(This is from the Critical Care Nurse's Instructor Outline, Renal Module, from SBCH, no representations are made for accuracy or errors/omissions, use your clinical judgement 3/31/02.)                        return to sbneph.com

CARING FOR THE PATIENT WITH ACUTE RENAL FAILURE

Lecture Time: 180 minutes Objectives

1. Compare and contrast the etiology, pathophysiology, and treatment of prerenal, intrarenal, and postrenal failure.

2. Describe the three phases of intrarenal failure.

3. List four major patient problems in acute renal failure and describe the related appropriate plan of care for each.

4. Describe the modes of renal replacement and indications for each mode.

5. Discuss the impact of chronic renal failure on other body systems.

6. Describe potential alterations to a plan of care for the patient with chronic renal failure.

Content Outline

I. Introduction

A. Definition: Acute renal failure is a clinical syndrome characterized by sudden deterioration in renal function resulting in a decrease in glomerular filtration rate (GFR). (Key is abrupt onset and reversibility: decrease in GFR results in failure to excrete end products of cellular metabolism and to regulate fluid, electrolytes, and acid base balance: represents major clinical challenge. When critically ill experience this additional insult disrupting normal homeostasis, overall adaptive capacity to withstand alterations in other major systems is severely compromised: can result in 60-90% mortality rate)

B. Determinants of renal function (Quick review of the determinants of renal function: impact on any of these can result in acute renal failure)

Slide #2-1 (Processes of the kidney) (demonstrate the processes of the kidney)

1. Renal perfusion (determines filtration)

2. Tubular function (determines secretion and absorption)

3. Post renal structures (responsible for excretion)

II. Types of Failure (Type of renal failure determined by location of cause)

A. Prerenal (Most common type seen in acute care setting)

1. Pathophysiology (Diminished renal perfusion)

a. Decreased renal blood flow leads to decreased renal perfusion resulting in decreased GFR (Decreased renal perfusion causes decrease in renal artery pressure: results in decreased pressure in afferent arteriole: when pressure falls below 70 mm/Hg the autoregulatory response is lost: afferent arteriole constricts, rather than dilating to increase renal perfusion, in attempt to shunt blood to heart and brain: result is decreased GFR)

Slide #2-2 (Renal blood flow and GFR)

b. No damage to kidneys

c. Unable to filter effectively due to hemodynamic compromise

d. If process not reversed result may be irreversible ischemia (Result is intrarenal failure)

2. Etiology (Anything that diminishes renal blood flow)

a. Decreased intravascular volume

1) internal fluid shifts (Burns, peritonitis, pancreatitis, ileus, third spacing)

2) external fluid losses (Hemorrhage, vomiting, diarrhea, diuresis)

b. Cardiovascular failure

1) decreased cardiac output (CHF, MMl, cardiogenic shock, dysrhythmias, pulmonary embolism)

2) increased intravascular capacity (Sepsis, anaphylaxis, vasodilating drugs)

3. Clinical Presentation (Key to understanding cause is thorough assessment and history)

a. Oliguria (< 400 cc/24 hours)

b. Fluid deficit: hypotension, tachycardia, orthostatic, CVP < 5, dry mucous membranes, flat jugular veins, lethargy (Progressing to coma)

c. Cardiac failure: hypotension, tachycardia, peripheral and systemic edema, clammy skin, elevated pulmonary artery diastolic pressure, low cardiac output, pulmonary artery wedge pressure > 18 mmHg

4. Laboratory Findings (Tubular function normal so findings are result of diminished GFR. Try to understand why lab values are affected by thinking through what is happening in kidneys rather than memorizing)

