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CKD Esrd

Based on the information provided: - 57-year-old with history of hypertension (HTN) and chronic kidney disease (CKD) stage 5, indicating end-stage renal disease (ESRD) - Patient refused dialysis - Developed respiratory distress after upper respiratory viral infection - Prior to arrest, patient developed asystolic cardiac arrest - Was resuscitated by EMTs - Admitted to ICU This patient likely developed uremic frost due to extremely high blood urea nitrogen (BUN) levels from end-stage renal failure without dialysis treatment. Urea crystallizes on the skin when BUN levels are very elevated, appearing as a white, frost-like coating. The respiratory

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Rita Lakhani
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100% found this document useful (1 vote)
240 views83 pages

CKD Esrd

Based on the information provided: - 57-year-old with history of hypertension (HTN) and chronic kidney disease (CKD) stage 5, indicating end-stage renal disease (ESRD) - Patient refused dialysis - Developed respiratory distress after upper respiratory viral infection - Prior to arrest, patient developed asystolic cardiac arrest - Was resuscitated by EMTs - Admitted to ICU This patient likely developed uremic frost due to extremely high blood urea nitrogen (BUN) levels from end-stage renal failure without dialysis treatment. Urea crystallizes on the skin when BUN levels are very elevated, appearing as a white, frost-like coating. The respiratory

Uploaded by

Rita Lakhani
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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CKD/ESRD

&
Management
“Bones can break, muscles can atrophy,
glands can loaf, even the brain can go to
sleep without immediate danger to
survival. But -- should kidneys fail....
neither bone, muscle, nor brain could
carry on”.
-Homer Smith, Ph.D.

2
REVIEW
 Recall functions of the kidneys?

 Recall normal creatinine & BUN; other lab


tests?

 Review Diagnostic Tools


CKD- Elderly Risk (Review)
•Older Adult-normal aging (plus co-morbidities) > risk kidney dysfunction/renal failure
•Must:

•Identify/prevent damage
•Monitor/risk multiple RX/OTC meds (altered renal blood flow/dec. renal
clearance etc)
•Monitor/risk associated with dehydration (ie diuretics)
•Monitor/risk with dec ability to respond to changes to fluid/electrolyte
status (manifestation may be atypical
Functions of the Kidneys

 Regulates volume and  Vitamin D activation


composition of
extracellular fluid
 Acid-base balance
(HCO3 & H) regulation
 Excretion of nitrogenous
through process of
waste products _____, ____ and ______.
 BP control via renin-  Prostaglandin synthesis
filtration, secretion,
angiotensin-aldosterone reabsorpton
 Erythropoietin
system- Recall RAAS
production
Functions of the Kidneys
(cont)
 Erythropoietin Release
 If a patient has chronic renal failure, what
condition will occur?
 WHY???

EPO- glycoprotein hormone that controls


erythropoiesis, or red blood cell production

6
Diagnostic Tools for
Assessing Renal Failure
 Blood Tests
 BUN elevated (norm 10-20 mg/dl) (text 10-30mg/dl)
 Creatinine elevated (norm 0.6 - 1.2 mg/dl) (text 0.5-
1.5mg/dl)
 K elevated (text norm 3.5-5.0 mEq/L)
 PO4 elevated (text norm 2.8-4.5mg/dl)
 Ca decreased (text norm 9-11mg/dl)
 Urinalysis
 Specific gravity (text norm 1.003-1.030
 Protein (text norm 0-trace)
 Creatinine clearance (text norm 85-135ml/min)

7
BUN
 Normal 8 - 20 mg/dl (text 10-30mg/dl)
 Nitrogenous waste product of protein
metabolism
 Unreliable in measurement of renal function
 Relevance assessed in conjunction with serum
creatinine

8
Creatinine
 A waste product of muscle metabolism
 Normal value 0.6 - 1.2 mg/dl (text 0.5-
1.5mg/dl)
 2 times normal = 50% damage
 8 times normal = 75% damage
 10 times normal = 90% damage
 Exception - severe muscular disease can greatly 
serum creatinine levels

