NOTES Acute Renal Failure/Vascular/Trauma cmj
Module #12: Nursing Care of the Individual with Genitourinary disorders:
Vascular Disorders, Trauma to the Kidneys and Acute Renal Failure
Acute Renal Failure
A&P Review only (if you know A & P in Part I…glance and go!)
______________________________________________________
Part I
Etiology/Pathophysiology (general)
(HTN=HPN=hypertension)
A. Normal physiology as relates to renal function (review renal anatomy
and physiology; critical!) text p. 696-700; excellent online web sites!
B. Kidneys: A&P review:
RNSG 2432  227
1. Outside peritoneal cavity; either side of vertebral column at levels
of T12 – L3; Supported by 3 layers of connective tissue
a. Outer renal fascia: surrounds kidney and adrenal gland
b. Middle adipose capsule: cushions and holds kidney in place
c. Inner renal capsule: barrier against infection; protects
kidneys from trauma
2. Functions: (P. 695) Balance solute and water transport; Excrete
metabolic waste products; Conserve nutrients; Regulate acid-base
balance; Secrete hormones to help regulate blood pressure;
Erythrocyte production; Calcium metabolism; Form urine
3. Internal regions of each kidney
a. Cortex: outer region; contains glomeruli
b. Medulla: contains renal pyramids (formed from bundles of
collecting tubules); renal columns (extensions of cortex)
c. Pelvis: innermost region; continuous with ureter as leaves hilum
1) Major and minor calyces, branches of pelvis, extend
toward
2) Medulla and collect urine and empty into pelvis
3) Urine channeled through ureter into bladder for
storage
228  RNSG 2432
a) Wall of calyces, renal pelvis, and ureter contain
smooth muscle and move urine by peristalsis
d. Each kidney- about 1 million nephrons
1) Nephron: contains tuft of capillaries = glomerulussurrounded by glomerular capsule (Bowman’s space)
a) Renal corpuscle: glomerulus and capsule
b) Endothelium of capillaries of glomerulus- very
porous
c) Solute-rich fluid (filtrate) pass from capillaries
into capsule; then channeled into Proximal
Convoluted Tubule (PCT) of nephron
d) Peritubular capillaries reabsorb substances into
plasma from filtrate by: (1) Active transport:
glucose, sodium, potassium, amino acids, proteins,
vitamins; (2) Passive transport: 70% water,
chloride, bicarbonate
e) Filtrate moves into loop of Henle and is
concentrated
f) Filtrate moves to Distal Convoluted Tubule (DCT)
where solutes are secreted into filtrate
g) Collecting duct receives newly formed urine from
many nephrons and channels urine through calyces
of renal pelvis into ureter
e. Ureters
1) Bilateral tubes 10 – 12 inches long (25 – 30 cm)
2) Transport urine from kidney to bladder through
peristalsis
3) Wall of ureter -3 layers: Inner -epithelial mucosa;
Middle-smooth muscle; Outer-fibrous connective tissue
f. Urinary Bladder
1) Posterior to symphysis pubis vagina and uterus
2) Storage of urine
3) Trigone- smooth triangular portion of base of bladder
outlined by openings for ureters and urethra
4) Layers: Epithelial mucosa lining (Internal); Connective
tissue submucosa; Smooth muscle layer: detrusor
muscle made up of fibers arranged to allow bladder to
expand or contract according to amount of urine in it;
Fibous outer layer
5) Size-holds 300 – 500 ml before signals need to empty
6) Sphincters: Internal: relaxes in response to full bladder
and signals need to urinate; External: formed by skeletal
muscle, under voluntary control
g. Urethra
1) Thin-walled muscular tube- urine to outside of body
RNSG 2432  229
2) Extends from base of bladder to external urinary
meatus; Males: 8 inches long (20 cm) channels for
semen and urine; Protstate gland encircles urethra at
base of bladder; urinary meatus located at end of the
glans penis; Females: 1.5 inches long (3 -5 cm) anterior
to vaginal orifice
C. Urine formation (click here for an animination of urine formation)
1. Kidneys processes 180 liters (47 gallons) of blood-derived fluid each
day; 1% excreted as urine; rest is returned to circulation
2. By nephron via 3 processes: (*understand these processes) (click her
interactive…good visualization of process, multiple resources)
