Thelan’s Critical Care Nursing

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Slide 0 Copyright © 2010 Elsevier, Inc. All rights reserved.

Renal Disorders

Eileen Lischer MA, BSN, RN, CNN

Acute Dialysis


Objectives

• Briefly review Renal Anatomy and physiology • Describe the etiology and pathophysiology of acute kidney

injury. • Identify the clinical manifestations of acute kidney injury. • Explain treatment of acute kidney injury. • Discuss the nursing management of the patient with acute

kidney injury. • Describe 5 stages of Chronic Kidney Disease • Identify the differences between hemodialysis, peritoneal

dialysis, and continuous renal replacement therapy. • Describe the plan of care for the renal patient


Structures of the Kidney

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Renal Anatomy • Internally

– Cortex • Outer layer • Contains glomeruli,

proximal tubules, cortical portions of loops of Henle, distal tubules, and cortical collecting ducts

– Medulla • Inner layer • Made up of pyramids,

which contain medullary portions of the loops of Henle, vasa recta, and medullary portions of the collecting ducts


Nephron • Microscopic structure

and function – Nephron: functional units

of the kidney • 1.2 million nephrons per

kidney


Functions of the kidneys • Makes urine

• Manage fluid volume

• Removal of toxic wastes – BUN

– Creatinine

• Acid- base, electrolyte regulation

• Blood pressure control

• Secretion of hormones – Erthyropoietin

– Conversion of Vitamin D2 to active for Vitamin D3

• Blood Pressure and RAAS – Blood pressure regulation by

maintaining circulating blood volume

• Renin – Enters lumen of afferent arteriole;

released into general circulation from juxtaglomerular cells

• Angiotensin II Vasoconstrictor – Stimulates release of aldosterone

• Aldosterone – Released by adrenal cortex

– Expands intravascular volume by increasing sodium and water reabsorption

• System

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Questions?


Acute Kidney Injury (AKI) “… a potentially reversible condition that results in

acute suppression of renal function.”

Result from two kinds of insults:

1. Ischemia

2. Necrotizing effects of medications and poisons.

AKI in critically ill patients is associated with mortality rates of 38%-80%

Incidence

• 1% of acute hospital admissions

• Complicates 7% of inpatient episodes

• Greater incidence in older patients and in those with preexisting chronic kidney disease


RIFLE classification of AKI

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Mortality


Stages of AKIN Stage Serum Creatinine Urine Output

Stage 1 Increase in serum creatinine > 0.3mg/dl

(26.2mmol/L) or increase to > 150-199%

(1.5-1.9 fold) from baseline

Increase in CR X 1.5

or<0.5mL/kg/h for > 6h

Stage2 Increase in serum creatinine to 200-299%

( > 2-2.9 fold) from baseline

<0.5mL/kg/h for > 12h

Stage3 Increase in serum creatinine 300% (> 3

fold) from baseline or an absolute serum

creatinine > 4.0mg/dl (354mmol/L) with

and acute rise of at least 0.5mg/dl

(44mmol/L) or initiation of RRT.

<0.3mL/kg/h for > 24h

OR

anuria for >12h


Etiology of Acute Kidney Injury

• Prerenal Any condition that decreases blood flow, blood pressure, or renal perfusion

• Intrarenal Any condition that produces an ischemic or toxic insult directly at the site of the nephron

• Postrenal Any obstruction that hinders the flow of urine from beyond the kidney through the remainder of the urinary tract

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PRE RENAL AKI

• Pre renal AKI-ischemia

– Renal hypo-perfusion occurs

– Related to low cardiac output, bleeding, vasodilation, thrombosis

– Oliguria is a classic finding

– Monitor urine output closely


PRE RENAL Causes • Volume depletion

– GI, skin, over use diuretics, hemorrhage

– Third spacing- burns, nephrotic syndrome, ascites, acute pancreatitis

• Cardiac output – CHF with decreased

cardiac output

– Myocardial infarction

– Cardiac failure

– Cardiac tamponade

• Vasodilatation

– Shock

– Sepsis, Anaphylaxis

– Extreme acidosis

– Overtreatment with antihypertensives

• Renal vascular obstruction

– Renal artery thrombosis

– Renal artery stenosis

– Small vessel and glomerular damage as in diabetes and atherosclerosis

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PRE RENAL Assessment • Signs and symptoms of volume depletion

– Fever, V/N/D – Wounds/burns – Poor skin turgor

• Signs and symptoms of volume overload

– Distended neck veins – Peripheral and pulmonary edema – Ascites

• Low urinary output- less than 0.5mg/kg/hr

– anuria rare


PRE RENAL Treatment • Treat underlying cause quickly!!

