Transcript Thelan*s Critical Care Nursing

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Describe the priorities of the renal nursing
assessment.
Identify ways in which alterations of hemoglobin
and hematocrit levels can
signal fluid volume deficit or excess.
Explain the reason elevations of blood
urea nitrogen and creatinine signal renal
dysfunction.
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Chapter
19-1
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Kidney Anatomy
 Both kidneys are enclosed in a renal capsule
 Renal cortex is the outer layer of the capsule &
contains blood-filtering mechanism
 Renal medulla is the inner region, containing
pyramids
 Parynchema is the functional unit of the kidney
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Chapter
19-2
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Chapter
19-3
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Chapter
19-4
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Nephrons – selectively secretes & reabsorbs ions &
filtrates (fluid, wastes, electrolytes, acids, bases)
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Glomerulus – capillaries filter large plasma proteins &
blood cells
Tubules (PCT, DCT, Loop of Henle) – reabsorbs
electrolytes, filters fluid & converts it into urine
Bowman’s Capsule - surrounds the glomeruli

Glomerular filtrate (electrolytes, glucose, amino acids,
metabolic waste) from the blood is filtered, enters a fluid
filled space (Bowman’s space), then enters PCT (proximal
convoluted tubule)
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Chapter
19-5
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Chapter
19-6
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Excretion - the removal of end waste products from
body fluids
Elimination - the discharge of waste products into
the environment
Homeostatic regulation of blood plasma
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Regulating blood volume and pressure
Regulating plasma ion concentrations
Stabilizing blood pH
Conserving nutrients & controlling electrolyte balance
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Chapter
19-7
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ADH is produced by hypothalamus and secreted
from the posterior lobe of pituitary gland
ADH secretion is stimulated by dehydration or high
sodium intake & by a decrease in blood volume
ADH makes the DCT & collecting duct permeable to
water
Water is drawn out of tubules by osmosis & returns
to blood; concentrated urine remains in tubules to be
excreted
ADH is primarily responsible for reabsorption of
water by the kidneys
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Chapter
19-8
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When sodium increases, extra water is retained to
preserve osmotic pressure
Increased sodium & water increases blood volume &
blood pressure
When BP increases, glomerular filtration increases, &
extra water & sodium are lost; blood volume is
reduced, returning BP to normal
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Chapter
19-9
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Increases in serum potassium stimulates the
secretion of aldosterone
Aldosterone stimulates the DCT to secrete potassium
This action returns the serum potassium
concentration to normal
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Chapter
19-10
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Blood pH is controlled by maintaining the
concentration of buffer systems
Carbonic acid & sodium bicarbonate form the most
important buffers for neutralizing acids in plasma
Normal arterial pH is maintained by keeping the
ration of concentration of sodium bicarbonate to
carbon dioxide at 20:1
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Chapter
19-11
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Chief Complaint (onset, location, duration)
Renal Symptoms ( wt. gain >2lbs./day)
Predisposing Risk Factors (infections, OTCs, HTN)
Medical History
Previous Diagnostic Studies
Current Medication Usage
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NSAIDs, antibiotics, HTN meds, iodine dyes)
Social History and Family History
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Chapter
19-12
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Inspection of flank & abdomen
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Bleeding
 Grey-Turner’s sign – flank discoloration (trauma)
 Abdominal distention or firmness
 Blood in urine usually indicates bladder, not kidney trauma
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Volume Depletion/ Overload
 Neck veins nondistended supine (hypovolemia); remain
distended at 45° > 2cm above sternal notch (overload)
 Skin turgor & dryness of the mouth