a. Glomerular filtration
b. Tubular reabsorption
c. Tubular secretion
3. Glomerular filtration (*need to understand this…see text p.
698-699)
a. Definition: passive, nonselective process- hydrostatic
pressure forces fluid and solutes through a membrane
230  RNSG 2432
b. *Glomerular filtration rate (GFR): amount of fluid filtered
from blood into capsule per minute
c. GFR-influenced by*
1) Total surface area available for filtration
2) Permeability of filtration membrane
3) Net filtration pressure (proportional to GFR
d. Net filtration pressure responsible for formation of
filtrate
e. Net filtration pressure determined by 2 forces
(*important to understand)
1) Hydrostatic pressure (“push”) (push/moves H2O and
solutes across membrane)
2) Osmotic pressure (“pull”) (colloid osmotic pressure of
plasma proteins in glomerular blood “pulls”)
f. Normal GFR in both kidneys -120 – 125 ml/min in adults;
constant under normal conditions by
1) Renal autoregulation:** Diameter of afferent arterioles
responds to pressure changes in renal blood vessels
2) Increase in systemic blood pressure: renal vessels
constrict; Decline in blood pressure; afferent
arterioles dilate (*have drop in urine output…like in
shock)
3) Renin-angiotensin mechanism (think carefully!)
a) Juxtaglomerular apparatus located in distal
tubules respond to slow filtrate flow by releasing
chemical that cause intense vasodilation of
afferent arterioles
b) **Increase in flow of filtrate promotes
vasoconstriction, decreasing GFR
c) **Drop in systemic blood pressure triggers
juxtaglomerular cells to release renin; acts on
angiotensinogen to release angiotensin I
which is converted to angiotensin II causing
systemic vaso-constriction and causes
systemic blood pressure to rise
RNSG 2432  231
Renin-angiotensin and Blood Pressure Control
Angiotensinogen
RENIN
Angiotensin I
Angiotensin converting
enzyme made by lungs
Angiotensin II
Inc. aldosterone
Inc. sodium and
H2O retention
Inc. peripheral resistance
Inc. extracellular fluid
Inc. blood
pressure
Renin catalyzes splitting of plasma protein angiotensin into angiotensin I then into
angiotensin II which stimulates release of aldosterone from adrenal cortex to cause
Na and H2O retention to produce increased blood pressure.
8/26/2005
9
Ask yourself…how does renin-angiotensin affect BP? What is effect of
aldosterone? (p. 94 & 698)
4) Extrinsic control through sympathetic nervous system
a) extreme stress > *strong constriction of
b) afferent arterioles and inhibits filtrate
formation
c) *> release of renin, increasing systemic blood
d) pressure
g. *Filtrate: essentially same composition as blood plasma
without the proteins; blood cells and proteins usually too
large to pass through glomerular membrane. * If present,
there is a problem!!
*Ultrafiltration of blood by glomerulus initiates urine formation
a. Requires hydrostatic pressure supplied by heart, assisted by
vascular resistance {glomerular hydrostatic pressure} and
sufficient circulating volume
Pressure in Bowman’s capsule opposes hydrostatic pressure and
filtration: if glomerular pressure insufficient to forces substances out
of the blood into the tubules, filtrate formation stops. (*Look carefully
at the following slide) & review above information
232  RNSG 2432
4. Tubular reabsorption of water and electrolytes controlled by
antidiuretic hormone (ADH), released by the pituitary, and
aldosterone secreted by the adrenal glands
a. Proximal convolutes tubule constantly regulate and adjust
rate and degree of water and solute reabsorption according to
hormonal signals (ADH): reabsorption of certain constituents of
the glomerular filtrate: 80% of electrolytes and H2O, all glucose
and amino acids, and bicarbonate; secretes organic substances
and wastes.
b. Loop of Henle: reabsorption of sodium and chloride in the
ascending limb; reabsorption of water in the descending limb;
concentrates/dilutes urine
5. Tubular secretion
a. Substances (hydrogen and potassium ions, creatinine,
ammonia, organic acids) move from blood into tubules as
filtrate
b. Mechanism for disposal of substance such as medications
c. Rids body of undesirable substances that had been reabsorbed
& rids body of excess potassium ions (regulation of pH)
d. Distal convoluted tubule: secretes potassium, hydrogen
ions, and ammonia; reabsorbs H2O (regulated by ADH) and
bicarbonate; regulates calcium and phosphate concentrations.
