AKI CKD Flashcards

1
Q

What is the most accurate indicator of fluid loss or gain?

A

Weight

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2
Q

I kg of weight gain =

A

1000 mL

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3
Q

Acute Kidney Injury

A

It is a rapid loss of renal function r/t damage to the kidneys
Depending on severity and duration a wide range of life-threatening complications can occur:
Fluid & electrolyte imbalances
Metabolic acidosis
Goal of care:
Minimize complications
Reduce cause of injury
Prevent long term loss of renal function
Criteria for AKI
50% or greater increase in serum creatinine above baseline
Urine volume may be normal or changes may occur:
Oliguria, anuria, Nonoliguria

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4
Q

AKI Causes:

A

Causes of AKI that reduce blood flow to the kidney and impair kidney function:
Hypovolemia
Hypotension
Reduced cardiac output
Heart failure
Obstruction of kidney or lower urinary tract
Tumor
Blood clot
Kidney stone (not very common causes)
Bilateral obstruction of the renal arteries or veins

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5
Q

AKI Classifications

A

5 point classification system:
RIFLE- Risk, Injury, Failure, Loss , ESKD
Severity:
Risk, Injury, Failure
Outcomes: Loss, ESKD

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6
Q

Fluid Volume Deficit:

A

Manifestation:Acute weight loss ≥5%, decreased skin turgor, dry mucous membranes, oliguria or anuria, increased hematocrit, BUN level increased out of proportion to creatinine level, hypothermia
Management: Fluid challenge, fluid replacement orally or parenterally

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7
Q

Fluid Volume Excess

A

Manifestations: Acute weight gain ≥5%, edema, crackles, shortness of breath, decreased BUN, decreased hematocrit, distended neck veins
Management: Fluid and sodium restriction, diuretic agents, dialysis

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8
Q

Hyponatremia

A

Manifestation: Nausea, malaise, lethargy, headache, abdominal cramps, apprehension, seizures
Management:
Diet, normal saline or hypertonic saline solutions

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9
Q

Hypernatremia

A

Manifestations: Dry, sticky mucous membranes, thirst, rough dry tongue, fever, restlessness, weakness, disorientation
Management: Fluids, diuretic agents, dietary restriction

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10
Q

Hypokalemia

A

Anorexia, abdominal distention, paralytic ileus, muscle weakness, ECG changes, dysrhythmias

Management: Diet, oral or parenteral potassium replacement therapy

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11
Q

Hyperkalemia

A

Diarrhea, colic, nausea, irritability, muscle weakness, ECG changes
Management:
Dietary restriction, diuretics, IV glucose, insulin and sodium bicarbonate, cation-exchange resin, calcium gluconate, dialysis

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12
Q

Hypocalcemia

A

Manifestations: Abdominal and muscle cramps, stridor, carpopedal spasm, hyperactive reflexes, tetany, positive Chvostek or Trousseau sign, tingling of fingers and around mouth, ECG changes
Management: Diet, oral or parenteral calcium salt replacement

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13
Q

Hypercalcemia

A

Deep bone pain, flank pain, muscle weakness, depressed deep tendon reflexes, constipation, nausea and vomiting, confusion, impaired memory, polyuria, polydipsia, ECG changes
Management: Fluid replacement, etidronate, pamidronate, mithramycin, calcitonin, glucocorticoids, phosphate salts

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14
Q

metabolic acidosis

A

Headache, confusion, drowsiness, increased respiratory rate and depth, nausea and vomiting, warm flushed skin
management:
Bicarbonate replacement, dialysis

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15
Q

metabolic alkalosis

A

Depressed respirations, muscle hypertonicity, dizziness, tingling of fingers and toes
Management:
Fluid replacement if volume depleted; ensure adequate chloride

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16
Q

hypoalbuminemia

A

Chronic weight loss, emotional depression, pallor, fatigue, soft flabby muscles
Management:
Diet, dietary supplements, hyperalimentation, albumin

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17
Q

hypomagnesemia

A

Dysphagia, muscle cramps, hyperactive reflexes, tetany, positive Chvostek or Trousseau sign, tingling of fingers, dysrhythmias, vertigo
management:

