Renal day 2 Flashcards
Urine Output
Standards
Daily output averages 1000 – 2400 ml / day
Normal adult approximately 1500 mL/day
Acute Care Setting: 30 ml / hour (720 ml / day)
Oliguria: 100 – 400 ml / day
Aging kidney’s lose ability to concentrate
Older adults may be oliguric with volumes of 600 – 700 / day
Anuria: < 100 ml / day
Acute Renal Failure: Causes
Primary causes in Acute Care:
Hypotension
Hypovolemia
Pre-Renal
Intra-Renal
Post-Renal
Pre-Renal Causes
Issues that interfere with renal perfusion
Circulatory volume depletion
Volume shifts
“3rd Spacing”
Decreased cardiac output
Decreased PVR
Vascular Obstruction
General Symptoms
High specific gravity & osmolarity
Normal sediment
May have Hyaline/Granular casts
BUN / Cr significantly elevated (10:1 – 40:1)
Proteinuria & sodium excretion not significant
Intra-Renal Causes
Parenchymal changes caused by disease or nephrotoxins
Acute tubular necrosis (75%)
Muddy brown granular casts
Glomerulonephritis
Hematuria
RBC & Hemoglobin casts
Vascular lesions
Cortical necrosis (Prolonged vasospasm)
Tissue damage - Elevated
Serum creatinine
Phosphokinase
K+
General Symptoms:
Fixed specific gravity
Edema
Weight gain
Hemoptysis
Elevated LV EDP
Weakness (Anemia)
Hypertension
High urine sodium
Proteinuria
Post-Renal Causes
Issues that cause obstruction of urinary tract
BPH
Calculi
Tumor
Surgical accident
Spinal cord injury
Neurogenic bladder with retention (decreased bladder emptying)
“Functional” obstruction
General Symptoms
Fixed specific gravity
Elevated urine sodium
Little or no proteinuria
Sediment normal
Indications of obstruction
Anuria / Polyuria: Intermittent?
Acute Kidney Injury: Elderly Considerations
Decreased GFR with aging
More susceptible to AKI & decreased ability to recover
Dehydration
Polypharmacy (Diuretics, laxatives)
Illness
Immobility
Hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders, surgery, infection, & contrast medium
Renal Replacement Therapies (RRT) still an option
Acute Kidney Injury: Oliguric Phase
U.O. < 400 ml / day
Occurs: 1 – 7 days of injury (24 - hours ischemia)
Duration: 10 – 14 days to months
Longer phase = poorer prognosis
50% patients non-oliguric; > 400 mL urine/day
Urinalysis; Casts, RBCs, WBCs, Protein
Specific gravity 1.010 (Fixed)
Osmolality 300 mOsm/kg
Acute Kidney Injury: Oliguric Phase cont
Hypovolemia may exacerbate AKI
Decreased urine output leads to fluid retention
Neck veins distended
Bounding pulse
Edema
Hypertension
Fluid overload can lead to:
CHF
Pulmonary edema
Pericardial or pleural effusions
Leukocytosis: Infection may be fatal
Urinary & respiratory
Waste product accumulation; Increased BUN & Cr
Neurologic disorders
Fatigue
Difficulty concentrating
Seizures, stupor, coma
Metabolic acidosis
Kidneys cannot excrete Hydrogen or acid products of metabolism
Serum bicarbonate production decreased; Reabsorption & regeneration defective
Severe acidosis develops; Kussmaul respirations (increase exhaled CO2)
Results from
Impaired ability of kidneys to excrete excess acid
Defective reabsorption & regeneration of bicarbonate
Plasma bicarbonate level usually falls to approximately 16 to 20 mEq/L (16 to 20 mmol/L)
Hyponatremia
Increased excretion of Na+ d/t damaged tubules
Can lead to cerebral edema
Hyperkalemia
Impaired ability to excrete K+
Usually asymptomatic; Peaked T waves, Wide QRS, ST depression
Increased risk with massive tissue trauma
Weakness, cardiac arrhythmias
EKG Monitoring / Remote Telemetry
Treatment:
K+ restriction
Potassium removal
Dialysis
Kayexalate
Acute Kidney Injury: Diuretic Phase
Lasts 1 – 3 weeks
Daily U.O. 1 - 3 Liters (up to 5 Liters)
Osmotic diuresis from high urea
Low specific gravity; Nearly iso-osmolar