Slide #2-3 (Laboratory Findings in Renal Failure)

a. Urine Na⁺ < 10-15 mEq (Tubules have maintained adequate reabsorptive capacity; they reabsorb Na⁺ and H2O in an attempt to increase effective arterial blood volume: thereby stabilize BP and maintain adequate perfusion to heart and brain. Value is not reliable in presence of metabolic alkalosis or osmotic and loop diuretics - all will increase urine Na⁺. If patient is to get a diuretic and urine Na⁺, obtain urine first, if possible)

b. FENa < 1 % (fractional excretion of Na⁺ ) (One of best tests for distinguishing type of failure: it is ratio between amount filtered and amount excreted is indicative of tubular function)

c. Specific gravity (SG) > 1.015 (Because of attempt to hold onto H2O, urine is concentrated)

d. BUN elevated (Best indicator of renal perfusion)

e. Serum creatinine slightly elevated (Best indicator of tubular function, increases slowly because of decreased filtration rate)

f. BUN/Creatinine ratio > 20:1 (Problem is perfusion and not function: BUN will rise more quickly than creatinine, can be as high as 40:1)

g. Urine osmolality > 500 mOsm/kg (Represents concentrated urine)

h. Urine sediment normal (Tubules intact so no abnormal sediment should be seen)

5. Management: Goal is to reestablish renal perfusion and prevent necrotic renal damage (Expand intravascular volume or increase cardiac output to increase renal perfusion, thereby increasing GFR and urine output)

a. Restore effective arterial blood volume

1) Fluid challenge (Diagnostic as well as a treatment: start with 500 cc NS and if renal function is normal, kidneys will have ability to respond to increased fluid: monitor closely for fluid overload)

2) Diuretics (Efficacy not conclusive but may prevent progression if given within 24 to 48 hours: may convert oliguric failure to non-oliguric)

a) furosemide (Diminishes Na⁺ reabsorption in proximal tubule and loop of Henle: also nephrotoxic and may enhance nephrotoxicity of other drugs)

b) mannitol (Osmotic diuretic: inhibits Na⁺ reabsorption and increases plasma osmolality: dose 12.5-25 gm: if not effective, don't repeat as will cause fluid overload and intracellular dehydration)

c) ethacrynic acid (Loop diuretic that may potentiate action of other diuretics)

3) volume expanders (Increase intravascular volume and renal perfusion)

4) dopamine (1-2 mcg/kg/min) (Not proven effective but small doses may dilate renal arteries and increase perfusion if not already fully dilated)

b. Improve cardiac output (treat cardiac failure) (Enhance contractility and optimize filling pressures)

c. Decrease intravascular capacity (IV fluids) (Possibly vasopressors depending on cause)

B. Intrarenal (Intrinsic failure) (Actual damage to nephrons, primarily tubules)

1. Pathophysiology (Insult results in either cortical or medullary involvement)

a. Cortical involvement (Not commonly seen in critical care setting)

1) swelling (Proliferation of cells), causing cellular debris and obstruction of glomeruli

2) results in decreased GFR

b. Medullary involvement (Commonly referred to as acute tubular necrosis or ATN, most common type seen in critical care)

1) pathogenesis controversial with different theories (Won't cover those theories: regardless of the cause the following results)

2) initial insult causes vascular swelling and results in self perpetuating ischemia

3) results in damage to glomerular filtration process and decreased GFR

4) initial insult can be ischemic or nephrotoxic

a) ischemic - prolonged decreased renal perfusion affects proximal and distal tubular segments (Destroys cells in the basement membrane that can't regenerate)

b) nephrotoxic - direct chemical effect that affects primarily proximal tubular segments (Effects epithelial cells that can regenerate)

2. Etiology

a. Cortical

1) infections

2) vascular damage

3) immunological processes

b. Medullary

1) ischemic: same causes as prerenal only more extensive and prolonged

2) nephrotoxic

a) antibiotics: aminoglycosides

b) radiographic contrast media

c) pesticides and fungicides

d) pigments: hemoglobin, myoglobin

e) nonsteroidal anti-inflammatory agents

3. Clinical Phases

a. Oliguric

1) obstruction of tubules causing inability to excrete fluids and metabolic wastes (Significant decrease in GFR)