Edema
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Chapter
19-13
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Edema (cont’d)
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Definition: the presence of fluid in interstitial space
Can indicate volume overload
However, loss of albumen from vascular space (d/t
circulatory compromise) can cause peripheral edema with
hypovolemia or normovolemia
A key feature to distinguish the two is that edema does not
reverse with elevation of extremity when volume overload
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Chapter
19-14
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Auscultation
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Heart
 3rd or 4th sound may be heard with bell of stethoscope
 Increased HR WITH decreased BP (hypovolemia)
 Friction rub – pericarditis d/t uremia
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Blood pressure
 Orthostatic hypotension = drop in SBP >20; DBP >10; or rise in
HR >15 bpm
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Lungs – crackles, dyspnea, gasping with periods of apnea =
severe acid-base imbalance
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Chapter
19-15
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Palpation
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To determine shape & size of kidneys
Rarely done in critically ill pts.
Capturing – placing one hand posteriorly under flank & the
other anteriorly below rib cage, then bringing them
together while pt. exhales
Right kidney is more easily palpable (lower)
Abnormal: mass (cancer), irregular surface (polycystic
kidney), size differences, extending significantly lower than
rib cage (trauma)
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Chapter
19-16
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Percussion
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Kidneys (dull is normal) – pain may indicate infection or
trauma
Abdomen (to assess fluid status)
 Ascites or severe fluid distention (dull)
 Fluid wave (Figure 19-1 p. 394) differentiates ascites from
distortion d/t solid bowel contents
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Chapter
19-17
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Other Observations
Fluid and electrolyte imbalances
 Mental status changes
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Chapter
19-18
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Weight
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Check weight on admission & daily
Weight gain or loss > 2lbs/ day indicates fluid rather than nutritional
factors
Differences in wt. from day to day are used to calculate the amt. of fluid
to remove during dialysis
Intake and Output
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Urine
 Oliguria = <30ml/ hr or 400 ml/ day
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 Anuria = < 100 ml/ day
Insensible losses (perspiration, stool, lung vapor)
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Chapter
19-19
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Hemodynamic Monitoring
CVP – most common cause of acute renal failure requiring
monitoring is severe sepsis & septic shock
 PAOP – “wedge pressure”
 MAP (70 – 100 mmHG) = SBP + (2 x DBP)
3
 Cardiac Output
 Cardiac Index = CO
BSA

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Chapter
19-20
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Blood Serum Analysis
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Blood Urea Nitrogen (BUN)
 A by-product of protein & amino acid metabolism
 Normal value = 5 – 25 mg/dl
 Increased when kidney function deteriorates d/t increased in
GFR and decreased urea excretion
 As BUN increases, uremia symptoms become more
pronounced
 BUN is never evaluated in isolation (must also know creatinine
level) because a decrease in GFR, therefore an increase in BUN,
may also be r/t hypovolemia, dehydration, nephrotoxic drugs,
or prolonged hypotension
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Chapter
19-21
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Blood Serum Analysis (cont’d)
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Creatinine
 A by-product of muscle & normal cell metabolism
 Appears in serum in proportion to body muscle mass
 Normal = 0.5 – 1.5 mg/dl
 Is easily excreted by renal tubules & not significantly
reabsorbed or secreted in tubules
 Creatinine clearance – measuring the amount of creatinine in
urine & blood over 24 hrs. provides a reliable & accurate
estimate of GFR (kidney function)
 Normal = 110 to 120 ml/ min (Box 19-3 p.396)
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Chapter
19-22
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Blood Serum Analysis (cont’d)
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Osmolarility
 Reflects the concentration or dilution of vascular fluid &
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measures the dissolved particles in the vascular fluid
Normal = 275 – 295 mOsm/L
Elevated Osmolarility indicates hemoconcentration or
dehydration
Decreased Osmolarility indicates hemodilution or volume
overload
ADH regulates serum Osmolarility (increases to increase water
resorption & decreases to increase excretion)
Bedside calculation = (2 x Na) + (BUN/3) + (Gluc/18)
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Chapter
19-23
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Blood Serum Analysis
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Anion Gap
 Is a calculation of the difference between the measurable
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extracellular cations (mainly Na) & the measurable
intracellular anions (mainly chloride & bicarb.)
Represents the remaining unmeasurable ions in the
extracellular fluid (phosphates, sulfates, ketones, lactate)
Normal = 1 – 12 mEq/L
An increased anion gap level reflects overproduction or
decreased excretion of acid products (metab. acidosis) & a
decreased anion gap indicates metab. alkalosis)
Na+ – (Cl- + HCO3-)
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Chapter
19-24
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Blood Serum Analysis (cont’d)
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Hemoglobin and Hematocrit
 H & H levels can indicate increases or decreases in
intravascular fluid volume
 Hemoglobin (Hgb) transports O2 & CO2 & is important
in cellular metabolism & acid-base balance (13.5-17.5
g/dl)
 Hematocrit (Hct) is the proportion of RBCs in a volume of
whole blood. > 54% indicates fluid volume deficit & <
37% may indicate fluid volume excess (normally 3x the
Hgb level)
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Chapter
19-25
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Blood Serum Analysis (cont’d)