Kidneys able to excrete waste, but not concentrate urine
Patients who develope oliguria will have greater diuresis than those who do not
Monitor for:
Hypovolemia,
Hypotension
Hyponatremia
Hypokalemia
Dehydration
Acute Kidney Injury: Recovery Phase
Begins when GFR increases
Allows BUN & Cr to plateau & then decrease
Major improvements occur in first 1 – 2 weeks
May take up to 12-months to stabilize
AKI: Diagnostics
Thorough history
Serum BUN / Cr
Serum electrolytes
Urinalysis
Renal ultrasound
Renal CT scan
Renal biopsy
Contraindications: Contrast
MRI or MRA with Gadolinium (May be fatal)
Contrast-induced nephropathy
Metformin: Hold 48-hours before & after use of contrast; Risk for lactic acidosis
If contrast needed for high-risk patients - Use low-dose & ensure optimal hydration
AKI: Interprofessional Care
Goals of Care:
Eliminate cause
Manage signs/symptoms
Prevent complications
Ensure adequate intravascular volume & cardiac output
Loop diuretics: Furosemide (Lasix)
Osmotic diuretics: Mannitol
Closely monitor fluid intake during Oliguric phase
Fluid restriction: All fluid losses for previous 24 hours + 600 mL
Expected outcomes:
Regain & maintain normal fluid & electrolyte balance
Adhere to treatment regimen
No complications
Complete recovery
Electrolytes
K+ (3.5 – 5.0 mEq/L)
Na+ (136 – 145 mEq/L)
Mg+ (1.3 – 2.1 mEq/L)
Phosphorous (3.0 – 4.5 mg/dL)
Ca+ (Parathyroid function)
Total 9.0 – 10.5 mg/dL
Ionized 4.5 – 5.6 mg/dL
Exchange Resins
Kayexalate & Sorbitol
Questions re: efficacy versus risks
Contra-indicated with ileus (Intestinal necrosis)
Patiromer (Veltassa)
Powder for oral suspension in water
Taken daily; Delayed action - Not for emergency use
Indications for Renal Replacement Therapy (RRT)
Volume overload
Hyperkalemia
Metabolic acidosis
BUN > 120 mg/dL
Significant change in mental status
Pericarditis, pericardial effusion, or cardiac tamponade
Clinical status of patient
Hemodialysis (HD): Emergent therapy
Peritoneal dialysis (PD)
ICU Setting Only:
Continuous Renal Replacement Therapy (CRRT)
Continuous cannulation (24-hours) of artery & vein
AKI: Nutritional Therapy
Maintain adequate caloric intake
Primarily carbohydrates, increased fats, adequate protein to prevent breakdown
Restrict Na+, K+, Phosphate
Calcium supplements or phosphate-binding agents
Enteral / parenteral nutrition
Acute Care
Accurate I & O
Daily weights
Assess for hypervolemia or hypovolemia
Assess for K+ & Na+ disturbances
Meticulous aseptic technique
Careful use of nephrotoxic drugs
Skin care measures
Oral care
Patient Teaching for Post-Acute Ambulatory Care
Monitor kidney function
Regulate protein & potassium intake
Follow-up care
Teaching
Appropriate referrals
Chronic Kidney Disease (CKD)
Progressive, irreversible loss of kidney function
Low glomerular filtration rate (GFR); <60 mL/min/1.73m2 for longer than 3 months
More than 26 million American adults have CKD
Increased prevalence: Aging population, increased obesity, increased diabetes & HTN
Increased incidence: Blacks, Native Americans, & Latinos
Underdiagnoses & untreated; Many with CKD are asymptomatic; Approximately 70% aware
Uremia
Syndrome; Kidney function declines to point that symptoms occur in multiple body systems
Often occurs when GFR is less than or equal to 15mL/min
Manifestations vary depending on cause, co-morbidities, age, & adherence to medical regimen
Diagnostic Studies
H & P
Dipstick evaluation of protein; Albuminuria
Urinalysis
Renal ultrasound, scan, CT scan, biopsy
Albumin-to-creatinine ratio (1st AM void)
Serum BUN, creatinine, creatinine clearance, electrolytes, lipids, hemoglobin, hematocrit
GFR
Stages of Chronic Kidney Disease
1
≥ 90
Diagnosis and treatment; CVD risk reduction; slow progression