– Autoregulation by kidney to preserve renal blood flow. At systolic B/P of <70 maximal afferent dilation has occurred.

• Blood Pressure <70 stimulates intense sympathetic and renin angiotensin activity is counter-product to autoregulation.

– Pre renal azotemia frequently precedes or contributes to the development of acute intra renal injury.

• ***BUN:CR ratio >15:1

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Pre RENAL Treatment • Usually give 250-500mls fluid challenge over 30

min.

• TOO MUCH FLUID IS TOXIC

• In Cardiac failure-inotrops+/ vasodilating agents, Na restriction.

• Surgery for reno-vascular correction


INTRA RENAL AKI Ischemic or toxic insult directed

at the of nephron

• Ischemia related to prolonged hypotension or low cardiac output

• Toxic insult is related to substances that damage the renal tubular endothelium (antimicrobials, contrast dye, ethylene glycol poisoning)

• Endogenous toxins-Rhabdomyolysis, post streptococcol infections, tumor lysis syndrome, Multiple myeloma

• Auto immune diseases-Lupus, Goodpastures, TTP, Sickle cell


INTRA RENAL • When internal filtering structures

are affected, this is known as acute tubular necrosis (ATN) 76% of critically ill patients

• Damage prevents normal concentration of urine, filtration of wastes and regulation of acid base. Electrolyte and water balance.

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Ischemic ATN

• Ischemia most common cause!

– Medulla (tubules)is severely compromised with

hypoperfusion. • MAP<50-70 for 25 mins= mild damage-reversible

• MAP<50-70 for 40-60 mins=severe damage- may recover in 2-3 weeks

• MAP <50-70 for 60-90 mins= permanent damage

• Disruption of basement membrane

• Patchy necrosis


Nephrotoxic ATN

• Damage occurs over a matter of days to weeks following exposure

• Nephrotoxic agents 30-40% of ATN cases

• Damages the tubular cells

• UR concentration- concentrates toxic substances and sustains repeated exposure.

• Lesions uniform and localized to proximal and distal tubules


Treatment of Intra renal AKI

• Treatment specific to the cause

– Volume replacement

– Removal of toxic substance

– Support B/P -Inotrops

– Support immune system- steroids, anti-neoplasctic medications

– Supportive therapy –dialysis, Apheresis

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Acute Kidney Injury (AKI)


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AKI-Cast Nephropathy


POST RENAL AKI

• Caused by any obstruction that impedes urine flow beyond kidney- not common

– Enlarge prostate (frequency, urgency, post void dribble, difficulty initiating stream, decrease force of stream.

– Stones

– Foley obstruction- check patentcy

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SUMMARY AKI


Assessment and Diagnosis AKI

• Laboratory assessment

– Acidosis

– BUN- azotemia

– Serum creatinine

– Creatinine clearance

– Fractional excretion of sodium


Assessment and Diagnosis (continued)

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At-Risk Disease States and Acute Kidney Injury

• Underlying chronic kidney disease • Risk of AKI

– Older age – Diabetes – Hypertension – Heart failure – Respiratory failure – Sepsis – Trauma – Contrast-induced nephrotoxic injury – Ethylene glycol ingestion


Questions?


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Chronic Kidney Disease

CKD is the irreversible loss of renal function that affects all organ systems

Normal Creatinine clearance?

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CKD classification /Creatinine Clearance

• Normal 100-125ml/min • CKD 1 > 90 mls/min with kidney damage • CKD 2 60-89mls/min with kidney damage • CKD 3 30-59 mls/min • CKD 4 15-29 mls/min • CKD 5 <15 or on dialysis ESRD (end stage renal

disease) – Dialysis initiated when patient becomes symptomatic-

confusion, lack of appetite, HA, HTN, respiratory distress, Acid base imbalances


Slide 34

Hemodialysis: Vascular Access

Vascular access for hemodialysis Acute- direct access to vein from skin

IJ vein catheters Femoral vein catheters-Highest risk for infection Subclavian vein-least preferred d/t probability

of stenosis.

