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Sophomore 2 Test 5 > ARF/CRF/Renal Transplant > Flashcards

ARF/CRF/Renal Transplant Flashcards

1
Q

Functions of the Kidneys and Urinary System

A
  1. Removing waste and extra fluid from the blood to form urine
  2. Produce erythropoietin
  3. Secrete and store renin, an enzyme that assists in regulating blood pressure
  4. Makes an active form of Vitamin D
  5. Maintains acid-base balance
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2
Q

Acute Kidney Injury (AKI)

A
  • Occurs when there is an abrupt decrease in kidney function
  • Occurs quickly (within a few hours to days)
  • There will be a 50% or greater increase in serum creatinine above baseline
  • May have normal urine volume, oliguria (less than 0.5mL/kg/hr), or anuria (less than 50 mL/day)
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3
Q

Pathophysiology of AKI

A

Although it is not always known what causes AKI; however, there is usually a specific underlying causes. Most types of AKI are reversible if diagnosed and treated early.

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4
Q

Causes of AKI (categories)

A
  1. Pre-renal
  2. Intrarenal
  3. Post-renal
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5
Q

Pre-Renal Failure Causes of AKI

A
  1. Renal vasoconstriction
  2. Loss of plasma volume
  3. Hemorrhage
  4. Hypovolemia
  5. Hypotension
  6. Reduced cardiac output
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6
Q

Pre-Renal Failure is the result of what (patho)?

A

It is the result of impaired blood flow to the kidney leading to poor perfusion. There is a decrease in the GFR - which is a decrease in filtration pressure
** Failure to restore blood volume or blood pressure and oxygen delivery may cause acute tubular necrosis or acute cortical necrosis

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7
Q

Where is the damage in Intrarenal AKI?

A

Intrarenal is where there is injury to the glomeruli, tubules or the interstitium (the space between the tubules)

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8
Q

Intrarenal Failure AKI Causes

A
  1. Acute tubular necrosis (most common)
  2. Infections
  3. OB complications
  4. Severe burns
  5. Invading tumors
  6. Glomerulonephritis
  7. Hypotension associated with hypovolemia
  8. Nephrotoxins
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9
Q

Examples of Nephrotoxins

A
  1. Aminoglycosides
  2. Heavy metals
  3. Myoglobin ethylene glycol
  4. Radiocontrast dye
  5. Uric acid
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10
Q

Four Phases of AKI

A
  1. Initiation
  2. Oliguria
  3. Diuresis
  4. Recovery
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11
Q

Initiation Phase

A
  • Begins with initial insult and continues until oliguria develops
  • Gradual accumulation of nitrogenous waste (increase in serum creatinine, BUN)
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12
Q

How long does the Initiation Phase last?

A

Lasts hours to days

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13
Q

Oliguria Phase

A
  • UOP of 100-400mL/24 hours with no response to fluid challenges or diuretics
  • Increase in BUN, creatinine, potassium, phosphate, Mg, Ca, bicarb (metabolic acidosis)
  • Some may have decreased kidney function with increased nitrogen retention with normal UOP called nonoliguric form of kidney failure. This sometimes happen post-exposure to nephrotoxic agents, burns, traumatic injury, or use of certain anesthetics
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14
Q

How long does the Oliguria Phase last?

A

Lasts 7-21 days

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15
Q

Diuresis Phase

A
  • Sudden onset within 2-6 weeks after oliguric stage
  • UOP increases rapidly over a period of several days (can be up to 10L/day) - urine is very diluted
  • Loss of electrolytes typically precede
  • Observe closely for dehydration
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16
Q

If there is dehydration in the Diuresis Phase there can be uremic symptoms which includes …

A
  1. Confusion
  2. LOC
  3. Oliguria
  4. Dry mouth
  5. Tachycardia
  6. Excessive thirst
  7. Fatigue
  8. Weakness
  9. Pallor
  10. Bleeding problems
  11. Edema
  12. N/V
  13. Severe anorexia
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17
Q

Recovery Phase

A
  • Patient returns to normal levels of activity
  • Functions at a lower energy level; has less stamina than before the illness
  • Residual renal insufficiency may be noted through regular monitoring of renal functioning
  • May never return to pre-illness levels, but function is adequate enough for a long healthy life
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18
Q

