N254N254

Renal Nursing CareRenal Nursing Care

Mary Moon, RNC, FNPMary Moon, RNC, FNP

Fall 2009Fall 2009

Renal CirculationRenal Circulation

Bowman’s CapsuleBowman’s Capsule

DiffusionDiffusionSmall molecules make easily movement by diffusion in a cell

limited by the cell’s semi permeable membrane

In liquid: Equally sweet

In air: Equally smell

Coffee

Sugar

Perfume

Room

Ex. RBCEx. RBC

Isotonic=In Equilibrium

Solutes: materials-- sugar, salt.

Solvent: Liquid material that dissolve--waterSolution: A mixture of two.

Tonicity: A state of amount of dissolved material in them.

O.9% NaCl

99.1% H20

0.9% Plasma NaCl

99.9% H20

Tonicity: By NaClTonicity: By NaCl

Osmosis:From: 0.9% NaCl

99.1% H20To:

3% NaCl

97% H20

Osmosis: [H20] [H20]

99.1 H20

0.9 NaCl

0% NaCl

100% H20

Hyper tonic

Hypo tonic

So, H20 will move into RBC. So., RBC will rupture

OsmosisOsmosis

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.

KidneyKidney

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% Brain: 14%Heart: 4%

Skeletal: 15% Skin: 6% Bone: 6%

Miscellaneous: 7%

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.FA.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 RenalPre Renal

Causes---> Consists of factors outside the kidneys that impair renal blood flow and lead to decreased glomerular perfusion

Problem corrected --> no ARF

PrerenalPrerenal

55-70%55-70%

Intravascular volume depletion, decreased CO, Intravascular volume depletion, decreased CO, vascular failure secondary to vasodilation or vascular failure secondary to vasodilation or obstruction---HTN, MI, severe dehydration, & obstruction---HTN, MI, severe dehydration, & shock ( not enough volume circulating).shock ( not enough volume circulating).

Reversible—can be corrected by establishing Reversible—can be corrected by establishing renal perfusion & preventing necrotic renal renal perfusion & preventing necrotic renal damage by fluid challengedamage by fluid challenge

Irreversible ischemiaIrreversible ischemia

Intra RenalIntra Renal

Conditions of actual damage to the renal tissue leading to malfunctioning of nephrons---> APN may lead ARF

Ex) acute tubular necrosis-

renal ischemia

Nephrotoxic drugs

Glomerulonephritis

IntrarenalIntrarenal

25-40%25-40%Kidney itself damaged to the kidney tissues and Kidney itself damaged to the kidney tissues and structures & includes tubular necrosis, structures & includes tubular necrosis, nephrotoxicity & alterations in renal blood flownephrotoxicity & alterations in renal blood flowInjuries @kidney glomeruli or tubules—90% due Injuries @kidney glomeruli or tubules—90% due to ATN--- glomerulonephrits, toxins, trauma, to ATN--- glomerulonephrits, toxins, trauma, crushing injuries, surgery, sepsis, CV collapse, crushing injuries, surgery, sepsis, CV collapse, MOF, ABX like aminoglycosides, street drugs, MOF, ABX like aminoglycosides, street drugs, chemo, nephrotoxic drugschemo, nephrotoxic drugsDon’t get confused w/ prerenal caused by blood Don’t get confused w/ prerenal caused by blood volume—dehydration & hypovolemiavolume—dehydration & hypovolemia

Post RenalPost 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.

PostrenalPostrenal

5%5%

Obstruction of urine between the Obstruction of urine between the kidney and the urethral meatuskidney and the urethral meatus

Calculi BPH Tumors stricturesCalculi BPH Tumors strictures

B/C the obstruction, urine backflowsB/C the obstruction, urine backflows

PreventionPrevention

A. High Risk

Hospital Pt. --> Massive trauma, major surgical procedure, extensive burns, sepsis.

B. Industrial chemicals and nephrotoxic drugs.

A.R.F PhasesA.R.F PhasesA. Onset phaseA. 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 PhaseA. Onset Phase

Initial injury to the kidneyInitial injury to the kidney

ReversibleReversible

Preventable with early interventionPreventable with early intervention

UO:20% of normalUO:20% of normal

Unable to regulate electrolytesUnable 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

and the adequate concentrating ability of tubules.

Capillary

urea H20

H20 H20 H20 H20H20 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 PhaseDiuretic Phase

Electrolytes are lost—deficit in Electrolytes are lost—deficit in concentrating ability of tubules and concentrating ability of tubules and osmotic diuretic effect of increased osmotic diuretic effect of increased BUN, slowly increased excretion of BUN, slowly increased excretion of metabolic wastes, hypovolemia, loss metabolic wastes, hypovolemia, loss of Na, K, increased BUN initially then of Na, K, increased BUN initially then gradually return to baselinegradually return to baseline

Diuretic PhaseDiuretic Phase

S/S: postural hypotension, tachycardia, S/S: postural hypotension, tachycardia, improving mental alertness and improving mental alertness and activity, weight loss, thirsty, dry activity, weight loss, thirsty, dry mucous membrane, decreased skin mucous membrane, decreased skin turgorturgor

K replacement may requireK 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 PhaseRecovery Phase

Increased GFRIncreased concentrating ability.Urine SG -- 1.003-1.030Urine osmolarity:Normal 300-1300Mortality Rate: 30% to 60% Most common cause of death secondary

to infection

Prevention of ARFPrevention 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 GoalsTreatment 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.

