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Education is a progressive

discovery of our own ignorance

- Will Durant -

CCRN REVIEW PART 2

Sherry L. Knowles, RN, CCRN, CRNI

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TOPICS Renal Alterations

Acute Renal Failure Electrolytes

IV Fluid Therapy

Neurological Alterations

AVMs & CerebralAneurysms

Intracranial Hemorrhage

Stroke

CCRN REVIEW PART 2

Metabolic Alterations

DKA & HNNK DI & SIADH

DIC

Shock States

Sepsis

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OBJECTIVES1. List the main functions of the kidney.

2. List the common diagnostic tests associated with renal function.

3. List the complications associated with acute renal failure.

4. Describe the common treatments of acute renal failure.

5. List the major signs & symptoms associated with electrolyte disturbances ofsodium, potassium magnesium and calcium and phosphorus.

6. Define serum osmolality.

7. List the intracellular & extracellular fluid compartments of the body.

8. Describe the effects of hypotonic, isotonic and hypertonic IV fluids.

9. Describe the different treatments for intravascular depletion verses cellulardehydration.

10. Identify the risk factors and signs & symptoms of brain aneurysms andAVMs.

11. Explain the current treatments available for brain aneurysms and AVMs.

12. Describe the different types of intracranial hemorrhage and their associatedsigns & symptoms.

CCRN REVIEW PART 2

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OBJECTIVES13. List the potential complications of associated with intracranial hemorrhages,

brain aneurysms and AVM repairs.

14. List the types of CVAs, their risk factors and related pathophysiology.

15. Identify the recommended treatments for CVAs.16. Differentiate between the signs and symptoms of DKA and HHNK.

17. Describe the treatment of DKA and HHNK.

18. Differentiate between the signs and symptoms of DI and SIADH.

19. Describe the treatment of DI and SIADH.

20. List the signs & symptoms of Disseminated Intravascular Coagulation.

21. Explain the treatments for disseminated intravascular coagulation.

22. Understand the different stages of shock.

23. Differentiate between different types of shock.

24. Identify the different treatments used for the different types of shock.

25. Describe the stages of the sepsis syndrome.

26. Explain the treatment of septic shock.

CCRN REVIEW PART 2

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Acute Renal Failure

Electrolytes

IV Fluid Therapy

RenalAlterations

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AcuteRenalFailure WHAT DO THE KIDNEYS DO?

Filter blood

Regulates electrolytes

Regulate blood pressure

Renin-angiotensin system (RAS)

Maintain acid/base balance

Removes wastes, detoxifies blood

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AcuteRenalFailure WHAT ELSE DO THE KIDNEYS DO?

Stimulate RBC production

Make erythopoietin

Make corticosteroids

Regulate kidney function

Increase calcium absorption

Convert Vitamin D to its active formCalcitriol

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TheKidney

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TheNephron

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Glomerulus Network of capillaries

Bowmanscapsule Membrane that surrounds

the glomerulus

Renal Tubules Travel from cortex to

medulla and back to cortex

Collecting duct Within the medulla

TheNephron

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TheKidney

The Renal Cortex Contains Bowman's Capsules

Glomerulus Proximal Tubules

Distal Convoluted Tubules

The Renal Medulla Contains

The Pyramids Loop of Henle

Collecting Duct

Blood Vessels

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Lies within Cortex

Controls the activity of

the nephron

Plays major role in therenin-angiontension-

aldosterone system

The Juxtaglomerular Apparatus

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UrineFormation
http://en.wikibooks.org/wiki/Image:Anatomy_and_physiology_of_animals_Summary_of_the_processes_involved_in_the_formation_of_urine.jpg

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AcuteRenalFailure DEFINITIONS

Sudden interruption of kidney function resulting

from obstruction, reduced circulation, or diseaseof the renal tissue

Rapid deterioration of renal function

increase of creatinine of >0.5 mg/dl in

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AcuteRenalFailure TERMINOLOGY

Anuria: No UOP (or

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AcuteRenalFailure PERSONS AT RISK

