Download Serum Creatinine

Nursing Care of Individuals
with Genitourinary
Disorders:
Renal Trauma
Renal Vascular Problems
Acute Kidney Injury
5/25/2017
1
The Kidney
Primary function
◦ Regulate volume and composition of ECF
(extracellular fluid)
◦ Excrete waste products
 Other functions
◦ Regulate acid-base balance
◦ Control BP
◦ Produce Erthyropoietin
◦ Activate Vitamin D

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Kidney- macrostructure

kidney anatomy
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Kidney- microstructure

nephron
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The Nephron

Why is it called the functional unit of the
kidney?
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Glomerular Filtration Rate
Glomerular filtration rate
 Used to assess how well the kidneys are
working

Estimates how much blood passes through the
glomeruli each minute
 The amount of filtrate formed per minute by
the two kidneys combined

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Glomerular Filtration Rate

For average male GFR is 125ml/min
◦ That would create180 L/d!

More than 99% of the filtrate is reabsorbed
◦ Average 1mL/min of urine excreted
◦ 1-2 L/day

Older people will have lower normal GFR
levels, because GFR decreases with age
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GFR
GFR too high
◦ increased urine output
◦ threat of dehydration and electrolyte
depletion
 GFR too low
◦ insufficient excretion of wastes

GFR of 60 or higher is in the normal range
 GFR below 60 may mean kidney disease
 GFR of 15 or lower may mean kidney failure

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The Kidney
Primary function
◦ Regulate volume and composition of ECF
(extracellular fluid)
◦ Excrete waste products
 Other functions
◦ Regulate acid-base balance
◦ Control BP
◦ Produce Erthyropoietin
◦ Activate Vitamin D

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Functions of the Kidneys
Regulates acid-base balance
◦ HCO3 and H+
 Controls Blood Pressure:
◦ Renin Release

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RAAS
Kidney senses low perfusion
 Renin released by kidney

Angiotensinogen (from liver) acivated into
angiotensin I
 Converted to Angiotensin II by ACE

Angiotensin II stimulates release of aldosterone
 Na+ and H2O retained

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Functions of the Kidneys

Erythropoietin Release
◦ If a patient has chronic kidney disease or
chronic renal failure, what condition will
occur and why?
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Functions of the Kidneys

Erythropoietin promotes the formation of
RBC’s  in response to decreased O2 carrying
capacity

Anemia from impaired erythropoietin
production and platelet abnormalities >
bleeding risk
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Functions of the Kidneys

Activated Vitamin D
◦ Necessary to absorb Calcium in the GI tract.
There is decrease in synthesis of D3, the active
metabolite of Vitamin D
If a patient has renal failure, what will happen to
the patient’s serum calcium level?
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Functions of the Kidneys

Inability of kidneys to activate vitamin Dhypocalcemia > parathyroid gland > secretes
PTH > stimulates bone demineralization >
release calcium from bones

Low serum calcium level/elevated phosphate

Why do you have a elevated serum phosphate?
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ReviewFunctions of the Kidney

Regulate
◦ Volume & composition of extracellular fluid
◦ F&E balance
Acid/Base balance
 Blood pressure regulation
 Erythropoetin release
 Vitamin D activation

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Acute Kidney Injury

Rapid decline in renal function that leads to
accumulation of nitrogenous wastes in the blood
(azotemia)

Etiology of AKI:
◦ Pre-renal
◦ Intra-renal
◦ Post renal
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Acute Kidney Injury
Pre-renal
Hypovolemia
dehydration, shock, burns
Decreased cardiac output
CHF, MI, arrhythmias
Decreased vascular resistance
septic shock
Renal vascular obstruction
renal artery stenosis, thrombus
Causes related to decreased blood flow to
the kidneys
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Acute Kidney Injury
Intra-renal
Conditions causing direct damage to renal
tissue causing damage to nephrons
Result from ischemia
 Nephrotoxins
 Hemoglobin released from hemolysis of red
blood cells
 Myoglobin released from necrotic muscle cells

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Acute Kidney Injury
Intra-renal
Primary Renal Disease
◦ Acute glomerulonephritis/pyelonephritis
◦ Systemic lupus