6. Collecting ducts: receives urine from distal convoluted tubules and
reabsorb water (regulated by ADH); Normal adult produces 1
liter/day urine.
a. Normal Composition and Volume of Urine: result of
countercurrent exchange of fluid through tubes of loop of Henle
and vasa recta (tiny capillaries)
b. Dilution or concentration of urine largely determined by action
of antidiuretic hormone (ADH)
c. Urine by volume: 95% water; 5% solutes; most of weight from
urea
7. Clearance of waste products*
a. Renal plasma clearance: What is it? (ability of kidney to clear
given amt. of plasma of particular substance in given time)
b. *Waste products cleared by kidneys: Urea-nitrogenous
waste product from breakdown of amino acids by liver (BUN)
blood urea nitrogen; Creatinine: end product of creatine
phosphate found in skeletal muscle); Uric acid: metabolite of
nucleic acid metabolism; Ammonia; Bacterial toxins;
Water-soluble drugs
RNSG 2432  233
c. Renal clearance (creatinine clearance): ability of kidneys to
clear solutes from plasma; 24 hour collection of urine required;
depends upon several factors:
1) How quickly substance is filtered across glomerulus
2) How much of substance is reabsorbed along tubules
3) How much of the substance is secreted into tubules
4) **Most useful to measure creatinine clearance =
glomerular filtration rate (GFR) and is calculated as
follows:
(volume of urine{mL/min/min}x urine creatinine {mg/dL})
______________________________________________
serum creatinine (mg/dL)
The normal adult GFR is about 100-120 mL/min.
See table 27.2 p. 751 for normal lab values especially
serum creatinine. . (You need to know this!)
1) BUN: 8-20 mg/dl
2) Serum creatinine: .5-1.2 mg/dl
3) Creatinine clearance: 100-135 ml.min (varies slightly with
men/women)
4) Serum albumin: 3.2-5g/dL
5) K: 3.5-5 mEq/L
6) NA: 135-145mEq/L
7) Ca 4.5-5.5 mEq/L
8) Phosphorous: 3-4.5 mg/dl
9) Red blood cell count: 4.0-6.2 million/mm3 (range here)
8. Blood pressure control
a. Kidneys regulate blood pressure partly through
maintenance of volume (formation/excretion of urine)
1) Rennin-angiotensin system (see above)
9. *Erythropoietin: hormone produced by kidneys in response to low
oxygen levels in arterial blood >stimulates increased (RBC)
production.
10. Renal hormones
a. Activation of Vitamin D: absorption of calcium and phosphate
1) Vitamin D enters body though dietary intake or action of
ultraviolet rays on cholesterol in skin
2) Activated first in liver then kidneys under stimulation by
parathyroid hormone
b. Natriuretic hormone (Recall from heart failure-BNP-should
sound familiar)
1) Released by right atrium of heart in response to inc.
volume and stretch
234  RNSG 2432
2) Inhibits ADH secretion >makes collecting tubules less
porous > produce large amount dilute urine
Kidney Disease/Kidney Failure
*Review in textbook information on glomeronephritis, nephritic syndrome
and polycystic kidney disease P. 744-755
What is the above image? If you said-polycystic kidneys-right! Click onto
the link to access a web site of a gentleman who is living with polycystic
kidney disease!
What are typical manifestation of polycystic kidney disease? (p. 745 & 746)
List prioity nursing diagnosis for the client with kidney disease? (756)
RNSG 2432  235
Part II
____________________________________________________________
Vascular Disorders of the Kidney
I.
Hypertension
See p. 755-756)
Etiology/Pathophysiology
1.
2.
3.
Sustained elevation of systemic blood pressure results from or
causes kidney disease
Damages walls of arterioles and accelerates process of
arthrosclerosis including afferent and efferent arterioes and
glomerular capillaries of kidney
Untreated malignant hypertension (dialstolic BP > 120) >lead to
rapid decline in renal function with decline GFR and tubular
function; have proteinuria and hematuria (Why does this occur?
Recall A&P-p. 698)
Management
1.
Control blood pressure vital
II. Renal Artery Occlusion
Etiology/Pathophysiology
1.
2.
3.
Primary process affecting renal vessels
Due to emboli, clots. other foreign materials
Risk factors include:
a. Severe abdominal trauma
b. Vessel trauma from surgery or angiography
c. Aortic or renal artery aneurysms
d. Severe aortic or renal artery atherosclerosis
e. Emboli from atrial fibrillation, post myocardial infarction,
vegetative growth on heart valves from bacterial endocartitis,
fatty plaque in aorta.
