AKI and Dialysis

Question 1

What are 2 main types of insults in AKI?

Answer 1

1) Acute ischemia –> Patchy lesions along proximal and distal tubules, basement cell membrane is affected and necrosis is present
2) Acute toxic –> Basement membrane usually left intact, tubular destruction ranges from swelling to necrosis, damage is generalized and widespread

Question 2

What are the 3 main categories of AKI?

Answer 2

1) Prerenal
2) Intrarenal
3) Postrenal

Question 3

What is prerenal failure?

Answer 3

Physiological response to insult that occurs before blood reaches kidney.
Result in renal hypoperfusion, decrease GFR, oliguria.
Nephrons remain normal and can recover

Question 4

What are causes of pre-renal failure?

Answer 4

Local causes: Emboli, thrombus, surgery, hepatorenal syndrome

General causes: Hypoperfusion, decreased CO

Question 5

What is intra-renal failure?

Answer 5

Parenchymal damage to nephrons resulting from disease or nephrotoxic agents. Damage can involve both glomerulus and tubular epithelium

**ATN (Acute Tubular Necrosis)

Question 6

What causes intra-renal failure / ATN?

Answer 6

Nephrotoxic or ischemic injury to the renal tubular epithelium. Damage can extend to the basement membrane

Question 7

What are the differences between Ischemic vs toxic ATN?

Answer 7

Ischemic: Damage is irregular along PCT and DCT, failure of autoregulatory properties of afferent and efferent arterioles that regulate GFR. ***Basement membrane damaged and necrotic

Toxic: Some nephrotoxins are vasoconstrictors (contrast dye), uniform widedspread damage to tubules range from swelling to necrosis. ***Basement membrane not as severely injured

Question 8

What is pathophys of ATN?

Answer 8

Inflammatory process 
Tubular swelling, cast formation (cellular debris)
Obstruction decrease capillary BF
Ischemia, cell injury 
Decrease O2, ATP
Decrease cell function 
O2 free radicals attract Ca intracellularly
Decrease serum Ca
Further injury

Question 9

Why do AKI pts become anuric?

Answer 9

Glomerular pressure equals hydrostatic pressure.

Obstructions increase tubular hydrostatic pressure that eventually equals filtration pressure

Question 10

What is postrenal failure?

Answer 10

Physiological response caused by disruption of urine flow from urinary tract to bladder.
Rare but accounts for most anuric cases.

Question 11

What are the 4 stages of acute renal failure?

Answer 11

1) Initiation (onset phase)
2) Maintenance (oliguric / anuric phase)
3) Diuretic
4) Recovery

Question 12

What happens in initiation phase?

Answer 12

Time of onset to cell damage, decrease in GFR due to impaired renal BF. Glomerular filtrate backleaks into tissues.

Pt has fatigue, fluid retention, anemia, decreased UO

Question 13

What happens in maintenance phase?

Answer 13

Oliguria, severe decrease GFR with excessive H2O retention leading to dilutional hyponatremia

Increased K –> due to decreased excretion, muscle breakdown
Increased H+ –> leading to metabolic acidosis
Anemia –> due to suppressed erythropoietin
Creatinine, urea, phosphate elevated –> Muscle breakdown and inability to excrete waste
Hypocalcemia –> Decreased gut absorption due to decreased Vit D activation in kidney and O2 free radicals attracting calcium intra-cellularly
Azotemia (Buildup of metabolic waste)

Question 14

What happens in the diuretic stage?

Answer 14

GFR begins to increase, reabsorption might not follow for a while. Gradual increase in UO

May have polyuria and dehydration d/t INABILITY TO CONCENTRATE URINE

Kidneys can clear volume but not solutes

Question 15

What happens in recovery stage?

Answer 15

GFR returns to 70-80% normal
BUN and Cr may never completely normalize
Final stage is ability to concentrate urine

Question 16

What is the best imaging test for AKI?

Answer 16

Renal ultrasound

Question 17

What is medical management of AKI?