2
60–89
Estimation of progression
3a
45–59
Evaluation and treatment of complications
3b
30–44
More aggressive treatment of complications
4
15–29
Preparation for RRT (dialysis or transplant)
5
Less than 15 or dialysis
RRT if uremia present and patient desires treatment; necessary to maintain life
CKD: Sodium / Magnesium
HYPOnatremia (Dilutional)
Confusion, seizures, coma
Fluid restriction for self-correction
HYPERmagnesemia
Decreased reflexes, mental status, B/P, respiratory failure
Avoid:
Dark green veggies
Grains, seeds, nuts
Legumes
Antacids with Mg+
Osmotic laxatives (Milk of Magnesia, Magnesium Citrate)
CKD: Calcium / Phosphorous
HYPOcalcemia
Decreased intestinal Ca+ absorption
Synthesis of 1,25 dihydroxyycholecalciferol
HYPERphosphatemia furthers low Ca+
Increased parathyroid hormone excretion leads to bone resorption
Osteomalacia
Osteitis fibrosa
Osteosclerosis
HYPERphosphatemia
Hypocalcemia
Increased risk for fractures, CKD-MBD
Avoid:
Dairy products & foods containing dairy products
Milk
Ice cream
Cheese
Yogurt
Pudding
Protein sources contain Phosphate
Phosphate binders
As Glomerular Filtration Rate (GFR) Falls
Parathyroid hormone levels increase
Activated form of Vitamin D falls
Old thinking: This was just decreased production of 1,25(OH)2D
New understanding: Degradative pathways are up-regulated (some induced by FGF-23)
Fall in 1,25(OH)2D is physiological with CKD
Makes sense because you do not want a lot of 1,25(OH)2D around to cause more calcium & phosphorus absorption when you cannot excrete these ions
Mechanisms of CKD-MBD
Systemic disorder of mineral & bone metabolism results in:
Skeletal complications (Osteomalacia, osteitis fibrosa)
Soft tissue complications (Vascular calcifications)
Phosphate not restricted until patient requires RRT
Then Phosphate restricted to < 1 g/day
Hypertension & Elevated Triglycerides
HTN; Cause & consequence of CKD
Aggravated by Na+ & H20 retention
Increased renin production may contribute
HTN, ECF volume overload, & anemia may develop into LV hypertrophy, which may lead to cardiomyopathy & HF
HTN can cause retinopathy, encephalopathy, nephropathy
B/P control; One of most important goals
Dysrhythmias; Hyperkalemia & Decreased coronary artery perfusion
Hyperinsulinemia stimulates hepatic production of triglycerides
Altered lipid metabolism
Decreased levels of enzyme lipase (Important in breakdown of lipoproteins)
Increased VLDLs & LDLs
Decreased HDLs
CKD & CV Disease Are Closely Linked
Death often r/t MI, ischemic heart disease, PAD, HF, cardiomyopathy, and/or stroke
Traditional CV risk factors; HTN & Elevated lipids
Nontraditional CV risk factors; Vascular calcification & arterial stiffness
Calcium deposits associated with stiff blood vessels
Vascular smooth muscle cells change
High Ca+ & phosphate
Impaired renal excretion
Drug therapies to treat bone disease
Altered Carbohydrate Metabolism
Caused by impaired glucose metabolism (Cellular insensitivity to normal action of insulin)
Mild-moderate hyperglycemia
Hyperinsulinemia
Uremic patients with DM may require less insulin than before onset of CKD
Excretion of insulin dependent on kidneys
Insulin dosing must be individualized
May improve after starting dialysis
CKD: Hematologic Changes
Decreased production of erythropoietin
Other factors:
Nutritional deficiencies
Decreased RBC life span,
HD & Increased hemolysis
Blood sampling
GI bleeding
Increased Parathyroid hormone
Decreased iron stores
Folic acid lost in dialysis
Bleeding tendencies
Defect in platelet function
Infection
Change in WBC function
Altered immune response & function
Hyperglycemia
External trauma
CKD: Every Part of GI System Affected
Cause: Excessive Urea
