N254
Renal Nursing Care
Mary Moon, RNC, FNP
Fall 2009
Renal Circulation
Bowman’s Capsule
Diffusion
Small molecules make easily movement by
diffusion in a cell
limited by the cell’s semi permeable
membrane
Coffee
In liquid: Equally sweet
Sugar
In air: Equally smell
Perfume
Room
Ex. RBC
O.9% NaCl
99.1% H20
0.9% Plasma NaCl
Isotonic=In Equilibrium
99.9% H20
Solutes: materials-- sugar, salt.
Solvent: Liquid material that dissolve--water
Solution: A mixture of two.
Tonicity: A state of amount of dissolved material
in them.
Tonicity: By NaCl
Osmosis:
From:
0.9% NaCl
99.1% H20
To:
3% NaCl
97% H20
Osmosis: [H20]
99.1 H20
0.9 NaCl
0% NaCl
100% H20
[H20]
Hyper tonic
Hypo tonic
So, H20
will move
into RBC.
So., RBC
will
rupture
Osmosis
A special type of diffusion between NACl & water.
Water: Small, unchanged molecules
NaCl: Changed molecules
*** Changed molecules are hard to move--- H20
move freely from a weaker solution to a more
concentrated one.
NaCl: Electrolytes that regulate vascular osmotic
pressure.
Kidney
Purify (Filter) and reabsorb 5 inches long, level
with T12 and L1~L3
Urine: collected by the pelvis
20% to 25% of the resting cardiac output
(approx. 1200 mL per Min.) passes through
kidney.
Liver: 27%
4%
Brain: 14%
Skeletal: 15%
6%
Miscellaneous: 7%
Skin: 6%
Heart:
Bone:
Each region of the nephron:
filtration, re absorption, and secretion.
(Bowman’s Capsule)
(Tubules and Collecting Duct)
180 liters of filtrate a day
upper limit (transport maximum):
glucose
225 mg/min
(BS: 180 mg/dl)
at higher concentration,
glucose begins to be lost in urine.
Right one more
volunable
Nephron:
Functional unit of
Kidney.
1/4 of nephron
needed for living.
Excretion of waste nitrogen (urea, uric acid, creatin)
protein--> ammonia--> harmless urea--> kidney
American food ( protein)
Detoxification of ammonia -->
¤ Liver, Kidney failure
H20 and electrolytes
Hypothalamus (Osmoreceptor)
Sense blood
¤[
] = H20, lytes.
A.R.F
Is a clinical syndrome characterized by
a renal shut down--> acute tubular
necrosis, obstruction, acute tubular
insufficiency--> Most occur in
previously healthy individuals.
Generally follows an identifiable
trauma contact with a nephrotoxic
agent. The most cause of ARF is related
to surgical procedures.
Pre Renal
Causes---> Consists of factors outside
the kidneys that impair renal blood
flow and lead to decreased glomerular
perfusion
Problem corrected --> no ARF
Prerenal
55-70%
Intravascular volume depletion, decreased CO,
vascular failure secondary to vasodilation or
obstruction---HTN, MI, severe dehydration, &
shock ( not enough volume circulating).
Reversible—can be corrected by establishing
renal perfusion & preventing necrotic renal
damage by fluid challenge
Irreversible ischemia
Intra Renal
Conditions of actual damage to the renal
tissue leading to malfunctioning of
nephrons---> APN may lead ARF
Ex) acute tubular necrosisrenal ischemia
Nephrotoxic drugs
Glomerulonephritis
Intrarenal
25-40%
Kidney itself damaged to the kidney tissues and
structures & includes tubular necrosis,
nephrotoxicity & alterations in renal blood flow
Injuries @kidney glomeruli or tubules—90% due
to ATN--- glomerulonephrits, toxins, trauma,
crushing injuries, surgery, sepsis, CV collapse,
MOF, ABX like aminoglycosides, street drugs,
chemo, nephrotoxic drugs
Don’t get confused w/ prerenal caused by blood
volume—dehydration & hypovolemia
Post Renal
Mechanical Obs. Of urinary outflow. As the
flow of urine is blocked. Urine backs up into
the renal pelvis. The most common causes are
renal calculi, trauma, tumors.--> usually
anuria rather than oliguria
Ex) Calculi, bladder tumor. Stricture
(Compression)--BPH
Basement membrane is not destroyed.
Trauma to back, pelvis, perineum strictures,
spinal cord disease.