2) lasts about 1 to 2 weeks

b. Diuretic

1) indicates returning tubular function

2) gradual increase in urea excretion and decrease in sodium loss (Mobilization of urea causes osmotic diuresis: interstitial fluid being mobilized: tubules can't reabsorb filtrate and concentrate urine yet)

3) lasts 7 to 14 days (Gradual improvement in renal function)

c. Recovery

1) begins when diuresis stops

2) occurs slowly - can take up to 2 years (May still have mild to moderate residual dysfunction)

4. Clinical Presentation - same as prerenal except patient may be either Oliguric or nonoliguric (Nephrotoxic insult often results in nonoliguric failure: associated with lower mortality rate: fewer problems with fluid and electrolytes. Always consider ATN in patient with hypovolemia especially very young and elderly: they are more sensitive to small transitory fluid changes)

5. Laboratory Findings (Findings are reflective of actual tubular damage)

Continue Slide #2-3 (Laboratory Findings in Renal Failure)

a. Urinary sediment: RBC casts and cellular debris (Reflects damage to tubular structure)

b. SG < 1.010 (Lose ability to concentrate urine)

c. Urine osmolality < 350 mOsm/kg (Reflective of dilute urine)

d. Urine Na⁺ > 30 mEq (First tubular function lost is the ability to hold onto Na+)

e. . FENa > 3 % (Indicative of Na⁺ wasting and increased excretion)

f. BUN > 25 mg/dL

g. Creatinine elevated (Tubules no longer able to reabsorb creatinine: value not as important as change from baseline: doubling in creatinine means loss of 50% of nephrons but value may be in normal range)

h. BUN/Creatinine. ratio < 20:1 (BUN and creatinine now rise at same rate so normal ratio is maintained: with critically ill, creatinine may not rise as high: shown that production of creatinine decreases)

6. Management (Specific management will be discussed with patient care problems: key is prevention: anticipate patients at high risk i.e. advanced age, dehydration, diabetes mellitus, renal insufficiency, proteinuria, and those receiving renal toxic agents)

a. Maintain fluid balance

b. N-acetylcysteine - reduces renal injury

c. Fenoldopam - improves renal circulation

b. Prevent further renal damage

1) prophylactic diuresis (Prior to a potential insult to kidneys [i.e. dye study or other nephrotoxic agents], give Mannitol and fluid to enhance renal flow)

2) adjust dosages and scheduling of medications (As indicated by specific medications)

3) cytoprotective agents (No conclusive data: may block entry of calcium into cell and protect from cell death if given prior to prolonged ischemia)

c. Manage complications

C. Postrenal (Dysfunction in postrenal structures)

1. Pathophysiology

a. Partial or complete obstruction of lower urinary tract causes increased hydrostatic pressure in tract (Glomerular filtration determined by pressures, a change in these results in impact on GFR)

b. Opposes filtration pressure resulting in decreased GFR

2. Etiology

a. Mechanical

1) structural obstruction (In the ureters, bladder, or urethra)

2) renal stones, ureteral stricture, tumors, benign prostatic hypertrophy, blood clots (Anything that blocks passage of urine either partially or completely)

b. Functional

1) neurogenic problems (Mechanical dysfunction of ureters, bladder or urethra)

2) diabetic neuropathy, spinal cord disease, atonic bladder (Most common causes)

3. Clinical Presentation

a. Oliguric or anuric (< 70 - 75 cc/24 hours) (Depends on location and degree of obstruction or neurogenic impairment)

b. Fluid excess (Can result in cardiomegaly, CHF, pulmonary vascular congestion, cerebral edema: assess for signs of fluid overload, e.g. bibasilar crackles, S3, confusion)