CRFCRF

CRFCRF

Slow, progressive, irreversible damageSlow, progressive, irreversible damage4 stages4 stagesDiminished Renal Reserve ---50% of Diminished Renal Reserve ---50% of

nephrones are lost, asymptomatic, no S/Snephrones are lost, asymptomatic, no S/SRenal Insufficiency---75% nephrones lost, Renal Insufficiency---75% nephrones lost,

azotemia, anemia, polyuria, nocturiaazotemia, anemia, polyuria, nocturiaRenal Failure---pt needs temporary or Renal Failure---pt needs temporary or

permanent dialysispermanent dialysisEnd Stage Renal DiseaseEnd Stage Renal Disease

CRFCRF

An irreversible loss of nephrons. A symptomatic until 70-90% 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 CRFEtiology 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 TreatmentMedical 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

AntiHTN: triamiterene spironolactone, amiloride

* 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 a-acidosis

Nutrition in Renal DiseaseNutrition in Renal Disease

Sodium: major ECF Caution, important in acid-base 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 (OS-call, 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 ConsiderationGeriatric 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.

HemodialysisHemodialysis

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 AccessAV Access

AV Shunt: Temporary while internal graft is healing Machine

Artery

VeinRinse

Fistulas:Cephalic/radial Artery

Basilic vein

Thigh or forearm

Grafts (looped graft)

Bovin--> relatively resistant to infectious organism.

Antecubital vein

Brachial arteryLooped graft

NSG: 14-16 G needle A thrill/bruit can be felt by palpating

***** NO VENIPUNCTURE, BP ON THE AFFECTED ARM*****

NSG ManagementNSG 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 ---> outflow

15-30 min. 4 hr/d 15-30 min.

10 hr/n

* continuous 24 times/day

* at night 8 hrs cycler machine

TransplantationTransplantation

A living or cadaveric donor

the life expectancy for patients on dialysis is 6-7 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 BleedingTo 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.

DefinitionDefinition

Infection of the kidney and renal pelvis.

Every PN is secondary

APNAPN

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.

CPNCPN

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.

PathogensPathogens

Gram-neg Bacilli: Escheria coli, proteus, Pseudomonas, Enterobacter, kebsiella, Serratia, and Citrobacter species.

Gram-pos cocci: Staphylo. S Strepto. A

Ascending InfectionAscending 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 ManifestationsClinical Manifestations

Rapidly over a few hrs. or a dayRapidly over a few hrs. or a day

Temp>39.4 C (103)FTemp>39.4 C (103)F

Shaking chillsShaking chills

N/V diarrheaN/V diarrhea

Sxs of cystitis may or may notSxs of cystitis may or may not

TachycardiaTachycardia

Flank painFlank pain

Generalized muscle tendernessGeneralized muscle tenderness

Marked tenderness on deep pressure on CVA or on Marked tenderness on deep pressure on CVA or on deep abd. Palpationdeep abd. Palpation

Significant leukocytosisSignificant leukocytosis

Pyuria with leukocyte castsPyuria with leukocyte casts

Bacteria on gram stains of unspun Bacteria on gram stains of unspun urineurine

Hematuria in acute phase of diseaseHematuria in acute phase of disease

Elderly: no classic sxs., urinary Elderly: no classic sxs., urinary incontinence (new onset), decreased incontinence (new onset), decreased appetite, confusion, lethargyappetite, confusion, lethargy

Children: not clear, low grade fever, Children: not clear, low grade fever, irritable, decreasedirritable, decreased appetite, n/v, appetite, n/v, diaper urine smells, no s/s of UTIdiaper urine smells, no s/s of UTI

Older Children: abd. Pain, Older Children: abd. Pain, frequency, flank pain, frequency, flank pain, dysuria, difficulty controlling dysuria, difficulty controlling urine.urine.Severe PN-fever subsides Severe PN-fever subsides more slowly and may not more slowly and may not disappear for several days. disappear for several days. Even after appropriate Even after appropriate antibiotic tx. antibiotic tx.

Medical ManagementMedical 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 glomeruliEtiology: 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 osmoticpressure-->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, bpPatient education--> avoid infection, fatigue, f/u medical care Sx renal fail---MD

Nursing Management

Nutrition Na & protein control. Small frequent feedings Medication--- steroids, diureticsChecks for SEs, resp. assess patient teaching---meds, nutrition,self assessment/fluids call MD--inc. edema, DOE, fatigue, HA, infection

KidneyKidney