Stomatitis with exudates & ulcerations
Uremic fetor (Urine odor to breath)
Anorexia, nausea, vomiting
Diabetic gastroparesis
GI bleeding
Constipation significant problem
Phosphate-binding medications are constipating
Cannot be managed by increasing PO fluids, or taking Magnesium or fiber / bulk forming laxatives
Probiotics, stool softeners, use of footstool when defecating
CKD: CNS Manifestations
CNS depression
Lethargy, apathy
Decreased ability to concentrate
Fatigue, irritability
Altered mental ability (late sign)
Seizures
Coma
Hypertensive encephalopathy
Peripheral neuropathy
Restless legs syndrome
Paresthesias
Motor involvement
Foot drop
Muscle weakness & atrophy
Loss of deep tendon reflexes
Muscle twitching, jerking, asterixis, & nocturnal leg cramps
CKD: Metabolic Changes
Carbohydrate intolerance
Peripheral insulin antagonism
Impaired insulin secretion
Prolonged insulin half-life
Abnormal circulating insulin
** Short acting insulin functions as longer acting
** Patients on dialysis may need less insulin for glucose control
Elevated triglycerides
Metabolic acidosis
Pericarditis
Acid-Base Balance
Normal pH: 7.35 – 7.45
Normal Base Excess: 0 +/- 3 mEq / L
Calculated with ABG results using pH, PC02 & HCT
Represents amount of buffering ions in blood
Largest = HCo3-
Hemoglobin, Proteins, Phosphates, Etc…
Negative (-) BE indicates metabolic (lactic) acidosis
Positive (+) BE indicates metabolic alkalosis or compensation to respiratory acidosis
CKD: Reproductive & Other Manifestations
Infertility & decreased libido
Experienced by both sexes: Low sperm counts, amenorrhea
Sexual dysfunction; Physical, psychological, & medication side effects
Pregnancy during dialysis poses significant risk to mother & fetus
Pruritus
Calcium-phosphate deposits
Sensory neuropathy
May be intense
Leads to bleeding or infection
Uremic frost
Urea crystalizes on skin
BUN > 200 mg/dL
CKD: Renal Diet
Adequate calories
30 – 35 kcal / Kg
Primarily from Carbs & Fat (30 – 40% to prevent / reduce catabolism)
Protein
0.8 – 1.0 Gm / Kg / day
Avoid high-protein, fad diets
Greater needs in end-stage
K+ / Na+ regulated to plasma levels
Restrict Na+ to prevent edema
Phosphate restriction
1 gram per day
Avoid foods high in phosphate (Meat & dairy)
Most foods high in phosphate are high in protein
Phosphate binders essential with dialysis
CKD: Interprofessional Care
Overall goals
Preserve existing kidney function
Reduce risks of CV disease
Prevent complications
Provide for comfort
Early recognition and treatment important
Nephrology referral
Identify & treat reversible causes
Management Stage 1 to 4: Control:
HTN
Hyperparathyroidism
CKD-MBD
Anemia
Dyslipidemia
Correct ECF overload or deficit
RRT
Treat CV disease
Nutritional therapy
Drug therapy
Medications for CRF
Antihypertensives
Diuretics
Calcium
Prophylactic antibiotics
Vitamins, Minerals & Phosphate binders
Antihypertensives: Angiotension-Converting Enzyme (ACE) Inhibitors
Slow progression or delay onset of Diabetic nephropathy (Example: Captopril)
Dilate arterioles & veins
Reduce blood volume (effect on kidneys)
Reduce glomerular filtration pressure
Suppress formation of Angiotension II
1st dose hypotension
Hyperkalemia
Vasodilation
Increase bradykinin (Inhibit Kinase II)
Cough & angioedema
Angiotension II Receptor Blockers (ARB’s)
Prevent Angiotension II mediated vasoconstriction & release of Aldosterone
Produce effects similar to ACE inhibitors
No cough
No angio-edema
Diabetic nephropathy
Irbesartan (Avapro)
Losartan (Cozaar)
Diuretics
Furosemide (Lasix)
Blocks re-absorption of Na+ & Cl- at ascending LOH
Diuresis despite low renal blood flow & GFR
Onset: 5-minutes
Duration: 2-hours
Hypotension
Hypokalemia
Ototoxicity (IVP: 20 - 40 mg over 1 - 2 minutes)