9
Diagnostic Tools
 Ultrasound
 X-Rays
 Biopsy *most definitive

10
Chronic Renal Failure/
Chronic Kidney Disease (CKD)
 Slow progressive renal disorder related to
nephron loss, occurring over months to years

 Culminates in End Stage Renal Disease


(ESRD)

11
Characteristics of CKD > ESRD

 Cause & onset often unknown


 Loss of function precedes lab abnormalities
 Lab abnormalities precede symptoms
 Symptoms (usually) evolve in orderly sequence
 Renal size is usually decreased

12
Causes of CKD
 *Diabetes
•Neoplasms
 *Hypertension •Obstructive disorders
 Glomerulonephritis •Autoimmune diseases
 Cystic disorders (lupus)
 Developmental - •Hepatorenal failure
Congenital •Scleroderma
•Amyloidosis
 Infectious Disease
•Drug toxicity-(overuse some
common drugs, as aspirin, NSAID as
ibuprofen, cocaine and
acetaminophen)
NSAIDs-…cause prerenal ARF by blocking prostaglandin production > also alters
local glomerular arteriolar perfusion… (reduces renal blood flow)

13
Glomerular Filtration Rate (GFR)-determine stage
CKD (most accurate evaluation)

 24 hour urine for creatinine clearance


 Formula- urine creatinine X urine volume
 serum creatinine
 Can estimate creatinine clearance by:
140 – {age x weight (kg)}
72 x serum creatinine

 What is normal GFR?


90 - 120 mL/min
14
Stages of CKD (“old”
terminology)
 Reduced Renal Reserve
 Renal Insufficiency
 End Stage Renal Disease (ESRD)

15
Stages of CKD
NKF Classification System

Stage 1: GFR > 90 ml/min despite kidney


damage
Stage 2: Mild reduction (GFR 60 – 89
ml/min)
1. GFR of 60 may represent 50%
loss in function.
2. Parathyroid hormones starts to
increase. (why?)
*kidneys unable to reabsorb calcium, blood calcium levels fall,
stimulating continual secretion of parathyroid hormone to maintain
normal calcium levels in blood.
16
During Stage 1 - 2
 No symptoms

FYI-older adult- may


 Serum creatinine doubles* impaired renal function even in
presence of normal serum

(Up to 50% nephron loss


 creatinine

17
Stages of CKD
NKF Classification System

Stage 3: Moderate reduction (GFR 30 – 59


ml/min)
1. Calcium absorption decreases
(from the GI tract)
2. Malnutrition onset
3. Anemia
4. Left ventricular hypertrophy

18
Stages of CKD
NKF Classification System

Stage 4: Severe reduction (GFR 15 – 29


ml/min)
1. Serum triglycerides
2. Hyperphosphatemia
3. Metabolic acidosis
Oops- 4. Hyperkalemia
trouble!

K Effect & EKG


19
During Stage 3 - 4

 Signs and symptoms worsen if kidneys stressed


 ability to maintain homeostasis
 75% nephron loss
 glomerular filtration rate, solute clearance,
ability to concentrate urine and secrete hormone
 Symptoms: BUN & Creatinine, mild
azotemia, anemia
20
Stages of CKD-NKF Classification System
Stage 5: Kidney failure (GFR < 15 ml/min) ESRD!!!