Diet, oral or parenteral magnesium replacement therapy

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18
Q

hypermagnesemia

A

Facial flushing, nausea and vomiting, sensation of warmth, drowsiness, depressed deep tendon reflexes, muscle weakness, respiratory depression, cardiac arrest
management:
Calcium gluconate, mechanical ventilation, dialysis
– causes prolonged PR interval, increased QRS duration, and prolonged QT interval. Can cause complete heart block or cardiac arrest
Calcium gluconate – displaces and neutralizes the effects of magnesium in the body

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19
Q

hypophosphatemia

A

Deep bone pain, flank pain, muscle weakness and pain, paresthesia, apprehension, confusion, seizures
Management:
Diet, oral or parenteral phosphorus supplementation therapy

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20
Q

AKI life threatening complications

A

Fluid & electrolyte imbalances
Metabolic acidosis

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21
Q

Criteria for AKI

A

Criteria for AKI
50% or greater increase in serum creatinine above baseline
Urine volume may be normal or changes may occur:
Oliguria, anuria, Nonoliguria

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22
Q

AKI Causes

A

Hypovolemia
Hypotension
Reduced cardiac output
Heart failure
Obstruction of kidney or lower urinary tract
Tumor
Blood clot
Kidney stone (not very common causes)
Bilateral obstruction of the renal arteries or veins

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23
Q

AKI classification

A

RIFLE – Risk, Injury, Failure, Loss, ESKD
(used to identify kidney injury and improve outcomes for patients)

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24
Q

R- RIsk

A

Increased serum creatinine 1.5 x baseline or GFR decreased greater than or equal to 25%
0.5 mL/kg/hr for 6 hours

