Acute Kidney Injury Flashcards
(53 cards)
1
Q
CKD
A
Progressive, irreversible loss of kidney function
2
Q
AKI
A
- a potentially reversible, abrupt decline in kidney function leading to increased creatinine, decreased urine output or both
3
Q
AKI is usually associated with…
A
other life-threatening conditions
4
Q
AKI follows: (3)
A
Follows severe, prolonged hyptension, hypovolemia, or exposure to a nephrotoxic
5
Q
How quickly do symptoms of AKI develop
A
Develops over hours to days
6
Q
Onset of AKI
A
sudden
7
Q
Most common cause of AKI
A
Acute tubular necrosis
8
Q
Diagnostic criteria AKI
A
Acute reduction in urine output, elevation in serum creatinine, or both
9
Q
Reversibility of AKI
A
potentially
10
Q
Morality of AKI
A
High
11
Q
Primary Cause of Death AKI
A
Infection
12
Q
Onset of CKD
A
Gradual, often over many years
13
Q
Most common cause of CKD
A
Diabetic nephropathy
14
Q
Diagnostic Criteria of CKD
A
GFR<60 for >3 mo, kidney damage >3 mo or both
15
Q
Reversibility of CKD
A
Progressive and irreversible
16
Q
Primary cause of death in CKD
A
Cardiovascular disease
17
Q
RIFLE Criteria
A
R - risk
I - Injury
F - Failure
L - loss
E - ESRD - end-stage renal disease
This is one of the most commonly used classification systems for AKI. uses serum creatinine, GFR, and urine output to identify these five criteria
18
Q
Clinical Manifestations of AKI
A
Range from mildly elevated serum creatinine to anuric renal failure
19
Q
Causes Leading to AKI: Prerenal
A
- External to the kidneys (hypovolemia or meds) that impact renal blood flow.
- Usually, reversible
Although renal tubular and glomerular function is preserved, glomerular filtration is reduced as a result of decreased perfusion.
20
Q
Prerenal Causes of AKI - Hypovolemia
A
Hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, and vascular obstruction cal all decrease the effective circulating volume of the blood. With reduced circulation, autoregulatory mechanisms that increase aldosterone, angiotensin II, norepinephrine and AHD attempt to preserve blood flow to essential organs. Prerenal azotemia (or accumulation of nitrogenous waste products) result in reduced excretion of sodium, increased salt and water retention, and decrease urine output
21
Q
Other cause of prerenal AKI: vasoactive medications
A
- ACE inhibitors
- ARBs
- Epinephrine and/or dopamine that cause intrarenal vasoconstriction leading to hypoperfusion of the glomeruli.
22
Q
Result of prolonged prerenal AKI
A
Prerenal AKI can lead to result in acute tubular necrosis, but if the prerenal cause is dealt with promptly, usually, renal function can be regained
23
Q
Causes Leading to AKI: Intrarenal
A
- Conditions that cause direct damage to renal tissue (parenchyma) –> impaired nephron function (ATN due to ischemia, nephrotoxins, or sepsis)
- Due to prolonged ischemia OR the presence of nephrotoxins (gentamycin or CT contrast). Hgb from hemolyzed RBC’s (sickle cell disease) or myoglobin released from necrotic muscle cells
- infrarenal causes of AKI can be due to untreated prerenal causes OR they can begin with direct damage to the renal
- SLE or acute glomerulonephritis may also cause AKI
24
Q
Causes Leading to AKI: Postrenal
A
- mechanical obstruction of urine outflow (BPH, prostate Ca, renal calculi, tumors)
- Usually reversible if identified before permanent kidney damage occurs
25
Prerenal and postrenal AKI correctible
ADDRESS THE CAUSE
- If the AKI hasn't caused intrarenal damage usually resolves quickly with correction of the cause.
if tissue damage HAS occurred from either cause or from intrarenal causes, acute tubular necrosis results and/or the course of AKI is prolonged
26
Untreated prerenal and postrenal causes +/- or infrarenal causes leads to
Acute Tubular Necrosis
27
ATN has three phases
- what happens if the pt doesnt recover?
- initiation
- maintenance
- recovery
In some situations, the patient does not recover from AKI and CKD develops
28
Initiation Phase: characterized by (2)
- increased serum creatinine + BUN
- decreased urine output
29
Maintenance Phase: how long does it last?
days to weeks
30
Maintenance Phase: Nonoliguric
Dilute urine but uremic toxins present (low specific gracity) kidneys are unable to filter out urea toxins into the urine
30
Urine output in Maintenance Phase
May be anuric: RARE, oliguric, or nonoliguric
31
Maintenance Phase: Oliguric
- manifestations (3)
- how long does this phase last?
- less than 400ml/day or 20ml/hr
- lasts 10-14 days usually. the longer it is prolonged, the poorer to outcome
- changes in urinary output
- fluid and electrolyte abnormalities
- uremia
32
Maintenance Phase - Oliguric: Urinary Changes
Decreased U/O to <400mL/24h.