Postrenal
5%
Obstruction of urine between the
kidney and the urethral meatus
Calculi BPH Tumors strictures
B/C the obstruction, urine backflows
Prevention
A. High Risk
Hospital Pt. --> Massive trauma,
major surgical procedure, extensive
burns, sepsis.
B. Industrial chemicals and
nephrotoxic drugs.
A.R.F Phases
A. Onset phase
begins with precipitating event-Hypovolemia, or nephrotoxin exposure
Ends when the oliguric-anuric phase
begins.
Time Span: Up to two days
urine output: 20% of normal.
A. Onset Phase
Initial injury to the kidney
Reversible
Preventable with early intervention
UO:20% of normal
Unable to regulate electrolytes
B. Oliguric Phase
Spans the period when urine is less
than 400 cc/d
Time Span: 8-14 days (1-2 wks)
urine output: 5% of normal.
Can not excrete fluid or waste
products
Oliguria--> caused by reduction in
the GFR
C. Diuretic Phase
Gradual increase in urine output of
1-3L up to 4-5 L/day. The high vol. Is
due to osmotic diuresis from high urea
concentration
urea
H2 0
H2 0
H2 0
H2 0
H2 0
Capillary
H 20
and the adequate concentrating ability
of tubules.
cells
Lab. Value stop rising, decreased SG:
Diluted urine and poss.
Excessive diuresis when lab value
stops dropping. Ends when they
stabilize.
Time span: 10 days
U.O:
Early 150%
Late: 200%
Diuretic Phase
Electrolytes are lost—deficit in
concentrating ability of tubules and
osmotic diuretic effect of increased
BUN, slowly increased excretion of
metabolic wastes, hypovolemia, loss
of Na, K, increased BUN initially then
gradually return to baseline
Diuretic Phase
S/S: postural hypotension, tachycardia,
improving mental alertness and
activity, weight loss, thirsty, dry
mucous membrane, decreased skin
turgor
K replacement may require
D. Recovery Phase
(convalescent phase)
Begins when lab. Values stabilize, ends
when renal function returns to normal.
Time Span: 4-6 mo.
Up to 12 mo.
U.O: 100%
Recovery Phase
Increased GFR
Increased concentrating ability.
Urine SG -- 1.003-1.030
Urine osmolarity:
Normal 300-1300
Mortality Rate: 30% to 60%
Most common cause of death secondary
to infection
Prevention of ARF
CHF, dehydration, shock. To minimize
the risk.
1. Keep the patient hydrated (esp.
before and after OR)
2. Continuously monitor the
dosages and effects of ABX and
other drugs (nephrotoxic)
3. Assess renal function regularly
Treatment Goals
1. Correcting the underlying problem
2. Preventing infection
3. Treating fluid and electrolytes
imbalance
4. Correcting metabolic acidosis
5. Treating clinically significant anemia.
How does one differentiate acute from chronic renal
failure?
1. History-medical records.
2. Hypo calcemia, hyper phosphatemia, anemia. --> has
been associated more often with CRF.
* Calcium, phosphorous, acid-base derangement
are often seen in ARF as early as 48-72 hours after onset
of illness.
* Anemia: nonspecific indicator.
3. Reliable indicator of CRf
Small kidney with a decreased or absence of renal cortex
as assessed by UTZ (0.5 cm)
Abnormal: Kidney length of less than 9 cm
--> CRF or significant renal dz.
> 1.5 cm in renal length: unilateral/asymmetric renal dz.
CRF
CRF
Slow, progressive, irreversible damage
4 stages
Diminished Renal Reserve ---50% of
nephrones are lost, asymptomatic, no S/S
Renal Insufficiency---75% nephrones lost,
azotemia, anemia, polyuria, nocturia
Renal Failure---pt needs temporary or
permanent dialysis
End Stage Renal Disease
CRF
An irreversible loss of nephrons. A symptomatic until 7090% of the nephron is destroyed.
(Divided into four stages)
1. Diminished renal reserve: nephron loss without the
loss of measured renal function. Normal BUN, CR, no sxs.
2. Renal insufficiency: a measurable decline in renal
function. Loss of ability to concentrate urine --> nocturia,
polyuria, often associated HTN fatigue, weak. Ha.
3. Renal failure /ESRD
4. Uremia: a clinical syndrome with severe decline in
renal function, associated with dysfunction of multiple
organ systems.
Etiology of CRF
1. 30%: Diabetic nephropathy
2. 26%: Hypertension
3. 14%: other urological disease (
hydronephrosis, polycystic kidney.)
4. Congenital malformations
5. Nephropathy associated with the human
immunodeficiency virus.