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25
I (injury)
Increased serum creatnine 2 x baseline or GFR decreased greater than or equal to 50% 0.5 mL/kg/hr for 12 hours
26
F (failure)
Increased serum creatnine 3x baseline or GFR decreased greater than or equal to 75% or serum creatnine greater or equal to 354 mmol/L with an acute rise of at least 44 mmol/L or < o.3 mL/kg/hr for 24 hours or anuria for 12 hours
27
L (loss)
Persistent actute kidney injury = complete loss of kidney function > 4 weeks
28
E (ESKD)
ESKD > 3 months
29
Pre renal
Hypoperfusion Sudden and severe shock or interruption of blood flow to the kidneys from severe injury of illness Hypoperfusion resulting from - Volume depletion - Hemorrhage - GI loss (vomiting, diarrhea, NG suctioning) - Renal loss (diuretics) - Burns - Impaired cardiac efficiency (hypotension) - Heart failure - Dysrhythmias - MI - Cardiogenic shock - Vasodilation - Anaphylaxis - Sepsis - Antihypertensive medications causing vasodilation - Stenosis of the renal arteries
30
Gerontologic Considerations:
They may develop atypical signs and symptoms * Fluid deficit can lead to  Constipation  Falls  Medication toxicity  Urinary or respiratory tract infections  Delirium, seizures  Delayed wound healing Recognition in this older group can be hampered by underlying chronic conditions, or just mistaken with the aging process
31
Hyperkalemia Treatment explained
Insulin helps drive potassium back into the cells Glucose facilitates this process and prevents hypoglycemia with this treatment NaBicarb – helps move potassium back into the cells from the blood Calcium gluconate to prevent arrhythmias Cation resins bind potassium in the gut and send it into the GI tract Chvostek sign – twitch of facial muscles when gently tapping the cheek Trousseau sign – adduction of the thumb, flexion of the wrist Etidronate and pamidronate – slows bone formation and breakdown in the body
32
Protein deficit
Hyperalimentation – iv administration of nutrients
33
Creatnine and Urine lab values
Normal value of creatinine is < 1mg/dL Oliguria – less than 0.5 ml/kg/hr (the production of abnormally small amounts of urine) Anuria – less than 50 ml/day (failure of kidneys to produce urine) Non-oliguria – greater than 800 ml/day (a well-maintained urine output)
34
Intra-renal
Intra-renal (damage caused by) ATN (acute tubular necrosis) characteristics: - Intratubular obstruction - Tubular back leak (abnormal reabsorption and decreased urine outflow) - Vasoconstriction - Glomerular permeability - These result in GFR decreasing, progressive azotemia (increase in BUN and creatinine), and fluid/electrolyte imbalances Causes of Intra renal failure: - CKD - Hypertension - Diabetes - Cirrhosis - Prolonged ischemia - Trauma, burns, crush injuries - Infectious processes: acute glomerulonephritis, acute polynephritis - Nephrotoxic agents: certain antibiotics (gentamycin, tobramycin), lead, mercury, NSAIDs, radiopaque contrast agents, solvents and chemicals (arsenic) Acute glomerulonephritis Acute pyelonephritis
35
Post renal
Post-renal: (obstruction of the urinary tract) Pressure rises in the tubules and the GFR decreases Causes: - Blood clots - Stones - Tumors - Strictures - BPH - Pregnancy
36
Phases of AKI
-Initiation Begins with initial insult and ends when oliguria develops -Oliguria Accompanied by an increase in urea, creatinine, uric acid, organic acids, and K+ and Mg++ Urine output decreases below 400 mL in 24 hours (or 0.5 mL/kg/hr) Hyperkalemia develops -Diuresis Gradual INCREASE in urine output…glomerular filtration starts to recover Lab values stabilize and improve UOP may reach normal (or even greater than normal) levels Labs may still be abnormal Medical/Nursing mgmt. still continuing until the recovery phase -Recovery Improvement of renal function and may take from 3-12 months Labs return to normal (or clients’ baseline level) 1-3% reduction in GFR may occur; however, is not clinically significant
37
AKI Phases Notes
Oliguria phase: - The minimum amount of urine needed to rid the body of waste products is 400 ml in 24 hours - Uremic symptoms appear first: fatigue, nausea, loss of appetite, confusion, metallic taste - Uremia is when there is an abnormally high level of waste products in the blood - The hyperkalemia develops Diuresis phase: - Still need to be monitored closely to make sure the patient doesn’t end up developing dehydration
38
AKI: assessment & diagnostics
Urine Changes: Urinary output Urine color, clarity, odor, etc Hematuria Specific gravity decreases (one of the earliest manifestations) Decreased sodium in urine Renal sonogram, CT or MRI to determine abnormalities with anatomy BUN and creatinine increase Hyperkalemia may lead to dysrhythmias (VTACH) and cardiac arrest strict Is and Os, daily weights, foleys
39
Progressive metabolic acidosis
r/t inability to eliminate daily acid-type substances produced in body Buffering fails Decreased serum CO2 and pH levels
40
Phosphate levels increase in blood
decreased calcium levels in blood (decreased absorption in the intestines
41
Anemia