Symptoms of Pre-Renal AKI

A
  1. Hypotension
  2. Tachycardia
  3. Decreased cardiac output
  4. Decreased central venous pressure
  5. Decreased urinary output
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19
Q

Symptoms of Intrarenal/Post-Renal AKI: Cardiac

A
  1. HTN
  2. Tachycardia
  3. JVD
  4. ECG changes: tall T-waves
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20
Q

Symptoms of Intrarenal/Post-Renal AKI: Respiratory

A
  1. SOB
  2. Rales or crackles
  3. Pulmonary edema
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21
Q

Symptoms of Intrarenal/Post-Renal AKI: GI

A
  1. Anorexia
  2. N/V
  3. Flank pain
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22
Q

Symptoms of Intrarenal/Post-Renal AKI: Neuro

A
  1. Lethargy
  2. HA
  3. Tremors
  4. Confusion
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23
Q

Symptoms of Intrarenal/Post-Renal AKI: General

A
  1. Weight gain

2. Generalized edema

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24
Q

AKI Labs: Urine

A
  • Low specific gravity (<1.005)
  • Prerenal azotemia (low urine Na)
  • Intrarenal azotemia (high urine Na)
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25
Q

AKI Labs: Blood

A
  • High BUN, creatinine, potassium, phosphorus, magnesium
  • Low calcium
  • Sodium can be high, low, or normal
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26
Q

AKI Labs: Arterial Blood Gas

A
  • pH (low or WNL)
  • Low Bicarbonate
  • Low PaCO2
    • Metabolic Acidosis - cannot eliminate daily metabolic load of acid-type substances produced by normal metabolic processes
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27
Q

What should you assess for to prevent AKI?

A
  1. Nephrotoxic medications
  2. Chronic use of NSAIDs
  3. Radiocontrast induced neuropathy (CIN)
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28
Q

Nephrotoxic Medications

A
  1. Aminoglycosides
  2. Colistimethane
  3. Polymyxin B
  4. Amphotericin B
  5. Vancomycin
  6. Cyclosporine
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29
Q

Aminoglycosides

A
  1. Gentamycin
  2. Tobramycin
  3. Amikacin
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30
Q

How can chronic use of NSAIDs cause AKI?

A

Chronic use of NSAIDs may cause interstitial nephritis and papillary necrosis. High risk patients are those with heart failure or cirrhosis with ascites are at high risk for NSAID-induced renal failure

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31
Q

Radiocontrast Induced Neuropathy (CIN)

A

Major cause of AKI. Anyone who has a baseline creatinine level of greater than 2 mg/dL is considered high risk.

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32
Q

Is there a way to prevent radiocontrast induced neuropathy (CIN)?

A

Administration of N-acetylcysteine and sodium bicarbonate before and after procedures reduces risk, but pre-hydration with saline is considered the most effective way to prevent CIN

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33
Q

General Management Goals for AKI

A
  1. Eliminate the underlying cause
  2. Avoiding fluid excess
  3. Providing renal replacement therapy
    * * Depending on the location of the AKI, depends on the management of treatment
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34
Q

Prerenal azotemia treatment

A

Treated by optimizing renal perfusion

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35
Q

Post-renal failure treatment

A

Treated by getting rid of the obstruction

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36
Q

Intrarenal azotemia treatment

A
  1. Supportive therapy
  2. Removal of causative agents
  3. Aggressive management of pre and post renal failure
  4. Avoiding associated risks
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37
Q

General Interventions for AKI

A
  1. Maintaining fluid balance
  2. Assess for SOB, tachycardia, distended neck veins, crackles, pulmonary edema, presacral and pretibial edema
  3. Administer dialysis
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38
Q

Hemodialysis

A

Circulating blood through a dialyzer to remove waste products from the blood and restores chemical and electrolyte imbalance
** Passes the patient’s blood through a semipermeable membrane to perform filtering and excretion functions of the kidney

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39
Q

Peritoneal dialysis

A

Uses the peritoneal membrane to exchange fluid and solute

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40
Q

Continuous Renal Replacement Therapy (CRRT)

A

Circulating blood through the dialyzer continuously 24 hours a day to remove waste

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41
Q

Pharmacologic Therapy for AKI

A
  1. Mannitol
  2. Furosemide (loop diuretic)
  3. Albumin (given if hypovolemic due to hypoproteinemia)
  4. Normal saline, LR
  5. Fresh frozen plasma
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42
Q

