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Lisa M. Soltis, APRN, MSN, CCRN-CSC, CCNS,

FCCM

Recognizing Renal Failure

Renal Physiology

� Rid body of endogenous (bilirubin, urea, uric acid, creatinine) & exogenous wastes (medications).

� Maintain Homeostasis by regulating fluid, electrolyte, and acid- base balance.

Renal Physiology

�Secretion, excretion, & metabolism of hormones:

�Epoetin

�Calcitrol (active form of Vitamin D)

�Insulin (metabolism)

Renal Physiology

� The kidneys increase epoetin production in response to hypoxia.

� The kidneys release bicarbonate in response to respiratory acidosis.

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Renal AnatomyRenal Structure

�Nephrons:

� Approximately 1 million per kidney. After age 40, amount decreases by 10% every 10 years.

�Leads to decreased GFR

�Decreased ability to concentrate urine can lead to dehydration

Nephron Structure

� Each nephron is comprised of a glomerulus, which is made up of about 50 capillaries that are covered by epithelial cells.

� Bowman’s capsule covers each glomerulus.

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Renal Physiology

� The afferent & efferent arterioles constrict & dilate depending on blood pressure & blood flow.

� This allows alterations in GFR & tubular reabsorption rates depending on the body’s needs.

� Normal plasma volume of 3 L is filtered approximately 60 times per day.

� Normal GFR is 100-150 ml/min

� This causes rapid removal of wastes.

� Without auto-regulation, there would be large GFR swings & possibly excessive urine production.

GFR

Glomerular Filtration Glomerular Filtration Rate (GFR)

�High GRF with normal to higher blood pressures.

�Decreased GRF & increased fluid retention during hypotension.

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Creatinine Clearance

� Byproduct of muscle metabolism, excreted at a constant rate

� Reliable indicator of renal function

� CrCl = urine creatinine x urine volume/24 hrs

Renal Assessment

� Color, clarity, amount of urine

� Difficulty initiating urination or changes in stream

� Changes in urinary pattern

� Dysuria, nocturia, hematuria, pyuria

Assessment

� History of urinary problems

� Urinary or abdominal surgeries

� Smoking, alcohol use, number of sexual partners and type of sexual relationship

� Chance of pregnancy

� History of diabetes or other endocrine disorders

� History of kidney stones

Physical Assessment

� Obtain clean-catch urine specimen

� Color, odor, clarity

� Vital signs and skin assessment

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Diagnostic Tests

� Clean-catch urine

� 24-hour urine

� Culture and sensitivity

� BUN, creatinine and creatinine clearance

� Intravenous pyelogram (IVP)

� CT scan

� Renal scan

Diagnostic Tests

� Ultrasound

� Bladder scan

� Cystoscopy

� Uroflowmetry

Acute Renal Failure

� Sudden decline in kidney function, which results in decreased glomerular filtration rate (GFR) and decreased excretion of nitrogenous wastes, causing azotemia.

� Associated with oliguria &/or anuria.

� Overall incidence is up to 25% of hospitalized patients.

Acute Renal Failure Stages

Onset – 1-3 days with increased BUN and creatinine and possible decreased UOP

� Oliguric – UOP < 400/d, increased BUN,Creat, Phos, K, may last up to 14 d

� Diuretic – UOP as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement

� Recovery – things go back to normal or may remain insufficient and become chronic

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Etiologies

Causes divided into three classes:

• Pre-Renal (50%)

Pre-Renal Azotemia (high BUN)

• Intrinsic Renal

• Post-Renal

(< 10%)

Acute Renal Failure

� 70% of ARF patients have either Acute Tubular Necrosis (ATN) or pre-renal azotemia.

� Overall mortality is 25-64%.

� Patients with non-oliguric ARF have the best chance of recovery.

Acute Oliguric Renal Failure

� Urine output < 400 ml/day

� Severe renal dysfunction requiring some form of renal replacement therapy.

� Usually done to facilitate fluid removal.

Post-Obstructive Uropathy

� Functional or mechanical obstruction of urine outflow.

�Urine backflows

�Increased pressure on Bowman’s capsule leads to decreased GFR.

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Etiologies of Post-Renal ARF

� Stones

� BPH or Prostate Cancer

� Ureteral Stricture

� UTIs, Bladder Tumors

� Blood Clots Blocking the Foley!!!

� Medications

Right Hydronephrosis

Hyrdro-nephrosis

Tumor

Management

� Diagnosis confirmed by hydronephrosis on renal ultrasound, CT Abdomen/Pelvis

� Treatment: Treat underlying cause!