r/t reduced erythropoietin production uremic GI lesions, blood loss from GI tract
42
AKI Prevention
Continually assess renal function (urine output, laboratory values) when appropriate. Monitor central venous and arterial pressures and hourly urine output of critically ill clients to detect the onset of kidney disease as early as possible. Pay special attention to wounds, burns, and other precursors of sepsis. Prevent and treat infections promptly Infections can produce progressive kidney damage. Prevent and treat shock promptly with blood and fluid replacement. Take precautions to ensure that the appropriate blood is given to the correct client to avoid severe transfusion reactions, which can precipitate kidney disease.
43
AKI Prevention II
Provide adequate hydration to clients at risk for dehydration, including: Before, during, and after surgery Clients undergoing intensive diagnostic studies requiring fluid restriction and contrast agents (e.g., barium enema, IV pyelograms), especially older clients who may have marginal renal reserve Clients with neoplastic disorders or disorders of metabolism (e.g., gout) and those receiving chemotherapy Clients with skeletal muscle injuries (e.g., crush injuries, compartment syndrome) Clients with heat-induced illnesses (e.g., heat stroke, heat exhaustion)
44
AKI prevention III
To prevent infections from ascending in the urinary tract give meticulous care to clients with indwelling catheters Remove catheters as soon as possible To prevent toxic drug effects closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys Treat hypotension promptly
45
AKI medical management
Eliminating underlying cause: Shock (any type); however, sepsis is most common Maintaining fluid balance Daily weights Measuring CVPs Serum and urine concentrations Fluid losses Maintaining BP Parenteral/oral intake, UOP, gastric drainage, stools, wound drainage, and perspiration are basis for fluid replacement
46
AKI Medical Management II
Avoid fluid excesses Dyspnea, tachycardia, and JVD Crackles auscultated in lungs edema Mannitol, furosemide, or ethacrynic acid may be prescribed for diuresis IV fluids and blood / blood product transfusions For prerenal causes Dialysis to prevent complications of AKI Hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema
47
AKI: pharmacologic therapy
Hyperkalemia: EMERGENCY!!! Potassium level greater than 5 mEq/L ECG changes (tall, tented, or peaked T waves) Irritability, abdominal cramping, diarrhea, paresthesia, and generalized muscle weakness Generalized muscle weakness, slurred speech, difficulty breathing, and paralysis Treatment: Kayexalate**** Hemodynamic instability: Low BP, AMS, and/or dysrhythmia Treatment: IV Dextrose 50%, insulin, and calcium replacement to shift potassium back into cells (temporary…so, dialysis will still be needed)
48
AKI pharmacologic therapy
Renal dosing of medications Since many meds utilize the kidneys to filter; pharmacy can adjust medications accordingly Common meds: antibiotics, digoxin, phenytoin, ACE inhibitors, and magnesium-containing agents Sodium bicarbonate: Since client is typically more acidotic, sodium bicarb may be given; however, dialysis may still be needed for long-term effect Phosphate-binding agents: Treatment of hyperphosphatemia Calcium or lanthanum carbonate decrease levels by decreasing absorption from the intestinal tract
49
CKD: Chronic Kidney Disease
An umbrella term describing kidney damage decrease in the glomerular filtration rate (GFR) that lasts for 3 months or longer Untreated CKD can result in end-stage kidney disease (ESKD) Final stage of CKD Results in retention of uremic waste products Need for RRT (renal replacement therapy) Dialysis, or kidney transplant Damage to kidneys is thought to be caused by prolonged acute inflammation Early stages: There can be significant damage with
50
CKD: Risk Factors / causes
Cardiovascular disease Diabetes (primary cause) More than 35% of the US population over 20 years of age has CKD Leading cause of kidney disease in patients starting renal replacement therapy Hypertension (second-leading cause) Obesity Glomerulonephritis Pyelonephritis Polycystic disorders Nephorsclerosis Hereditary disorders More than 60 Congenital disorders Renal cancers
51
Stage 1 of CKD
Stage I: GFR > or equal to 90mL/min/1.73 m2 Kidney damage with normal or increased GFR
52
Stage 2:
Stage II: GFR = 60-89 mL/min/1.73 m2 Mild decrease in GFR
53
Stage 3:
Stage III: GFR = 30-59 mL/min/1.73 m2 Moderate decrease in GFR dialysis
54
Stage 4:
Stage IV: GFR = 15-29 mL/min/1.73 m2 Severe decrease in GFR dialysis
55
Stage 5:
Stage V: GFR < 15 mL/min/1.73 m2 End-stage kidney disease (ESKD) or chronic kidney disease dialysis
56
CKD: what to expect
Elevated serum creatinine levels Abnormal creatinine clearance -24 hour sample Anemia Decreased erythropoietin Metabolic acidosis Abnormal calcium and phosphorus levels Fluid retention (edema and CHF) As the disease progresses: Electrolyte disturbances heart failure worsens HTN more difficult to control
57
CKD: Medical Management