S/Sx of Hyperkalemia

A
  1. Irritability
  2. Abdominal cramping
  3. Diarrhea
  4. Generalize muscle weakness
  5. EKG changes (tall or peaked T waves)
  6. Dysrhythmias
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43
Q

Treatment for Hyperkalemia

A 
Polystyrene sulfonate (if stable)
- PO or rectally

Dextrose 50%, insulin (regular), calcium
- IV

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44
Q

Medications that are excreted via the kidneys and therefore dosages need to be reduced for those with AKI

A
  1. Aminoglycosides
  2. Digoxin
  3. Phenytoin
  4. ACE inhibitor
  5. Magnesium containing agents
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45
Q

Why do AKI patients need nutritional therapy?

A

AKI causes extreme nutritional deficits, due to nausea and vomiting contributing to poor dietary intake
** Nutritional support is based on the underlying cause of AKI

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46
Q

Diet for AKI

A 
At first...
1. High carbohydrate
2. Low protein
3. Low potassium
4. Low phosphorus
After diuretic phase...
1. High protein
2. High calories
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47
Q

Chronic Renal Failure

A

When a patient has sustained enough kidney damage to require renal replacement therapy on a permanent basis, the patient has moved into the end stage kidney disease or chronic kidney disease

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48
Q

Pathophysiology of Chronic Renal Failure

A

As renal function declines, the end products of protein metabolism are retained in the blood. Uremia develops and adversely affects every body system. The greater the build-up of waste, the more prominent the symptoms.
** Tends to progress more rapidly in patients who excrete a considerable amount of protein or have elevated blood pressure than those who do not.

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49
Q

Causes of Chronic Renal Failure

A
  1. HTN
  2. Diabetes
  3. Chronic glomerulonephritis
  4. Reoccurring pyelonephritis
  5. Autoimmune disorders such as systemic lupus erythematosus
  6. Arteriosclerosis
  7. Urinary blockage and reflux related to frequent infections, stones, or anatomical abnormality
  8. Excessive medications that are metabolized through the kidneys
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50
Q

Clinical Manifestations of Chronic Renal Failure: Neurological

A
  1. Fatigue
  2. Lethargy
  3. Confusion
  4. Burning of soles of feet
  5. Restlessness of legs
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51
Q

Clinical Manifestations of Chronic Renal Failure: Integumentary

A
  1. Grayish-bronze in color
  2. Flaky
  3. Dry
  4. Pruritis
  5. Coarse thinning hair
  6. Nails are thin and brittle
  7. Uremic frost (related to increased urea)
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52
Q

Clinical Manifestations of Chronic Renal Failure: Cardiovascular

A
  1. HTN
  2. Pitting edema (hands, feet, sacrum)
  3. Distended neck veins
  4. Hyperkalemia
  5. Hyperlipidemia
  6. Periorbital edema
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53
Q

Clinical Manifestations of Chronic Renal Failure: Pulmonary

A
  1. Crackles
  2. Thick, tenacious sputum
  3. Uremic pneumonitis
  4. Depressed cough reflex
  5. Tachypnea
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54
Q

Clinical Manifestations of Chronic Renal Failure: GI

A
  1. Ammonia breath
  2. Metallic taste
  3. Constipation or diarrhea
  4. GI bleed
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55
Q

Clinical Manifestations of Chronic Renal Failure: Hematologic

A
  1. Anemia

2. Thrombocytopenia

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56
Q

Clinical Manifestations of Chronic Renal Failure: Reproductive

A
  1. Infertility
  2. Amenorrhea
  3. Decreased libido
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57
Q

Clinical Manifestations of Chronic Renal Failure: Musculoskeletal

A
  1. Muscle cramps
  2. Bone fractures
  3. Renal osteodystrophy
58
Q

Lab Values that Indicate the progression of ESKD

A
  1. Low GFR
  2. Low creatinine clearance
  3. High BUN (not definitive indicator)
  4. High serum creatinine (most sensitive indicator)
59
Q

What happens with calcium and phosphorus with the progression of ESKD?

A

They have a reciprocal relationship. As one increases the other lowers. Because the kidney does not filter properly, there is an increase in serum phosphorus and decrease in serum calcium. This causes the release of parathormone from the parathyroid gland. However, in renal failure the body does not respond normally to the increase secretion of parathormone. The result is that calcium leaves the bone, causing disease of the bone as well as calcification of major blood vessels.