 Azotemia

 Residual function < 15% of normal

 Excretory, regulatory, hormonal functions severely


impaired
 Metabolic acidosis (Kussmaul breathing)

 Marked : BUN, Creatinine, Phosphorous


 Marked : Hemoglobin, Hematocrit, Calcium

 Fluid overload

21
During Stage 5
 Uremic syndrome develops- affecting all body
systems
 can be diminished with early diagnosis & treatment
 Last stage of progressive CKD
 Fatal if no treatment

22
Manifestations of Chronic
Uremia
Syndrome-
combination
of common
symptoms
*greater
build-up
waste
products =
greater
symptoms

Fig. 47-5

23
What happens when kidneys
don’t function correctly?

24
Manifestations of CKD -
Nervous System
 Mood swings
 Impaired judgment
 Inability to concentrate and perform simple math
functions
 Tremors, twitching, convulsions
 Peripheral Neuropathy
 restless legs

 foot drop
Manifestations due to inc nitrogenous waste products, electrolyte imbalances, metabolic
acidosis and axonal atrophy and demyelination of nerve fibers & dec erythropoietin*

25
Manifestations of CRF
Skin
 Pale, grayish-bronze color
 Dry scaly
 Severe itching
 Bruise easily, petechiae, ecchymosis
 *Uremic frost
*Manifestations due to…calcium-phosphate deposition in skin, sensory
neuropathy, platelet abnormalities; urea crystallizes (uremic frost) >if
BUN extremely high

26
Medical Mystery? What do lab studies, etc indicate ? What causes uremic frost?

*57-year-old with HTN and CKD (Stage 5), refused dialysis found in respiratory distress after week
of upper respiratory symptoms due to viral infection

Before admission to hospital >developed asystolic cardiac arrest, was resuscitated by EMT, admitted to ICU,
required vasopressor support.

PE- diffuse deposits tiny white crystalline material on skin > lab studies- BUN 208 mg/dl; creatinine 15 mg/dl;
bicarbonate level 5 mmol per liter; anion gap-26; arterial pH of 6.74, and arterial partial pressure of carbon
dioxide of 50 mm Hg. Blood cultures- revealed-Staphylococcus aureus pneumonia, likely due to prior
Walsh S and Parada N. N Engl J Med 2005;352:e13
influenza infection. *Aggressive care measures withdrawn after consultation with patient's family >patient
died.

*Uremic frost- uncommon skin manifestation due to profound azotemia;


occurs when urea and other nitrogenous waste products accumulate in sweat
and crystallize after evaporation.
Manifestations of CKD
Eyes
 Visual blurring
 Occasional blindness
 “Red eye”

Due to calcium-phosphate deposits


in eyes

28
Manifestations of CKD
Fluid - Electrolyte - pH
 Volume expansion and fluid overload
Due to impaired kidneys unable to excrete acid load (mostly
 Metabolic Acidosis from NH3); defective reabsorption/regeneration of HCO3.
 Electrolyte Imbalances
Due to dec excretion by kidneys, breakdown of cellular
 Potassium protein, bleeding, metabolic acidosis, food, drugs, etc

 Magnesium Kidneys unable to excrete (too much magnesium


causes hyporeflexia and can lead to cardiac arrest)

 Sodium Kidneys retain > water retention> fluid overload

29
Manifestations of CKD
GI Tract/Bleeding Risk
 Uremic fetor
 Anorexia, nausea, vomiting
 GI bleeding Due to GI irritation, platelet defect; diarrhea from hyperkalemia
 Anemia
 Platelet dysfunction
Anemia-due to insufficient production of erythropoietin, protein
naturally produced in functioning kidneys…circulates through
bloodstream to bone marrow, stimulating production of RBCs.

Platelet dysfunction-subnormal platelet aggregation -due to fibrinogen fragments,


usually absent in normal human blood but present in uremic plasma may lead to
platelet dysfunction in uremia.

30
Manifestations of CKD-Musculoskeletal

 Muscle cramps
 Soft tissue calcifications
 Weakness
 Related to calcium phosphorous imbalances
 RENAL OSTEODYSTROPHY
 Fracture risk!

31
Manifestations of CKD- Heart & Lungs

 Hypertension
 Heart failure > pulmonary edema
 Pericarditis due to uremia
 Pulmonary edema
 Pleural effusions- “Uremic Lung”
 Atherosclerotic vascular disease*
 Cardiac dysrhythmias (from HF, electrolyte
imblaances)
*Major Problem!