Albumin
 More than 50% of total plasma protein is albumen
 Is made in the liver & is responsible for maintaining colloidal
osmotic pressure which hold fluid in vascular space
 Normal = 3.5 – 5 g/dl
 Blood vessel walls prevent albumen from leaving the vascular
space
 Decreased levels of albumen creates edema (burns, sepsis,
renal failure, protein malnutrition, liver disease/ injury, severe
portal HTN → ascites)
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Chapter
19-26
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Urine Analysis (Table 19-3 p.397)
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Urine pH
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Specific Gravity / Osmolality

Glucose
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Protein
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Electrolytes
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Urea
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Hematuria

WBC/ Bacteria
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Chapter
19-27
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24 Hour Urine Collection (Silvestri p. 928)
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Creatinine clearance
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Uric acid test (gout & kidney disease)
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Vanillylmandelic test (pheochromocytoma – tumor of the
adrenal gland)-avoid certain foods x 2 days
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Nursing Considerations
 Encourage fluids
 Avoid tea, coffee & some medications
 Discard 1st sample (start time)/ keep last sample (end time)
 Keep collections on
ice or refrigerated
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Chapter
19-28
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KUB – to evaluate presence of calculi & masses
Bladder scanning (US) – bladder volume; cysts
CT/ MRI – provide cross-sectional views
IV Pyelography (IVP) – internal kidney tissues
Renal angiography – renal blood flow
Cystoscopy/ biopsy – bladder mucosa examined for
inflammation, calculi or tumors
Renal biopsy (closed vs. open) – to obtain kidney
tissue sample
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Chapter
19-29
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Describe the stages of acute tubular necrosis.
Identify the priorities of nursing management
in acute renal failure.
Identify the differences among hemodialysis,
peritoneal dialysis, and continuous renal displacement
therapy.
Describe the etiologies of acute renal failure.
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Chapter
19-30
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Definition: characterized by a sudden decline in
glomerular filtration rate (GFR)
 Waste product retention
 Electrolyte, acid-base, & fluid volume imbalances
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Chapter
19-31
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Etiology (Box 20-2 p.402)
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Pre-Renal: any condition that ↓ blood flow, BP, or renal
perfusion before arterial blood reaches the kidney
Intra-Renal: any condition that produces an ischemic or
toxic insult directly at the site of the nephron
Post-Renal: any obstruction that hinders the flow of urine
from beyond the kidney
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Chapter
19-32
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Acute Tubular Necrosis (Intra-Renal): results from
injury that damages the renal tubular epithelium and
may extend to basement membrane
Over 90% of episodes of acute renal failure are d/t
ATN as a result of ischemic or toxic injury (Box 20-3)
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Ischemic Injury – occurs as a result of vasodilation
associated w/ sepsis (prolonged hypotension or low CO)
Nephrotoxic Injury – common cause is radiopaque
(contrast) dye
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Chapter
19-33
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Description
Abrupt decline in glomerular filtration
rate (GFR)
 Retention of metabolic waste products
 Disruption of fluid volume
 Mortality is high without treatment
 Associated complications are frequent

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Chapter
19-34
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Pathophysiology
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Tubular obstruction – cellular debris accumulates due to
lack of filtrate/ blood flow
Tubular edema exacerbates obstruction
Tubular cell injury - ischemia
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Chapter
19-35
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Onset Phase
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From when an insult occurs until cell injury
GFR decreases because of impaired renal blood flow &
decreased glomerular filtration pressure
Lasts hours to days, depending on cause
If tx is initiated during this time, irreversible damage can be
alleviated
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Chapter
19-36
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Oliguric / Anuric Phase
Lasts 5 – 8 days in nonoliguric patients & 10 – 16 days in
oliguric patients
 Necrotic cellular debris in the tubular space blocks the flow
of urine & causes damage to tubular wall & basement
membranes
 GFR is greatly reduced