Acute Tubular Necrosis (ATN)
◦ Necrosis of tubular cells which slough and
plug tubules
◦ Potentially reversible
◦ Most common cause of intra-renal AKI
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Acute Tubular Necrosis(ATN)
◦ Renal ischemia
 Disruption basement
membrane;destruction
tubular epithelium
◦ Nephrotoxic agents
 Necrosis tubular
epithelium… plug
tubules; basement
membrane intact.
Renal
ischemia
◦ Potentially reversible IF
 Basement not destroyed
and tubular epithelium
regenerates
Nephrotoxic
agents
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Acute Kidney Injury
Intra-renal

Acute Tubular Necrosis (ATN)

Nephrotoxic drugs/chemicals (ATN)
◦ Aminoglycosides*
◦ Radiographic contrast agents
◦ Arsenic, lead, carbon tetrachloride
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Acute Kidney Injury
Intra-renal

Hemolytic blood transfusion (ATN)

Trauma
◦ crushing injuries which release myoglobin
◦ damaged muscle tissue and blocks tubules
(rhabdomyolysis)(ATN)

What is Rhabdomyolysis?
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Healthy
ATN
Compare & Contrast
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Lupus Nephritis
 ‘Flea bite’ look

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Acute Kidney Injury
Post-renal






Mechanical
obstruction of
urinary outflow
urine backs up into
renal pelvis
BPH
Calculi
Trauma
Prostate cancer
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Stages of Acute Kidney Injury
Initiating Phase
◦ Time of insult until signs and symptoms become
apparent
 Oliguric Phase
◦ Usually appears 1-7 days of initiating event
 Diuretic Phase
◦ Start varies, usually within10-12 days of onset
oliguric phase
 Recovery
◦ Usually within a month, recovery takes up to 12
months
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

Urine output in AKI varies widely & does
NOT provide clinical correlation to the
degree of injury!!!!!

Must look at GRF
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Oliguric Phase
Onset- 1-7 days
 Duration- 10-14 days
 Urine Output- Less than 400 ml/24 hours in 50% of
patients (Can have non-oliguric AKI)


Signs & Symptoms to anticipate Specific gravity fixed at 1.010 in oliguria in intra renal
failure – may be elevated in pre & post
 Fluid overload
 Urine with RBCs, casts, WBCs, protein (if glomerulus
damaged)
 K+ likely elevated
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Oliguric Phase

Metabolic acidosis
 kidneys unable to synthesize HCO3, cannot excrete H+
and acid metabolites, serum bicarbonate decreased
because used to buffer H+
 Kussmaul breathing

Calcium deficit & phosphate excess
 decreased GI absorption of Ca (Vit D)
 increase in Calcium secretion

Nitrogenous product accumulation
◦ unable to eliminate urea and creatinine > elevated BUN,
serum creatinine
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Treatment – Oliguric phase

Fluid Challenge/Diuretics
◦ Done to r/o dehydration as cause of ARF and
to blast out tubules if ATN
◦ 250-500cc NS given I.V. over 15 minutes
◦ Mannitol (osmotic diuretic) 25gm I.V. given
◦ Lasix 80mg I.V. given
◦ Should see what within 1-2 hours?
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Treatment – Oliguric phase
If fluid challenge fails- intake limited
 Fluid restriction
◦ 600ml + u.o. past 24 hours


Patient’s u.o. yesterday was 300ml. What will be
the allowed fluid intake today?
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Diuretic Phase
Onset- days to weeks
 Duration- 1-3 weeks
 Urine Output- 1-3 liters/day

Signs & Symptoms to anticipate
 Elevated BUN and Serum Creatinine
 What happens to intravascular volume?
 What happens to BP?
 Urine Na?
 K+ elevated or decreased?

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Recovery Phase
Onset- When BUN and Creatinine stabilized
 Duration- 4-12 months
 Urine Output- Normal


Signs & Symptoms
◦ Continue to monitor for signs and symptoms of F & E
imbalances
◦ All body systems for effects of fluid volume changes
◦ What are some key nursing interventions?
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Diagnostic tests in AKI
BUN (blood urea nitrogen)
 Measurement of amount of urea in blood
 Normal -6-20 mg/dl

What is urea?
 BUN fluctuates
 BUN elevated when?
 BUN decreased when?