32
Manifestations of CKD- Endocrine -
Metabolic
 Erythropoietin
 Hypothyroidism
 Insulin resistance
 Growth hormone
 Gonadal dysfunction
 Parathyroid hormone and Vitamin D 3
 Hyperlipidemia

33
Treatment Options
 Conservative Therapy * (Severe restrictions, dietary,
fluids maintain renal function as long as possible- if GFR >
10ml/min)
 Hemodialysis
 Peritoneal Dialysis
 Transplant
 Nothing > Death

34
Conservative Treatment Goals
 Detect/treat potentially reversible causes of
renal failure
 Preserve existing renal function
 Treat manifestations
 Prevent complications
 Provide for comfort

35
Conservative Treatment
 Control
 Hyperkalemia
 Hypertension

 Hyperphosphatemia

 Hyperparthryoidism

 Anemia

 Hyperglycemia

 Dyslipidemia

 Hypothyroidism
Depends on lab values-usually low
 Nutrition : Describe a renal diet?NA, K, restricted protein,
phosphorous, & fluids (See text)
36
Hemodialysis
 Removal of soluble substances and water from the blood by
diffusion through a semi-permeable membrane.

 Early animal experiments began 1913


 1st human dialysis 1940’s by Dutch physician Willem Kolff (2
of 17 patients survived)
 Considered experimental through 1950’s, No intermittent
blood access; for acute renal failure only.
 1960 Dr. Scribner developed Scribner Shunt-1960’s machines
expensive, scarce, no funding.
 “Death Panels” panels within community decided who got to
dialyze.

37
Hemodialysis Process
 Blood removed from patient into
extracorporeal circuit.
 Diffusion and ultrafiltration take place in
dialyzer.

 Cleaned blood returned to patient.

38
Extracorporeal Circuit

39
How Hemodialysis Works

40
.
How Dialysis Works-Interactive!
An Introduction to Dialysis-How
Stuff Works! (Step by Step)
YouTube- Hemodialysis! Great!

                                                                            

                                                                            
Vascular Access (click)
 Arterio-venous shunt (External Shunt) *used
now for Continuous Renal Replacement
Therapy (CRRT)-temporary access
 Arterio-venous (AV) Fistula (AKA-native or primary
fistula)
 PTFE Graft
 Temporary catheters
 “Permanent” catheters

42
External Shunt (Schribner Shunt)
 External- one end into
artery, one into vein.
 Advantages
 place at bedside
 use immediately
 Disadvantages
 infection
 skin erosion
 accidental separation
 limits use of extremity
 *Used now only for
CRRT-temporary

43
Arterio-venous (AV) Fistula
Primary (native) Fistula
 Patients own artery and vein surgically anastomosed.
 Advantages
 patient’s own vein/artery

 longevity

 low infection and thrombosis rates

 Disadvantages
 long time to mature, 1- 6 months

 “steal” syndrome

 requires needle sticks davita.com

44
PTFE (Polytetraflourethylene) Graft
 Synthetic “vessel” anastomosed into an artery and vein.
 Advantages
 for people with inadequate vessels

 can be used in 1-4 weeks

 prominent vessels

 Disadvantages
 clots easily

 “steal” syndrome more frequent

 requires needle sticks

 infection may necessitate removal of graft

45
Temporary Catheters
 Dual lumen catheter placed into a central vein-
subclavian, jugular or femoral.
 Advantages
 immediate use

 no needle sticks

 Disadvantages
 high incidence of infection

 subclavian vein stenosis

 poor flow-inadequate dialysis

 clotting

 Restricts movement
46
Cuffed Tunneled Catheters (Dacron cuff)
 Dual lumen catheter with Dacron cuff
surgically tunneled into subclavian,
jugular or femoral vein.
 Advantages
 immediate use; *permanent/long
term use
 can be used for patients that can have
No other permanent access
 no needle sticks
 Disadvantages
 high incidence of infection
 poor flows result in inadequate
dialysis
 clotting

47
Above Native fistula (in place for over 20 “Temporary” vascular access catheters- if tunnelled,
years) with Dacron cuff, can be used long-term as
Permacath, below.
*Remember- assess circulation-listen for bruit,
feel for thrill!