4. Laboratory Findings (Result of decreased filtration rate and excretion not impairment with kidney function)

Continue slide #2-3 (Laboratory Findings in Renal Failure)

a. Elevated BUN

b. Elevated Creatinine

c. BUN/Creatinine ratio < 20:1 (Decreased excretion of both)

d. SG variable

e. Urine Na⁺ variable (Usually high normal)

f. FENa > 3%

5. Management - goal is to optimize renal perfusion, and if possible, diuresis.

a. ultrasound to exclude obstruction

b. Removal of obstruction if problem is mechanical

c. Post obstruction diuresis

1) first 48-72 hours danger of fluid deficit - replace hourly urine output

2) monitor electrolytes and acid/base balance

3) if no diuresis, expect renal damage

III. Patient Care Problems (Leading causes of death without renal replacement are hyperkalemia, fluid overload, infection, and major hemorrhage: risk diminished with renal replacement)

A. Oliguric phase: goal is to control fluids, regulate electrolytes, control and promote excretion of metabolic waste products, and reduce tissue catabolism (Complications depend on extent and duration of renal injury, volume of urine produced, and condition of other organs)

1. Alteration in fluid status - fluid excess (Not a problem with nonoliguric failure)

a. Fluid assessment

1) fluid overload (Resulting in pulmonary edema, peripheral edema, and CHF)

2) fluid distribution (Uremic toxins cause increased capillary permeability: retention of Na⁺ and H2O cause increased hydrostatic pressure: both affect fluid distribution)

b. Strict intake and output - remember insensible losses (400­700 cc/24hrs)

c. Daily weights (1 kg gain represents 1 liter of fluid)

d. Careful fluid administration

e. Maintain fluid restriction

f. Diuretics

g. Renal replacement therapies (Will be discussed later)

2. Alteration in electrolyte balance (Resulting from impaired renal excretion - with nonoliguric failure, electrolytes are more readily excreted and easier to manage. Specific management of fluid and electrolyte imbalances will be discussed in the fluid and electrolyte section of this module)

a. Hyperphosphatemia

b. Hypocalcemia (Increased binding of calcium with phosphate ions)

c. Hypermagnesemia

d. Hyponatremia (Clue to fluid overload: do not give Na+)

e. Hyperkalemia (Major cause of death)

Slide #2-4 (ECG changes with hyperkalemia)

1) myocardial dysfunction is major risk (Absolute value not as crucial as rapidity with which K⁺ increased: review ECG changes briefly: < 6.5 have peaking or tenting of T wave; > 6.5 flattening of P, prolonged P-R, widening of QRS; > 8.0 deep S or sine wave, ventricular fibrillation)

2) reduce production/decrease intake (Dying cells release K⁺; control breakdown of body tissues; administer fresh blood, older blood even if not expired has more K⁺ secondary to death of cells; maintain acid-base balance - metabolic acidosis increases serum K)

3) promote excretion (Exchange resin such as Kayexalate)

4) promote movement into cells (Sodium bicarbonate causes H⁺ to move out of cells and K⁺ will move in: glucose with help of insulin will move into cells and take K⁺ with it)

5) antagonize effects on cardiac membrane (Calcium chloride or gluconate blocks effect of K⁺ on cardiac membrane: does not change serum level; another measure to decrease K⁺ needs to be done in conjunction)

3. Potential for infection - common sites: wounds, respiratory and urinary tracts (Uremia causes depression of cellular immune response: change in mucous membranes provide portal of entry for bacteria: fluids in respiratory tract increase risk: recent statistics show 80%^-develop infections: of those 50% result in sepsis or death)

a. Maintain skin integrity

b. Monitor temperature and note trends (Urea is hypothermic agent: any temp is significant)

c. Avoid indwelling catheters and invasive procedures

d. Administer antibiotics (Be aware of route of excretion and need to adjust dosages)

e. Monitor WBC and differential

4. Alteration in acid-base balance

a. Causes

1) renal excretion of H⁺ ions not functioning

2) inability of tubules to reabsorb bicarbonate

3) catabolism and hyperkalemia

b. Balance dependent on lungs ability to compensate

1) maximize respiratory status (Good pulmonary hygiene)