Chronic AV fistula- preferred AV grafts Tunneled catheter- tunneled under skin before

entering the vein.


Slide 35

Fistula vs Graft

FIGURE 20-4 Methods of vascular access for hemodialysis. A, Arteriovenous fistula between vein and artery. B, Internal synthetic graft corrects artery and vein.

Created from

patients

natural veins

Synthetic graft

material used

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Vascular access management Vas Caths

• Hemodialysis or ICU trained nurses only to access any dialysis access.

• Vas caths- dressing with biopatch. If needs changing notify dialysis staff.

• Femoral lines- do not elevate head of bed >45 degrees.

• Check q shift to ensure they have not migrated out of vessel. No traction to catheter.


Vascular management Fistulas/grafts

• Check for bruit/thrill q shift and record • No B/P or lab draws from access arm • NO PICCS • Check distal circulation • Observe for S/S infection • Steal syndrome • Avoid constriction of flow- no watch or carrying

purse on that arm. • Post dialysis – check for bleeding- apply direct

pressure as to not occlude flow for 10 minutes.


Renal Replacement Therapy

• The circuit- fluid pathways

• Hemodialyzer

• How it works

– Diffusion

– Ultrafiltration- patient fluid removal

– Convection

– Anti-coagulation

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Slide 39

RRT circuit

FIGURE 20-2 Components of a hemodialysis system.


Hemodialyzer


Renal replacement therapy

• Diffusion

• Ultrafiltration- patient fluid removal

• Hemodialyzer

• Flow paths

– Blood

– Dialysate

Anticoagulation

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Intermittent vs Continuous RRT

– Choice of blood purification method is a medical decision-

– Early initiation and adequate dose affects outcomes

– 24hr of CRRT =3.5 hours of IHD


Renal Replacement Therapy


Continuous Renal Replacement Therapy CRRT

• 24 hour replacement therapy – SCUF

– CVVH

– CVVHD

– CVVHDF

Same amount of clearance as our 3.5 hr treatment

Used for patient who are hemo-dynamically unstable or cannot tolerate rapid fluid electrolyte shifts. Facilitates nutritional support.

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Complications of RRT Machine related

– Air embolism

– Filter clotting

– Poor ultra-filtration

– Blood leaks

– Broken filter-highly unlikely

– Recirculation/disconnection

– Access failure

– Catheter dislodgment


Patient complications RRT

– Code/emergency situation

– Dehydration

– Hypotension

– Electrolyte imbalances-especially hypokalemia

– Acid-base imbalances

– Blood loss/hemorrhage

– Hypothermia

– Infection


Peritoneal Dialysis

• Indications – Can be used as an emergent treatment – Can be used in acute or chronic kidney disease – Low frequency of use- 8% of dialysis population

• Description – Access is via a catheter placed in peritoneum – Using the peritoneal lining as the semipermeable

exchange membrane, excess fluid and solutes cross peritoneal membrane to clear solutes and fluid.

– Essentially a lavage- three cycles-fill-dwell-drain

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Peritoneal Dialysis (continued)


Peritoneal Dialysis (continued)


Peritoneal Dialysis

• Advantages of PD – No blood loss – Liberalize diet – Portability – Independence Disadvantages Requires a partner/specialized training Peritonitis Works better with renal reserve High dextrose solutions- scar peritoneal membrane Peritoneal overfill and distention

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Slide 51

Peritoneal Dialysis—Complications

Complications

Low potassium levels

Infection-Hi WBC, temperature, malaise, abdominal pain, exudate from catheter site

Failure to drain- constipation

Loss of exchange membrane


Care plan for patients with Renal impairment

• I. Fluid Management

• II. Electrolyte management

• III. Acid base regulations

• IV. CKD considerations – Anemia of renal disease

– Hypertension/Cardiac

– Bone mineral metabolism

– GI complications

– Medications


Care of dialysis patient

• V. Infection

• VI. Access management

• VII Psycho-social issues

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Fluid Balance – Absolutely critical data- Daily Intake and output and daily

weight. ALL MODALITIES

– Daily weight • 1 kg of weight gain over a 24-hour period = 1000 mL of fluid retention

– S/S of pulmonary edema, dependent edema, cough when supine

– Retained water leads to hypertension, triggers kidney to release renin to close afferent arteriole and protect pressure in glomerulus leading to worsening hypertension.