Major surgery

Major trauma

Receiving nephrotoxic medications

Hypovolemia > 40 minutes

Elderly

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SIGNS & SYMPTOMS Azotemia

Hyperkalemia Electrolyte Disturbances

K+ phosphateNa+ calciumCr BUN

Metabolic acidosis

Nausea/Vomiting

Oliguria - anuria

HTN Hypovolemia

Pulmonary edema

Ascites

Metabolic acidosis

Asterixis

Encephalopathy

AcuteRenalFailure

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AcuteRenalFailure COMPLICATIONS

Results in retention of toxins, fluids, and endproducts of metabolism

May be reversible with medical treatment

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DIAGNOSTIC TESTS

H&P

BUN, creatinine, sodium, potassium, pH,bicarb, Hgb and Hct

Urine studies

US of kidneys

24 hour urine for protein and creatinine

Urine eosinophils

AcuteRenalFailure

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OTHER DIAGNOSTIC TESTS

Albumin, glucose, prealbumin

KUB

Abd and Renal CT/MRI

Retrograde pyloegram

Renal biopsy Post-void residual or catheterization

AcuteRenalFailure

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AcuteRenalFailure PHASES

Onset 1-3 days with BUN and creatinine and

possible decreased UOP Oliguric

UOP < 400/day, BUN, Cr, P04, K, maylast up to 14 days

Diuretic

UOP to as much as 4000 mL/day but withoutwaste products, may begin to see improvement atend of this stage

Recovery Things go back to normal or may remain

insufficient and become chronic

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AcuteRenalFailure CAUSES

Pre-renal (hypoperfusion)

Renal (intrinsic)

Post-renal (obstructive)

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AcuteRenalFailure SPECIFIC CAUSES

Prerenal Hypovolemia, shock, blood loss, embolism,

pooling of fluid due to ascites or burns,cardiovascular disorders, sepsis

Intrarenal ATN, nephrotoxic agents, infections, ischemia

acute tubular necrosis, acute nephritis, polycystic

kidney disease

Postrenal Stones, blood clots, BPH, urethral edema from

invasive procedures, renal calculi

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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

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TREATMENT Make/consider the diagnosis

Treat life threatening conditions Identify the cause if possible

Hypovolemia

Toxic agents (drugs, myoglobin)

Obstruction

Treat reversible elements Hydrate

Remove drug

Relieve obstruction

AcuteRenalFailure

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NURSING CARE Fluid and dietary restrictions

Protein, potassium & phosphate restriction Maintain electrolytes

D/C or reduce causative agent

Adjust medication doses

May need dialysis to jump start renal function

May need to stimulate production of urine withIV fluids, Dopamine, diuretics, etc.

AcuteRenalFailure

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DIALYSIS

Hemodialysis

Peritoneal Dialysis

Continuous Renal Replacement Therapy (CRRT)

AcuteRenalFailure

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TREATMENT

Strict I&O

Daily weights

Watch for heart failure

Monitor lab results

Watch for hyperkalemia

Watch forhyper/hypoglycemia

Maintain nutrition

Mouth care

Monitor skin

S & S of Hyperkalemia: Malaise, anorexia,parenthesia, muscle weakness, EKG changes

Chronic RenalFailure

S & S

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BREAK

CCRN REVIEW PART 2

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ElectrolyteDisturbances

Na+

Ca++

Cl-

Mg+

K+

PO4

NH3

Cu

HCO3-

NaCl

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Dominant intracellular electrolyte

Primary buffer in the cell

K+

Potassium (K+)

Normal serum K+ level: 3.5-5.5 mEq/L

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INVOLVED IN Muscle contraction

Nerve impulses Cell membrane function

Attracting water into the ICF

Imbalances interfere with neuromuscular function

and may cause cardiac rhythm disturbances

Potassium (K+)