2) prevent atelectasis and maintain maximum lung expansion

c. Replace bicarbonate as needed

d. Monitor ABGs

e. Assess for acidosis

1) mental changes

2) Kussmaul respirations

3) hyperkalemia

4) cardiovascular effects (pH < 7.2) (Decreased cardiac output, decreased BP, arrhythmias)

5. Alteration in nutritional status

a. Primary goal is to reduce protein catabolism

b. Hypermetabolic state

1) give carbohydrates to spare protein stores

2) 35 Kcal - 55 Kcal/kg per day (Amount needed dependent on degree of catabolism)

3) maintain low protein, low sodium, low potassium diet as well as fluid restriction (Need to maintain intake of high essential amino acids)

4) monitor BUN, electrolytes, serum protein and albumin

c. Frequent oral hygiene

d. Enteral/parenteral feedings as needed (Combination of hyperalimentation and dialysis shown to increase survival rates)

6. Alteration in excretion of metabolic wastes (Even with nonoliguric failure, kidneys unable to excrete metabolic wastes)

a. Maintain in anabolic state (Decrease nitrogen produced - all cells release protein)

b. Uremic syndrome (usually with BUN > 100) (Keeping BUN < 100 shown to lower mortality rates), note distinction with azotemia.

1) anemia/bleeding

a) decreased erythropoietin and decreased red cell life span, hemodilution

b) impaired platelet function (Interferes with activation of platelet factor III)

c) monitor platelet count and Hct

d) guaiac stools (Urea causes capillary fragility and irritation of mucosal surfaces)

e) assess for active bleeding

f) transfuse PRBCs as necessary

2) nervous system dysfunction (Frequent neurological assessment)

a) peripheral neuropathy (Sensory and motor loss begins distally)

b) uremic encephalopathy (Range from confusion and drowsiness to coma: may have tremors or seizures - need to avoid overstimulation)

3) pericarditis (serous vs. hemorrhagic)

a) accumulation of metabolic wastes

b) assess for pleuritic pain, friction rub, fever, ECG changes (Pleuritic pain increases with inspiration: if friction rub disappears may be that patient has developed effusion: check for a paradox with BP)

7. Alteration in pulmonary status (Result of volume overload and change in capillary permeability)

a. Monitor arterial blood gases

b. Administer OZ as needed

c. Frequent position changes

d. Maintain pulmonary hygiene (Cough, deep breath, incentive spirometry)

e. Assess for pulmonary edema/pulmonary effusion

8. Alteration in GI function (Urea changed to ammonia in intestine: gives patient foul taste: additionally, there is change in mucosal surface of gut)

a. Anorexia

b. Diarrhea or constipation

c. Stomatitis, gastritis with bleeding (GI hemorrhage from stress ulcers is a leading cause of death)

d. Nausea/vomiting

e. Frequent oral care

f. Laxatives as needed

B. Diuretic phase: goal is to maintain adequate fluid balance and regulate electrolytes

1. Fluid loss (Nephron can't conserve Na⁺ or H2O)

a. Monitor BP, HR, skin turgor (Hypotension, tachycardia, orthostatic)

b. Daily weights (Better indicator than intake and output)

c. Fluid replacement - urine output can be 150-200% of normal (Usually replace with 2/3 previous hour + 30cc for insensible loss)

2. Alteration in electrolytes

a. Hypo/hyperkalemia (Depends on rate of urinary excretion)

b. Hypophosphatemia

c. Hypercalcemia (Especially seen if cause was rhabdomyolysis)

C. Recovery phase: goal is supportive care and to prevent further insults to kidney

1. Assessment of renal function (Monitor BUN, creatinine, and electrolytes)

2. Keep patient well hydrated and free from infection

3. Prevent further insults (May have residual insufficiency and will always be at increased risk for renal failure)

IV. Dialysis (Shown to decrease complications and increase survival rates: requires specialized training so will only introduce principles; types, etc.)