60
Q

Why can ESKD patients experience metabolic acidosis?

A

Because they are unable to excrete acid

61
Q

Why can ESKD patients experience anemia?

A
  1. Inadequate erythropoietin production
  2. Shortened lifespan of RBCs
  3. Nutritional deficits
  4. The tendency to bleed
62
Q

1,25-dihydroxycholecalciferol

A

The active metabolite of Vitamin D that decreases as renal failure progresses

63
Q

Complications of EKSD that can be preventable or delayed by administering

A
  1. Calcium and phosphorus binders
  2. Antihypertensive and cardiovascular agents
  3. Antiseizure agents
  4. Vitamins and minerals
  5. Synthetic erythropoietin
64
Q

Calcium and Phosphorus Binders

A
  1. Calcium carbonate
  2. Calcium acetate
  3. Sevelamer hydrochloride
65
Q

Sevelamer hydrochloride

A

This is administered if serum calcium is high or calcium-phosphorus product exceeds >55 mg/dL

66
Q

Calcium carbonate and calcium acetate

A

These bind dietary phosphorus in the GI tract

  • Must take with meals
  • Do not take at the same time as digoxin (at least 2 hours apart)
  • High risk of hypercalcemia
67
Q

Antihypertensive and cardiovascular agents given to ESKD patients

A
  1. Digoxin

2. Dobutamine

68
Q

Digoxin

A
  • Used when heart failure induces renal failure or makes it worse
  • IV (initial dose) or PO
  • Take pulse (apical) before administration, hold if less than 60 bpm
  • Watch for toxicity (0.8-2.0 is normal range)
69
Q

Dobutamine

A

Given for EKSD to improve creatinine clearance

70
Q

Antiseizure Agents given for ESKD patients

A
  1. Phenytoin

2. Diazepam

71
Q

Vitamins and minerals given to ESKD patients

A
  1. Folic acid and Ferrous sulfate
    • Administered when patient loses these due to dialysis
    • Take these after dialysis
    • Ferrous sulfate with OJ or meals
    • May cause dark stools
    • Take stool softeners with iron as it causes constipation
72
Q

Epoetin Alfa

A
  • A synthetic erythropoietin
  • Prevents anemia by stimulating red blood cell growth and maturation in bone marrow
  • IV or SC
  • Watch for side effects
73
Q

Side Effects of Epoetin Alfa

A

Report…

  1. Chest pain
  2. SOB
  3. HTN
  4. Rapid weight gain
  5. Seizures
  6. Skin rash or hives
  7. Edema of feet or ankles
    * *Can induce serious cardiovascular problems such as an MI
74
Q

Side Effects of high Phosphorus level

A

Itching

- Diphenhydramine may be given to alleviate this

75
Q

Why would heparin be given to a ESKD patient?

A

Prevents clotting during dialysis

- Administered SC or IV

76
Q

Foods that ESKD patients should avoid

A
  1. Foods that are high in sodium
  2. Avoid cheese except for cream cheese
  3. Avoid biscuits, whole grain breads, long grain rice
  4. Avoid dried fruits
77
Q

What kind of patient needs acute dialysis?

A
  1. High increasing level of serum potassium
  2. Fluid overload
  3. Impending pulmonary edema
  4. Increasing acidosis
  5. Pericarditis
  6. Severe confusion
  7. To remove certain medications or toxins
78
Q

What kind of patient needs chronic dialysis?

A
  1. ERSD (end stage renal disease)
  2. Presence of uremic s/sx
  3. Hyperkalemia
  4. Fluid overload with no response to diuretics and fluid restriciton
  5. General lack of well being
  6. Pericardial friction rub
79
Q

Types of Vascular Access for Dialysis

A
  1. Arteriovenous fistulas (AVFs)

2. Arteriovenous grafts (AVGs)

80
Q

Arteriovenous Fistula

A
  • Most commonly created in the forearm
  • It is an anastomosis between an artery and a vein (usually cephalic)
  • Arterial blood flow is essential to provide the rapid blood flow required for hemodialysis
  • Increased pressure of the arterial blood flow through the vein makes the vein dilate and become tough, making it amenable to repeated venipuncture in approximately 4-6 weeks
  • AVFs have the best overall patency rates and least number of complications of all vascular accesses
81
Q

How long before hemodialysis is initiated should the AVF be placed?