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Diagnostic tests in AKI

Serum Creatinine
◦ End product of muscle and protein metabolism
◦ Excreted by the kidneys at a constant rate
◦ Normal = 0.6 – 1.3 mg/dl
◦ Directly related to GFR
 2 X normal (2.4) = 50% nephron fx loss
 10 X normal (12) = 90% nephron fx loss
More accurate indicator of renal function than
BUN
 BUN:Creatinine ratio 5/25/2017
Normal= 12:1 to 20:1

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Diagnostic tests in AKI

Creatinine clearance
 Normal= 120-125ml/minute
◦ Most accurate indicator of Renal Function
◦ Reflects GFR
◦ Involves a 24 hr urine/serum creatinine
◦ Formula:
urine creatinine X urine Volume
serum creatinine
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24 hour urine
What is the nurses role in the collection of a 24
hour urine?
 What if they have a foley cath?

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Diagnostic tests in AKI
Urine Specific Gravity
 Normal= 1.003-1.030
 Will be fixed a 1.010 usually in AKI due to
kidneys losing ability to concentrate urine


Serum Electrolytes
 Sodium
 Potassium
 Calcium
 Phosphorus
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Diagnostic tests in AKI
Serum Electrolytes
 Serum Sodium
 Normal= 135-145

May be high, low, or normal
 When would it be high/low?

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Diagnostic tests in AKI
Serum Electrolytes
 Serum Potassium
 Normal= 3.5-5 meq/L

Almost always increased in renal failure
 Why? Two major reasons


If > 6.0 treatment to prevent….
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Diagnostic tests in AKI
Serum Electrolytes
 Serum Phosphorus
 Normal=2.8-4.5mg/dl


Almost always increased. Why?

What other process is occurring to increase
serum phosphorus?
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Diagnostic tests in AKI
Serum Electrolytes
 Serum Calcium
 Normal=9.0-11.0 mg/dl


Almost always decreased, why?

What other process is occurring to decrease
serum calcium?
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Diagnostic tests in AKI
ABGs
 Metabolic acidosis-due to decreased
ability of kidneys to excrete acid metabolite
(uric acid)
 So the pH will be high or low?


Bicarb- decreased due to bicarb being used up
to buffer excess H+ ions
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Management of AKI

Treat the primary disease/condition

Prevention
◦ Frequent monitoring for early signs of AKI in
at risk patients
◦ What are these signs?
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Management of AKI

Assess for FVD vs FVE
◦ VS
◦ Strict I&O
◦ Daily weights
◦ Monitor labs- which ones?

Metabolic acidosis
◦ Administer NaHCO3 IV as ordered
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Management of AKI

Hyperkalemia
◦ Insulin and glucose
 K+ moves back into the cells when insulin is given.
 Glucose to prevent hypoglycemia
◦ Sodium Bicarbonate
 Correct acidosis and shifts K+ into cells
◦ Kayexalate
 Pulls K+ out through GI tract
◦ Dietary restrictions
 Bananas, avocado, apricots, potatoes, white beans
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Management of AKI

Calcium imbalance
◦ Calcium Gluconate

Phosphorus imbalance
◦ Calcium supplements, Phosphate binders

Hypertension
◦ Lasix, Amlodipine, Metoprolol
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Management of AKI
Anemia
◦ Administer epogen/procrit as ordered
◦ PRBC’s
 Diet
◦ Fluid restriction
◦ Low K+, low Na
◦ Low protein- why?
 Emergency dialysis
◦ K+>6.0, FVE, uremia, metabolic acidosis

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Renal Trauma
Etiology:
 Men under age 30
Blunt force from falls
MVA
Sports injuries
Knife/gunshot wounds
Impalement injury, rib fractures
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Renal Trauma

Common Manifestations:
◦ Hematuria-microscopic to gross
◦ Pain- Flank or abdominal
◦ Decreased Urine Output- oliguria or anuria
◦ Localized swelling, tenderness
◦ Turner’s sign
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renal trauma
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Renal Trauma

What are some diagnostic tests used in renal
trauma?
◦ CT scan, MRI, renal ultrasound, renal
arteriogram, IVP with cystography

What serum levels can be useful?
UA (hematuria),
H & H (decreasing values)
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Renal Trauma-Interventions

Minor Trauma
◦ Bedrest and close observation.
◦ Monitor for S & S of what?

