renal megan mcclintock, rn, ms 10/27/11 “to pee is to live”

RenalMegan McClintock, RN, MS

10/27/11

“TO PEE IS TO LIVE”

"Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But should the kidneys fail … neither bone, muscle, gland, nor brain could carry on.”

Smith HW: Fish to philosopher, Boston, 1953, Little, Brown.

KIDNEY DISEASE

Acute kidney injury (AKI) Chronic kidney disease (CKD)

• Sudden onset• Acute decrease in

urine output and/or increase in creatinine

• Potentially reversible• Mortality 60%

• Usually die from infection

• Gradual onset• GFR < 60 mL/min for >

3 months

• Progressive and irreversible

• Mortality 19-24% (need dialysis to survive)

• Usually die from CV disease

ACUTE KIDNEY INJURY

• Prerenal causes – external to the kidney, sudden reduction in blood flow to the kidneys• Usually resolve quickly with correction of cause

• Intrarenal causes – infections, toxins, drugs, or direct trauma, ATN

• Postrenal causes –urinary tract obstructions• Usually resolve quickly with correction of cause

ACUTE KIDNEY INJURYCLINICAL COURSE

• Oliguric Phase (10-14 days)– Urine output less than 400 mL/day– UA w/ casts, RBCs, WBCs, SG fixed at 1.010,

urine osmo of 300 mOsm/kg (may have proteinuria)

– Volume depletion but oftentimes fluid retention– Metabolic acidosis– Sodium imbalance– Potassium increase– Hematologic disorders– Waste product accumulation– Neuro disorders

ACUTE KIDNEY INJURY CLINICAL COURSE

• Diuretic Phase (1-3 weeks)– Begins with a gradual increase in daily

urine output to 1-3 L– Nephrons still not fully functional– Kidneys can excrete waste, but still

can’t concentrate the urine– Hypovolemia– Hypotension– Hyponatremia, hypokalemia

ACUTE KIDNEY INJURY CLINICAL COURSE

• Recovery Phase (12 months)– Begins when the GFR increases– BUN and creatinine plateau, then

decrease

ACUTE KIDNEY INJURYTREATMENT

• Eliminate the cause, manage signs & symptoms, prevent complications– #1 goal is to ensure adequate cardiac

output and intravascular volume– Careful monitoring of I/Os– Prevent hyperkalemia– Use RRT (renal replacement therapy)

only if needed– Nutritional management

ACUTE KIDNEY INJURYTREATMENT

• Avoid exposure to contrast media• Watch for nephrotoxic drugs• ACE inhibitors• Meticulous aseptic technique• Meticulous skin care• Meticulous mouth care

ACUTE KIDNEY INJURYNURSING DIAGNOSES

• Decreased cardiac output• Excess fluid volume• Risk for infection• Imbalanced nutrition: less than body

requirements• Fatigue• Anxiety• Dysrhythmias • Sensory/perceptual alterations

CHRONIC KIDNEY DISEASE

CHRONIC KIDNEY DISEASE

• Frequently asymptomatic• Early on have no change in urine

output, may even have polyuria • Uremia develops when GFR is <10

mL/min• Persistent proteinuria• Tend to die of CV disease before

needing dialysis

Fig 45-3 clinical manisfestations of chronic uremia

CHRONIC KIDNEY DISEASE

TREATMENT• Treat high potassium• Control HTN• Treat anemia (EPO)• Treat hyperlipidemia• Restrict proteins• Restrict fluids• Restrict sodium, potassium, phosphates• Lots of teaching and reteaching

TREATING HYPERKALEMIA

• Insulin• Sodium Bicarbonate• Calcium Gluconate IV• Dialysis• Sodium Polystyrene Sulfonate

(kayexalate)• Dietary Restriction

Dialysis

Peritoneal Dialysis (PD) Hemodialysis (HD)

PERITONEAL DIALYSIS

• Three phases of PD

• Manual vs Continuous

• Complications

Fig 45-12

Temporary catheters

Fig 45-13 placement of jugular vein temporary dialysis catheter

Fig 45-14 components of hemodialysis system

HEMODIALYSIS

• Pre & Post Dialysis Interventions• Complications

– Hypotension– Muscle cramps– Blood loss– Hepatitis

PYELONEPHRITIS

• Cause – Bacteria (most common)• S/S – abrupt onset of chills, fever,

vomiting, malaise, CVA pain, dysuria, urinary urgency and frequency

• Labs – UA w/ pyuria, bacteriuria, hematuria, WBC casts; CBC w/ left shift (increase in bands)

• Cx – Urosepsis leading to septic shock and death, chronic pyelonephritis

Pyelonephritis: glomerular hemorrhage

Pyelonephritis - papillary necrosis

PYELONEPHRITIS INTERVENTIONS

• Early tx for cystitis• Take antibiotics as prescribed• Follow-up urine culture• Drink at least 8 glasses of fluid daily• Rest

GLOMERULONEPHRITIS

• Cause – Antibody-induced injury (exposure to drugs, immunizations, microbial/viral infxn)

• S/S – generalized edema, HTN, oliguria, hematuria, proteinuria, abd/flank pain

• Labs – UA w/ proteinuria, hematuria, WBC casts; increased BUN and creatinine, ASO titer

• Cx – Renal insufficiency, destruction of renal tissue

GLOMERULONEPHRITIS INTERVENTIONS

• REST• Diuretics, restricted sodium and fluids• Restrict dietary protein if in BUN.• Treat severe HTN with anti-

hypertensives• No abx unless infection still present• Prevention - Take the FULL course of

antibiotics (treat strep)

NEPHROTIC SYNDROME

• Cause – systemic disease, allergens, drugs, infxn, glomerulonephritis

• S/S – edema, massive proteinuria, HTN, hypoalbuminemia, hyperlipidemia

• Labs – low albumin, low protein, high cholesterol

• Cx – Infection, thromboembolism, skin breakdown, malnourishment, body image problems

NEPHROTIC SYNDROME INTERVENTIONS

• ACE inhibitors, corticosteroids, diuretics, lipid-lowering agents

• Low sodium, low-moderate protein diet (focus on preventing malnutrition)

• Strict I/Os, daily weights• Protect skin• Prevention of infection

Minute paper

• On the provided 3x5 card answer the following:

1)What was the most important thing you learned today.

2)What important point remains unclear to you?