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Hyperkalemia

SIGNS & SYMPTOMS

Weakness, malaise, lethargy

Anorexia

Muscle cramps

Paresthesias

Dysrhythmias

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K > 5.5 -6

Tall, peaked Ts

Wide QRS

Prolong PR

Diminished P

Prolonged QT QRS-T wave

merge = sine wave

Hyperkalemia

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TREATMENT Calcium Gluconate (carbonate)

Calcium Chloride Sodium Bicarbonate

Insulin/glucose

Kayexalate

Lasix

Albuterol

Hemodialysis

Hyperkalemia

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SIGNS & SYMPTOMS Malaise

Skeletal muscle weakness

Decreased reflexes

Hypotension

Vomiting

Excessive thirst

Cardiac arrhythmias and cardiac arrest

Flattened T wave

U wave

Hypokalemia

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Hypokalemia

CAUSES

Reduced dietary intake

Poor absorption by the body

Vomiting and/or diarrhea

Renal disease

Medications (typically diuretics)

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SIGNS & SYMPTOMS Cold, clammy, pale skin

Nervousness

Shakiness, lack of coordination, staggering gait Irritability, hostility, and strange behavior

Difficulty concentrating

Fatigue

Excessive hunger

Headache

Blurred vision and dizziness

Abdominal pain or nausea

Fainting and unconsciousness

Hypoglycemia

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SIGNS & SYMPTOMSCardiovascular Signs

Palpitations

Tachycardia

Anxiety

Irritability

Diaphoresis

Pale, cool skin

Tachypnea

Neurological Signs

Agitation

Confusion

Slurred Speech

Staggering Gait

Paraplegia

Seizures

Coma

Acute Hypoglycemia

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SIGNS & SYMPTOMS Thirst

Polyuria Dehydration

Nausea, vomiting

DKA

HNNK

Hyperglycemia

Normal serum Glu level: 70 - 110 mg/dL

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SIGNS & SYMPTOMS

Excess sodium in the blood

Hypertension

Muscle twitching

Mental confusion

Coma

Hypernatremia

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Activates many enzymes

50% is insoluble in bone

45% is intracellular

5% is extracellular

Mg+

Magnesium (Mg+)

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

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CAUSES

Alcoholism

Malabsorption

Starvation

Diarrhea

Diuresis

Hypomagnesemia

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SIGNS & SYMPTOMS Peaked T wave

Bradycardia

CNS Depression

Areflexia

Sedation

Respiratory paralysis

Hypermagnesemia

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CAUSES

Not common

Occurs with chronic renal insufficiency

Treatment is hemodialysis

Hypermagnesemia

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INVOLVED IN Blood clotting

Nerve impulse

Muscle contraction

Ca++

Calcium (Ca++)

Excreted through urine, feces, and perspiration

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SIGNS & SYMPTOMS Tetany(cramps/convulsions in wrists and ankles)

Weak heart muscle Increased clotting time

Prolonged QT interval

May lead to Torsade de Pointes

Abnormal behavior Chvostek's sign (facial twitching)

TrousseausSign (carpopedal spasm)

Paresthesia

Hypocalcemia

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CAUSES

Renal insufficiency

Decreased intake or malabsorption of Calcium

Deficiency in or inability to activate Vitamin D

Hypocalcemia

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SIGNS & SYMPTOMS Kidney stones

Bone pain

Hypotonicity of muscles(decreased tone)

Altered mental status

Cardiac arrhythmias

Shortened QT interval

Hypercalcemia

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INVOLVED IN

Energy metabolism

Genetic coding

Cell function

Bone formation

PO4

Phosphorus (P, PO4)

Normal serum PO4 level: 2.5-4.5 mg/dL

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CAUSES Severe infections

Kidney failure

Thyroid failure

Parathyroid Failure

Often associated with hypercalcemia orhypomagnesemia or too much Vitamin D

Cell destruction - from chemotherapy, when thetumor cells die at a fast rate

Can cause tumor lysis syndrome

Hypophosphatemia

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SIGNS & SYMPTOMS

Elevated blood phosphate level

There are no symptoms of hyperphosphatemia

Hyperphosphatemia

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TREATMENT

Calcium Carbonate tablets

Aluminum hydroxide

Can cause aluminum toxicity

Hyperphosphatemia

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IV Fluid Therapy

OSMOLALITY

Concentration of a solution

Concentration of solutes per kilogram

The higher the osmolality the greater

its pulling power for water

Normal serum osmolality is 275 to 295mOsm/L

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Isotonicsame osmolality as serum