Manifestations
1.
2.
3.
Slow onset; may be asymptomatic
If acute occlusion, what symptom? (p. 755)
Emboli can cause-what side of heart would emboli originate from?
(p. 755)
Diagnostic tests:
a. WBC: leukocytosis
b. Elevated renal enzymes: AST, LDH
236  RNSG 2432
c. Acute renal failure (ARF) on lab (elevated serum creatinine,
creatinine clearance, K, etc (if bilateral arterial occlusion and
infarction)
Therapeutic Interventions/Collaborative Care
1.
2.
III.
Surgery-restore blood flow to affected kidney with acute occlusion
Management: anticoagulant therapy, hypertension control,
supportive.
Renal Artery Stenosis
See stenotic lesion of the
renal artery?
Etiology/Pathophysiology
1.
Narrowing one or both renal arteries due to arthrosclerosis or
structural abnormalities; due by hypertension in 2-5% of the cases.
Manifestations
1.
2.
3.
Hypertension before age 30 or after 50 without prior history
Epigastric bruit
Diagnostic tests
a. Renal ultrasound shows small and atrophied kidney
b. Captopril test for renin activity shows higher levels of rennin
c. Renal angiography visualizes renal stenosis
RNSG 2432  237
Therapeutic Interventions/Collaborative Care
1.
2.
Dilation of stenotic vessel by percutaneous transluminal angioplasty
Surgery: bypass graft of renal artery beyond stenosis
IV. Renal Vein Occlusion
Etiology/Pathophysiology
1.
2.
3.
Pathophysiology unclear; thrombus forms in renal vein
Adults usually with nephrotic syndrome What is nephrotic
syndrome? (see p. 748)
Gradual/acute deterioration of renal function-only manifestation
Manifestations/Therapeutic Interventions/Collaborative Care
1.
2.
3.
If thrombus breaks loose; result is pulmonary embolism
Why pulmonary?...think location
Diagnosis: visualization of thrombus on renal venography
Treatment: thrombolytic drugs to dissolve clot; anticoagulant
therapy; treat embolism
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V.
Renal Trauma (here for actual series of renal trauma slides)
The retroperitoneum opened, revealing large laceration to lower pole of right kidney
Etiology/Pathophysiology
1.
2.
3.
Kidneys damaged by blunt force or penetrating injury
Minor injuries: contusion, small hematoma, capsule or cortex
laceration
Major injuries
238  RNSG 2432
a. Kidney fragmentation; *significant blood loss, urine
extravasation
b. Tearing of renal artery or vein
c. Renal artery, vein or pelvis laceration
Manifestations
1.
2.
3.
4.
5.
6.
Hematuria, gross or microscopic
Flank or abdominal pain
Localized swelling, tenderness, ecchymosis in flank area
Turner’s sign: bluish discoloration of flank
*Acute blood loss: signs of shock: hypotension; tachycardia,
tachypnea, cool pale skin, altered level of consciousness
Diagnostic tests:
a. Falling hemoglobin and hematocrit levels
b. Urinalysis: hematuria
c. AST levels rise
d. Renal ultrasound reveal renal bleeding and damage
e. CT scan
f. IVP
g. Renal arteriography
Therapeutic Interventions/Collaborative Care
1.
2.
3.
4.
Minor kidney injuries
a. Conservative treatment: bedrest and observation
b. Minimal bleeding and self-limiting
Major kidney injuries
a. *Immediate treatment to control hemorrhage, prevent and
treat shock (Major concern)
b. Surgery including surgical repair, partial or total nephrectomy
c. Percutaneous arterial embolization during angiography
Nursing management
a. Accurate assessment
b. Monitor H & H levels for bleeding
c. Bedrest; close observation; evaluate for signs and symptoms
of shock
d. Prevent complications; monitor urine output
Nephrectomy (see text p. 756; Nursing Care of Client Having a
Nephrectomy; see also p. 759 Fig 27-4 ) Nephrectomy- also by
laproscope; less invasive)
RNSG 2432  239
a. Indications:
1) tumor removal; infected, non-functioning kidney
2) major trauma to kidney, if repair not possible
b. Pre/Post op care: (Important to recognize prioriities)
1) Preparation for procedure
2) Careful monitor intake and output; initially hourly I
& O; urine to at least 30 cc per hour; check for
bleeding
3) Note placement, status ALL drainage tubes,
stents; label clearly; irrigate ONLY if specifically
ordered
4) Maintain gravity drainage; prevent any occlusion
*Important-encourage turn, cough, deep
breathe; use incentive spirometry-incision in
flank area just below diaphragm.
