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Dialysis
Removal of waste & extra fluid the kidneys can’t handle
Hemodialysis
Removal of waste by the use of an artificial kidney (dialyzer)
toxins and wastes in blood are removed by diffusion (higher concentration (blood) to an area of lower concentration (dialysate: circulates the machine), heparin to prevent clotting
Immediate vascular access
Central catheter
Double lumen, large bore in right/ left jugular/ femoral vein in leg (temporary, removed once permanent access is established)
Risks: hematoma, bleeding, pneumothorax, increased infection, thrombosis, inadequate flow
Fistula
Connects artery to vein
Takes 3 months to mature
2 IVs (arterial: goes to dialyzer then return via the venous segment
Longer lifespan
Graft
Used if blood vessels aren’t compatible for a fistula
synthetic tubing connects artery to vein
Quick placement
In arm, thigh, chest
Increased risk of infection
Nursing actions before dialysis
assess graft/ fistula
Baseline vitals
Hold key meds (BP)
Baseline weight
Nursing actions during dialysis
monitor vitals
Assess blood loss
Monitor muscle cramps
Nursing actions after dialysis
Monitor vitals
Assess access site for bleeding
Weights
Peritoneal dialysis
Peritoneum used as a membrane to perform dialysis
dialysate infused through a catheter & into peritoneal cavity ( catheter is clamped & dialysate filters the waste in the abdomen then drained out)
Diffusion occurs as waste moves from blood to the dialysate through the peritoneum
Complication of peritoneal dialysis
Peritonitis (swelling of belly)
redness, swollen, distended stomach, pain, tenderness, cloudy fluid, exit site red w/ pus, fever, N/V
Nursing management for HD & PD
Pre treatment: labs weight, vitals, review new orders
During: document vitals & catheter/fistula site
After: weight, vitals
HD complications: change in vitals, pain, arrhythmias
PD complications: peritonitis, leakage, bleeding
Education: fluid restriction, proper diet, family education
Continuous renal replacement therapy (CRRT)
Double linen catheter is placed in femoral artery or jugular vein
connected to hemofilter where solutes are removed so the blood is filtered of toxins
ICU setting
Every hour monitoring
Usher when too unstable for HD or PD
Function of kidney
Maintains volume & composition of body fluids
Clears waste from protein metabolism & maintains acid base & electrolyte balance
Excretes drugs
Regulates vitamin D activation (helps maintain & regulate calcium)
Regulates BP (RAAS)
Production & secretion of erythropoietin (RBCs)
Blood urea nitrogen
Measures the amount of urea nitrogen in blood (7-20)
Creatinine
A waste product produced by muscle metabolism (0.6-1.2)
eGFR
Amount of plasma filtered through the glomeruli per unit of time (90-120)
considered the best measure of overall function of the kidney
Urine specific gravity
Indicates how well the kidneys are concentrating urine (1.010-1.030)
Kidney diagnostic tests
Renal ultrasound (obstructions & abnormalities of GU)
CT (masses of vascular abnormalities)
Renal scan
Biopsy (cause of kidney disease, most definitive)
RIFLE
Classification of AKI, used to identify kidney injury and improve outcomes
Risk, Injury, Failure, Loss, ESKD
Risk, injury, & failure are grades of AKI severity
Loss & ESKD are outcomes of loss that require RRT
AKI
Rapid loss of renal function
causes build up of nitrogenous waste products & impairs F&E balance
Tx: dialysis, RRT, restore normal chemical balance (treat underlying cause: hypovolemia, infection, HF, kidney stones), maintain F&E (I&Os, weight, BP), nutrition support (low sodium & potassium, high carb)
Most common indicator is azotemia (accumulation of nitrogenous waste in blood and a decrease in GFR)
S/S: 50% or greater increase in creatinine, increased BUN & sudden decrease in urine
Monitor for complications, assess progress of interventions, pretty infection, support
Prerenal AKI