Hypotoniclower osmolality than serum

Hypertonichigher osmolality than serum

IV Fluid Therapy

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IV Solutions

D5W Hypotonic in the body

Hypotonic

Solutions

Used for cellular dehydration

Not used with head injuries

Isotonic

SolutionsHydrates extracellular compartment

Hypertonic

SolutionsPulls fluid into vascular space

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IV Solutions

D5W

D10W

D50W

NSNS

D51/2 NS

D5NS

D5W Hypotonic in the body

Isotonic

Hypertonic

Hypertonic

HypotonicIsotonic

Hypertonic

Hypertonic

Hypertonic

Isotonic

Hypertonic

HypertonicHypertonic

Hypertonic

Hypertonic

3% NaCl

LR

D5LR

AlbuminDextran

Hetastarch

PRBCs

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Daily Fluid Balance

Intake:

1-1.5 L

Insensible Loss

- Lungs 0.3 L

- Sweat 0.1 L

Urine: 1.0 to 1.5 L

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Intracellular

(2/3)

Extracellular

(1/3)

Solids 40% of Wt

H2O H2O

Na

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Intra-

vascular

(1/4)

E.C.F.

COMPARTMENTS

Interstitial (3/4)

H2O H2O

NaNa

Colloids

& RBCs

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1 liter 5% Dextrose

Total body water

ECF=1/3 = 300ml ICF=2/3 = 700ml

Intravascular

=1/4 of ECF~75ml

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CerebralSpinalFluid

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

brain, the cavity of the spinal cord, and the subarachnoid space

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Spinal Cord Nerve Tracts

Ascending

Sensory

Tract

Descending

Motor Tract

(Corticospinal Tract)

(Spinothalmic Tract)

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Brown-Squard syndrome

Incomplete

Spinal Cord

Injury

(Hemi-section)

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Intracranial Aneurysms

Usually occur at bifurcations and branches of the

large arteries located in the Circle of Willis

The most common sites include the:

Anterior Communicating artery (30 - 35%)

Bifurcation of the Internal Carotid and Posterior

Communicating artery (30 - 35%)

Bifurcation of Middle cerebral (20%) Basilar artery bifurcation (5%)

Remaining posterior circulation arteries (5%)

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Types of Aneurysms

Saccular aneurysm

Occurs at bifurcations

Fusiform aneurysm

Often in basilar artery

Dissecting aneurysm

Ruptured aneurysm

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Brain Circulation

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Arterial Circulation in the Brain

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SIGNS & SYMPTOMS Usually asymptomatic until rupture

Cranial Nerve Palsy

Dilated Pupils Double Vision

Pain Above and Behind Eye

Localized Headache

Warning signs prior rupture

Localized Headache Nausea & Vomiting

Stiff Neck

Blurred or Double Vision

Sensitivity to Light (photophobia)

Loss of Sensation

Intracranial Aneurysms

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Treatment of Brain Aneurysms

Surgery

Craniotomy and clipping

Endovascular coiling

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Aneurysm Post-Op Risks

Rebleeding Most frequently within the first 24 hours

Up to 20% of patients rebleed within 14 days

Main preventative measure is control of blood pressure(preferably beta blockers)

Vasospasm Usually occurs before 3 days or after 10 days (post bleed)

May require hypervolemic therapy

Hydrocephalus Hyponatremia

Fluids / Electrolytes

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Arterio-Venous Malformation

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The arteries and veins have a direct connection,

bypassing the capillary network

Presents with ongoing headaches, seizures,

hemorrhage, or progressive neurological

dysfunction


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SIGNS & SYMPTOMS Seizures

Headaches

Whooshing" Sound (Bruit)