 Increased BUN (azotemia) & creatinine
 Hyperkalemia, hyperphosphatemia, hypocalcemia
 Metabolic acidosis, Changing anion gap
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Chapter
19-37
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Diuretic Phase
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Lasts 7 – 14 days
Characterized by an increase in GFR & sometimes polyuria
Tubular obstruction has passed, but edema & scarring are
present
GFR returns before the ability of the tubules to function
normally and the kidney can remove volume but not
solutes
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Chapter
19-38
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Recovery Phase
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Both oliguric & nonoliguric patients will have increased
urine output
Renal function slowly returns to normal or near normal
If renal parenchymal damage has occurred, BUN &
creatinine levels may never return to normal
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Chapter
19-39
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Normal Laboratory Assessment (Table 20-3 p.404)
Sodium: 135 – 145 mEq/L
 Potassium: 3.5 – 4.5 mEq/L
 Chloride: 98 – 108 MEq/L
 Calcium: 8.5 – 10.5 mg/dl
 Phosphorus: 2.7 – 4.5 mg/dl
 Magnesium: 1.5 – 2.5 mEq/L
 Bicarbonate: (CO2) 24 – 28 mEq/L

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Chapter
19-40
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Assessment & Diagnosis
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Acidosis (pH below 7.5) is one of the trademarks of ARF
Radiologic Findings – CT scan & angiography
Hemodynamic Monitoring
Fluid Balance
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Chapter
19-41
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Underlying chronic kidney disease
RIFLE (risk, injury, failure, loss, end-stage kidney
dis.)
Older Age (> 65 years)
Heart Failure-HTN- or cardiovascular disease
Respiratory Failure-54%-84% with ARF had Resp
failure
Sepsis-shock, renal hypoperfusion-inflammatory
changes
Trauma-crushing injuries and Rhabdomyolysis
Contrast-Induced Nephrotoxic Injury(1% of all
contrast procedures)
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19-42
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Hemodynamic & Fluid Balance Monitoring
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Hemodynamic Monitoring (CVP, PAOP, CO, CI)
Daily weight
Physical assessment
 ECF depletion sx: thirst, ↓ skin turgor, lethargy
 Intravascular fluid overload sx: pulm. congestion, ↑ heart
failure & BP
 Edema
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Chapter
19-43
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Medical Management (Electrolytes)

Hyperkalemia
 ECG changes: peaked T waves, widening QRS, VT/F
 Tx: diuretics; 10U insulin & 50 ml 50% dextrose (to force K into
cells); Kayexalate (binds K in bowel)
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Hyponatremia tx w/ fluid restriction or dialysis
Hypocalcemia tx w/ supplements, Vit. D & synthetic
calcitrol
Lower phosphorus levels (to increase calcium) with binding
agents (PhosLo, Renagel, Fosrenol)
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Chapter
19-44
Hyperkalemia
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Chapter
19-45
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Medical Management (Goals)
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Prevention
Correcting the causative mechanism
Regeneration of functional capacity
Management is based on category of ARF
 Pre-renal
 Intra-Renal
 Post-Renal
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Chapter
19-46
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Medical Management (Volume)
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Fluid Resuscitation (NS) for trauma, hemorrhage,
hypotension, contrast dye injury
Crystalloids and Colloids (volume management)
 Crystalloids (NS 0.9% & 0.45%, LR w/ caution-contains K)
 Colloids expand IV volume (albumen, Hetastarch)
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Fluid Restriction to prevent circulatory overload &
interstitial edema with oliguria
Fluid Removal – diuretics, hemodyalisis
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Chapter
19-47

Pharmacologic Management (Table 20-7)

Diuretics stimulate urinary output (controversial)
 Loop (Lasix) – inhibit Na & Cl (Monitor electrolytes)
 Thiazides (Zaroxolyn, Diuril) – in addition to Lasix since they
work on distal tubule to inhibit Na & Cl
 Osmotic (Mannitol) - ↑ flow of fluid from tissues by ↑ plasma
osmolality
 K-sparing (Aldactone) – exerts (weak) effect on collecting
tubule/ used in heart failure (monitor for hyperkalemia)
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Chapter
19-48

Pharmacologic Management (cont’d)
Dopamine (renal dose) to stimulate renal blood flow
 Acetylcysteine (Mucomyst) to vasodilate tubule &
“scavenge” free radicals
 Fenoldopam (Corlopam) to lower blood pressure
 Dietary – Phosphorous Binders