Most common, decrease in renal blood flow
caused by:
loss of extra cellular fluid volume: GI losses (vomit, diarrhea, NG suction), hemorrhage, renal losses (diuretics, osmotic diuresis)
impaired perfusion: arrhythmias, cardiogenic shock, hf, mi
vasodilation: anaphylaxis, anti HTN meds, sepsis hemorrhage
Main symptom: low UO
Intrarenal AKI
Results from conditions that cause damage (ischemia) to structures within the kidney (parenchyma, vessels, tubules, interstitium
anemia, rhabdomyolysis, ACE inhibitors, heavy metals, NSAIDS, acute glomerulonenephritis, acute pyelonephritis
Postrenal AKI
Result from obstruction of urine flow (calculi, stictures, tumors, prostatic hyperplasia *, blood clots)
Initiation phase of AKI
Initial, ends when oliguria occurs
Oliguric phase of AKI
Decreased urine output, increase in BUN & CR, uremic symptoms first appear, hyperkalemia
Diuretic phase of AKI
Recovery begins, gradual increase in urine output, labs stabilize, monitor for dehydration
Recovery phase of AKI
Recovering (up to 12 months), labs are normal
CKD
Damage of decrease in GFR for more than 3 months, permanent loss of nephrons = kidney failure
caused by prolonged inflammation that isn’t organ specific (HTN, diabetes, obesity)
Albuminuria** key sign
Azotemia** key early sign
Stage GFR: 1 (>90), 2 (89-60), 3 (59-45), 4 (44-30), 5 (29-15) ESKD (<15)
S/S: increased CR, decreased GFR & RBCs (anemia), edema, HF, fluid retention, F&E imbalance, puritus (result of too much phosphorus)
Monitor labs, treat underlying cause, encourage exercise, low sodium/potassium/phosphorus, smoking cessation
CKD in kids
Causes severe growth impairment
developmental delays, delay in sexual maturation, bone abnormalities, psychosocial problems
Physical/cognitive development are significantly slowed
CKD management
Treat underlying cause, early referral
Treat hyperglycemia, manage anemia, encourage smoking cessation, weight loss, exercise program, reduce salt and alcohol intake, minimize nephrotoxins
ESKD
Severe kidney damage, RRT required permanently
uremia develops
Disease progresses faster if excreting excess amounts of proofing and show HTN
Severity of symptoms dependent on amount of kidney impairment
Meds: vitamins, anti HTN, erythropoietin, dialysis
Monitor: labs, sodium, acidosis, anemia
Nephrotic syndrome
Increased glomerular permeability and proteinuria, results from glomerular damage
leak of massive amounts of protein (albumin)
Causes: acute glomerulonephritis, cancer, drugs, bee sting/pollen, HIV, hepatitis, mono, syphillis, malaria, diabetes
S/S: pitting edema everywhere, proteinuria, hypoalbuminemia, frothy, foamy urine, high cholesterol, hyperlipidemia, hypercoagulability (increased risk for DVT, renal VT, PE
Dx: 24 hr urine
Mangement: treat underlying cause, prevent AKI, meds, relieve symptoms, measure abd. girth, I&Os, weight, low sodium/ fluid diet, monitor for blood clots
Meds: diuretics, albumin infusions, corticosteroids, ACE/ ARBS
Acute nephritic syndrome (glomerulonephritis)
Inflammation of glomerular capillaries (leakage of RBCs, mild protein loss)
causes: infections, beta hemolytic strep infections, HIV, Hepatitis B, Epstein Barr, autoimmune diseases
S/S: HTN, hematuria, edema, azotemia, severe flank pain, headache, mild proteinuria, tea colored urine, pus, cellular & granular casts in urine
Labs: low GFR, high BUN/ CR
Mangement: monitor BP, I&Os, potassium, edema, diet (low sodium & fluid)
Tx: meds depend on cause, ‘treating the symptoms’ → corticosteroids, antibiotics, manage HTN, control proteinuria
Diet: low protein & sodium
Chronic glomerulonephritis
Kidney shrinks to 1/5 their size, glomeruli scarred
can progress to CKD if not managed
May have no symptoms
S/S: high BUN/ CR, proteinuria, HTN, poor nourishment, periorbital/peripheral edema, neuro changes, nocturia, headaches, dizziness, digestive disturbances
Management: manage symptoms, daily weights, diuretics, dialysis,education, monitor labs
Avoid NSAIDS