Other Signs

Subtle behavioral changes

Communication or thinking disturbances

Loss of coordination and balance

Paralysis or weakness in one part of the body

Visual disturbances

Abnormal sensations

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COMPLICATIONS

Hemorrhage(into surrounding tissue)

Ischemia

Seizures

Brain Cell Death

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DIAGNOSIS

MRI (including MR Angiography) as well as CT

Angiography help identify AVMs

Cerebral Angiographyis a prerequisite to

treatment

To identify the precise anatomy and configuration

of both the lesion and the feeding and drainingvessels

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TREATMENT

Surgery

Usually delayed

Open ligation and/or resection of the AVM

Radiosurgery

Embolization

Usually as adjunct to surgery

Observation

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RADIOSURGERY

Believed to "work" by initiating an "inflammatory"

response in the pathological blood vesselsultimately resulting in their progressive narrowing

and ultimate closure

The risk for hemorrhage is not reduced during this

lag time

There is the added risk of radiation necrosis of

adjacent healthy brain tissue or brain cyst formation

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Brain Radiosurgery

ADVANTAGES

Noninvasive

Can access all anatomic locations of the brain

DISADVANTAGES

Can only treat smaller lesions

(

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AVM Post-Op Risks

Perfusion-breakthrough bleeding

Endovascular occlusion

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Sudden onset of the worst headache of my life

IntracranialHemorrhage

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Epidural

Subdural

Subarachnoid

Intraparencymal

Intraventricular

Cerebellar

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ICH is a dynamic, not a static process

Hemorrhage volume can increase over time

CT scan is the most important diagnostic tool

Managing blood pressure is extremely important

Must aggressively manage fever and seizures

Consider hyperventilation and paralytics in setting

of increased ICP and deterioration


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Treatment of ICH

KEY CONCEPTS

1) Intracranial Pressure

Elevated when ICP >20 mm Hg

2) Cerebral Perfusion Pressure

CPP = MAP - ICP

Must maintain CPP > 70 mm Hg Example: MAP = 100, ICP = 20

CPP = 80 mmHg

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Subarachnoid Hemorrhage (SAH)

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

area of the skull surrounding the brain (the subarachnoid

space) rapidly fills with blood

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SIGNS & SYMPTOMS

Sudden, intense headache

Neck pain

Nausea or vomiting

Neck stiffness

Photophobia

Sudden onset of the worst headache of my life

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SAH may be spontaneous or traumatic

Spontaneous SAH causes

Cerebral aneurysms

AV malformations

Trauma

Uncommon causes

Neoplasms, venous angiomas, infections

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Warning bleeds are relatively common

Sentinel headache 30-50%

Early diagnosis prior to rupture will improve outcomes

50% of patients die within 48 hours irrespective of

therapy

Subarachnoid Hemorrhage

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Often accompanied by a period of unconsciousness

(50% never wake up)

Common signs include neck stiffness, photophobia,

headache

20% have ECG evidence of myocardial ischemia

Subarachnoid Hemorrhage

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Complications of SAH

Hydrocephalusmay develop within the first 24hours because of obstruction of CSF outflow in theventricular system by clotted blood

Rebleedingof SAH occurs in 20% of patients in thefirst 2 weeks. Peak incidence of rebleeding occurs the dayafter SAH and may be from lysis of the aneurysmal clot

Vasospasmfrom arterial smooth muscle contraction(symptomatic in 36% of patients)

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Re-bleeding After SAH

Re-bleeding occurs most frequently within the first 24 hrs

Up to 20% of patients rebleed within 14 days

The main preventative measure is to control the bloodpressurepreferably beta blockers

Early clipping of the aneurysm allows hypertensive andhypervolemic therapy to prevent vasospasm

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Vasospasm After SAH

Worst time is day 7 to day 10 (most frequent time forvasospasms)