Moderate/Major Trauma
◦ Embolization or open surgery to stop bleeding
or repair
◦ Partial or total Nephrectomy
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Renal Trauma-Interventions
Nursing Management
 Bedrest
 Prevent complications
 Close Observation for s/sx shock
◦ H&H
◦ I&O
◦ Daily weights
◦ VS

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Renal Surgery-Nephrectomy

Indications for
Nephrectomy:
◦ Renal tumor
◦ Massive Trauma
◦ Polycystic Kidney
Disease
◦ Donating a Healthy
kidney
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Renal Surgery-Nephrectomy

Post Op Nursing Management
◦ Strict I & O
 Urine output should be at least _____.
 What should output be if patient had bilateral
nephrectomy? ______.
◦ Observe ACC of urine
◦ TCDB & incentive spirometery
 Incision in flank area, 12th rib removed
◦ Medicate for pain as ordered
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Renal Vascular Problems
Nephrosclerosis

Caused by chronic or malignant HTN

Renal dysfunction and renal failure are two
major complications of HTN

Sustained elevation of the systemic blood
pressure can result from or cause kidney
disease---How?
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Patho of Nephrosclerosis

Development of arterio sclerotic lesions in
the arterioles and glomerular capillaries
↓
Decreased blood flow which leads to
ischemia and patchy necrosis
↓
Destruction of glomeruli
↓
Decrease in GFR
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Renal Vascular Problems
Renal Artery Stenosis

Narrowing of one or both
renal arteries due to
atherosclerosis or
structural abnormalities

Uncontrollable HTN

How could a renal artery
stenosis result in HTN?
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Renal Artery Stenosis

Treatment/Collaborative Care
 Anti-hypertensive Medications
 Dilation of renal artery by Percutaneous
Transluminal Angioplasy
 Bypass Graft of Renal Artery
 Nephrectomy
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Renal Vein Thrombosis/Occlusion

Partial occlusion in one or both renal veins due to
atherosclerosis or structural abnormalities in vein
by a thrombus

Risk Factors
 Nephrotic syndrome
 Use of birth control pills
 Certain malignancies
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Renal Vein Thrombosis/Occlusion

Pathophysiology/etiology
◦ Thrombus forms in renal vein
◦ Cause unclear
◦ Trauma, nephrotic syndrome
◦ Gradual loss of kidney function

Common manifestations/complications
◦ Decreased GFR
◦ Signs of renal failure
◦ Pulmonary embolus
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Renal Vein Thrombosis/Occlusion
Treatment/Collaborative Care
 Diagnosis
◦ Renal venography


Management
◦ Thrombolytic drugs
◦ Anticoagulant therapy
◦ Surgical thrombectomy
◦ Corticosteroids
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Your patient develops AKI after
being on Amphotericin for 1 week:

The patient’s AKI is primarily related to:
◦ A. spasms of the renal arteries
◦ B. blood clots in the loops of Henle
◦ C. low cardiac output
◦ D. acute tubular necrosis
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Your patient’s K+ level is elevated.
The physician orders Kayexalate
because it:
A. increases sodium excretion from the colon
 B. releases hydrogen ions for sodium ions
 C. increases calcium absorption in the colon
 D. exchanges sodium for potassium in the colon

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Clinical scenario
You are a student nurse on day shift and you hear
in report that your patient is scheduled to have
an IVP this am….
What do you know about an IVP?
 What do you teach the patient about preparing
for this procedure?
 What nursing interventions or orders should
you anticipate?

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The client’s BUN is elevated in AKI.
What is the likely cause of this finding?

a-fluid retention

b-hemolysis of red blood cells

c-below normal protein intake

d-reduced renal blood flow
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Activity

The RN is taking care of a group of patients.
One of the patients is taking glucophage 500mg
orally every morning. What does the RN need
to know prior to administration of this
medication?

Another client is scheduled to get a CT with
contrast of their abdomen and is at risk for ARF,
what does the RN need to know?
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A 24 hours urine for creatinine clearance is
ordered. Which task is appropriate to
delegate to the the clinical assistant?
a) instruct patient to collect all urine with each
voiding
 b) explain the purpose of collecting a 24 hour
urine
 c) ensure that the 24 hour urine collection is kept
on ice
 d) assess urine for color, odor, sediment

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Which urinary symptom is the
most common initial manifestation
of AKI?
a-dysuria
 b-anuria
 c-hematuria
 d-oliguria

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