– Dialysis can take off 2 liters/hr

– Hemodynamic monitoring • Central venous pressure, pulmonary artery occlusion pressure,

cardiac output, and cardiac index- None of these are good indicators of patient fluid volume status


Nursing Actions Rationale

Measure all sources of I&O. Weigh routinely. Aids in evaluating fluid status, especially when compared with weight. Weight gain between treatments should not exceed 0.5 kg/day.

Monitor BP, pulse. Hypertension and tachycardia between hemodialysis runs may result from fluid overload and/or HF.

Note presence of peripheral/sacral edema, respiratory rales, dyspnea, orthopnea, distended neck veins, ECG changes indicative of ventricular hypertrophy.

Fluid volume excess due to inefficient dialysis or repeated hypervolemia between dialysis treatments may cause/exacerbate HF, as indicated by signs/symptoms of respiratory and/or systemic venous congestion.

Note changes in mentation. Fluid overload/hypervolemia may potentiate cerebral edema (disequilibrium syndrome).

Monitor serum sodium levels. Restrict sodium intake as indicated.

High sodium levels are associated with fluid overload, edema, hypertension, and cardiac complications.

Restrict PO/IV fluid intake as indicated, spacing allowed fluids throughout a 24-hr period.

The intermittent nature of hemodialysis results in fluid retention/overload between procedures and may require fluid restriction. Spacing fluids helps reduce thirst.


Electrolyte Imbalances

• Potassium – Hyperkalemia may lead to lethal cardiac

dysarrhythmias-Sr K >6

– Treatment may include • Diuretics (if producing urine)

• Intravenous insulin and glucose

• Kayexalate

• Fludrocortisone Florinef- (inc NA retention wastes K)

– Hypokalemia- post dialysis • Do not draw electrolytes til 2 hours post dialysis

• PD liberalize diet

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Electrolyte Imbalance (continued)

• Sodium – Usually hypernatremic with thirst drive

• Restrict Na to a point and water

• Slow Na correction via dialysis no more than 8-10mEq/24 hours

– Dilutional hyponatremia

– Correct with fluid restriction or dialysis

Medications

Tolvaptan


Electrolytes-Bone Mineral

• Calcium and phosphorus – Hypocalcemia

– Hyperphosphatemia

• Calcium replacement – Calcium supplements, vitamin D, calcitrol-active Vit D

• Dietary-phosphorus binding drugs – Limit dietary intake-sources of PO4??

– Give calcium salts or phosphate binders

– Must be given with food!!!!!


Ca/Phos Bone Mineral Disease FGF 23

production

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BMD

• FGF 23 promotes the excretion of PO4

• Elevated in CKD 3

• Chronic disruption in CA/Phos regulation leads to hyperparthyroidism.

• Leads to calcification of vessels, calciphylaxis

• Labs- hi phos, normal or low Ca and Hi PTH


Acid Base Balance

• Protein metabolites= Cr and BUN

• Acid production w/o ability to remove via Kidney – Increased respiratory rate

– Metallic taste in mouth

– In very high levels-uremic frost

– Treat with more dialysis and sodium bicarb

– Reduce hi BUN slowly to prevent disequilibrium syndrome/seizures


CHRONIC KIDNEY DISEASE-CKD

• Anemia- role of kidney

– Role of ESAs-erthyropoieten stimulating agents

• Procrit

• Epogen

• Aranesp

• Omontys

– Iron deficiencies

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Cardiac

• Volume overload leads to distended cardiac muscle, leads to edema and CHF.

• Electrolyte imbalances interfere with conduction • Elevated BUN/CR can lead to pericarditis • Anemia compromises cardiac oxygenation • Heart stretch receptors trigger Kidney to waste

water and NA (aldosterone release) • Bone mineral disease of CKD and heart • CKD 3 have cardiac impairment • Monday/Tuesday MIs


GI involvement

• Chronic acid state leads to GI ulcers and bleeds.

• Increased BUN interferes with platelet cohesiveness increasing bleeding risk

• Decreased gastric mobility leading to constipation. (binders)

• Dietary fluid restrictions dry out stool.

• PD patients- must have BM daily or interfers with fluid drainage.