Diagnosed by neurologic exam, transcranial doppler andangiography

May use calcium channel blockers

Reduces vasospasm, neurological deficit, cerebral infarction

and mortality

May use some antispasmodics

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Vasospasm & HHH Therapy

Hemodilution

Hct 30-35%

Hypertension

Phenylephrine / Norepinephrine

BP titration to CPP/exam

Hypervolemia Colloids/crystalloids

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Other Vasospasm Therapy

Angioplasty

BP management during procedure

Reperfusion issues

Timing

Papaverine Infusion

Side effects

Repeated trips

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Neurologic deficitsfrom cerebral ischemia, peaks at days 4-12

Hypothalamic dysfunctioncauses excessive sympathetic

stimulation, which may lead to myocardial ischemia or labile BP

Hyponatremiamay result from cerebral salt wasting / SIADH

Nosocomial pneumoniaand other such complications

Pulmonary edemaneurogenic & non-neurogenic

Other Complications of SAH

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1) Identify and treat the causative lesion

Thus preventing re-bleeding

2) Treat hydrocephalus

3)

Treating and prevent vasospasm

Treatment of SAH

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Maintain systolic BP >130mmHg

Use vasopressors if necessary to maintain CPPand reduce ischemic complications from vasospasm

Generally avoid vasodilators (except calcium

channel blockers)

Treatment of SAH

CCRN REVIEW PART 2

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BREAK

CCRN REVIEW PART 2

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Stroke

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Stroke

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RISK FACTORS TIA

CAD

High Blood Pressure High Cholesterol

Smoking

Heart Disease

Diabetes

Excessive alcohol

Family History

Age

Sex

Race

Obesity

Annual risk of stroke: Increases with age

Stroke

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Computed Tomography (CT)

Magnetic Resonance Imaging (MRI)

Cerebral Angiography: identify responsible vessel

Carotid Ultrasound: carotid artery stenosis

Echocardiogram: identify blood clot from heart

Electrocardiogram (ECG): underlying heart conditions

Heart monitors, blood work and more tests!!

Stroke Tests

a

es.ht

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CT MRI

p://www.strokecente

r.org/education/ais_

ct_tool/ct04/

ct04-fr

http://www.strokecenter.org/education/ais_ct_tool/index.htm

T t t f I h i CVA

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Tissue plasminogen activator (tPA) can be givenwithin three hours from the onset of symptoms

Heparin

Intra-arterial thrombolysis

Hemicraniectomy

In addition to being used to treat strokes, thefollowing can also be used as preventative measures

Anticoagulants/Antiplatelets

Carotid Endarterectomy

Angioplasty/Stents

Treatment of Ischemic CVA

T t t f H h i CVA

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Surgery is often required to remove pooled blood

from the brain and to repair damaged blood vessels

Prevention:

An obstruction is introduced to prevent rupture and

bleeding of aneurysms and AVMs

Surgical Intervention

Endovascular Procedures

Treatment of Hemorrhagic CVA

P ti f CVA

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Control high Blood Pressure

Lower cholesterol

Quit smoking Control diabetes

Maintain healthy weight

Exercise

Manage stress

Eat a healthy diet

Prevention of CVA

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BREAK

CCRN REVIEW PART 2

Metabolic Alterations

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DKA & HHNK

DI & SIADH

DIC

Shock States

Sepsis

MetabolicAlterations

Diabetic Ketoacidosis

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What is DKA?


A life-threatening complication seen with

Diabetes Mellitus Type 1

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HHNK

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HHNK

What is HHNK?

Hyperglycemic Hyperosmolar Nonketonic Coma

A life threatening complication seen with

Diabetes Mellitus Type 2

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DKA vs HHNK

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DKA vs HHNK

DKA

Faster Onset

Glucose 300-800

Acidosis

Fruity Breath

Kussmaul Respirations

HHNK

Slower Onset

Glucose 600-2000

No Acidosis

Normal Breath

Shallow Respirations

Treatment of DKA & HHNK

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Treatment of DKA & HHNK

Reverse Dehydration

NS, then NS

Restore Glucose Levels

D5 NS When Glu 250

Restore Electrolytes

Diabetes Insipitus

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Diabetes Insipitus

What is Diabetes Insipitus?