Answer 17

1) Prevention –> Avoid nephrotoxins, IV contrast
2) Correct causative agent
3) Maintain fluid balance –> Replacement vs restriction vs removal
4) Restore/maintain electrolyte balance (K, Na, Ca, Po4)
5) Manage nutrition
6) Medication –> DIuretics, vasodilators, inotropes, Ca+ ch blockers

Question 18

How are electrolytes managed in AKI?

Answer 18

Increased K –> Diuretics, insulin/glucose, sodium bicarb, kayexelate

Decreased Na –> Fluid restriction vs hypertonic saline, dialysis

Decreased Ca –> Supplement Ca and Vit D

Increased Po4 –> From bones attempt to free Ca, decreased excretion. Administer aluminum hydroxide to bind with phosphate and excrete in feces

Question 19

Nursing diagnosis for AKI?

Answer 19

Impaired oxygenation d/t: Anemia from loss of erythropoietin, poor g/e from fluid in alveoli
–> Suction, monitor ABGs, Hgb, give EPO, blood, diuretics, monitor fluid status

Skin breakdown d/t: Generalized pitting edema, altered skin perfusion, pruritis caused by uremic toxins
–> Skin care, turns, nutrition

Question 20

What is the purpose of dialysis?

Answer 20

Remove excess electrolytes, fluid, and toxins from blood via filtering through a semi-permeable membrane.

Does NOT improve renal function, indicated when there is buildup or uremia leading to changes in pt condition

Question 21

What are the basic principles of dialysis?

Answer 21

1) Diffusion (movement of solutes)
2) Osmosis (movement of water)
3) Hydrostatic pressure (force of fluid pushing out)
4) Ultrafiltration (removal of fluid from vascular space)

Question 22

What is uremia and what is its effect?

Answer 22

Accumulation of substance in blood ordinarily eliminated in urine.

Decrease LOC, metabolic acidosis, increased PO4, K,Cr, BUN, decreased Ca

Causes pulmonary edema, CHF, positive fluid balance, drug toxicity

Question 23

What are contraindications to HD?

Answer 23

1) Inability to obtain vascular access
2) Hemodynamic instability
3) Coagulopathy

Question 24

What is the process of intermittent HD (IHD)?

Answer 24

Blood mechanically pulled from pt through PVC tubing system to dialyzer. Diffusion and ultrafiltration occurs, wastes removed and blood is pumped back to pt.

**Blood volume removed approx 250-300mls
Treatment lasts 3-4 hrs given every other day or daily

Question 25

How does blood flow relate to dialysate flow?

Answer 25

Always counter-current, enhancing diffusion

Question 26

Pros and cons of IHD?

Answer 26

Pros: Remove large amount of fluid volume, decreases cardiac workload, correct cardiac arrythmias d/t hyperkalemia, improve metabolic acidosis, pt can mobilize

Cons: Not for hemodynamically unstable, drops in BP, potential for bleeding, blood clotting in circuit results in loss

Question 27

Nursing considerations of IHD

Answer 27

Monitor hemodynamics, pt may need inotropes or albumin, accurate I/Os, daily monitoring of lytes, pre-and post IHD K level, observe for bleeding

Question 28

What is Continuous renal replacement therapy (CRRT)? Pros/cons?

Answer 28

For pts who cannot tolerate IHD.

Pros:
100-200ml blood removed at once outside of body
Slower blood flow, continuous controlled removal
Continuous control of acid-base and lytes
Rate of fluid removal can be altered
Gentle dialysis for hemodynamically unstable

Cons: 
Gradual correction 
Unable to mobilize pt
Infection risk 
Circuit clotting, issues

Question 29

What is sustained low efficiency daily dialysis (SLEDD)?

Answer 29

Similar to IHD but lasts longer, done over 8-10 hrs, usually at night, does not interfere with mobilization. One HD nurse can monitor many pts

Question 30

What is peritoneal dialysis (PD) and what is the process?

Answer 30

Diasylate solution infused into peritoneal membrane and osmotic ultrafiltration achieved by amount of GLUCOSe in the solution.

Osmosis and active transport causes excess fluid and solutes to move from the peritoneal capillary fluid through capillary wall through peritoneal membrane into dialysis fluid.

Process:

1) Infusion of dialysate bath (1-2L)
2) Dwell time (Variable, up to 2 hrs)
3) Drainage (over 10 mins)