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complex care 2 > AKI > Flashcards

AKI Flashcards

1
Q

DEFINITION OF AKI

A
  • Rapid loss of kidney function
  • Rise in serum creatinine or reduction of urine output
  • Can develop azotemia (increase in nitrogenous waste)
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2
Q

AKI most common causes

A

-Hypotension, Hypovolemia, Exposure of nephrotoxic agents

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3
Q

most common reason for AKI in the hospital

A
  • prerenal causes

- acute tubular necrosis (ATN)

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4
Q

Pre renal

A
  • is due to factors external to the kidney that reduce circulation causing reduction in renal blood flow and decreased glomerular perfusion
  • body will compensate in prerenal AKI to increase blood flow by increasing blood volume angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone to.
  • can lead to intrarenal.
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5
Q

Intrarenal

A
  • caused by direct damage to the kidney tissue which leads to impaired nephron functioning
  • Causes for this can be prolonged ischemia, nephrotoxins, hemoglobin release from hemolyzed RBCs, or myoglobin released from necrotic muscles cells
  • ATN could be a cause
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6
Q

post renal

A
  • caused by mechanical obstruction of urinary flow and is below the kidneys
  • 10% of AKI
  • most common cause is BPH, prostate CA, calculi, trauma, or external tumors
  • If you have bilateral ureter obstruction this can lead to hydronephrosis.
  • If a blockage is fixed within 48 hours there generally is complete recovery.
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7
Q

acute tubular necrosis (ATN)

A
  • Caused by disruption in the basement membrane and patchy destruction of the tubular epithelium
  • Nephrotoxic agents cause tubular epithelial cells to slough off and plug the tubules.
  • nephrotoxic agents build up and plug the tubules of the kidney which alters the ability of the kidney to filter appropriately.
  • can be reversed death from AKI in the hospital can be high
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8
Q

Risk stage of RIFLE

A
  • Serum creatinine incresed by 1.5 or GFR decreased by 25 %

- urine output is less than 0.5 ml/kg/hr fro 6 hr

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9
Q

Injury phase of RIFLE

A
  • serum creatinine increased by 2 or GFR decreased by 50%

- UO less than 0.5 for 12 hours

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10
Q

Failure stage of RIFLE

A
  • serum creatinine increased by 3 or greater than 4 mg with acute rise of more than 0.5 mg GFR decreased by 75%
  • UO less than 0.3 for 24 hours (oliguria) or anuria for 12 hours
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11
Q

Loss stage of RIFLE

A
  • persistant acute kindey failure; complete loss of function > 4 weeks
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12
Q

end stage kidney disease stage of RIFLE

A

-complete loss of kidney function > 3 months

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13
Q

oliguric phase

A
  • reduction of urine output of less than 400mL/day and can occur within 1-7 days of injury
  • lasts 10-14 days
  • 50 % of people may not experience this
  • The longer in the oliguric phase the poorer the prognosis
  • changes in UO do not always correspond to changes in GFR. Rather the changes in urine output can help determine the cause. Further diagnostics can be done to determine the cause of AKI.
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14
Q

difference in oliguria and nonoliguria

A
  • Nonoliguric have a higher GFR than oliguric patients and/or they may reabsorb less in the tubules.
  • The difference in urine output between oliguric and nonoliguric ATN may be due to variations in GFR or in the rate of tubular reabsorption
  • Treatment based on oliguria vs. nonoliguria
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15
Q

diuretics with oliguric ATN

A
  • does not shorten the duration of renal failure, decrease the requirement for dialysis, or improve survival and might delay timely initiation of dialysis.
  • Among patients with oliguria and established ATN, diuretics should not be used as a possible therapy of ATN. -Diuretics may be given for a short length of time for volume control, but such use should not postpone the initiation of dialysis (if required).
  • However, giving crystalloids maybe appropriate depending on the cause like if the person is hypovolemic.
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16
Q

clinical manifestations during the oliguric phase

A
  1. fluid volume- retention to due to hypovolemia
  2. metabolic acidosis: not excreting enough hydrogen
  3. Sodium balance: cannot conserve sodium so urine has high sodium and serum has low to normal levels
  4. Potassium excess: K+ > 6mEqL emergency
  5. Hematologic disorders: leukocytosis
  6. Waste product accumulation: increase urea
  7. Neurologic disorders: build up of waste = fatigue, difficulty concentrating, stupor, coma
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17
Q