A

The AVF should be placed at least 3 months before hemodialysis is initiated

82
Q

How is the AVF accessed?

A

Using 2 large gauge needles

83
Q

AVFs are difficult to place in what kind of patients?

A
  1. History of severe PVD
  2. Prolonged IV drug use
  3. Obese women
    * * For these patients, synthetic grafts are best
84
Q

Arteriovenous Grafts (AVGs)

A
  • These are made up of synthetic material and form a “bridge” between the arterial and venous blood supplies
  • Grafts are placed beneath the skin and are surgically anastomosed between and artery and a vein
  • Because the grafts are made of artificial material, they are more likely to become infected and have a tendency to become thrombogenic
85
Q

How long before hemodialysis is initiated should the AVG be placed?

A

A healing time of at least 2-4 weeks is necessary to allow the graft to heal, but some centers may use it earlier

86
Q

How is an AVG accessed?

A

Two large gauge needles (14G-16G)

87
Q

What kind of patients usually get AVGs?

A

This is a graft that is created when the patient’s vessels are not suitable for creation of a fistula. It is seen with diabetics and other types of compromised vascular status

88
Q

Are water soluble medications easily removed from the blood during dialysis?

A

Yes

89
Q

Are fat soluble medications easily removed from the blood during dialysis?

A

No

90
Q

CRRT

A

Continuous Renal Replacement Therapy

  • Used in ICU when patients are too unstable for traditional dialysis
  • It pulls fluid off at a slower pace than traditional dialysis
91
Q

CVVH

A

Continuous Venovenous Hemofiltration

  • Used to manage acute renal failure (ARF)
  • Continuous slow fluid removal
  • Does not require arterial access
92
Q

CVVHD

A

Continuous Venovenous Hemodialysis

  • Similar to CVVH
  • Hemodynamic effects are mild
  • Does not require arterial access
93
Q

Should heart and BP medications be given before or after dialysis?

A

AFTER

94
Q

Complications of Hemodialysis

A
  1. Failure of permanent dialysis access
  2. Hypotension
  3. Muscle cramps
  4. Loss of blood
  5. GI ulcers/GI problems
  6. Dysrhythmias
  7. Air embolism (rare)
  8. Chest pain
  9. Disequalibrium Syndrome
  10. Insomnia
95
Q

Potential Complications of Hemodialysis: Hypotension

A

Due to the removal of fluid - hypovolemia

  • Decreased cardiac output
  • Light headedness
  • N/V
  • Seizures
  • Visual changes
  • Chest pain
96
Q

Potential Complications of Hemodialysis: Hypotension Treatment

A

Decrease the volume of fluid being removed and administer 0.9% NS

97
Q

Potential Complications of Hemodialysis: Muscle Cramps

A
  • Poorly understood; factors include hypotension, hypovolemia, high ultrafiltration rate, and use of low-sodium dialysis solution.
  • Cramps are more frequently seen in the first month after initiation after dialysis begins
98
Q

Potential Complications of Hemodialysis: Muscle Cramps Treatment

A

Reducing the ultrafiltration rate and administering of fluids (saline, glucose, mannitol)

  • Hypertonic saline is not recommended since the sodium can be problematic
  • Hypotonic glucose administration is preferred
99
Q

Potential Complications of Hemodialysis: Loss of Blood

A
  • From blood not being completely rinsed from the dialyzer, accidental separation of blood tubing, dialysis membrane rupture
  • Too much heparin or clotting disorders can cause post-dialysis bleeding
100
Q

Potential Complications of Hemodialysis: Loss of Blood Treatment

A
  1. Rinse back all blood
  2. Monitor heparinization to avoid excess anticoagulation
  3. Hold firm but not occlusive pressure on access sites
101
Q

Potential Complications of Hemodialysis: GI Ulcers/GI problems

A

Related to the physiologic stress of chronic illness, medication, and related problems

102
Q

Potential Complications of Hemodialysis: GI Ulcers/GI problems Treatment

A
  1. H2 Blocker
    • Ranitidine, Famotidine
  2. Proton Pump Inhibitor (PPI)
    • Omeprazole
103
Q