Cerebral

• Blood brain barrier

• Clearance from vascular side faster than brain

• Sets up disequilibrium

– HA

– Seizures

– Confusion

– Lethargy

– Time patient teaching to non dialysis days

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Dietary restrictions

• Protein- limit 30-45 gms per day (0.6-0.75g/kg)

– Reduce production of acid wastes-BUN/CR

Sodium (2 Gms) and Water(1 Liter)- to prevent fluid overload, HTN, and cerebral edema

Potassium 1mEq/kg/dy- to prevent cardiac events

Phosphorous- to control bone mineral disease 800-1000mg

Calories-30-35 kcals/kg If diabetic- limits carbohydrates

If cardiac- limit fats


Dietary helps

• Such hard sour candy to stimulate parotids to secrete saliva for thirst

• Rinse and spit vs swallow • Ice chips vs water-count in I and O • Biotene rinse • Boil food and discard water midway to remove electrolytes-

ie potato, apple sauce vs apple • Read food labels- sports drinks, and flavored waters high in

Phosphorous.- TAKE BINDERS WITH FOOD • Eat good sources of protein-egg, chicken- Tend to have low

albumin levels from protein restriction- predictor or poorer outcomes.


Pharmacologic Management

– Eliminate any nephrotoxic medications

– Diuretics- if renal reserve

– Antihypertensives-target B/P 130/80 • ACE-Angiotension Converting Enzyme blockers

• ARBS-Angiotension Receptor Blockers

• Calcium Channel blockers

• Beta blockers

• Adrenergic blockers

• Do not hold B/P meds prior to dialysis unless ordered to do so.

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Pharmacologic management Phosphate binders

• Phosphate binders-include Calcium products, aluminum based products and PO4 polymer binding agents

• Calcium based=Phoslo, Os-Cal, Tums- can result in Hypercalcemia

• Aluminum based=Amphojel Alternagel, Basajel-Not used too much anymore

• Polymers=Sevelamer, (renalgel)- • Lanthanum carbonate=Fosrenal • MUST BE GIVEN WITH FOOD IN THE STOMACH


Bone Mineral

• Calcimimetics- treat secondary hyperparathyroidism and hypercalcemia in parathyroid tumors.

• Cinacalcet (Sensipar)


Pharmacologic management Vitamins

• Water soluble vitamin replacement

– Without vitamin C- Nephrocaps

• GIVE AFTER HEMODIALYSIS

– Vitamin D- (hypocalcemia and hyperparathyroidism)

• Act like Vit D or enhance Ca absorption providing neg feedback to parathyroid gland

– Cacitriol (calcijex, Rocaltrol)

– Doxercalciferol (Hecotorol)

– Paricalciol (Zemplar)

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Pharmacologic management

• Stool softeners

• Prokinetics-Reglan

• Proton pump inhibitors

• Histamine (H1)blockers- itching

• Histamine (H2) blocker- reduce gastric irritation

• Glucocorticoids-treat underlying K disease

• Insulin for diabetics- kidney metabolizes insulin so insulin needs may decrease with loss of function.


PolyPhamarcy

• Multiple medications

• Multiple schedules

• Confusion of renal disease

• Elderly

• Is it really poor compliance?


Psycho-social

• Quality of life

• Dependence on machine

• Limited freedoms of choice in food selections

• Isolation

• Anemia

• Multiple MDs to manage

• Depression

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Slide 75

Kidney Transplant

Transplant procedure

Ureter, renal vein, renal artery, and kidney are dissected

Living donor surgery

Cadaver donor surgery

Can be maintained 48 to 72 hours before it must be transplanted

Extended criteria donors

Lollipop transplants


Slide 76

Recipient Surgery

FIGURE 20-8 Placement of the kidney graft into the iliac fossa. A, The incision depicted is for the right side of the abdomen, representing kidney graft implantation in the right iliac fossa. B, The iliac vessels are exposed. (Modified from Smith SL: AACN tissue and organ transplantation: implications for professional nursing practice, St Louis, 1990, Mosby.)


Slide 77

Medical and Nursing Management Post-Transplant

Close monitoring of patient Fluid status-

Urine Output daily weights

Electrolyte balance Bleeding risk Immunosuppressive therapy-hyperglycemia Infection risk

Viral Yeast

Rejection

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Questions?

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Thelan’s Critical Care Nursing