fluid volume in oliguric phase

A
  • retention is occurring because of hypovolemia.
  • By repleting fluids, issues can be resolved.
  • However, in some cases there can be fluid overload such with anuria where neck veins could be distended or other complications like pulmonary edema or HF can occur.
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18
Q

metabolic acidosis in oliguric phase

A

-This can occur because the kidneys cannot excrete hydrogen. Acid builds up. Serum bicarbonate is depleted and production is decreased.

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19
Q

sodium balance in oliguric phase

A
  • The damaged tubules cannot conserve sodium so urine has high amounts of sodium and normal to lower levels of serum NA.
  • Always be careful on replacement of NA because excess intake of NA can cause volume expansion. Likewise, hyponatremia can lead to cerebral edema.
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20
Q

potassium excess in oliguric phase

A
  • Kidneys normally excrete potassium
  • with AKI they are not able to do that.
  • monitor for peaked T waves and widening of the QRS and ST segment depression.
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21
Q

hematologic disorders in oliguric phase

A

-Leukocytosis (high WBC) is often present with AKI and the most common cause of death in AKI is infection.

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22
Q

waste product accumulation in oliguric phase

A

Normally kidneys excrete urea the end product of protein metabolism, this will be increased with AKI.

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23
Q

neurologic disorders in oliguric phase

A

as nitrogenous waste builds people can experience fatigue and difficulty concentrating and eventually seizures, stupor and/or coma.

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24
Q

Urine analysis for oliguric phase

A
  • RBCs
  • Casts
  • WBCs
  • Specific gravity 1.010
  • Osom: 300 mOsm/kg (this is the same osom of plasma which means there is tubular damage and the kidneys can no longer concentrate urine)
  • Proteinuria (if related to glomerular membrane dysfunction)
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25
Q

diuretic phase

A
  • Begins with gradual increase in UO
    • May last 1-3 weeks
    • normalizing of acid-base
    • electrolyte and waste product parameters indicate improvement of renal failure
  • Nephrons still cannot concentrate urine, but the kidneys can now excrete wastes
  • Assess for hypovolemia and hypotension from fluid loss – replace fluids
  • Assess for hyponatremia, hypokalemia and dehydration (Since the nephrons can excrete waste now but not concentrate it)
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26
Q

recovery phase

A
  • Begins when Glomerular Filtration Rate increases, allowing BUN and creatinine levels to plateau/decrease
  • Improvement can occur up to 12 months
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27
Q

AKI dx

A
  • Hx
  • UA
  • Labs
  • Ultrasound
  • Renal scan
  • CT
  • Renal biopsy
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28
Q

prerenal causes

A

hx of cardiac dx, dehydration, blood loss

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29
Q

intrarenal causes

A

nephrotoxic meds, blood transfusion, exposure to contrast media

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30
Q

postrenal causes

A

hx changes in urinary stream, hematuria, stones, ca of bladder or prostate

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31
Q

MRI advisory with AKI

A
  • People in AKI should not get a MRI/MRA with contrast because gadolinium (the dye) could be potentially fatal.
  • anyone with kidney issues can get contrast induced nephropathy.
  • For patients with diabetes metformin should be held for 48 hours prior to and after the use of a contrast dye to decrease the risk of lactic acidosis.
32
Q

contrast induced nephropathy that causes AKI

A

-see the serum creatinine increase and peak around day 4 and return to normal around day 10.

33
Q

AKI interprofessional care

A
  • Prevention/eliminate cause, prevent complications
  • Hydration: Maintain intravascular volume and CO
  • Manage signs/symptoms while kidneys repair themselves
  • Monitor exposure to nephrotoxins
  • Diuretic therapy and volume expanders to prevent fluid overload
  • Very close monitoring of I&Os (every mL counts!)
  • Watch for hyperkalemia: can be fatal
  • Nutritional support: adequate calories, energy from carbohydrates, increase fats, sodium restricted * to prevent edema monitor labs
34
Q

when to start renal replacement therapy

A
  • volume overload
  • elevated potassium levels
  • metabolic acidosis
  • extremely elevated BUN (>120mg/dL)
  • significant change in LOC
  • pericarditis
  • pericardial effusion
  • cardiac tamponade.
  • RRT can be peritoneal dialysis, hemodialysis, or continuous renal replacement therapy.
35
Q