Treat underlying cause(s) Keep blood pressure BELOW 130/80 Renal replacement therapies (RRT) Early referral Prevent complications Controlling cardiovascular risk factors Treating hyperglycemia Managing anemia Smoking cessation Weight loss Exercise Reduction in salt and alcohol intake labs before and after dialysis
58
Dialysis
Dialysis or renal replacement therapy is indicated when advanced uremia and/or serious imbalances are present. Dialysis is typically the first-line treatment vs. kidney transplantation Dialysis is divided into 2 categories: Hemodialysis Peritoneal dialysis Continuous renal replacement therapy (CRRT) is a ‘gentler’ form of dialysis that can be done in critical care settings ONLY!
59
Hemodialysis
Hemodialysis is basically an artificial kidney Acute, chronic, ESKD Prevents death, but does not cure kidney disease A hemodialysis system consists of 3 parts: Blood delivery system Dialyzer Dialysis fluid delivery system During dialysis, blood moves from an artery through the tubing and blood chamber, then back into the body through a vein…this occurs via an AV fistula Diffusion, osmosis, ultrafiltration Heparin is given to prevent clotting during the dialysis circuit Most persons are dialyzed three times a week for 3-4 hours each time Always assess fistula sites! You don’t give heparin because it’s a part of dialyzer.
60
Before Dialysis
Before Dialysis: Assess Fluid status Weigh (current & previous) Vital signs Assess Fistula (shunt) Feel a thrill (vibration) Hear a bruit (swooshing
61
Hemodialysis deadly complication
Deadly complication – DDS (dialysis disequilibrium syndrome) Restless & disoriented Vomiting Headache Priority action: Stop or slow infusion, & report to provider (can happen during or after hemodialysis)
62
Hemodialysis Hold meds:
A (ACE & ARBS) Lisinopril, Losartan B (Beta blockers) Atenolol, metoprolol C Ca Channel Blockers Nifedipine, Verapamil, Diltiazem D Diuretics Furosemide, Hydrochlorothiazide D Dilators Nitroglycerin
63
Hemodialysis washed out meds
Washed out Antibiotics Digoxin Water soluble vitamins (B, C, & folic acid)
64
Hemodialysis Monitor for
Monitor for: Infection Bleeding Feel a thrill
65
Hemodialysis the 5Ps
The 5 P’s Pale skin “pallor” Paresthesia (numbness or tingling) Pulses diminished Poor capillary refill Pain (distal to shunt) First 2 P’s are serious and need to be addressed quickly (they can loose their fistula, or worse, their extremeties
66
Hemodialysis Teaching: Nos
NO Nos No restrictive clothing or jewelry No BP on affected arm No sleeping on arm No cream or lotions (infections) No lifting over 5 lbs. (no purse)
67
AV Fistula
Best choice for hemodialysis made by connecting an artery to a vein optimal blood flow lowest chance of infection
68
Goals of peritoneal dialysis
Goals of PD are to remove toxic substances and metabolic wastes to reestablish normal fluid and electrolyte balance
69
Peritoneal Dialysis- Treatment of choice for
Treatment of choice for clients with kidney disease who are unable or unwilling to undergo hemodialysis or kidney transplantation
70
A typical candidate for PD:
Diabetes Cardiovascular disease Those at risk for adverse effects from systemic heparin Clients with other conditions that haven’t been responsive to hemodialysis, will sometimes do well with PD.
71
What happens during peritoneal dialysis?
A sterile dextrose dialysate fluid is introduced into the peritoneal cavity via an abdominal catheter Once this solution is in the peritoneal cavity, uremic toxins begin to be cleared from blood.
72
Peritoneal Dialysis Advantages
More freedom More control over daily activities A more liberal diet (less fluid restrictions) Improve BP control
73
Peritoneal Dialysis Disadvantages
7 days a week Need to increase protein & K+ in diet
74
Peritoneal Dialysis Indications
Willingness, motivation & ability to do Strong support (family & community) Problems with HD (failing access devices, severe HTN, severe anemia, post dialysis HA HTN, uremia, and hyperglycemia easier to manage with PD
75
Peritoneal Dialysis Contraindications
Adhesions from previous surgery Chronic back pain or disc disease Severe arthritis or poor hand strength
76
Parameters and Acronyms for peritoneal dialysis
Acute intermittent peritoneal dialysis Not indicated for long term Usually someone who requires immediate dialysis (referred late in stage of CKD) CAPD Continuous ambulatory peritoneal dialysis Done during the day CCPD Continuous cyclic peritoneal dialysis Done at night while you sleep All PD involves a series of exchanges: Installation of dialysate (by gravity) Dwell time Drainage of fluid (by gravity
77
CRRT: Continuous replacement therapy
ONLY DONE IN ICU- patient is very unstable Dialysis that is carried out continuously instead of over 3-4 hours, as in traditional hemodialysis cases Benefits: Can be initiated quickly Do not affect hemodynamics as often as traditional hemodialysis Used in critical care units Indicated for clients who have acute or chronic kidney disease in the following cases: Too clinically unstable for traditional hemodialysis Fluid overload secondary to oliguric kidney disease Client with kidneys that cannot handle acutely high metabolic or nutritional needs