5) Keep medicated for pain
6) Protect remaining kidney; avoid UTS; fluid intake to
2000-2500 ml/24 hours
7) Post-op teaching-avoid contact sports; no lifting, care
of remaining stents, catheters, need to report any
signs, symptoms of infections
240  RNSG 2432
Renal Failure (ARF)
Definition: kidneys unable to remove accumulated metabolites from
blood >leads to altered fluid, electrolytes and acid-base balance;
remember kidneys require 20-25% CO to maintain GFR!
1.
Result from kidney disease (primary) or disease in another organ or
systemic (secondary)
Classified as Acute:abrupt onset/may be reversible or Chronic:
develops slowly, insidiously with few symptoms until kidneys are
severely damaged and unable to meet body’s excretory needs due to
a. Diabetes, Polycystic kidney disease, chronic
glomerulonephritis, and nephrotic syndrome (review
pathophysiology); see text p. 745, 746-748. (chronic)
b. *While helpful, drugs, NSAIDS and ACE inhibitors interfere
with normal autoregulatory mechanisms of kidney >lead to
hypoperfusion and eventual ischemia. Note-“ACE inhibitors reduce
2.
protein loss in associated with nephritic syndrome.” p. 751-thus also
protective of kidney)
Acute renal failure
ARF:
I.
rapid decline in renal function with azotemia (retention in blood of
excessive amount of nitrogenous compounds; toxic; due to kidneys
inability to remove urea form blood; characteristic of uremia)> fluid
and electrolyte imbalances.
Etiology/Pathophysiology related to underlying cause
(*differentiate among the different causes; See text p. 762, Table 27-5
Causes of Acute Renal Failure) Know the difference.
Causes of ARF
A.
Pre-renal
1.
2.
B.
55-60% cases of ARF
Due to conditions that affect renal blood flow and perfusion
(ischemia primary cause; if allowed to continue more than 2
hours> produces irreversible damage to renal tubules, extent
varies)
a. Decreased vascular volume (hemorrhage, diuretic therapy)
b. Decreased cardiac output (heart failure; MI)
c. Decreased vascular resistance (septic shock; anaphylaxis,
vasoactive drugs)
Intra-renal
1. 35-40% cases of ARF
2. Due to acute damage to renal parenchyma and tubules
RNSG 2432  241
3.
Causes:
a. Acute glomerulonephritis (review p. 747))
b. Vascular disorder including vasculitis, malignant
hypertension, arterial or venous occlusion
c. Acute tubular Necrosis (ATN): destruction of tubular
epithelial cell; abrupt decline in renal function (recovery
possible if basement membrane that surrounds tubules
remains intact and problem identified and treated
promptly.) (*need to understand how & why recovery
can occur with ATN, see p. 763…read carefully)
1)
2)
3)
4)
Prolonged ischemia
Nephrotoxins such as aminoglycosides antibiotics;
radiologic contrast media; NSAIDS, heavy metals
Rhabdomylosis: excess myoglobin from skeletal
muscle injury clogs renal tubules
Hemolysis: red blood cell destruction as with
transfusion reaction (clogs tubule)
C.
Post-renal
1. <5% of cases of ARF
2. Cause:
a. Obstruction >prevent urine excretion>lead to kidney
hypertrophy eventually to intra-renal failure.
1) Benign prostatic hypertrophy
b. Renal or urinary tract calculi or tumor
D.
Stages of ARF (Text describes 3 stages; other references
describe 4 stage approach: Initiation event; Oliguric; Diuresis and
Recovery…think overall process…
1.
Onset or Initiating Event Phase
a. Onset: 1-7 days of causative agent…such as lack of
perfusion to kidney (nephroxic agent, obstruction to urine
outflow…various causes…thus onset and manifestations
vary…) may last hours to days
b. Manifestations depend upon underlying problem
c. Critical to recognize/treat here!
2.
Oliguric or maintenance stage (days to weeks after initial
insult) *Kidneys not producing!
a. Urine output typically less than 400 cc/24 hours (oliguria
or anuric)
b. Can have “normal” urine output but “fixed” urine
specific gravity. (kidney produces urine, but not
removing “waste” products…unable to “concentrate”
242  RNSG 2432
c.
d.
e.
f.
urine….specific gravity typically remains at 1.010
regardless of fluid intake.)