Slide #2-5 (Osmosis and diffusion in dialysis)

A. Principle: Dialysis is diffusion of dissolved particles from one fluid compartment to another across semipermeable membrane (One fluid compartment is always the blood; the membrane and other compartment will change depending on type of dialysis)

B. Indications

1. Volume overload (Not responsive to diuretics)

2. Uncontrolled hyperkalemia

3. Uncontrolled acidosis

4. Symptomatic uremia (BUN > 100 mg/dL)

5. Pericarditis

C. Modes

1. Hemodialysis - blood is one fluid compartment and dialysate is the other with an artificial semi-permeable membrane.

a. Indications (Not just renal failure)

1) rapid removal of toxins, poisons or drugs

2) removal of waste products

3) removal of excess water through ultrafiltration

b. Contraindications (Causes rapid fluid shifts)

1) labile cardiovascular states

2) recent MI

3) hypotension

c. Complications

1) hypotension (Secondary to fluid loss)                     

2) air embolism

3) arrhythmias (Fluid shifts and electrolyte changes)

4) infection

5) disequilibrium syndrome (Rapid shifts in osmolality between cerebral spinal fluid and blood can lead to cerebral edema)

6) coagulopathies (Heparin used during dialysis to prevent clotting of blood outside of body)

d. Management

1) assessment of fluid and hemodynamic status (May need to administer volume expanders and vasopressors)

2) adjust timing and dosages of medications (Know how medications are excreted and metabolized)

3) monitor coagulation studies

2. Peritoneal Dialysis

a. Blood is one fluid compartment, dialysate the other with peritoneum as semi-permeable membrane (Cannula is placed into the peritoneum: dialysate is infused and allowed to remain for period of time then drained: may be done manually or by machine)

b. Indications (Less expensive, less training: if done manually does not require dialysis nurse)

1) hemodialysis not available

2) vascular access not available

3) contraindications exist for hemodialysis

c. Contraindications

1) peritonitis

2) abdominal surgery

3) abdominal adhesions 4) pregnancy

d. Complications

1) peritonitis

2) respiratory distress (Increased pressure against diaphragm from fluid in peritoneum: less room for lungs to expand)

3) atelectasis/pneumonia

4) perforation of bowel/bladder

e. Management

1) assessment of fluid, hemodynamic and respiratory status

2) monitor for signs of infection

3) provide pulmonary hygiene (Cough, deep breath, incentive spirometry)

3. Continuous renal replacement therapy (CRRT) - provides continuous ultrafiltration of extracellular fluid and clearance of uremic toxins in slower, more controlled manner (May be best type for critically ill, especially if hemodynamically unstable: is not new but still not used in many areas)

a. Types

1) hemofiltration

a) blood pumped from artery or vein through hemofilter and back into venous circulation (Requires cannulation of large artery and vein or double venous catheter: blood flows from artery (or vein) through porous hemofilter and back into vein: oncotic pressure holds fluid within plasma: hydrostatic pressure created by MAP > 70 (or pump if vein is used) becomes the driving force: when this exceeds oncotic pressure fluid is forced out through filter)

b) loss of large quantities of water through ultrafiltration (Ultrafiltration rate controlled by gravity drainage system or augmented by suction: replacement fluid must be given)

c) urea, creatinine and Na⁺ are carried with water (Plasma and blood cells are too large)

d) requires large volumes of fluid (20-40 L/24hrs)

2) hemodialysis

a) same principle as traditional hemodialysis

b) addition of dialysate to filter

c) less removal of water (Don't have to rely just on H2O movement for removal of waste products and electrolytes)

3) systems

Slide #2-6 (CAVH system)

a) CAVH - continuous arteriovenous hemofiltration (Movement of blood from artery through filter and back to vein) - moderate fluid removal and clearance of solutes

Slide #2-7 (CA VHD system)

b) CAVHD - continuous arteriovenous hemodialysis (Addition of dialysate) - most closely resembles hemodialysis - aggressive fluid and urea removal

c)            CVVH - venovenous hemofiltration (Movement of blood from vein with addition of pump through filter and back to vein) - recognized as most appropriate for critical care setting- requires double lumen catheter