Care for hyperkalemia

A
  • Insulin IV
  • IV Ca Gluconate: Temporarily blocks K effect on the heart; stabilizes cardiac cells
  • Kayexalate: Given PO/NG or by retention enema
  • IV Sodium Bicarbonate: increasing the pH of the serum also moves K into the cells (lasts about 2 hours)
  • Dialysis
  • Dietary Restriction of Potassium
36
Q

ACE inhibitors and AKI

A
  • ACE inhibitors can decrease perfusion and cause hyperkalemia, they may need to be reduced or stopped
  • ACE inhibitors also prevent proteinuria and progression of kidney disease
37
Q

other special considerations for AKI

A
  • Infection is the leading cause of death with AKI
  • Monitor for both local (redness, swelling, pain) and systemic (fever or leukocytosis) signs of infections
  • Patients may not have a temperature with AKI
38
Q

movement of solutes with dialysis

A
  • solutes and water, moving across the membrane from The blood to the dialysate or vice versa based on concentration Gradients
  • Urea, creatinine, uric acid and electrolytes move from blood to dialysate with
  • The net effect of lowering their concentration in the blood
  • Glucose is added to dialysate to create an osmotic gradient across the membrane To remove excess fluid from the blood.
39
Q

when to start dialysis

A
  • GFR <15 ml/min/1.73m2
  • Lack of donated organs
  • Unable to get a transplant
  • Don’t want a transplant
40
Q

semipermeable membrane and dialysis

A
  • Diffusion: moves urea, creatinine, uric acid and electrolytes
  • Osmosis: add glucose pulls fluid from the blood
41
Q

in PD what is the membrane

A

the peritoneal membrane is the semipermeable membrane

42
Q

In HD what is the membrane

A

there is an artificial membrane

43
Q

ultrafiltration

A

you have water and fluid removed this is generally created through the addition of glucose in PD and increasing the pressure in HD

44
Q

what is PD

A

-Catheter Placement
-Peritoneal access is obtained by surgically inserting a catheter through the anterior abdominal wall (will take a few weeks for fibrosis to grow and hold the catheter)
-Tip of the catheter rests in the peritoneal cavity and has many perforations to allow fluid to flow in and out of the catheter
-will do several exchanges through the night per order
–infuse the solution, let it sit so osmosis happens, then drain

45
Q

3 phases of PD

A
  • all three called exchange)
  • Inflow: 2L infused over 10 minutes
  • Dwell: 4-6 hours
  • Drain: 15-30 minutes
46
Q

PD systems

A
  1. Automated PD – uses a cycler that times and controls the fill, dwell and drain times
    - allows for PD while they sleep
    - machine cycles each exchange and allows for 4 or more exchanges/night
    - May DC from the PD in am and keep fluid in the abdomen during the day
    - may need 1-2 daytime exchnages
    - Continuous Cycle PD
    - Intermittent PD
    - Nightly PD
  2. Continuous Ambulatory PD – manually exchanging 2L of peritoneal dialysis usually 4X/day with dwell times of 4hrs
47
Q

PD complications: infection

A
  1. at catheter site
  2. Peritonitis
    - Due to improper technique
    - Abdominal pain, rebound tenderness, cloudy peritoneal effluent, maybe a fever
    - Formation of adhesions can occur after repeated infections
48
Q

other PD complications

A
  • Hernias: due to the pressure from the dialysate
  • Lower back programs: due to increased intraabdominal pressure
  • Bleeding: at the catheter site especially after the first few exchanges
  • Pulmonary complications: atelectasis, PNA, and bronchitis due to the upward placement of the diaphragm
  • Protein loss: can be worse if someone gets peritonitis
49
Q

contraindications of PD

A
  • History of multiple abdominal surgeries or abdominal pathologies
  • Recurrent abdominal wall or inguinal hernias
  • Excessive obesity
  • Preexisting vertebral disease
  • Severe obstructive pulmonary disease
50
Q