Characterized by significant fall in GFR (much less than
100-135 ml/min
No waste elimination; develop: azotemia, fluid retention,
electrolyte imbalance including
1) *Hyperkalemia, hypocalcemia, hyperphosphatemia,
acidosis-impaired hydrogen ion elimination.
Explain why these alterations occur- hyperkalemia,
metabolic acidosis. (p. 764-765)
2) Anemia after several days due to suppressed
erythropoietin secretion; impaired immune function
(Why?)
3) *Salt and water retention > hypertension >risk
for heart failure and pulmonary edema
4) What are signs/symptoms of *hyperkalemia? (p.
98-99) cardiac dysrhythmias and EKG changes,
muscle weakness, nausea, diarrhea, ileus
5) Signs/symptoms uremia-confusion, disorientation,
agitation or lethargy, hyperreflexia, possible seizures,
coma; vomiting, decreased or absent bowel sounds
Manifestations depend upon electrolyte imbalances and comorbitity
Two typical components: Oliguric (initial) then
Diuretic as recovery starts.
1) Oliguric (or anuria) (little or urine; identify and
remove cause- fluid challenge to rehydrate initiallyprevent overload; careful monitoring of electrolytes)
(discuss later with treatment)
2)
Diuretic (*diuresis as kidney recovers: BUN,
creatinine, potassium and phosphate remain high, but
stabilized)
a) Gradual increase in daily urine output to 1-3 L per
day, may reach 3-5 L per day
b) High urine volume due to osmotic diuresis from
high urea concentration on glomerular filtrate and
inability of the tubules to concentrate the urine.
*Understand this concept
c) May develop hypovolemia and hypotension;
carefully monitor for hyponatremia, hypokalemia
and dehydration; may last 1-3 weeks.
d) Careful monitoring for fluid replacement;
cc/cc…Kidneys not recovered!
g. Prognosis depends upon early recognition and appropriate
treatment!!
RNSG 2432  243
3.
Recovery Phase (BUN, creatinine stabilized; duration 412 months)
a. Progressive tubular cell repair/regeneration: return of GFR
to pre-ARF levels
b. Renal function improves rapidly first 5-15 days,
improvement may continue up to a year.
II. Assessment/Diagnostic Test ARF; findings similar to chronic renal
failure (anuric/oliguic/non-oliguric stage = a GFR of 10-20 ml/min as
normal of 100/120 ml/min! (see chart p. 765-766)
A.
Determine if ARF (and type) or if Chronic Renal Failure
1.
*Cause of oliguria/anuria & altered lab values-especialy
BUN, creatinine at on set
a. Pre-renal “oliguria” cause or an “intra-renal” cause
ARF
1) Pre-renal oliguira: no damage to renal tissueoliguria d/t decrease in circulating blood volume
> causes autoregulartory mechanisms that increase
angiotensin II, aldosterone, norepinephine, and
antidiuretic hormone in attempt to preserve flow to
essential organs.
Pre-renal oliguria-have urine with high specific
gravity and low sodium concentration. *Can
recover with appropriate renal re-perfusion
2) Intra-renal: actual damage to renal tubules
 ATN (acute tubular necrosis); most common
intrarenal type ARF (ischemia & nephrotoxic drugs
-90% )
 Prolonged ischemia > patchy necrosis and damage
to basement membrane in proximal convoluted
tubule and loop of Henle
 Nephrotoxic drugs/injury (recognize them!!) >
proximal tubular damage, recovery more likely to
regenerate
 Urine in intra-renal ATN: normal specific
gravity; high sodium concentration (injured
tubules unable to respond to autoregulartory
mechanisms)*understand this
Explain why patient with ARF due to shock will have
urine with a low urine sodium concentration.
b. Renal ultrasound-identify any obstruction, differentiate
acute from chronic renal failure; CT scan: identify
obstruction and kidney size (*small, atrophied reflects
chronic renal disease)
244  RNSG 2432
c. IVP, retrograde xylography or antegrade
pyelography
d. Renal biopsy: determine cause, differentiate acute
from chronic
B.
“Common” findings with ARF-require daily lab monitoring
*Need to understand “why”of these changes…
1.
