSVR Lactate Levels Lactate Levels

TREATMENTTREATMENT– Epinephrine Epinephrine

– IVFIVF

– VasoconstrictorsVasoconstrictors

– Support/Maintain AirwaySupport/Maintain Airway

Anaphylactic ShockAnaphylactic Shock

EARLY STAGE (Hyperdynamic)EARLY STAGE (Hyperdynamic)Normal BPNormal BP TachycardiaTachycardiaConfusion Confusion Agitation (or listless)Agitation (or listless) Respiratory RateRespiratory Rate TemperatureTemperatureNormal ColorNormal Color Normal or Normal or UOP UOPNormal PAWPNormal PAWP CO CO SVR SVR

LATE STAGE (Hypodynamic)LATE STAGE (Hypodynamic)Low BPLow BP TachycardiaTachycardiaOrthostatic Hypotension Orthostatic Hypotension RestlessnessRestlessnessConfusion Confusion Agitation (or listless)Agitation (or listless)Thirst Thirst PallorPallorCool, Clammy SkinCool, Clammy Skin UOP UOP COCO PAWP PAWP CVPCVP SVR SVR Lactate LevelsLactate Levels

Septic ShockSeptic Shock

TREATMENTTREATMENT– IVF (150cc/hr or wide open)IVF (150cc/hr or wide open)

– Treat Cause (Pan culture, antibiotics)Treat Cause (Pan culture, antibiotics)

– Vasoconstrictors in warm phaseVasoconstrictors in warm phase– Treat Temp as neededTreat Temp as needed

Septic ShockSeptic Shock

Obstructive ShockObstructive Shock

CAUSESCAUSESPulmonary EmbolusPulmonary Embolus TamponadeTamponade

Tension PneumothoraxTension Pneumothorax Aortic AneurysmAortic Aneurysm

TREATMENTTREATMENTTreat the CauseTreat the Cause

SIRS Sepsis Severe Septic MODS DeathSIRS Sepsis Severe Septic MODS DeathInfection Infection Sepsis Shock Sepsis Shock

Sepsis SyndromeSepsis Syndrome

Sepsis– SIRS’ response with presumed/confirmed infectionSIRS’ response with presumed/confirmed infection

Severe Sepsis– Sepsis associated with organ dysfunction, hypoperfusion Sepsis associated with organ dysfunction, hypoperfusion

(lactic acidosis, oliguria, altered mental status etc.), or (lactic acidosis, oliguria, altered mental status etc.), or hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)

Septic Shock– Sepsis with perfusion abnormalities and hypotension Sepsis with perfusion abnormalities and hypotension

despite adequate fluid resuscitationdespite adequate fluid resuscitation

Sepsis SyndromeSepsis Syndrome

Homeostasis Gets LostHomeostasis Gets Lost

3.3. Improve PerfusionImprove Perfusion– Prevent organ dysfunctionPrevent organ dysfunction

2.2. Treat The CauseTreat The Cause – Seek primary site of infectionSeek primary site of infection

– Direct therapy to primary causeDirect therapy to primary cause

1.1. Stabilize The PatientStabilize The Patient– Fluids (lots of fluids)Fluids (lots of fluids)

– VasoconstrictorsVasoconstrictors

Treatment for SepsisTreatment for Sepsis

THE ENDTHE ENDPART 2PART 2

PCCN REVIEWPCCN REVIEW

THANK YOU!THANK YOU!


GOOD LUCK!GOOD LUCK!


ResourcesResourcesAmerican Stroke Association. (2007). Acute and Preventative Treatments. Retrieved American Stroke Association. (2007). Acute and Preventative Treatments. Retrieved

March 4, 2007 from March 4, 2007 from http://http://www.strokeassociation.org/presenter.jhtml?identifierwww.strokeassociation.org/presenter.jhtml?identifier=2532=2532

Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14, July 2001. Nursing:15(4):1–14, July 2001.

Balk, R. A. (2000). Severe sepsis and septic shock. Critical Care Clinics; (2)179-92.Balk, R. A. (2000). Severe sepsis and septic shock. Critical Care Clinics; (2)179-92.

Block, C., and Manning, H. (2002). Prevention of acute renal failure in the critically ill. 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.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. Brenner, B. M., and Rector, F.C. (2000). The kidney (6th ed), Vol I. Philadelphia: W.B. Saunders Company; (1)399-416.Saunders Company; (1)399-416.

Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN Clinical Issues; Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN Clinical Issues; (16)515-525.(16)515-525.

Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial aneurysms? Lancet; Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial aneurysms? Lancet; (366)783-785. (366)783-785.

Campbell, D. (2003). How acute renal failure puts the breaks on kidney function. Campbell, D. (2003). How acute renal failure puts the breaks on kidney function. Nursing 2003; (33)59-63.Nursing 2003; (33)59-63.

Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. In A. C. 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: Guyton & J. E. Hall. Textbook of medical physiology (10th ed.). Philadelphia: W.B. Saunders Company; pg. 264-379.W.B. Saunders Company; pg. 264-379.

Impact of Stroke. (2007). American Stroke Association. Retrieved March 4, 2007 from Impact of Stroke. (2007). American Stroke Association. Retrieved March 4, 2007 from http://http://www.strokeassociation.org/presenter.jhtml?identifierwww.strokeassociation.org/presenter.jhtml?identifier=1033=1033

Resources ContinuedResources ContinuedKhurana, V. G., Friedman, J. A., Meyer, F. B. (2004). Chapter 11: Biology of Cerebral Khurana, V. G., Friedman, J. A., Meyer, F. B. (2004). Chapter 11: Biology of Cerebral

Blood Vessels and Blood Flow. In Le Roux, P. D., Winn, H. R., Newell, D. W. Blood Vessels and Blood Flow. In Le Roux, P. D., Winn, H. R., Newell, D. W. (eds). Management of Cerebral Aneurysms, Philadelphia, WB Saunders, pp 139-(eds). Management of Cerebral Aneurysms, Philadelphia, WB Saunders, pp 139-167, 2003.167, 2003.

Marino, P. L. (2006, September). The ICU Book. Lippincott Williams & Wilkins: Marino, P. L. (2006, September). The ICU Book. Lippincott Williams & Wilkins: Philadelphia.Philadelphia.

Metheny, N. (2000). Fluid and Electrolyte Balance: Nursing Considerations (4th ed.) Metheny, N. (2000). Fluid and Electrolyte Balance: Nursing Considerations (4th ed.) Philadelphia: Lippincott Williams & Wilkins; (4)158-200.Philadelphia: Lippincott Williams & Wilkins; (4)158-200.

Nettina, S. M. (2005). Diseases and Disorders in Lippincott Manual of Nursing Practice Nettina, S. M. (2005). Diseases and Disorders in Lippincott Manual of Nursing Practice Handbook (3rd ed.), page 414. Handbook (3rd ed.), page 414.

Rivers, E. P. (2006, February). Early goal-directed therapy in severe sepsis and septic Rivers, E. P. (2006, February). Early goal-directed therapy in severe sepsis and septic shock: converting science to reality. Chest; 129(2):217-8. shock: converting science to reality. Chest; 129(2):217-8.

Rucker, D. (2006, June). Diabetic Ketoacidosis. Retrieved Feb 28, 2007 from Rucker, D. (2006, June). Diabetic Ketoacidosis. Retrieved Feb 28, 2007 from http://www.emedicine.com/emerg/topic135.htm.http://www.emedicine.com/emerg/topic135.htm.

Schmidt, T. (2000). “Assessing a Sodium and Fluid Imbalance”, Nursing 2000; (30) Schmidt, T. (2000). “Assessing a Sodium and Fluid Imbalance”, Nursing 2000; (30) Number 1, p18.Number 1, p18.

Sterns, R.H., Silver, S. M., Spital, A., Robertson, G. L., Seldin, D. W., Giebisch, G. Sterns, R.H., Silver, S. M., Spital, A., Robertson, G. L., Seldin, D. W., Giebisch, G. (2000). The Kidney: Physiology & Pathophysiology. Philadelphia PA: Lippincott (2000). The Kidney: Physiology & Pathophysiology. Philadelphia PA: Lippincott Williams & Wilkins, Inc; pgs. 1133–52 & 1217–38.Williams & Wilkins, Inc; pgs. 1133–52 & 1217–38.

Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188. 188.

Urden, L., Lough, M. E. & Stacy, K. L. (2005). Thelan's Critical Care Nursing: Diagnosis Urden, L., Lough, M. E. & Stacy, K. L. (2005). Thelan's Critical Care Nursing: Diagnosis and Management (5th ed). S and Management (5th ed). S