33
Maintenance Phase - Oliguric: Fluid volume excess (5)
- JVD
- edema
- hypertension
- pulmonary edema
- pericardial and.or pleural effusions
34
Maintenance Phase - Oliguric: Metabolic Acidosis
- Kussmaul's resps (deep rapid) to increase blowing off Co2
- lethargy/stupor (if prolonged)
- kidneys can't synthesize ammonia, which is needed for hydrogen ion excretion or to excrete acid products of metabolism. Serum bicarb levels decrease b/c bicarb is used up buffering H+ ions
35
Maintenance Phase - Oliguric: Sodium Balance
Hyponatremia
Damaged tubules cannot conserve sodium, therefore, the urinary excretion of sodium may increase resulting in hyponatremia
36
Maintenance Phase - Oliguric: Potassium Excess
hyperkalemia -> tall, peaked T waves
occus b/c the normal ability of the kidneys to regulate and excrete potassium is impaired. May be precipitated by a number of causes: massive tissue trauma; bleeding and blood transfusion may cause cellular destruction; acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid.
Prompt treatment is essential
37
Maintenance Phase - Oliguric: Hematological Disorders
Anemia, increased bleeding, decreased WBC
- anemia r/t impaired erythropoietin production. Uremia reduces platelt adhesiveness, leading to bleeding.
WBCs are altered leading to immune deficiency. Infection in association with AKI is associated with double the mortality rate
38
Maintenance Phase - Oliguric: Calcium and Phosphate
- hypocalcemia
- hyperphosphatemia
Activated Vit D must be present for GI absorption of calcium. Only functioning kidney's can activate Vitamin D, therefore, in damaged kidneys, serum calcium decreases in response the parathyroid gland releases PTH, stimulating bone demineralization. Phosphate is released as well, leading to hyperphosphatemia, worsened by the reduced excretion of PO4 by the kidneys
39
Maintenance Phase - Oliguric: Waste Product Accumulation
- increased creatinine
- increased BUN
- decreased eGFR
Kidneys are the primary exretors for urea, the end product of protein metabolism and creatinine, and end product of endogenous muscle metabolims. BUN results have to be interpreted carefully because other things can increased BUN.
40
Maintenance Phase - Oliguric: Neurological Disorders
Fatigue/difficulty concentrating --> seizures, stupor, coma
41
Recovery Phase
Marked by return of BUN, Creatinine and GFR towards normal states
Diuresis --> fluid & electrolyte abnormalities
- patients acid-base, electrolyte and waste product values begin to normalize
- Renal function may take up to 12 months to stabilize
42
Recovery Phase: Diuresis
- Begins 1-3L/24 h --> 3-5L/24h
- pts must be monitored for hyponatremia, hypokalemia and dehydration
- may last 1-3 weeks
The high urine output occurs d/t osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine. Hypovolemia and hypotension can occur form massive fluid losses
43
AKI - Diagnostic Studies (5)
- Urinalysis - sediment WITH casts, cells, or proteins -> intrarenal disorders
- urine specific gravity, sodium content, osmolality --> helps differentiate different types of AKI
- renal ultrasound: anatmy and function
- Renal CT: can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk
- MRI and MRA are NOT recommended
44
Goals of care AKI (3)
1) eliminate the cause
2) manage signs and symptoms
3) prevent complications
45
IMPORTANT CONSIDERATIONS IN AKI COLLABORATIVE CARE
- Is there sufficient intravascular volume and cardiac output to perfuse the kidneys?
46
Collaborative Care: Diuretic Therapy
- Loop diuretics (Lasix)
- Osmotic diuretic (mannitol)
Diuretics will not help the prerenal or postrenal
Sometimes they can be helpful for the infrarenal causes.
47
Collaborative Care
- Fluid restriction: 600mL (insensible losses) + previous 24h losses
- treatment of electrolyte imbalances
- Renal Replacement Therapy - hemodialysis
48
What is AKI is already established?
Fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications
49
Nutritional Therapy
- main challenge --> balancing adequate calories to prevent catabolism despite restriction required to prevent electrolyte and fluid disorders
- energy from fat and carb sources prioritized to prevent ketosis
- 25-35kCal/kg
- Electrolyte replacement in accordance with serum levels
- sodium is restricted
- hyperphosphatemia, hypermagnasemia and hypocalceia
Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)
50
AKI - Nursing Managenent: Health Promotion (VERY IMPORTANT)
- ID high-risk populations for AKI (hypovolemic, dehdyrated, shockym poor cardiac output, advanced liver disease with low albumin- be thinking about renal perfusion)
- Control nephrotoxic drugs (IV contrast, gentamicin, NSAIDS, ACE inhibitors and ARBs, PipTaz and Vanco have special dosing for renal patients)
- Prevent prolonged episodes of hypovolemia or hypotension (treat low BP where it is warranted, the earlier the better)
51
Prevention and AKI
- essential d/t high morality rates associated with AKI. For patients with ANY level of renal insufficiency (esp those with diabetes or older adults), special attention must be given to prevent nephrotoxic events secondary to contrast dye.
- Adequate hydration before and after the test is critical
- Preventing prolonged episodes of hypovolemia INCLUDES monitoring output (esp when pts receiving ++ diuretic therapy, or in those with excessive diarrhea/NG/vomiting)
52
AKI Acute Nursing Interventions (6)
- Managing fluid and electrolyte balance
- Monitoring AND recording accurate intake and output
- Daily weights (at the same time; same scale) 1kg = 1L of fluid
- Reducing risk of infection: blunted febrile response (infection is the leading cause of death in AKI, meticulous aseptic technique required)
- Correct dosing of antibiotics for renal impairment
- Skin care and month care (edema and decreased muscle tone, mouth care d/t ammonia in saliva causing breakdown of mucous membranes)