6. Myeloma Kidney
Evaluation: To establish the degree of
renal impairment.
To identify reversible factors
-infection, obstruction, volume deficit,
nephrotic drugs, less than optimal cardiac
output with, without HTN, uncontrolled
HTN, hypercalcemia and hyperuricemia
-orthostatic Bp. Pulse
-U/A with microscope/dipstick, serum
electrolyte, BUN, CR, CBC, evaluation of
post void residual, UTZ
U/A: the simplest, most cost effective evaluation
Urine SG: 1.010 or less
Urine pH: less than 7.0
8.0: the question of infection
Dipstick: glucose in DM or CRF
Proteinuria: the hall mark of intrinsic renal disease.
Nephrotic-range of proteinuria is seen in glomerular
lesions and 1-2 gm of protein excretion in interstitial
dzs.
RBC: active renal dz of a glomerular or vascular
etiology.
WBC: infection
Medical Treatment
A. Most hypervolemic--> kidney can’t eliminate amount of
H20 and electrolytes. ** Hypovolemia
(Increased HCT)
B. Anemia/Bleeding
The main cause of anemia-->
Decreased production of erythropoietin by the kidney
C. Nutritional deficiency
Decreased RBC life
increased hemolysis of RBC bleeding from G I tract
dialyzer may contribute to the anemic state.
Folic Acid: Essential for DNA Synthesis and normal
maturation of RBC.
D. Dialysis
1) Hemodialysis: within 1-2 Hr. bring K+ to normal
2) Peritoneal dialysis: 4-8 hrs.
E. Phosphate binders
(aluminum or magnesium containing antacids)-->
CA-Phos.
An inverse relationship to bind excessive CA in ECF-> Decreased serum Ca level phosphate binders-->
urinary acidifier to help prevent calcium stones
F. Diet
the major goal of nutritional management is to
decrease catabolism of the body’s protein. No more
than 0.8-1 gm of protein/kg/day.
F. Diet
the major goal of nutritional management is to
decrease catabolism of the body’s protein. No more
than 0.8-1 gm of protein/kg/day.
G. HTN
1. NA-fluid restriction
2. Diuretic--Lasix
*3. Anti HTN drugs
A. Ace inhibitors-- enalapril, captopril
B. beta-adrenergic--inderal (decreased rennin
released)
C. Calcium channel blockers: diltiazem,
verapamil
H. Neurologic Function
No. TX. Available without dialysis
neuro Change--> renal failure progress
* contraindicated
amiloride
AntiHTN: triamiterene spironolactone,
* 10 unit regular insulin + D 50 ampule.
NaHCO3 bolus or 75~ 100 cc/hr- hyperkalemia tx.
* Albuterol: Potassium lowering effect
Increased nitrogenous waste products,
electrolytes imbalances --> demylination of
nerve fiver, axonal atrophy.
** Safety: due to weak muscle
general depression of CNS--> lethargy, fatigue,
decreased concentration, dialysis dementia due
to aluminum toxicity
Complications: UGI bleeding
a major Cx and 3-7% of deaths. Superficial
mucosal abnormalities. Duodenitis and gastritis
(10-60%)
TX: Cimetidine (H2-receptor antagonist)
Death is usually due to infection, G-I
bleed, myocardiac infarction. Kidney
can no longer remove toxic wastes
and water from blood. Two means
are mimicking the body’s lost
capabilities.
Uremia is a clinical situation in which
azotemia progress to systematic state.
Azotemia; an excess of urea or other
nitrogenous compounds in the blood.
Fetor: offensive odors
halitosis: offensive odors of the
breath.
CV: CHF, HTN, pericarditis, arrythmia,
hematopoietic anemia, peripheral/systemic edema.
Neuro: Drowsy, confusion, tremor, coma,
irritability, convulsion, twitching, peripheral
neuropathy
Integ: pallor, yellowish color, dryness, pruritis,
ecchymosis
Skeletal:
Hypocalemia, soft tissue, calcification, alteration in
coagulation, increased infection
GI: Anorexia, N/V, gastrtitis, uremic halitosis,
diarrhea, constipation
Resp: Pul. Edema, Pneumonia, Kussmaul Resp.
Asterixis:
A motor disturbance by sustained
contraction of muscles.
Kussmaul Breathing--> Deep to
rapid breathing to increase excretion
of CO2
--> a compensatory mechanism of aacidosis
Nutrition in Renal Disease
Sodium: major ECF Caution, important in acidbase balance, fluid balance, cell permeability, and
muscle action.