Buttonhole technique-individual cannulates


own fistula
for home dialysis YouTube video
Care of Vascular Access
 NO BP’s, needle sticks to arm with vascular
access. This includes finger sticks.
 Place ID bands on other arm whenever
possible.
 Palpate thrill and listen for bruit.
 Teach patient nothing constrictive, feel for
thrill.

49
Potential
Complications of Hemodialysis
 During dialysis
 Fluid and electrolyte related
 hypotension
 Cardiovascular
 arrhythmias
 Associated with the extracorporeal circuit
 exsanguination
 Neurologic
 Disequilibrium Syndrome & seizures
 Musculoskeletal
 cramping
 Other
 fever & sepsis
 blood born diseases

50
Potential Complications of Hemodialysis
Long term (due to disease process
& management)
 Between treatments

 Hypertension/HypotensionMetabolic
 Edema
•Hyperparathyroidism
 Pulmonary edema
•Diabetic complications
 Hyperkalemia
•Cardiovascular
 Bleeding
CHF
 Clotting of access
AV access failure
Cardiovascular
disease
•Respiratory
Pulmonary edema
•Neuromuscular
51
Complications Hemodialysis- con’t-long term, ESRD

 Long term cont’d Long term cont’d


•Genitourinary
 Hematologic •infection
 anemia •Sexual dysfunction
 GI •Psychiatric
•depression
 bleeding
•Infection
 dermatologic •blood borne
 calcium pathogens
phosphorous
deposits
 Rheumatologic
 amyloid deposits
52
Dietary Restrictions-Hemodialysis

 Fluid restrictions Urine output + 500-600


 Phosphorous restrictions Approx 800-1200 mg/day
 Potassium restrictions Approx 1-2 g/day; 40 mg/kg/IBW
 Sodium restrictions Approx 1-2 g/day
 Protein to maintain nitrogen balance (complete)
 too high - waste products
 too low - decreased albumin, increased mortality

 Calories to maintain or reach ideal weight


53
Peritoneal Dialysis
 Removal of soluble substances and water from blood by diffusion through a
semi-permeable membrane (peritoneum) that is intracorporeal (inside
body).
 Solution warmed to body temperature prior to instillation into
peritoneal cavity via peritoneal catheter
 Metabolic waste products and excessive electrolytes diffuse into
dialysate while it remains in abdomen
 Fluid removal controlled by glucose (dextrose) concentration in
dialysate (acts as “osmotic” agent)
 Excess fluid/solutes removed- gradual/constant-
 Fluid drained by gravity into sterile bag at set intervals-
1. “Clear” solution ‘fills” abdomen
2. “Yellow” urine-like fluid drains out (like urine, clear)
3. Types of Peritoneal Dialysis
1. *CAPD: Continuous ambulatory peritoneal dialysis
2. CCPD: Continuous cycling peritoneal dialysis/Aka. *APD – Automated
Peritoneal Dialysis
3. IPD: Intermittent peritoneal dialysis (also)
54
Phases of Peritoneal
Dialysis Exchange

1. Fill (inflow): fluid infused into


peritoneal cavity (usually 10-15
min).

2. Dwell time (equilibrium):


time solution (dialysate) fluid
remains in peritoneal cavity
(duration depends on method- as
CAPD 4-5 exchanges/day).

3. Drain (equilibrium): time


fluid drains from peritoneal cavity CAPD
by gravity flow (usually 20-30
min); facilitate by gently
massaging abdomen, changing
position.