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Chapter
19-49
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Nutrition – restrict potassium, sodium, phosphorous,
protein, & fluids. Encourage carbs.
Nursing Management
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Infection Control
Optimize Fluid Balance
Electrolyte Balance
Prevent Anemia (kidney no longer produces erythropoitin)
Patient Education
Nursing diagnoses on p. 400 Box 20-3
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Chapter
19-50
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Hemodialyzer
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Exchanges of fluid, electrolytes, & toxins from blood to
dialysate bath through osmosis/ diffusion
Ultrafiltration – transmembrane pressure & results in
fluid extraction
Anticoagulation – to prevent clotting
Dialysis Process (Figures 20-4 & 20-6Definition
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Separating from the blood
Indications (Box 20-4)
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Chapter
19-51
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Vascular Access for Hemodialysis

Temporary Acute Access (Fig 20-5)
 Subclavian vein catheters
 Femoral vein catheters
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Permanent/ Chronic Access (Fig 20-5)
 AV Fistula (27%)– joining peripheral radial artery & cephalic
vein
 AV Grafts (47%)-synthetic graft between radial artery &
cephalic vein
 AV Shunt (23%) – temporary tunneled catheter
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Chapter
19-52
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Chapter
19-53
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Medical Management
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When to begin hemodialysis
When and where to place vascular access
Exact quantity of fluid and/ or solute removal based on lab
results and weights
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Chapter
19-54
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Nursing Management

Care of hemodialysis vascular access
 Assess patency (thrill & bruit)
 Assess extremity circulation
 No BPs, IVs, labs
 Heparinize

Patient education
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Chapter
19-55
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Venous blood is circulated through a highly porous
hemofilter using venous catheter (Figure 20-3)
The advantage is the continuous removal of fluid
from plasma, or ultrafiltrate, & IV replacement which
is controlled over many hours to several days)
Indications (Box 20-6)
Contraindications
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Hematocrit > 45%
Terminal illness
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Chapter
19-56

Four CRRT methods
SCUF – Slow Continuous Ultrafiltration
 CVVH – Cont. Venovenous Hemofiltration
 CVVHD – Cont. Venovenous Hemodialysis
 CVVHDF – Cont. Venovenous Hemodiafiltration

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Chapter
19-57
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Complications of CRRT (Table 20-11)
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Decreased Ultrafiltration Rate
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Filter Clotting
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Hypotension
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Fluid and Electrolyte Changes
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Bleeding
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Access Dislodgment

Access Infection
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Chapter
19-58

Medical Management of Hemodialysis and CRRT
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Choice of blood purification method is a medical decision
Often the acute clinical diagnosis, physician preference,
availability of CRRT, & physician/ RN knowledge of CRRT
are deciding factors
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Chapter
19-59

Nursing Management of Hemodialysis and CRRT
Surveillance for side-effects of dialysis
 Monitoring fluid balance
 Accurate I & O
 Maintaining catheter patency
 Preventing infection
 Patient education

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Chapter
19-60

Indications
Renal failure (uremia)
 Volume overload
 Electrolyte imbalance
 Hemodynamic instability
 Lack of access to circulation
 Removal of high molecular weight toxins
 Inability to anticoagulate (i.e.: subdural bleed)

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Chapter
19-61

Contraindications
Recent abdominal surgery
 Hx of abdominal surgeries w/ adhesions/ scarring
 Significant pulmonary disease
 Need for rapid fluid removal
 Peritonitis

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Chapter
19-62
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Infection – most significant risk
Medical Management – used for long term end-stage
renal failure
Nursing Management
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Prevention
Detection of complications (Table 20-12) p.414
Patient education for self-management Catheter placement
(Figure 20-7)
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Chapter
19-63
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Living Donor Surgery
Cadaver Donor Surgery
Recipient Surgery
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Chapter
19-64
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
Fluid Status
Electrolyte Imbalance ↓K, ↓Mg, ↓Ca
Bleeding Risk- Hct/Hgb
Urine Output-q 30’, assess bladder decompression,
clots
Immunosuppressive Therapy



Polyclonal antithymocyte/ antilymphocyte compound
Monoclonal antibody compound
Infection Risk
Copyright © 2004, Elsevier (USA). All
rights reserved.
Chapter
19-65

Rejection
Rescue therapy if biopsy is positive
 High dose IV steroids (mild rejection)
 Monoclonal antibody (mod. to severe rejection)
 oral immunosuppressant (chronic rejection)
 Treatment goal: to create a balance among medications that
allows the patient to fight off most infections & yet avoid
rejection

Copyright © 2004, Elsevier (USA). All
rights reserved.
Chapter
19-66