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Flashcards in AKI and Dialysis Deck (30)
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What are 2 main types of insults in AKI?

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


What are the 3 main categories of AKI?

1) Prerenal
2) Intrarenal
3) Postrenal


What is prerenal failure?

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


What are causes of pre-renal failure?

Local causes: Emboli, thrombus, surgery, hepatorenal syndrome

General causes: Hypoperfusion, decreased CO


What is intra-renal failure?

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

**ATN (Acute Tubular Necrosis)


What causes intra-renal failure / ATN?

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


What are the differences between Ischemic vs toxic ATN?

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


What is pathophys of ATN?

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


Why do AKI pts become anuric?

Glomerular pressure equals hydrostatic pressure.

Obstructions increase tubular hydrostatic pressure that eventually equals filtration pressure


What is postrenal failure?

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


What are the 4 stages of acute renal failure?

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


What happens in initiation phase?

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


What happens in maintenance phase?

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)


What happens in the diuretic stage?

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


What happens in recovery stage?

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


What is the best imaging test for AKI?

Renal ultrasound


What is medical management of AKI?

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


How are electrolytes managed in AKI?

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


Nursing diagnosis for AKI?

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


What is the purpose of dialysis?

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


What are the basic principles of dialysis?

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)


What is uremia and what is its effect?

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


What are contraindications to HD?

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


What is the process of intermittent HD (IHD)?

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


How does blood flow relate to dialysate flow?

Always counter-current, enhancing diffusion


Pros and cons of IHD?

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


Nursing considerations of IHD

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


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

For pts who cannot tolerate IHD.

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

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


What is sustained low efficiency daily dialysis (SLEDD)?

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


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

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.

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