Slide #2-8 (CVVHD system)

d) CVVHD - continuous venovenous hemodialysis (Addition of dialysate)

b. Type to be used determined by:

1) fluid balance (How much H20 needs to be pulled off and can be done safely)

2) electrolyte balance

3) metabolic status

4) severity of uremia (Hemodialysis needed for aggressive management)

5) vascular access (Artery versus double lumen venous) 6) blood pressure (Has to be able to overcome oncotic pressure)

c. Indications (Allows for slower volume removal: allows venous system to compensate with refilling from interstitial spaces)

1)       hemodynamic instability (Not only renal but HF, pulmonary edema, postoperative volume overload)

2)       contraindications to hemo/peritoneal dialysis

3) fluid management in patients with large daily fluid requirements (Not responsive to diuretics) 4)       patients with multiple organ dysfunction syndrome (Provides ability to administer pressors, blood products, and TPN without jeopardizing cardiovascular or respiratory status)

d. Complications

1) fluid imbalance - hypo/hypervolemia (Depends on ultrafiltration rate and intravascular volume requirements)

2) electrolyte imbalance (Hypokalemia, hyponatremia, hypocalcemia, and hypomagnesemia)

3) metabolic acidosis (Bicarbonate readily removed)

4) drug removal (Potential for removing most drugs)

5) hemorrhage (Heparin used as blood leaves body to prevent coagulation)

6) thrombosis/infection

7) hypo/hyperthermia (Temperature may be affected by temperature of fluid: may not be good indicator for infection)

e. Management (No detail will be provided here because requires more specific training depending on type used)

1) initiate and discontinue treatment

2) adjust rate of infusion hourly (Based on fluid balance)

3) asses hemodynamic and volume status

4) titration of heparin

5) assess ABGs and chemistries

6) troubleshoot circuit

V. Chronic renal failure (Caring for a critically ill patient who has underlying renal insufficiency can be a challenge for the critical care nurse. We'll review the physiology of chronic renal failure and review the common complications seen in these patients. We'll also briefly address special considerations when planning care for the critically ill, chronic renal failure patient.)

A. Definition: slow, progressive, irreversible damage to nephron

B. Stages

1. Diminished renal reserve

a. 50% nephron loss (Reflected by doubling in baseline creatinine)

b. Asymptomatic (Potentially dangerous with critically ill patients: creatinine within normal limits but diminished GFR: if suspected, obtain baseline creatinine clearance - looks at amount produced and excreted)

c. Protect kidneys from further insult

2. Renal insufficiency

a. 75 % nephron loss

b. Mild azotemia

c. Slightly impaired urinary concentrating ability

d. Anemia

e. Protect from infection, dehydration, cardiac failure and nephrotoxic drugs

3. End state renal disease (ESRD)

a. 90% nephron loss

b. Requires artificial support

c. Chronic and persistent impact on other systems

4. Uremic syndrome - same as acute renal failure

C. Complications (Result of chronic accumulation of metabolic waste products and inability to maintain homeostasis: won't discuss any in detail but important to be aware of potential complications)

1. Neurologic

a. uremic encephalopathy

b. peripheral neuropathy

c. neuromuscular irritability

2. Cardiovascular

a. uremic pericarditis/tamponade

b. hyperkalemia/cardiac arrest

c. arteriosclerosis

d. pulmonary edema, pericardial effusion

3. Pulmonary

a. pleural effusion, pleuritis

b. uremic pneumonitis

4. GI

a. peptic ulcers

b. malabsorption/diarrhea

5. Hematologic a. anemia b. GI bleeding

6. Integument

a.    ecchymosis, bruising b. calcium deposits c. infections

D. Management

1. Conservative

a. focus on fluid and electrolyte regulation

b. comfort measures (Symptom management)

2. Dialysis (May require hemodialysis 3x/week)

3. Renal transplantation

a. assess for and manage rejection

b. management of antirejection medications (Side effects include immunosuppression, fluid retention, impaired wound healing, bone marrow suppression)