Potential Complications of Hemodialysis: Dysrhythmias

A

From electrolyte and pH changes or from removal of antiarrhythmic meds during the procedure

104
Q

Potential Complications of Hemodialysis: Disequalibrium Syndrome

A

A complication of dialysis believed to result from too-rapid removal of electrolytes.
- It is characterized by neurological symptoms and signs attributable to cerebral edema that occurs due to fluid shifts into the brain following a relatively rapid decrease in serum and serum osmolality during hemodialysis

105
Q

Risk Factors for Disequalibrium Syndrome

A
  1. First dialysis treatment
  2. Large increase in blood urea concentration prior to dialysis
  3. Chronic kidney disease as compared to acute
  4. Severe metabolic acidosis
  5. Older age
  6. Pediatric clients
  7. Pre-existing neurologic disease
  8. Conditions characterized by cerebral edema
  9. Any condition that increases permeability of the blood brain barrier
106
Q

Conditions characterized by cerebral edema

A
  1. Hyponatremia
  2. Hepatic encephalopathy
  3. Malignant hypertension
107
Q

Conditions that increases permeability of the blood brain barrier

A
  1. Sepsis
  2. Vasculitis
  3. Encephalitis
  4. Meningitis
108
Q

Mild S/Sx of Disequalibrium Syndrome

A
  1. HA
  2. N/V
  3. Muscle cramps
109
Q

Severe S/Sx of Disequalibrium Syndrome

A
  1. Altered mental status
  2. Seizures
  3. Come
    * * Rarely death
110
Q

Treatment for Disequalibrium Syndrome

A
  1. Slower removal of fluid

2. CRRT

111
Q

Can hemodialysis halt the progression of ESKD?

A

No, it can slow the progression but not halt it. It can’t fully replace the normal metabolic and hormonal functions of the kidneys. It can ease many of the symptoms of CKD and, if started early, can prevent certain complications. However, it does not alter the accelerated rate of development of CV disease and the related high mortality rate.

112
Q

Nursing Interventions for the Patient undergoing dialysis

A
  1. Weigh the patient before and after dialysis
  2. Know the patient’s dry weight (post-dialysis)
  3. Discuss with MD if any medications should be withheld until after dialysis is complete
  4. Be aware of what events that occurred during the dialysis treatment
  5. Measure T, P, R, BP
  6. Assess for orthostatic hypotension
  7. Assess the vascular access site
  8. Observe for bleeding
  9. Asses the patient’s LOC
  10. Assess for headache, nausea, and vomiting.
113
Q

Nursing Interventions with all AVFs and AVGs

A
  1. No BP’s in the extremity in which the vascular access is placed
  2. No venipunctures or IVs in the extremity in which the vascular access is placed
  3. Palpate for thrills and auscultate for bruits q 4 hours while the patient is awake
  4. Assess distal pulses and circulation
  5. Elevate the affected extremity post-op
  6. Encourage routine ROM
  7. Assess for bleeding at needle insertion site or shunt tubing insertion sites (keep small clamps handy)
  8. Instruct the patient not to carry heavy objects or anything that compresses the access site
  9. Instruct the patient not to sleep on his/her body weight on the extremity in which the device is placed
114
Q

Likely Candidates for Peritoneal Dialysis

A
  1. Older patients
  2. Diabetics
  3. CV disease
  4. Risk for adverse effects of heparin
  5. Severe HTN
  6. Heart failure
  7. Pulmonary edema who do not respond well to treatment
    * * These are the patients who are susceptible to the rapid fluid, electrolyte, and metabolic changes that occur during hemodialysis
115
Q

Medications that can be added to the dialysate in peritoneal dialysis

A
  1. Heparin (LMWH/enoxaparin) may be added to prevent fibrin formation and resultant occlusion of the peritoneal catheter
  2. KCL to prevent hypokalemia
  3. Antibiotics may be added to treat peritonitis
  4. Regular insulin for diabetics: may receive a larger than normal dose because about 10% of the insulin binds to the wall of the dialysate container.
    * * All medications are added immediately before the solution is instilled.
    * * Aseptic technique is imperative.
116
Q

Why is the dialysate warmed to body temperature before the medications are added?