High NA+ Foods: Table salt, processed foods,
milk, fish, poultry, meat, eggs, carrots,k some
canned soup, beets, spinach, meat sauce, soy
sauce, salad dressings, potassium: major ICF,
important in acid-base balance, neuromuscular
activity, carbohydrate metabolism, and protein
synthesis.
High in K+ foods: meat, oranges,
potatoes, whole grains, bananas,
broccoli, beans, nuts, apricots, spinach,
dried fruits, melons, peas, fruit juices,
peaches, tomatoes, avocados, coffee,
wine, salt substitute, antibiotics.
Proteins: build, maintain, and repair
body tissues
Protein sources: eggs, milk, fish, poultry,
grains, legumes (dry beans, lentils, split
peas, soy beans)
Calories (carbohydrates, fats): to meet
body’s need for energy and to attain or
maintain ideal body weight. Fats are also
important in maintaining skin integrity
and forming complex lipid compounds.
Carbohydrate source: fruits, vegetables,
cereals, sugar, hard candy, jelly beans,
jams, jellies.
Fat sources: butter, margarine, oil, cream,
bacon, meat fat, salad dressing, egg yolk,
olives, nuts, avocados.
Vitamins and mineral supplements:
Vitamin C, B Complex Vitamins, calcium,
phosphorus, and vitamin D.
Calcium sources: calcium carbonate (OScall, Tums), calcium acetate (Phos-Low),
supplements given between meals.
Phosphorous binding agents: Calcium
acetate (Phos-Low), aluminum hydroxide
gel (Amphogel), aluminum carbonate
(Basalgel) binding agents given with
meals.
Vitamin D source; Calciferol (Hytakerol),
Calcitrol (Rocaltrol).
Iron sources: ferrous sulfate, parental
iron products.
Magnesium: not usually a problem
unless there is intake of
magnesium containing medicines
such as laxatives and antacids.
Geriatric Consideration
A. Decreased RRF (Reserved Renal Factor)
Decreased GFR
Decreased Clearance
B: Aging kidney is less able to withstand
changes in hydration, solute, load, cardiac
output. Aging itself is the primary risk factor.
Mortality: 5-25% higher in older than
younger.
Hemodialysis
An artificial Semi permeable membrane acts like
the kidney-> diffusion and osmosis
Excess fluid is removed by creating a pressure
differential BTN the blood and the dialysate
solution
(=balanced solution of electrolytes and fluid)
With a combination of positive pressure in the blood
compartment and/or negative pressure in the
dialysate compartment
2.5-4 hrs 3 times/week at home or dialysis center.
Quinton Catheter;
single, double, temporary
vascular access, 2-3 days
femoral, subclavian, internal
jugular veins.
AV Access
AV Shunt: Temporary while internal graft is
healing
Machine
Artery
Vein
Rinse
Fistulas:
Cephalic/radial Artery
Basilic vein
Thigh
or
forearm
Grafts (looped graft)
Bovin--> relatively resistant to infectious
organism.
Antecubital vein
Looped graft
Brachial artery
NSG: 14-16 G needle A thrill/bruit can
be felt by palpating
***** NO VENIPUNCTURE, BP ON THE
AFFECTED ARM*****
NSG Management
1. Hypovolemia/shock --due to rapid removal of vascular volume
* trendelenberg to improve cerebral blood flow
2. Analgesia: muscle cramps associated with significant discomfort
and pain
: neuromuscular hypersensitivity
Peritoneal dialysis
Principle---sterile dialyzing fluid infused into peritoneal cavity
through a catheter
Surgically implanted in the pt’s peritoneal cavity.
Inflow
---> dwell
15-30 min.
--->
4 hr/d
10 hr/n
outflow
15-30 min.
* continuous 24
times/day
* at night 8 hrs
cycler machine
Transplantation
A living or cadaveric donor
the life expectancy for patients on dialysis is 67 years < 60 years.
2-3 years > 60 years or diabetic
Survival years is 90% at 3 years with cadeveric
transplant
95%: Living
Ruptured AV Shunt
Subcutaneous hemorrhage--hypovolemia--shock-- cardiac arrest
Intervention
1. Control bleeding
2. Transfusion
3. Pain relief
hematoma-arm, cold compression
To Control Bleeding
1. Tie a tourniquet above the AV or BP
cuff. Don’t release until OR.
* pressure DSG, Arm.
2. IV fluid, O2 2L
3. Notify MD/surgical team
4. Type and cross match ---cont.
monitor the pt for signs of shock.