Hemodialysis (HD)

A

-Pump driven system
-Requires: Rapid blood flow, Access to large blood vessel
-“inpatient therapy” or could be done out pt
-Requires AV fistula for large bore IV access
-Emergent:
Jugular or femoral vein for catheter placement at the bedside
High rate of infection and should not be DC with

51
Q

HD: iv catheter access device

A 
Acute, temporary access
Red = “arterial”
Blue = “venous”
DO NOT use for other lab draws unless OK by protocol
DO NOT use for IV access
52
Q

HD: arteriovenous grafts

A
  • Synthetic graft
  • When pt has history of severe peripheral vascular disease, prolonged iV drug abuse, obese women
  • Grafts are implanted under the skin
  • Connect both artery and vein
  • Takes 2-4 four weeks to heal/access
  • Can be used right away- don’t require maturation
  • More likely to become infected and/or thrombotic
  • Can palpate a thrill and auscultate a bruit
  • Use large needles to access for HD
53
Q

HD arteriovenous fistula

A
  • Uses pt artery and vein to make fistula for hemodialysis
  • Vein becomes arterialized to allow for rapid blood flow for HD
  • Takes 6 weeks to mature and so a person has to plan ahead with PCP and plan on getting graft 3 months prior to needing to use it
  • Common access:
    1. Forearm by a side-to-side end-to-side or end-to-end anastomosis between an artery and a vein;
    2. fistula provides arterial blood flow, rapid blood flow through the vein (which dilates the vein)
    3. Over time the vein becomes tough and may be used for repeated venipuncture for repeated access
  • Native fistulas have best overall patency rates, least complications, can only be used if pt has good vascular health
  • Central venous stenosis or occlusion is common problem which leads to loss of vascular access for HD
54
Q

HD nursing considerations for AV fistulas and grafts

A
  • Assessment: Palpate for a thrill at site of anastamosis, listen for bruit – both created by arterial blood rushing through vein
  • Never perform BP or venipuncture on affected extremity with graft/fistula
  • Put sign up at HOB “no blood draws or IV in left or right arm”
55
Q

HD prior to dialysis

A

-LARGE bore needle required that is inserted into the fistula or graft
-When blood comes into contact with the dialyzer it tends to clot so heparin is added to the blood to prevent clotting (get order prior to dialysis)
-Pre-dialysis RN care: weight, BP, temp, assess peripheral edema, auscultate lung/heart sounds
1. Need to know how much fluid is in patient
2. Helps determine how fast and/or long HD will run
3. Difference between post dialysis wt and present pre-dialysis wt determines amount of wt to be removed
-During dialysis vital signs are taken every 30-60 minutes by the dialysis nurse.
-In-center HD
-Home HD
1. Requires good support
2. Daily or nocturnal with less complications: less meds, less side effects
3. Increased autonomy
<2% dialyze at home

56
Q

dialyzer

A
  • is a long plastic cartridge that contains many parallel hollow tubes or filters that are semipermeable membranes.
  • Blood is pumped into the top of the cartridge and is dispersed to all of the fibers.
  • Dialysate is pumped into the cartridge and bathes the outside of the filters w/ dialysis fluid.
  • Ultrafiltration, diffusion and osmosis occur across the pores of the semipermeable membrane.
  • When the dialyzed blood reaches the end of the thousands of semipermeable filters, it converges into a single tubing that returns to the patient.
57
Q

dialyzing procedure

A
  • Primed w/ NS, displaced by blood as it is drawn from the fistula
    1. Heparin added to blood as flows to dialyzer
  • Ultrafiltration controller equalizes + and − pressures to regulate amount of fluid removed
  • Blood is returned to pt via venous line
  • Dialysis is terminated by flushing dialyzer w/ NS
  • Firm pressure to graft site after removal of needles
58
Q

HD complications: hypotension

A

-Rapid removal of vascular volume, ↓ CO, and ↓SVR:
light headedness, N/V
seizures, vision changes
coronary ischemia
-TX: decrease the volume of fluid removed and infuse 0.9% saline. hold BP meds prior HD if pt has hx of ↓BP.