A
  1. Prevent patient discomfort and abdominal pain
  2. To dilate the vessels of the peritoneum to increase urea clearance.
  3. Solutions that are too cold cause pain, cramping, and vasoconstriction and reduce clearance.
  4. Solutions that are too hot burn the peritoneum.
  5. Dry heating (heating cabinet, incubator, or heating pad) is recommended.
  6. Do NOT MICROWAVE!!
117
Q

Peritoneal Dialysis: Performing the Exchange

A
  • Is the infusion, dwell, and drainage of the dialysate
    1. The dialysate is infused by gravity into the peritoneal cavity via Tenckhoff
    2. The tip of the catheter rests in the peritoneal cavity and has many perforations spaced along the distal end of the tubing allowing fluid to flow in and out of the catheter. A period of about 5-10 minutes is usually required to infuse 2-3L of fluid.
    3. At the end of the dwell time the drain cycle begins. Drainage is usually completed in 10-30 minutes.
118
Q

Peritoneal Dialysis: Drainage

A
  • The drainage fluid is normally colorless or straw colored and SHOULD NOT be cloudy.
  • Bloody drainage may be seen in the first few exchanges, but should not occur after that.
  • The removal of excess water during the PD exchange is achieved by using hypertonic dialysate with a high dextrose concentration. The higher the dextrose concentration the greater the osmotic gradient and the more water that will be removed.
  • The entire exchange should take about 30-45 minutes.
119
Q

Tenckoff

A

Used for peritoneal dialysis
- a silicone rubber catheter tubing about 60cm long and has one or two Dacron cuffs on its subcutaneous and peritoneal portions. These cuffs acts as anchors and prevent the migration of microorganisms down the shaft from the skin.

120
Q

Advantages of Peritoneal Dialysis

A
  1. Easy to learn
  2. Can be done in the home setting
  3. Less stressful
  4. Better control of blood pressure
  5. Less dietary and fluid restrictions
  6. Greater freedom
121
Q

Disadvantages of Peritoneal Dialysis

A
  1. Time consuming
  2. Protein wasting
  3. Sterile procedure
  4. Weight gain
  5. Peritoneum injury
  6. Chronic back pain
  7. Hernia development
122
Q

Potential Complications of Peritoneal Dialysis

A
  1. Peritonitis
  2. Leakage
  3. Bleeding
123
Q

Potential Complications of Peritoneal Dialysis: Peritonitis

A

Most common and most serious

  • Cloudy dialysate drainage
  • Diffuse abdominal pain and rebound tenderness
  • Signs of shock
124
Q

Potential Complications of Peritoneal Dialysis: Peritonitis Treatment

A
  1. Initially 1-3 rapid exchanges with a 1.5% dextrose solution without added medications
    - Washing out causes ↓’s inflammation & reduce abdominal pain.
  2. The fluid is examined for cell content and Gram stain and cultures are used to identify the organism to guide treatment.
  3. Antibiotics (such as aminoglycosides or cephalosporins) are added until results are available.
    - Antibiotic therapy will continue 10-14 days. Careful calculation of the antibiotic dosage helps prevent nephrotoxicity and further compromise renal function.
125
Q

Potential Complications of Peritoneal Dialysis: Leakage

A
  1. Through the catheter site may occur immediately after insertion.
  2. Will stop on its own if dialysis is withheld for several days to give the exit and incision site time to heal
  3. Want the patient to avoid abdominal muscle activity and straining during bowel movements
126
Q

Potential Complications of Peritoneal Dialysis: Leakage Treatment

A

Leakage can be avoided by using smaller volumes (500mL) of dialysate, gradually increasing the volume up to 2-3L.

127
Q

Potential Complications of Peritoneal Dialysis: Bleeding

A
  1. May be occasionally, but most often seen in young menstruating women.
  2. Hypertonic fluid pulls blood from the uterus through the opening of the fallopian tubes and into the peritoneal cavity
  3. Common during the first few exchanges after a new catheter insertion
  4. Invariably, bleeding stops in 1-2 days and requires no specific intervention
  5. May need more frequent exchanges during this time to prevent obstruction from blood clots
128
Q

Long Term Complications of Peritoneal Dialysis

A
  1. Hypertriglyceridemia
  2. Increased BP (leading to L ventricular hypertrophy)
  3. CV disease
  4. Abdominal hernias
  5. Low back discomfort
  6. Anorexia
  7. Constant sweet taste (related to the glucose absorption)
  8. Clots in the peritoneal catheter
129
Q