5. Dopamin Drip
--Pulmonary edema
secondary to fluid overload
6. Strict I & O
7. H & H Q 4-6 H
8. Monitor circulatory, motor,
neurofunction below hematoma.
Definition
Infection of the kidney and renal
pelvis.
Every PN is secondary
APN
Acute infection of the kidney, characterized by
acute inflammation and focal abscess, usually
unilateral, often accompanied by bacteremia.
Characterized by bacteriuria (generally >
100,000 colonies/ml) and pyuria. In acute
infections, a single infective pathogen usually
is found.
CPN
The result of repeated episodes of
APN leading to progressive renal
scarring.
Scars are usually asymmetric and
irregular and involve the renal cortex
and pelvocalyceal system. Negative
urine cultures and no evidence of
active infection.
Pathogens
Gram-neg Bacilli: Escheria coli,
proteus, Pseudomonas,
Enterobacter, kebsiella, Serratia,
and Citrobacter species.
Gram-pos cocci: Staphylo. S
Strepto. A
Ascending Infection
The most common cause of GU
tract infection
Female- short urethra
altered flora d/t
antibiotics, birth control
(spermicide and diaphragm)
urethral massage.
Direct extension from
other organ.
-Interaperitoneal
abscess
- Pelvic
inflammatory disease
- GU tract fistulas.
Clinical Manifestations
Rapidly over a few hrs. or a day
Temp>39.4 C (103)F
Shaking chills
N/V diarrhea
Sxs of cystitis may or may not
Tachycardia
Flank pain
Generalized muscle tenderness
Marked tenderness on deep pressure on CVA or on
deep abd. Palpation
Significant leukocytosis
Pyuria with leukocyte casts
Bacteria on gram stains of unspun
urine
Hematuria in acute phase of disease
Elderly: no classic sxs., urinary
incontinence (new onset), decreased
appetite, confusion, lethargy
Children: not clear, low grade fever,
irritable, decreased appetite, n/v,
diaper urine smells, no s/s of UTI
Older Children: abd. Pain,
frequency, flank pain,
dysuria, difficulty controlling
urine.
Severe PN-fever subsides
more slowly and may not
disappear for several days.
Even after appropriate
antibiotic tx.
Medical Management
A. Relieve obstruction prn
(may be contributing to the
infection)
B. C & S--> antibiotics/long
term
C. Check Creatinine, CBC
Nursing Management
may treat at home!
A. patient teaching
-continue antibiotics
- 3 liters fluid/day
- check urine output
- prevent infections
- call MD
AGN
Inflammatory reaction in
the glomeruli
Etiology: streptococcal
infection (2-3 wks after)
Pathophysiology
Antigen-antibody reaction
with glomerular tissue.
Inflammatory response--->
increased porosity &
decreased filtration--->
kidney congested, swollen
Clinical Manifestations
HA, malaise, edema, flank
pain, HTN,
CVA tenderness, SOB
Diagnostic Evaluation
Proteinuria, hematuria,
increased SG, edema,
HTN, decreased UO,
increased BUN & Cr.
Medical TX
Protect kidney + treat CX
promptly---ABX, BR,
dec.protein diet & Na diet,
anti-HTN, fluids, diuretics
Nephrotic Syndrome
Proteinuria, Hypoalbuminemia,
edema, hypercholesterolemia
Etiology
Conditions that manage glomerular
capillary membrane--- chronic GMN,
DM, SLE, pericarditis, allergic
reaction, CHF, pregnancy
Pathophysiology
Change in glom. Base membrane,
inc. porosity & loss of proteins--->
dec. albumin---> dec. serum
osmotic
pressure-->edema& dec. plasma
Vol.
---aldosterone--NA & H2O
retention--->!
Clinical Manifestations
Edema, proteinuria, dec. albumin,
inc. lipidemia, UO inc/dec-->
renal failure. Dec. appetite, fatigue
Medical Management
Dec. albuminemia, control
edema,
promote general health--Steroids, Diet--->
protein normal or inc, inc.
calories
Edema---dec. NA, diuretics,
check K+RUA, renal labs.
Nursing Management
Activity---bed rest--->ambulate!
Fluid management->assess/overload
, diet, bp
Patient education--> avoid infection,
fatigue, f/u medical care
Sx renal fail---MD
Nursing Management
Nutrition Na & protein control. Small
frequent feedings
Medication--- steroids, diuretics
Checks for SEs, resp. assess
patient teaching---meds, nutrition,
self assessment/fluids call MD-inc. edema, DOE, fatigue, HA,
infection
Kidney