� Irrigate the Bladder with Sterile Water

� Foley catheter, stents, nephrostomy tubes.

Pre-Renal Etiologies

� Anything that prevents adequate blood flow to the kidneys can cause pre-renal ARF

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Pre-Renal ARF (Pump)

�Decreased Cardiac Output:

� Cardiogenic Shock

� Heart Failure

� Arrhythmias

� Drugs: Digoxin, β-blockers

Pre-Renal ARF (Pressure)

�Systemic Vasodilation:

�Distributive Shock: Anaphylactic, Septic, Neurogenic, Adrenal

�Drugs: Anti-hypertensives, vasodilators such as nitrates, morphine, etc.

Pre-Renal ARF (Volume)

� INTRAVASCULAR VOLUME DEPLETION:◦ Burns

◦ GI Hemorrhage

◦ Dehydration

◦ Third Spacing

◦ Diuretics

◦ Diarrhea

◦ Excessive NGT Output

Pathophysiology

� Baroreceptors sense decreased BP

� Renin-angiotensin-aldosterone activated

� Vasoconstriction (angiotensin II)

� Na+ & H20 reabsorbed

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Pathophysiology

� Prolonged lack of blood flow due to hypotension or vasoconstriction can lead to destruction of the renal tubules.

� This is called acute tubular necrosis (ATN).

Etiologies of Intrinsic ARF/ATN

�Vasoconstriction:

�From prolonged shock

�Drugs: vasopressors

�Prolonged dehydration

Etiologies of ATN

�Toxicity:

�Drugs: Amphotericin, Aminoglycosides

�Ionic Contrast Dyes: CT, Angio, etc

�Pigments: Rhabdomyolysis

Vascular Causes of Intrinsic ARF

� Vascular Diseases:

� Lupus Vasculitis, Renal Scleroderma

� Renal Artery Stenosis

� Renal Vein Occlusion

� Thromboembolic Disease (emboli, TTP)

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ATN

� Inflammation:

� If it is caused by inflammation, multiple organs

are usually involved.

� I.E. Systemic Inflammatory Response (SIRS) &

Multi-Organ Dysfunction Syndrome (MODS)

ATN

� Majority of interstitial ARF cases

� Sloughing of tubular epithelial cells obstructs the lumen of the proximal tubule

� This obstruction causes back pressure

� This decreases GFR

Myoglobinuric ATN

� Rhabdomyolysis causes wide-spread muscle breakdown.

� Myoglobin causes renal tubular damage

� Direct nephrotoxin

� Can block renal tubules

Who Gets Rhabdo?

�Trauma:

�Crush injuries

�Long-bone fractures

�Other:

�Found down after prolonged period

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Diagnosis of Rhabdomyolysis

� Urine dips positive for occult blood

� No red blood cells on microscopy

� Creatnine rises usually > 2 mg/dl/day

� Elevated CK

Treatment

� Volume, Volume, Volume

� Alkalinize urine with bicarb drip (controversial)

� Watch for hyperkalemia

� Due to massive muscle breakdown

Radiocontrast Nephropathy

� ARF within 48 hours of administration of hyperosmolar ionic contrast dyes

� CT scans, arteriograms, cardiac catheterization

� Contrast induces vasoconstriction

� Leads to endothelial cell injury in the vessels of the renal medulla

Radiocontrast Nephropathy

� This leads to a rapid/sustained decrease in renal plasma flow (RPF)

� Induces medullary hypoxemia

� This causes ischemic tubular injury/ATN

� Can directly damage tubular cells

� Usually resolves in about 2 weeks

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RCN Risk Factors

� Common in diabetics with renal insufficiency

� Increased risk with:

� Dehydration

� Class III/IV Heart Failure

� Chronic Liver Disease

RCN Prevention

� N-acetylcysteine (Mucomyst)

� Fenoldopam (Corlopam)

� HYDRATION with NS

� Only intervention consistently shown in to

decrease incidence of RCN

Avoid Contrast, If Possible

� Avoid iodinated contrast scans--MRI/MRA dye is non-iodinated

� Abdominal Ultrasound instead of CT Scan

� If the test is absolutely necessary:

� Iso-osmolar contrast decreases risk of RCN

Lab Results

� Electrolytes

� Hyperkalemia possible

� Glucose

� May be high or low

� Creatnine/BUN

� Both elevated

� WBC, Hgb/Hct

� Determine if infection or anemia are causes

� Urinanalysis

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Diagnostic Tests

� Pre-Renal

� BUN/CREAT >20:1

� UA: normal

� Uosmo: > 500mOsm

� ATN

� BUN/CREAT: <15:1

� UA: granular casts

� Uosmo: <350mOsm

Treatment

�Treat underlying cause!!!!!