59
Q

HD compliocations: muscle cramps

A
  • from rapid removal of Na and H20 or from neuromuscular sensitivity,
  • TX:↓ ultrafiltration rate, NS bolus, glucose, mannitol
60
Q

other HD complications

A

-Thrombosis at graft sites
-Aneurysm
-Infection
-Blood loss: inadequate flush of dialyzer, separation of blood tubing or dialysis membrane rupture or bleeding out of fistula after dialysis; ↑risk b/c use of heparin
-Hepatitis: from blood transfusions
1. Hep C more prevelent (10% in dialysis patients)
2. Hep B less prevalent now, receive HepB vaccine
Sepsis: from infection of vascular access sites during dialysis
-TX: aseptic technique is essential

61
Q

disequilibrium syndrome

A

-Range of neuro symptoms that affect pt on HD- esp. if first started on dialysis or pt who have missed multiple consecutive dialysis tx
-rapid changes in extracellular fluid;
urea, Na and other solutes from blood then from the CSF and the brain
-differential creates ↑osmotic gradient in brain →↑fluid shifts in the brain → cerebral edema

62
Q

mani of disequilibrium syndrome

A
  • N/V, confusion, restlessness (progress to somnolence, confusion, disorientation, mania) HA, twitching and jerking, muscle cramps and hypotension; blurred vision
  • seizure, stupor, coma, death are the severe mani
63
Q

disequilibrium syndrome tx

A
  • slowing or stopping dialysis

- Infuse hypertonic saline solution albumin or mannitol to draw fluid from the brain cells back into circulation;

64
Q

dialysis comparison

A
  • Peritoneal Dialysis (PD): fluid is removed by ↑’ing the osmolality of dialysate (by adding glucose)
  • Hemodialysis (HD): fluid is removed by creating a difference in pressure between the blood compartment (positive) and the dialysate compartment (negative pressure)
65
Q

dialysis: crrt

A

Continuous renal replacement therapy (CRRT)

toxins and fluids can be removed from unstable patients

66
Q

crrt

A
  • CRRT as the more physiologic way of how the kidneys work slowly over the course of 24 hours.
  • Used in patients who are hemodynamically unstable or slow continuous removal of toxins is desired
  • Toxins and fluids are removed while acid-base status and electrolytes are adjusted slowly and continuously
  • Pts must not have life-threatening hyperkalemia or pericarditis that would require rapid resolution
67
Q

how is crrt different from hemodialysis

A
  • The big point for CRRT is that for any emergent situation related to potassium it is not a good choice.
  1. continuous rather than intermittent
    2) solute removal mechanism is by convection in addition to osmosis and diffusion
    3) causes less hemodynamic instability (e.g. hypotension) b/c of slower fluid removal
    4) ICU RN can perform CRRT, but does not require a specialized nurse like what is needed with HD
    5) Different equipment: doesn’t use a dialyzer, but a blood pump is needed for venovenous therapies
68
Q

crrt set up

A
  • access is similar to emergent HD using either the jugular or femoral vein
  • a person can have it for 30-40 days, but the hemofilter is changed every 24-48 hours.
  • In CRRT the removal of solutes occurs by convection, osmosis, and diffusion.
  • Vascular access like HD

-Exchange is slow, but continuous

  • Rate of ultrafiltration (removal of fluid/solutes) around 150mL/min
    1. typically on the lower side as system relies on patient’s BP to push blood through unit
    2. Newer units have a blood pump that increases the pressure gradient and fluid flow

-Anticoagulation to prevent blood clotting

69
Q

HX for dx of AKI

A
  • recent s/s, drug tx to determine the cause
70
Q

UA for dx of AKI

A

-UA: urine sediment containing abundant cells, casts or proteins suggests intrarenal disorders.

71
Q

labs for dx of AKI

A

-Labs: BUN/Cr and urine sodium levels

72
Q

ultrasound for dx of AKI

A

-Ultrasound- no nephrotoxic agents needed, done first, r/o obstruction

73
Q

renal scan for dx of AKI

A

-Renal scan-looks an renal blood flow tubular function

74
Q

CT scan for dx of AKI

A

-CT- identify lesion and masses, obstructions, vascular anomalies

75
Q

renal biopsy for dx of AKI

A

-Renal biopsy- best way to confirm intrarenal causes of AKI

complex care 2 (8 decks)

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