Mannitol (5% - 25%)
Creates osmotic force within nephron
Diuresis of fluid only
Onset: 30 – 60 minutes
Duration: 6 – 8 hours
Edema
May precipitate CHF / Pulmonary edema
Observe for crystals
Filter needle
Medications for Dyslipidemia
Statins (HMG-CoA reductase inhibitors)
Most effective for lowering LDL
Atorvastatin (Lipitor)
Fibrates (Fibric acid derivatives)
Used to lower triglyceride levels & increase HDL
Gemfibrozil (Lopid)
Vitamins, Minerals & Binders
Calcium
Cinacalcet (Sensipar)
Increases sensitivity of Ca+ receptors in parathyroid glands
Subtotal or total parathyroidectomy
Vitamin D: Calcitriol (Rocaltrol)
0.5 – 1.0 mcg / daily
Treats hypoparathyroidism & hypocalcemia
Serum phosphate must be lowered before Calcium or Vitamin D is administered
Avoid aluminum & magnesium preparations
Folic Acid
Phosphate binders (Reduce intestinal absorption)
Bind phosphate in bowel & then excrete
Ca+ based
Calcium carbonate (Caltrate)
Calcium acetate (PhosLo)
Ca+ free
Sevelamer (Renagel) – Lowers cholesterol & LDL
Treatments for Anemia
Iron supplements
If plasma ferritin <100 ng/mL
Side effects: GI irritation, constipation
May make stool dark in color
Folic acid supplements
Needed for RBC formation
Removed by dialysis
Avoid blood transfusions
Increase development of antibodies
May lead to iron overload
Epoetin alfa (Epogen, Procrit)
Darbepoeitin alfa (Aranesp)
Given IV or SQ
Expect increased H & H in 2 - 3 weeks
Side effects:
Thromboembolism, HTN
Inter-dialetic Weight Gain
Weight gain between dialysis treatments
Rationale for fluid restriction
Measure of adherence
1 – 3 Kg advised (2.2 to 6.6 pounds)
Fluid & Electrolyte Balance
Careful fluid replacement
Calculated fluid restriction = 24-hour loss + 600 ml insensible
Daily weights
Fluid restriction (1000 – 1500 mL / Day)
Diuretics
Furosemide (Lasix)
Bumetanide (Bumex)
Mannitol
Managing Fluid Restriction in Acute Care
1000 – 1500 mL/day (Average fluid restriction for CKD)
Acute Care RN responsible to supervise & maintain ordered fluid restriction from all sources:
PO
Enteral nutrition, & free water flushes
Parenteral nutrition
Maintenance IV
Continuous IV medications (Ex: Heparin, Nexium)
Intermittent IV medications (Ex: Antibiotics, others)
Dialysis Access: A Dialysis Patient’s Life Line
Temporary Dialysis Catheter
Double-lumen, non-tunneled CVAD
13 – 20 cm long, 13G or less, No cuff, Rigid
Permanent Dialysis Catheter (“PermCath”)
Tunneled, cuffed at skin/exit site
Arterio-venous Fistula (AVF)
Arterio-venous Graft (AVG)
HeRO Graft
Used when other options have failed
Bypasses venous system; blood flow directly from target artery from the heart
More difficult to assess Thrill / Bruit d/t no venous anastomosis
Peritoneal Dialysis Catheter
Temporary Vascular Access
Insertion at internal jugular or femoral vein when immediate access needed
Double lumen
Blood removal
Blood return
Risks:
Infection
Dislodgment
Malfunction
Assessment of Dialysis Access
A-V Fistula
A-V Graft
Assess for bleeding / bruising (after Hemodialysis)
Assess for patency
Auscultate for “Bruit”
Palpate for “Thrill”
Dry Weight
Usually reflects lowest weight a patient can tolerate without intra-dialytic symptoms or hypotension
Imprecise trial-and-error method
Does not account for changes in nutritional status & lean body mass
Difficult to determine over- or under-hydration
Used to calculate ultra-filtration (UF) volume & rates for dialysis treatment
Physiologic Dry Weight
Weight resulting from
Normal renal function
Vascular permeability
Serum protein concentration
Body volume regulation
Patients theoretically should be lower than physiologic to be prophylactic for inter-dialytic weight gain
Renal Replacement Therapies (RRT)