55
CAPD APD
 Catheter into peritoneal cavity  Automated Peritoneal
 Exchanges 4 - 5 times per day Dialysis- fluid exchanges
 Treatment 24 hrs; 7 days a week automatically by machine-
 Solution remains in peritoneal cavity (also known as continuous
except during drain time cycling peritoneal dialysis
 Independent treatment (CCPD), requires “cycler
machine”- programmable- to
automate filling and draining
process.
 Treatment at home, typically at
night (while sleeping-thus no
fluid in “the belly” at daytime

Click to play animation

Videos-Dialysis, all types!


Click to locate desired
Complications of Peritoneal Dialysis
 Infection
 peritonitis  Obesity
 tunnel infections  Hypokalemia
 catheter exit site  Hernia
 Hypervolemia  Cuff erosion
 hypertension  Low back pain
 pulmonary edema  Hyperlipidemia
 Hypovolemia
 hypotension
 Hyperglycemia
 Malnutrition
Peritoneal Catheter Exit Site

58
Advantages of PD
 Independence for patient
 No needle sticks
 Better blood pressure control
 Some diabetics add insulin to solution
 Fewer dietary restrictions
 protein loses in dialysate
 generally need increased potassium

 less fluid restrictions

59
Multi-prong system
occasionally used
with PD patients in
hospital settings
Which dialysis
“bags” have
already been
infused?

The “yellow”
ones!- dialysis
nurse sets up
bags, staff nurse
infuses, drains
according to
schedule.

60
Medications - Dialysis Patients & CKD (Stages 4-5)

 Vitamins - water soluble


 Phosphate binder - (Phoslo, Renagel, Calcium,
*Aluminum hydroxide-risks) Give with meals
 Iron - don’t give with phosphate binder or calcium
 Antihypertensives – typically hold prior to dialysis
 Erythropoietin
 Calcium Supplements - Between meals, not with iron
 Activated Vitamin D3 - aids in calcium absorption
 Antibiotics - hold dose prior to dialysis if it dialyzes out

62
Medications
 Many drugs or their metabolites are
excreted by the kidney
 Dosages - many change when used in
renal failure patients
 Dialyzability - many removed by dialysis
varies between HD and PD

63
Patient
Education
 Alleviate fear
 Dialysis process
 Fistula/catheter care
 Diet and fluid restrictions
 Medication
 Diabetic teaching

64
Case Study
A 48 year old female with a history of uncontrolled
diabetes presents to the ER. Her chief complaints are
nausea, vomiting and fatigue.
Lab: BUN 100; Creatinine 10; H&H 7.0/21.4;
K+ 6.0, PO4 5.5; Ca++ 7.5

What do you suspect? How would she possibly be treated?

*Access Evolve Apply Case Study- Chronic Renal Failure

*Access Renal Case Study

65
Transplantation

 Treatment not cure


View also Organ Donation video

66
Kidney Awaiting Transplant

67
“Old” kidneys typically left in place

68
Advantages Disadvantages
 Restoration of “normal”  Life long medications
renal function  Multiple side effects
 Freedom from dialysis from medication
 Return to “normal” life  Increased risk of tumor
 Reverses  Increased risk infection
pathophysiological  Major surgery
changes related to RF
 Less expensive than
dialysis after 1st year
Care of Recipient
 Major surgery with general anesthesia
 Assessment of renal function
 Assessment of fluid and electrolyte
balance
 Prevention of infection
 Prevention and management of rejection

70
Post-op Care
 ATN? (acute tubular necrosis)
 50% experience
 Urine output >100 <500 cc/hr
 BUN, creatinine, creatinine clearance
 Fluid Balance-careful monitor
 Ultrasound
 Renal scans
 Renal biopsy
71
Fluid & Electrolyte Balance
 Accurate I & O
 CRITICAL TO AVOID DEHYDRATION