Nursing Management of the Peritoneal Dialysis Patient

A
  1. Observe for s/sx of infection
  2. Strict I/O must be observed at all times
  3. Cardiac/respiratory assessment must be conducted frequently
  4. Pericarditis may result from build-up of uremic toxins
  5. Monitor for substernal chest pain, low grade fever, pericardial friction rub, pulsus paradoxus (a decrease in BP of more than 10mmHg during inspiration)
130
Q

Patients that are not considered for kidney transplants

A
  1. Advanced, uncorrectable cardiac disease (transplant worsens these symptoms)
  2. Metastatic cancer
  3. Chronic infection
  4. Severe psychological problems (alcoholism, chemical dependency)
  5. GI disorders, such as PUD and diverticulosis (will consider for transplant, but need to resolve these issues d/t large doses of steroids after transplant can worsen symptoms)
131
Q

Candidates that are considered for renal transplant

A
  1. Patients with a recent history of cancer –treated with dialysis d/t shortage of donor organs & limited life expectancy. In addition, drugs that are used post-transplant increase the risk of cancer. If more than 2-5 years have passed since eradication of the cancer, patient will be considered for transplant.
  2. Diabetes Mellitus and other endocrine problems—can receive a transplant, but will require intense observation,
  3. Most patients with ESKD are considered
132
Q

Two Types of Kidney Donors

A
  1. Living donors (relative or non-relative)

2. Non-heart beating donors (NHBD)

133
Q

Non-Heart Beating Donors (NHBD)

A
  1. Declared dead by cardiopulmonary criteria
  2. Removed (harvested) immediately post-death who have previously consented for organ donation
  3. If immediate removal must be delayed, kidney is preserved by infusing a cool preservation solution into the abdominal aorta after death is declared & surgery can be performed.
134
Q

Does the size of the kidney matter for donation?

A

Size is seldom a problem in adults - if transplanted from child, the kidney will become larger to meet adult needs within a few months

135
Q

Living Related Donors (LRDs)

A
  • Highest renal graft survival (90%)
  • Donor ages: usually 18-65 yrs
  • There is certain physical criteria that donor must meet such as absence of systemic infection, no history of CA, No HTN or kidney disease, and adequate renal function.
  • Donor must express a clear understanding of the surgery and the willingness to give up a kidney.
136
Q

Pre-Op Renal Transplant

A
  • Pre Op education is very important. Patient must understand that he/she will be on anti-rejection meds for the rest of their life
  • Potential complications include GI bleed and renal insufficiency
137
Q

Intraoperative Renal Transplant

A
  1. Will be placed on non-diseased side with
    diseased kidney side up.
  2. Opposite trunk area is flexed to increase
    exposure.
  3. Removal of 11th and 12th rib is done to better
    access the kidney
  4. Surgeon will remove kidney, tumor, renal artery, renal vein, and fascia. Adrenal gland is left intact. (Drain will be placed prior to closure.)
    **Radical nephrectomy is when local
    and regional lymph nodes are removed.
138
Q

Post-Op Renal Transplant Nursing Care

A
  1. Monitor for hemorrhage, adrenal insufficiency, and kidney functioning
  2. Inspect for abdominal distention
  3. Monitor BP
  4. Monitor Urine output
  5. Monitor HCT/HGB
  6. Monitor VS q 4 and PRN
  7. Daily weights
  8. Have patient TCDB; incentive spirometer x10 q1 hour
  9. Pain management
139
Q

Urine Output Post-Op Renal Transplant

A

Functional kidney is expected to provide adequate renal function, but may take days or weeks.

  - Assess urine output for the first 24 hrs. post op.  
  - Acceptable is 30-50mL/hr
  - Output of < 30mL you should suspect decreased renal blood flow  * * The sooner the kidney starts working, the better the prognosis.
140
Q

Pain Management for Post-Op Renal Transplant

A

Opioid analgesics (common) hydromorphone and morphine administered parentally

141
Q

Preventing Complications Post-Op Renal Transplant

A

Prevent infection, management of adrenal insufficiency.

 - Monitor q 8 hrs and PRN for manifestations of systemic infection or local wound infection.  
 - Adrenal insufficiency: although only one is affected, may not be able to secrete sufficient glucocorticoids immediately after surgery - steroid replacement may be needed.

Sophomore 2 Test 5 (4 decks)

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