Urinary output/urinalysis; dec. to less than 400 cc in 24
hours for 50 % of clients; urine may have casts (sloughing of
the lining of the tubules) (oliguric/anuric stage)
a. Fixed specific gravity-1.010-urine osmolality of 300
mOsm/kg (same as plasma if kidneys unable to
concentrate urine) *varies with underlying cause
b. *Proteinuria if glomerular damage
c. Presence of red blood cells (glomerular dysfunction, white
blood cells (inflammation), renal tubular epithelial cells
d. Brown color -iindicate hemoglobinuria or myoglobinuria
(ATN)
e. Cell casts (protein and cellular debris molded in shape of
tubular lumen)
2.
Fluid volume excess-due to fluid retention; may have neck
vein distention, bounding pulse> lead to CHF > pulmonary
edema, etc.
3.
Metabolic acidosis
a. Kidneys unable to synthesize ammonia needed for H+
ion excretion or excrete acid products of metabolism (uric
acid, NH3) > pH decreases
b. Bcarbonate levels dec. as bicarbonate used up to buffer
excess H+ ions in buffering hydrogen ions
c. Have defective reabsorption and regeneration of
bicarbonate ions
d. May develop Kussmauls respirations (rapid, deep
respirations) to increase the excretion of carbon dioxide.
Why are Kussmauls respirations effective in reducing
metabolic acidosis? (p. 124-125)
Sodium balance altered
a. damaged tubules cannot conserve sodium
1) urinary excretion of sodium-increased > normal or
below normal levels of serum sodium
2) increased or decreased serum Na (Normal = 135145 meq/l): inc. Na due to volume deficit
(dehydration); decreased Na due to damaged tubules
not conserving Na
4.
RNSG 2432  245
5.
6.
Potassium levels increased (usually)
a. Kidneys normally excrete 80-90% of body’s potassium
b. ARF due to massive tissue trauma
1) damaged cells from injury, bleeding, blood transfusion
release additional potassium into extracellular fluid
2) Acidosis: hydrogen ions enter cells and potassium
driven out of cells into extracelluar fluid (Know
concept!)
c. Normal K = 5-5.0 meq/l)
1) *Kidneys excrete 90% of K+ of total daily intake
2) If K=>6.0; treatment must be initiated to prevent
what complication(s) (p. 99) Life threatening
dysrhythmia; peaked narrowed T waves; ST segment
depression and shortened QT interval; skeletal muscle
weakness; diarrhea
Hematologic disorders
a. Anemia from impaired erythropoietin production & low iron
and folate levels
b. Platelet abnormalities leading to bleeding from multiple
sources
c. Altered WBC’s; also altered.
7.
Calcium deficit and phosphate excess
a. Low serum calcium level from decreased GI absorption
(needs activated vitamin D).
b. Hypocalcemia > parathyroid gland to secrete PTH which
stimulates bone demineralization > releasing calcium from
bones and phosphate too (inc. hyperphosphatemia)
(Normal= 9-11 mg/dl)
c. Elevated serum phosphate levels- dec. renal excretion
by kidneys. (Normal 2.0-4.5 mg/dl)
8.
Waste product accumulation
a. Inc. BUN ( blood urea nitrogen) end product or protein
metabolism Normal= 8-20mg/dl; BUN fluctuates; NOT
accurate indicator alone for renal function
b. Inc. serum creatinine, end product of endogenous muscle
metabolism: Normal = 0.6-1.5 mg/dl; levels normally
remain constant & are directly related to GFR; good
indicator of renal function; creatinine clearance most
accurate.
Value approximates loss of nephron function (quick
estimate)
2X normal creatinine (2.4) = 50% nephron fx loss
10X normal creatinine (12) = 90% nephron fx loss
246  RNSG 2432
c. Evaluate BUN to creatinine ratio (helps to determine
underlying cause…dehydration vs nephrotoxic drug)
BUN : creatinine ratio
Normal = 10:1 (normal ratio
as follows)
BUN
16
12
8
9.
Creatinine
1.6
1.2
0.8
Creatinine Clearance decreased: MOST ACCURATE
INDICATOR OF RENAL FUNCTION: REFLECTS GFR-involves
obtaining 24 hr. Urine collection & drawing a serum creatinine
(see Part I for formula)
10. Neurologic alterations
a. Nitrogenous waste products accumulate in brain and other
nervous tissue- uremic symptoms (uremia)
____________________________________________________________
**If ARF recognized early and treated effectively-client has a
good prognosis.