A Condition resulting from too little ADH

Why is it called Diabetes Insipitus?

The term Diabetes refers to polyuria

Diabetes Insipitus

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Diabetes Insipitus

SIGNS & SYMPTOMS

Polyuria

Severe Hypovolemia

Severe Dehydration

Elevated Serum Osmolality

Elevated Serum Sodium

Shock

Diabetes Insipitus

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Diabetes Insipitus

CAUSES

Decreased ADH

Neurological Surgery

Head Trauma

Dilantin or Lithium

Diabetes Insipitus

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Diabetes Insipitus

TREATMENT

Fluid Resuscitation

ADH Replacement

Vasopressin, Pitressin, DDAVP

Treat The Cause

SIADH

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SIADH

What is SIADH?

Syndrome of Inappropriate ADH

Too much ADH

SIADH

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SIADH

SIGNS & SYMPTOMS Hyponatremia

Low Serum Sodium

Serum NA < 135

Low Serum Osmolality

High Urine Osmolality

Elevated Specific Gravity

Urine specific gravity> 1.030

Elevated Urine Osmolality

Elevated ADH Level

Weight Gain Without Edema

Elevated CVP, PAP, PAWP

Hypertension

Concentrated And UOP

Headache

Altered LOC

Seizures

SIADH

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CAUSES

Head Trauma

Oat Cell Carcinoma

Other Cancers

Viral Pneumonia

SIADH

Medications

Stress

Mechanical Ventilation

SIADH

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TREATMENT Monitor Fluid Balance, Monitor I & O

Restrict Fluids Replace Na+ loss when necessary

May Give 3% (Hypertonic) Saline

May Give Dilantin or Lithium

May require PA Catheter For Monitoring

May Give Diuretics

SIADH

DI vs SIADH

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DI vs SIADH

DI

Too Little ADH

Dehydration

High Serum Sodium

High Serum Osmolality

Low Urine Osmolality

SIADH

Too Much ADH

Water Intoxication

Low Serum Sodium

Low Serum Osmolality

High Urine Osmolality

DI vs SIADH Treatment

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DI vs SIADH Treatment

DI

Lots of Fluids

Hold Dilantin

Hold Lithium

Give ADH

SIADH

Fluid Restriction

May Give Dilantin

May Give Lithium

3% Saline

DIC

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DIC

What is DIC?

Disseminate Intravascular Coagulation

A clotting disorder that ultimately causes

bleeding

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DIC

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SIGNS & SYMPTOMS

Bleeding

Thrombosis

Organ Failure

DIC

DIC

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DIC

DIC

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CAUSES Massive Tissue Injuries

Obstetric Emergencies

Septicemia

Cancers

Vascular Disorders

Systemic Disorders

Many More Causes

DIC

DIC Lab Results

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CLOTTING FACTORS DEPLETED

Platelets

Fibrinogen Protein Activated C

Antithrombin

DIC Lab Results

CLOTTING TESTS ELEVATED

PT

aPTT

Fibrin degradation products (D-dimer)

DIC

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TREATMENT

Treat the Cause

Replace Clotting Factors

Anticoagulation Therapy (Heparin)

DIC

CCRN REVIEW

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THE END

PART 2

CCRN REVIEW

CCRN REVIEW PART 2

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THANK YOU!

CC

CCRNREVIEW

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GOOD LUCK!

References

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References

American Stroke Association. (2007). Acute and PreventativeTreatments. Retrieved March 4, 2007 fromhttp://www.strokeassociation.org/presenter.jhtml?identifier=2532.

Block, C., and Manning, H. (2002). Prevention of acute renal failure inthe critically ill. American Journal of Respiratory and Critical CareMedicine; (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. AACNClinical Issues; (16)515-525.

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

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

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Documents

CCRNPart2