 Output normal - >100 <500 cc/hr, could be 1-2


L/hr
 Potential for volume overload/deficit

 Daily weights
 Hyper/Hypokalemia potential
 Hyponatremia
 Hyperglycemia

72
Prevention of Infection

 Major complication of transplantation due to


immunosuppression
 HANDWASHING
 Avoid Crowds, Kids
 Patient Education

73
Rejection
 Hyperacute - preformed antibodies to donor antigen
 function ceases within 24 hours
 Rx = removal
 Accelerated - same as hyperacute but slower, 1st week to month
 Rx = removal
 Acute - generally after 1st 10 days to end of 2nd month
 50% experience
 must differentiate between rejection and cyclosporine toxicity
 Rx = steroids, monoclonal (OKT 3), or polyclonal (HTG)
antibodies
 Chronic - gradual process of graft dysfunction
 Repeat rejection episodes- not completely resolved with
treatment
 4 months to years after transplant
 Rx = return to dialysis or re-transplantation
74
Immunosuppressant Drugs
 Cytoxic Agents-Azathioprine
 Corticosteroids-Prednisone (Imuran); Mycophenolate
 Prevents infiltration of T (*Cellcept), *Cytoxin (less
lymphocytes toxic than Imuran)
 Prevents rapid growing
 Side effects lymphocytes
 cushingoid changes
 Side Effects
 Avascular Necrosis  bone marrow toxicity
 GI disturbances  hepatotoxicity

 Diabetes  hair loss

 infection  infection

 risk of tumor
 risk of tumor
Immunosuppressant Drugs

 Calcineuin Inhibitors-
 Monoclonal antibody-
OKT3 - used to treat
Cyclosporin, Neoral, rejection/induce
*Prograft, *FK506 (more immunosuppression
potent than cyclosporin)  decreases CD3 cells within
 Interferes with production of 1 hour
interleukin 2 which is necessary  Side effects
for growth and activation of T
 anaphylaxis
lymphocytes.
 Side Effects  fever/chills
– Nephrotoxicity  pulmonary edema
– HTN
 risk of infection
– Hepatotoxicity
 tumors
– Gingival hyperplasia

– Infection
 1st dose reaction expected
& wanted, pre-treat with
Benadryl, Tylenol, Solumedrol
Immunosuppressant Drugs cont’d
 Polyclonal antibody-Atgam-treat rejection or induce
immunosuppression
 decreased number of T lymphocytes

 Side effects
 anaphylaxis

 fever chills

 leukopenia

 thrombocytopenia

 risk of infection

 tumor

77
Patient Education
 Signs of infection
 Prevention of infection
 Signs of rejection
 decreased urine output
 increased weight gain
 tenderness over kidney
 fever > 100 degrees F
 Medications
 time, dose, side effects

78
Transplants
Notes from Organ Donation slides

 Exclusion for Transplant not limited too


 Active vasculitis; or
 Life threatening extrarenal congenital abnormalities;
or
 Untreated coagulation disorder; or

 Ongoing alcohol or drug abuse; or

 Age over 70 years with severe co-morbidities; or

 Severe neurological or mental impairment, in persons


without adequate social support, such that the person
is unable to adhere to the regimen necessary to
preserve the transplant.

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Official Criteria for Deceased
Donors
 Usually irreversible brain injury
Usually irreversible brain injury
 MVA, gunshot wounds, hemorrhage, anoxic brain injury from
MI
 Must have effective cardiac function
 Must be supported by ventilator to preserve organs
 Age 2-70
 No IV drug use, HTN, DM, Malignancies, Sepsis, disease
 Permission from legal next of kin & pronoucement of death made
by MD
 *Brain Death is the complete cessation of all brain &
brainstem function. It is death.

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Official Criteria for Living Donors
 Psychiatric evaluation
 Anesthesia evaluation
 Medical Evaluation
 Free from diseases listed under deceased donor
criteria
 Kidney function evaluated
 Crossmatches done at time of evaluation and 1
week prior to procedure
 Radiological evaluation
Nurses Role in Event of
Potential Donation
 Notify TOSA of possible organ donation
 Identify possible donors
 Make referral in timely manner

 Do not discuss organ donation with family


 Offer support to families after referral is
made & donation coordinator has met with
family

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