� Volume depletion

� Colloid, Crystalloid

� Decreased Cardiac Output:

� Dobutamine, milrinone

� Diuretics (for ATN)

Treatment

� Stop any potentially nephrotoxic agents, unless absolutely necessary

� i.e.: Patient with fungal sepsis who is going into renal failure because of amphotericin B. Without the drug, he’ll die.

Chronic Renal Failure

�Medical treatment

� IV glucose and insulin

�Na bicarb, Ca, Vit D, phosphate binders

�Fluid restriction, diuretics

� Iron supplements, blood, erythropoietin

�High carbs, low protein

�Dialysis - After all other methods have failed

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Dialysis

� ½ of patients with CRF eventually require dialysis

� Diffuse harmful waste out of body

� Control BP

� Keep safe level of chemicals in body

� 2 types

� Hemodialysis

� Peritoneal dialysis

Peritoneal Dialysis

� Abdominal lining filters blood

� 3 types

� Continuous ambulatory

� Continuous cyclical

� Intermittent

03/05/2011

Dialysis

� Peritoneal dialysis

� Semipermeable membrane

� Catheter inserted through abdominal wall into peritoneal cavity

� Cost less

� Fewer restrictions

� Can be done at home

� Risk of peritonitis

� 3 phases – inflow, dwell and outflow

� Automated peritoneal dialysis

� Done at home at night

� Maybe 6-7 times /week

� CAPD

� Continous ambulatory peritoneal dialysis

� Done as outpatient

� Usually 4 X/d

Hemodialysis

� 3-4 times a week

� Takes 2-4 hours

� Machine filters

blood and returns it

to body

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Chronic Renal Failure

� Hemodialysis

� Vascular access

�Temporary – subclavian or femoral

�Permanent – shunt, in arm

� Care post insertion

� Can be done rapidly

� Takes about 4 hours

� Done 3 x a week

Types of Access

�Temporary site: subclavian or femoral

�Permanent: shunt, in arm

�AV fistula�Surgeon constructs by combining an artery

and a vein

�3 to 6 months to mature

�AV graft�Man-made tube inserted by a surgeon to

connect artery and vein

�2 to 6 weeks to mature

Hemodialysis

� Absolute Indications: Severe fluid, electrolyte imbalances, refractory acidosis, severe uremic symptoms

� Relative Indications: Moderate fluid or electrolyte imbalances, moderate uremic symptoms

Continuous vs. Intermittent Dialysis

�Continuous Renal Replacement Therapy (CRRT): Indicated in hemodynamically unstable patients who can’t tolerate dramatic fluid shifts. Can change Rx quickly.� OPTIMIZES FLUID BALANCE

�Hemodialysis: good if hemodynamically stable, better for rapid removal of toxins

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Temporary CatheterAV Fistula & Graft

What This Means For You

� No BP on same arm as fistula

� Protect arm from injury

� Control obvious hemorrhage

� Bleeding will be arterial

� Maintain direct pressure

� No IV on same arm as fistula

� A thrill will be felt – this is normal

Nursing Considerations

� Make sure the dressing remains intact

� Do not push or pull on the catheter

� Do not disconnect any of the catheters

� Always transport the patient and bags/catheters as one piece

� Never inject anything into catheter

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Dialysis Related Problems

� Lightheaded –give fluids

� Hypotension

� Dysrhythmias

� Disequilibration Syndrome

� At end of early sessions

� Confusion, tremor, seizure

� Due to decrease concentration of blood versus brain leading to cerebral edema

Complications of HD

�Myocardial Ischemia

�Osmotic Shifts: cerebral edema

�Bacteremia

Chronic Renal Failure

� Nursing diagnosis

� Excess fluid volume

� Imbalanced nutrition

� Altered renal perfusion

� Ineffective coping

� Risk for infection

� Risk for injury

Chronic Renal Failure

� Nursing care

� Frequent monitoring

� Hydration and output

� Cardiovascular function

� Respiratory status

� E-lytes

� Nutrition

� Mental status

� Emotional well being

� Ensure proper medication regimen

� Skin care

� Bleeding problems

� Care of the shunt

� Education to client and family

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Questions?