E. Implications for critically ill patient (Remember patients with CRF may be asymptomatic but still have diminished GFR)

1. Maintain adequate oxygenation (Pulmonary complications, in addition to severe anemia, which results in inability to transport sufficient oxygen)

2. Restrict fluid and Na⁺ intake (More likely to retain fluid: increased ADH and aldosterone release: decreased excretion: refractory to diuretics)

3. Prevent infection (Immunosuppressed: effects of urea and possible medications)

4. Maintain electrolyte balance

5. Prevent tissue breakdown (Generalized edema from change in osmotic gradient of cells and changes in skin increase chance of breakdown: causes hyperkalemia and increased chance for infection)

6. Maintain adequate cardiac output (Common complication is heart failure)

 

Case Study

Terry is a 54-year-old male admitted to the critical care unit for multiple trauma following a motorcycle accident. He lost a large volume of blood. Upon admission, he is lethargic and the following are his parameters:

BP       90/50            Urine output  10-15cc/hour

MAP   63            BUN            40 mg HR       124            Creatinine     0.8 mg FENa .9%

1) Based on the above information what is accounting for Terry's low urine output? Decreased renal perfusion secondary to hypovolemia

2) What does his BUN, Creatinine and FENa tell you about his renal function?

BUN is elevated representing hypoperfusion: creatinine is within normal limits and ratio is greater that 20:1 indicating normal tubular function: FENa is < 1 % indicating that lddneys are holding on to Na⁺ in attempt to increase volume)

3) Which of the following interventions would be most appropriate?

a) Administer Furosemide 20mgIV and monitor results.

b) Fluid challenge of 500cc normal saline and consider transfusion.

c) No intervention necessary as he is still producing urine.

d) Initiate continuous venovenous hemofiltration.

Terry is given a fluid challenge of 500cc and 2u PRBCs over the next 3 hours. His BP is now 118/80, HR 96 and urine output 100cc/hour.

4) What does this response indicate about his renal function?

Kidney function is normal and able to respond to increased perfusion by increasing urine output

24 hours later Terry is taken to surgery for internal injuries. After surgery it is determined that he suffered an intraoperative anterior MI. He is noted to have irregular and labored respirations and falling oxygen saturations. Oxygen is started at 3L/nasal cannula. Auscultation reveals crackles 1/3 up bilaterally. He has also gained 3kg since surgery despite furosemide. Parameters include:

BP 76/48 Urine output            10-15cc/hr HR 102 PAWP            18 mm/Hg

5) Based on the above information what laboratory tests would you want to see? Electrolytes, BUN, creatinine, FENa, urine for sediment, Na⁺, osmolality

Furosemide 40mg is given and Dopamine started for hypotension. There is no response to the furosemide. He is switched to norepinephrine for BP as the dopamine is at 30mcg/kg/min with no response. The following parameters are obtained..

Sodium   128 mEq/L

Urine Osmolality   374 mOsm/kg

BUN 64 mg

Sediment Casts - granular: Cells - epithelial

Creatinine   6.0 mg/dL

Potassium   5.0 mEq/L

6) Discuss the significance of these lab values.

BUN and creatinine are both elevated with a ratio of about 10:1 indicating diminished renal function: elevated K⁺ means tubules are not able to reabsorb: low Na⁺ can indicate fluid overload: osmolality indicative of very dilute urine: sediment reflects tubular damage

7) What type of renal failure is this? Intrarenal: Acute tubular necrosis

8) The most likely cause is:

a. Nephrotoxicity from furosemide

b. Renal constriction from norepinephrine

c. Diminished cardiac output

d. Toxins from death of myocardial cells

9) Identify 3 priorities for management of Terry's renal failure at this point.

Any of the major interventions are acceptable that relate to Terry i.e. enhance cardiac output: maintain fluid balance: electrolyte balance (primarily K⁺) prevent catabolism to decrease nitrogen produced: maintain acid/base balance: adequate nutrition