Intermittent (Hemodialysis, Peritoneal dialysis)
Continuous (CRRT) in Critical Care
Toxins/fluids removed
Acid-Base balance & electrolytes adjusted slowly in hemodynamically UNSTABLE patients
Access: Double-lumen catheter in Jugular or Femoral veins
Blood pump & anti-coagulation required
Renal Transplantation
Funding for Chronic Diseases
1972 Social Security Amendment - Medicare Coverage for all those:
65 or older
Under 65 with certain disabilities (DM, HTN) & those who have received Social Security Disability (SSDI) for 2-years
Any age with ESRD
1978: Congress established ESRD Network Organizations Program
1986: Program re-codified to 18 ESRD Network Organization areas, Funding for Renal Transplantation
Dialysis
Movement of fluid/molecules across semipermeable membrane from one compartment to another
Used to correct fluid & electrolyte imbalances, & remove waste products in kidney failure
Can be used to treat drug overdoses
Two methods available
Peritoneal dialysis (PD)
Hemodialysis (HD)
Nephrologist determines when to start; Usually uremia can no longer be adequately treated conservatively; GFR < 15 mL/min/1.73 m2
Uremic complications require dialysis
ESRD treated with dialysis because
Lack of donated organs
Some patients are physically or mentally unsuitable for transplantation
Some patients do not want transplantation
General Principles of Dialysis
Diffusion; Movement of solutes from an area of greater concentration to an area of lesser concentration
Osmosis; Movement of fluid from an area of lesser concentration of solutes to area of greater concentration
Glucose in dialysate creates osmotic gradient to pull fluid from the blood
Ultrafiltration; Water & fluid removal results when there is an osmotic gradient or pressure gradient across membrane, excess fluid moves into dialysate
PD: Glucose in dialysate
HD: Pressure gradient
Peritoneal Dialysis
Access obtained by inserting catheter through anterior abdominal wall
Technique for placement varies; usually done via surgery
PD may start right away or be delayed until site healed
Aseptic technique important to avoid peritonitis
Peritoneal Dialysis: Dialysis Solutions & Cycles
Dextrose in dialysis solution; Osmotic agent
Manual PD: 3-Phase Cycle (Called an “Exchange”)
Volume depends on size of peritoneal cavity
Inflow (fill); 2 to 3 Liters over 10-minutes
Dwell (equilibration); 20 - 30 minutes to 8-hours (Individualized)
Drain; 15 - 30 minutes
Continuous Ambulatory Peritoneal Dialysis (CAPD)
Manual exchange 4 x / Day
Automated Peritoneal Dialysis (APD)
Cycler delivers dialysate during sleep
Times & controls fill, dwell, & drain phases
Alarms & monitors for safety
Peritoneal Dialysis Complications
Exit site infection
Redness, tenderness, drainage
Treated with antibiotics
Peritonitis: Exit site or tunnel infection
Abdominal pain, rebound tenderness
Cloudy effluent with increased WBCs or bacteria, may have fever
GI: diarrhea, vomiting, distention, hyperactive bowel sounds
Treated with antibiotics
Repeated infections may cause adhesions
Hernias: Increased intra-abdominal pressure from dialysate
Treatment: hernia repair
Bleeding
Common with initial catheter placement
New; Active intraperitoneal bleeding; check BP & hematocrit
Pulmonary complications
Decreased lung expansion leads to atelectasis, pneumonia, or bronchitis
Elevate HOB, repositioning & deep breathing
Protein loss; Monitor nutrition
Lower back problems
Intraperitoneal infusion increases pressure
Treatment: binders and exercise
Peritoneal Dialysis – Effectiveness of Chronic PD
Short training program; 3 to 7 days
Advantages
Simplicity
Home-based program
Increasing patient participation
No need for special water systems