III. Nursing Care/Collaborative Care
(***May not initially recognize that patient had ARF: Initiation Phase:
however, recognize factors such as hemorrhage that would precipitate
AFR. Assess patient; what is urine output; is it above 30 cc per hour;
what signs/symptoms fluid overload; what “insults” to put patient at
risk?
A.
Initial & Oliguric Stage *Refer to text p. 774 Client with ARF
1.
2.
Identify problem: Alert physician; treat aggressively. Use IV
fluids and blood volume expanders to increase renal
perfusion
Start with fluid challenge and diuretics to rule out
dehydration as cause of ARF:
a. 250-500cc NS given IV over 15 minutes (treat potential
dehydration, flush renal tubules)
b. Mannitol (osmotic diuretic) 25gm IV given (where and
how does this drugs work?) **Refer to text p. 765-766
Med Adm
c. Lasix 80mg IV given (where and how does this drugs
work?)
RNSG 2432  247
d. Should see urine output >30 cc/hr within 1-2 hrs
e. Also manage HTN; ACE inhibitors; no nephrotoxic drugs
3.
**If fluid challenge fails, fluid intake limited to 500cc +
urine output past 24 hrs. The 500cc = patient’s
‘insensible” fluid loss; if more given than what client
able to eliminate > fluid overloaded.
Example the patient’s urine output on Mondays is 500cc for 24
hours; what will be his fluid intake on Tuesday? It should be
1000 cc
Note: strict I& O!
*Dopamine (Intropin) given to increase renal blood flow
and improve cardiac output. (1-3 g/kg) (What
classification is this drug; how does it work?)
4.
Assess for fluid volume deficit vs fluid versus overload
a. Strict I & O, vs q 2-4 hours; limit fluids as above**
500 + urine output for past 24 hours
b. **Daily weights 1 lb= 500cc; 1kg= 2.2 lb:
c. Assess for signs of CHF
d. **Fluid Management. Monitor for fluid overload. Typically
have period of oliguria followed by period of diuresis-at
high risk for overload or dehydration electrolyte
imbalance.. etc. careful assessment required
5.
Treat manifestation of metabolic acidosis
a. Give NaHCO3 IV as ordered to elevate the plasma pH
6.
Hyperkalemia; treat if serum K > 6.5 mEq/L (*know
why each of these drugs are use and explain…see p.
764-765!)
a. Identify signs and symptoms of hyperkalemia
b. Insulin & glucose IV to drive potassium into the cells
> lowers serum potassium levels temporarily. Also need
calcium gluconate to help protect heart from effect of high
potassium levels. How does this work?
c. Administer Kayexalate po or enema. Kayexalateexchanges sodium ion for potassium ion in intestinal tract.
Sorbital often administered in combination with kayexlate
to induce diarrhea –type effect to promote elimination.
d. Restrict K+ intake (Limit to 2 gm (50meq)/day)
248  RNSG 2432
Avoid foods high in K+ such as citrus fruits, bananas,
coffee and juices.
7.
EMERGENCY DIALYSIS INDICATED WHEN:
a.
b.
c.
d.
K+ > 6.5 (approx)
Volume Overload
Metabolic acidosis < 15 HCO3
BUN > 120mg/dl; serum creatinine greater than 9.5. client
in ESRD; elevated blood urea nitrogen; toxic level altered
sensorium
8.
Diet- protein limited to about 1g to .6/kg (generally limit
protein unless protein lost through dialysis or glomerular
membrane as with nephritic syndrome; need protein of high
biologic value) what kinds of protein ae of high biologic value?
Low in sodium foods & fluids
9.
Calcium/phosphorus imbalance
a. Calcium supplements as ordered (Phoslo, Oscal) and to
bind with phosphorous
b. Phosphate binders as Amphogel/Basaljel, Nephrox,
Renagel
10. Treat HTN: Give Lasix, Vasotec, Procardia, etc. as
ordered
11. Assess for anemia: Give Epogen/Procrit sc as ordered.
PRBCs as ordered
RNSG 2432  249
Diuretic Stage to Recovery
12. *As kidney function returns; urine output increases:
however; kidneys are not healed
a. BUN & creatinine still elevated high
b. Creatinine clearance low
13. Carefully monitor electrolytes; I & O & daily weights critical
a. Replace fluids cc per cc.
b. As healing continues; teach to prevent future insults to
kidney
250  RNSG 2432