AKI CKD Flashcards
What is the most accurate indicator of fluid loss or gain?
Weight
I kg of weight gain =
1000 mL
Acute Kidney Injury
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
AKI Causes:
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
AKI Classifications
5 point classification system:
RIFLE- Risk, Injury, Failure, Loss , ESKD
Severity:
Risk, Injury, Failure
Outcomes: Loss, ESKD
Fluid Volume Deficit:
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
Fluid Volume Excess
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
Hyponatremia
Manifestation: Nausea, malaise, lethargy, headache, abdominal cramps, apprehension, seizures
Management:
Diet, normal saline or hypertonic saline solutions
Hypernatremia
Manifestations: Dry, sticky mucous membranes, thirst, rough dry tongue, fever, restlessness, weakness, disorientation
Management: Fluids, diuretic agents, dietary restriction
Hypokalemia
Anorexia, abdominal distention, paralytic ileus, muscle weakness, ECG changes, dysrhythmias
Management: Diet, oral or parenteral potassium replacement therapy
Hyperkalemia
Diarrhea, colic, nausea, irritability, muscle weakness, ECG changes
Management:
Dietary restriction, diuretics, IV glucose, insulin and sodium bicarbonate, cation-exchange resin, calcium gluconate, dialysis
Hypocalcemia
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
Hypercalcemia
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
metabolic acidosis
Headache, confusion, drowsiness, increased respiratory rate and depth, nausea and vomiting, warm flushed skin
management:
Bicarbonate replacement, dialysis
metabolic alkalosis
Depressed respirations, muscle hypertonicity, dizziness, tingling of fingers and toes
Management:
Fluid replacement if volume depleted; ensure adequate chloride
hypoalbuminemia
Chronic weight loss, emotional depression, pallor, fatigue, soft flabby muscles
Management:
Diet, dietary supplements, hyperalimentation, albumin
hypomagnesemia
Dysphagia, muscle cramps, hyperactive reflexes, tetany, positive Chvostek or Trousseau sign, tingling of fingers, dysrhythmias, vertigo
management:
Diet, oral or parenteral magnesium replacement therapy
hypermagnesemia
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
hypophosphatemia
Deep bone pain, flank pain, muscle weakness and pain, paresthesia, apprehension, confusion, seizures
Management:
Diet, oral or parenteral phosphorus supplementation therapy
AKI life threatening complications
Fluid & electrolyte imbalances
Metabolic acidosis
Criteria for AKI
Criteria for AKI
50% or greater increase in serum creatinine above baseline
Urine volume may be normal or changes may occur:
Oliguria, anuria, Nonoliguria
AKI Causes
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
AKI classification
RIFLE – Risk, Injury, Failure, Loss, ESKD
(used to identify kidney injury and improve outcomes for patients)
R- RIsk
Increased serum creatinine 1.5 x baseline or GFR decreased greater than or equal to 25%
0.5 mL/kg/hr for 6 hours
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
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
L (loss)
Persistent actute kidney injury = complete loss of kidney function > 4 weeks
E (ESKD)
ESKD > 3 months
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
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
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
Protein deficit
Hyperalimentation – iv administration of nutrients
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)
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
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
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
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
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
Progressive metabolic acidosis
r/t inability to eliminate daily acid-type substances produced in body
Buffering fails
Decreased serum CO2 and pH levels
Phosphate levels increase in blood
decreased calcium levels in blood (decreased absorption in the intestines
Anemia
r/t reduced erythropoietin production
uremic GI lesions, blood loss from GI tract
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.
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)
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
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
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
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)
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
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
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
Stage 1 of CKD
Stage I:
GFR > or equal to 90mL/min/1.73 m2
Kidney damage with normal or increased GFR
Stage 2:
Stage II:
GFR = 60-89 mL/min/1.73 m2
Mild decrease in GFR
Stage 3:
Stage III:
GFR = 30-59 mL/min/1.73 m2
Moderate decrease in GFR
dialysis
Stage 4:
Stage IV:
GFR = 15-29 mL/min/1.73 m2
Severe decrease in GFR
dialysis
Stage 5:
Stage V:
GFR < 15 mL/min/1.73 m2
End-stage kidney disease (ESKD) or chronic kidney disease
dialysis
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
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
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!
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.
Before Dialysis
Before Dialysis:
Assess Fluid status
Weigh (current & previous)
Vital signs
Assess Fistula (shunt)
Feel a thrill (vibration)
Hear a bruit (swooshing
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)
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
Hemodialysis washed out meds
Washed out
Antibiotics
Digoxin
Water soluble vitamins (B, C, & folic acid)
Hemodialysis Monitor for
Monitor for:
Infection
Bleeding
Feel a thrill
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
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)
AV Fistula
Best choice for hemodialysis
made by connecting an artery to a vein
optimal blood flow
lowest chance of infection
Goals of peritoneal dialysis
Goals of PD are to remove toxic substances and metabolic wastes to reestablish normal fluid and electrolyte balance
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
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.
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.
Peritoneal Dialysis Advantages
More freedom
More control over daily activities
A more liberal diet (less fluid restrictions)
Improve BP control
Peritoneal Dialysis Disadvantages
7 days a week
Need to increase protein & K+ in diet
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
Peritoneal Dialysis Contraindications
Adhesions from previous surgery
Chronic back pain or disc disease
Severe arthritis or poor hand strength
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
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