Equipment set-up is relatively simple
Hemodialysis (HD) Vascular Access
Requires rapid blood flow & access to large blood vessel
Obtaining vascular access is one of most difficult problems
AV Fistula: Created in forearm or upper arm; Preferred access for HD
Allows arterial blood to flow through vein; becomes “arterialized; Increases vein size & wall thickness
Placed 3-months before HD; Needs to heal/mature
“Thrill” & “Bruit” (High velocity blood flow)
AV Graft: Synthetic material surgically placed under skin to form a “bridge” between brachial artery & antecubital vein
Temporary vascular access
AV Fistulas & Grafts
Healing: 2 to 4 weeks
More likely to get infected or form clots
If infected, may need removed
Risks:
Distal ischemia (Steal Syndrome)
Pain distal to access site
Numbness or tingling of fingers
Poor capillary refill
Aneurysms
Safety alert for AVF & grafts
No BP, venipunctures, or IV lines
Post signs in room & labeled arm band
Prevent infection & clotting
HeRO Graft (Hemodialysis Reliable Outflow)
Special bridge access used when other access options are exhausted
Two pieces
Reinforced tube to bypass blockages
Dialysis graft anastomosed to an artery; placed under skin
Bypasses venous system; blood flows from target artery to heart
Hemodialysis Dialyzer
Plastic cartridges that contain thousands of parallel hollow tubes or fibers; semipermeable membranes
Blood is pumped from top into fibers
Dialysate pumped from bottom & bathes outside of fibers
Ultrafiltration, diffusion & osmosis occur
When blood reaches end it is returned via single tube to patient
Hemodialysis Procedure
Fluid status assessed before HD treatment
Weight, BP, peripheral edema, heart & lung sounds
Last post-dialysis weight & current pre-dialysis weight determines amount of fluid to be removed
Assess vascular access & temperature
Two large bore needles placed in fistula or graft
One to pull blood from circulation to HD machine
Other to return dialyzed blood to patient
Dialyzer/blood lines primed with NaCL to eliminate air; Heparin added to prevent clotting
Dialysate delivery & monitoring system is used; VS every 30 - 60 minutes, Terminated with saline flush to return all blood to patient, Needles removed & firm pressure applied
Most in community-based center; Dialyzed 3 - 4 hours, 3 days/week
Other options; Short daily HD, Long nocturnal HD, Home HD
Hemodialysis Complications
Hypotension; Hypovolemia, decreased CO & SVR; Light-headed, nausea, seizures, vision changes, & chest pain
Treatment: Decrease volume of fluid removal & IV Normal Saline
Muscle cramps; Decreased BP, hypovolemia, increased ultrafiltration, & low-sodium dialysate
Treatment: Decrease ultrafiltration & give IV fluids
Blood loss; Blood not rinsed from dialyzer, accidental separation of tubing, dialysis membrane rupture or bleeding after needles removed; Heparin
Treatment: Rinse all blood back, avoid excess Heparin, hold pressure to access sites
Hepatitis C (8% to 10% develop): Infection control precautions
Hepatitis B: low incidence; administer vaccine
Hemodialysis Effectiveness
Cannot fully replace normal function of kidneys
Can ease many of symptoms
Can prevent certain complications
CV disease carries high mortality rate
Infectious complications 2nd leading cause of death
Individual adaptation
Positive
Ambivalent
Depressed
Nursing goals:
Help patient to:
have a healthy self-image
return to highest level of function
Wearable Artificial Kidney (WAK)1st Clinical Trial 2015 – 7 Patients
Battery operated
Requires only 370 mL water
Versus 40-gallons for HD
Early model 11-pounds
Latest model 2-pounds
Device connected via one catheter surgically inserted in 20-minute procedure under a local anesthetic