Polycystic kidney disease
Incurable genetic disorder
growth of fluid filled cysts in kidneys → kidney failure
Most common side effect is polyuria
Nephrosclerosis
Hardening of renal arteries
causes: HTN, diabetes, aging
Progresses elevation of BUN, CR
Mild proteinuria
TX: ACE inhibitors
Priority assessments & cues in kidney disorders
Assess for: anorexia, N/V, lethargy, fatigue = high BUN
Monitor for: neuro changes, itching, signs of fluid overload, hyperkalemia, metabolic acidosis (kussmaul breathing), anemia
Review OTC meds that may be toxic
Loop diuretics
Block chloride pump in the ascending loop of henle ( inhibits NA, K, Cl transporters)
greatest degree of diuresis
Furosemide, bumetanide, torsemide
Ototoxic so push slow
Monitor: electrolytes, vitals, I&Os, daily weights
SE: alkalosis, hypokalemia, hypotension, hypercalcemia
Potassium sparing diuretics
Prevent reabsorption of sodium in the distal tubule collect duct while holding on to potassium
not as powerful, used in conjunction with other diuretics
Spironolactone
Thiazide diuretics
Block the chloride pump in the distal convoluted tubule
keep chloride and sodium in the tubule to be excreted in the urine, thus preventing the reabsorption of Cl and NA in the vascular system
Doesn’t increase UO (urine will have high concentration of NA)
ASE: GI upset, F&E imbalances, hypotension
Hydrocholorothiazide, chlorothiazide
Trauma
Disordered psychic or behavioral state resulting from severe mental or emotional stress or physical injury
Types of trauma
Individual, collective
Individual trauma
Abuse, illness, sudden loss
Collective trauma
Disasters, historical trauma, generational trauma
PTSD
Disturbed pattern of behavior lasting at least 1 month, disrupts ADLs
follows a traumatic event, starting at 3 months post event
Caused by actual or potential threat
Feelings of intense fear, helplessness, terror
S/S: reexperiencing trauma (dreams, intrusive/recurrent thought), avoidance, negative cognition/thoughts, being on guard, hyperarousal
Risks: trauma, peri-trauma dissociation, existing psychiatric disorders, poor support, high stress
Adjustment disorder
Reaction causes problems, starts within 1 month & lasts no longer than 6 months
group of symptoms (stress, sadness, hopelessness) & physical symptoms that occur following a stressful event
Reaction is stronger than would be expected for the event that occurred
Acute stress disorder
Reexperiencing, avoidance, hyperarousal
starts 3 days to 4 weeks, PTSD can follow
Reactive attachment disorder
Occurs before 5, response to trauma of child abuse or neglect
Exhibits minimal social and emotional responses to others, lacks a positive effect, may be sad, irritable, or afraid for no apparent reason
Disinhibited social engagement disorder
Occur before 5, responded to trauma of child abuse or neglect
exhibits undelevtive socialization, allowing/ tolerating social interaction with all people, they lack hesitation approaching or talking to others
Dissociative amnesia
Disruption of memory
Dissociative identity disorder
> 2 identities/ personalities
Depersonalization/ derealization disorder
Detachment from body/self, dream like unreal environment, repressed memories
Assessment for PTSD
Appearance/motor behavior: hyper alert, anxious
Mood/ affect: angry, scared
Cognitive concerns: oriented until flashback, memory gaps
Self awareness: variable
Self concept: guilt, low self esteem
Relationship concern: difficulty maintaining them
Physiological concerns: insomnia, substance abuse
PTSD Treatment
Counseling, CBT (exposure therapy: addresses avoidance), cognitive restructuring/ processing (addresses negative thoughts), adaptive disclosure, SSRIs
PTSD caring interventions
Discuss self harm thoughts, help develop a plan for going to a safe place, grounding techniques, validate their feelings/fear, supportive touch, deep breathing, distraction techniques, establish support system, convey empathy, be nonjudgmental