(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


CARING FOR THE PATIENT WITH FLUID AND ELECTROLYTE DISORDERS

Lecture Time: 150 minutes Objectives

1. Explain the homeostatic mechanisms for maintaining fluid balance and electrolyte balance.

2. Differentiate between saline and water abnormalities.

3. Describe the clinical situations where abnormal potassium (K), calcium (Ca ++), and magnesium (Mg ++) levels are seen.

4. Compare the defining characteristics and nursing and medical management of each of the following:

a. Water excess/deficit

b. Saline excess/deficit

c. Hyper/hypokalemia

d. Hyper/hypocalcemia

e. Hyper/hypomagnesemia

Content Outline

I. Overview

A. Total body fluid (TBW)

1. 60% of body weight is water for an adult (Total body water distribution changes and amount decreases with age; also varies with fat content and sex)

2. Saline vs water (Fluid balance is achieved by regulating both water and saline which is a solution of 0.9% NaCl and H20; serum sodium [Na+] not reflective of saline balance; used as indicator of water concentration and osmolality)

B. Compartments Slide.#3-1 (Fluid distribution)

1. Intracellular (ICF) (Within the cell) - 2/3 of water

2. Extracellular (ECF) (Outside the cell) - 1/3 of water (This is further divided into two locations)

a. Interstitial fluid (Between cells)

b. Intravascular fluid (Fluid in blood vessels)

3. Transcellular (Fluid separated by epithelium from other ECF; may be considered part of ECF or separate) - digestive juices, cerebrospinal fluid, pleural fluid, intraocular fluid

C. Movement of body fluid (Balance of fluid and electrolytes must be maintained within narrow range; to understand process must understand some mechanisms which affect movement of fluid)

1. Movement between compartments determined by osmolality

a. Number of particles in compartment (Primarily electrolytes)

b. Water moves from area of low osmolality to area of high osmolality

c. Osmolality of ECF: 280 - 300 milliosmoles per kilogram (mOsm/kg) (Determined primarily by concentration of Na+ and glucose contained in ECF; osmolality of ICF determined by K+)

2. Hydrostatic pressure causes fluid to move into interstitial spaces

a. Pressure generated in blood by the heart

b. Varies within the capillary (Higher at the arteriolar end; water moves into interstitial space; results in decrease in hydrostatic pressure at the venous end)

3. Colloid osmotic pressure

a. Generated by plasma proteins within vessel (Primarily albumin; pressure fairly constant; plasma proteins do not cross capillary membrane under normal conditions; integrity of capillary membrane essential to maintain balance)

b. Pulls water back into vessel (Higher than hydrostatic pressure at the venous end causing water to be pulled back in; osmotic and hydrostatic pressure balance each other when normal)

II. Water balance

A. Regulation (Water moves freely between compartments; osmolality of TBW normally reflects equilibrium; osmolality is determinant of water balance; as osmolality increases, amount of water decreases; as osmolality decreases, water increases)

1. Thirst (Primary control of fluid intake; water intake dilutes osmolality of ECF and restores volume)

a. Thirst center located in hypothalamus

1) Contains osmoreceptors (Respond to changes in ECF osmolality)
2) (Possibly causes) Shrinkage of cells result in stimulation of thirst

b. Decreased renal perfusion secondary to hypovolemia

1) Activates renin/angiotensin (Result is release of Angiotensin II)
2) Stimulates hypothalamus (Angiotensin II stimulates the hypothalamus, resulting in thirst)

2. Renal regulation (Major control of output of water)

a. Regulates osmolality and volume of body fluids

b. Decreased renal perfusion - decreased urine output (With decreased perfusion, kidneys reabsorb water in attempt to enhance intravascular volume; results in decreased excretion)

3. Antidiuretic hormone (ADH)

a. Increased reabsorption of water in collecting ducts (Attempt to correct osmolality and volume of ECF)

b. Stimulation of secretion

1) Increased osmolality
2) Decreased vascular volume
3) Stress (Trauma, surgery, pain, hyperthermia, analgesics such as Demerol and morphine sulfate)

c. Inhibition of secretion (Distal tubule and collecting duct impermeable to water so increases excretion of water)

1) Decreased serum osmolality
2) Increased blood volume
3) Increased blood pressure

B. Water excess (water intoxication) (Hypotonic or hypoosmolar imbalance; excess of water in relation to solutes in ECF; dilution of ECF; movement of water to ICF due to osmosis; usually related to a water gain or solute loss; pure water excess rare)

1. Etiology

a. Excess water intake (Fluid not, containing electrolytes)

1)       Psychogenic disorders (Cause compulsive water drinking)
2) Multiple tap water enemas
3) Irrigating solutions (Such as with TURPs)
4) IV infusions of D5W (In the presence of acute renal failure [ARF], chronic renal failure [CRF], or cirrhosis)

b.   Decreased urine output

1) Renal disease
2) Decreased renal perfusion

c. Syndrome of inappropriate secretion of ADH (SIADH)

1) Decreased. renal excretion of water (Results in decreased serum Na+ and osmolality; kidney continues to excrete Na)
2) Etiology (Factors other than hyperosmolality or hypovolemia stimulate secretion of ADH)
a) Conditions associated with stress (Fear, pain, acute infection, brain trauma, surgery)
b) Medications (Analgesics - Demerol, morphine; anesthetics)
c) Tumors in body organs (Bronchogenic cancer most common cause)
d) Inflammatory conditions of lung or brain (TB, pneumonia, encephalitis)

2. Clinical presentation (Symptoms related to rate at which water excess occurred)

a. Neuromuscular (Swelling of brain cells)

1) Confusion progressing to coma
2) Lack of coordination
3) Convulsions (Chronic accumulation causes headache, muscle twitching, cramps)
4) Increased intracranial pressure (ICP) (Slow bounding pulse, widening pulse pressure)

b. Hyperventilation

c. Sudden weight gain (May have peripheral edema but not always)

d. Anorexia, nausea and vomiting (Seen with chronic or slow accumulation)

e. Lab findings

1) Decreased serum osmolality
2) Decreased hematocrit (Hct) (Dilutional effect)
3) Low serum Na-(Not always)

3. Management (Prevent by close assessment of all patients with increased water intake)

a. Water restriction (If asymptomatic - 500-1000mL/day: this is a good place consider the difference between a water restriction and a fluid restriction.)

b. Hypertonic (3-5%) saline infusion with diuretic (Used with severe symptoms; saline increases Na+ level and diuretic increases water loss; monitor patient closely when receiving; can result in intracellular dehydration)

1) Hourly I and O, daily weight
2) Serum Na monitoring (May be as often as every few hours)
3) Neuro assessments

c. Provide for patient safety (Potential for confusion and seizures)

C. Water deficit (Hyperosmolar or hypertonic imbalance; results from a water loss or solute gain; salt solution of > 0.9%; results in movement of water from ICF to ECF)

1. Etiology

a. Decreased water intake (Usually occurs with impaired mental status such as confusion or coma)

1) Loss of thirst (Or lack of response to thirst)
2) Inability to communicate thirst

b. Excess water loss (Lost in excess of electrolytes)

1) Diabetes insipidus (Inability to concentrate urine)
2) Watery diarrhea
3) Excessive osmotic diuresis
4) Increase in insensible water loss (Prolonged hyperventilation; massive burns)
5) Excessive diaphoresis (With no water replacement)

c. Excess intake of solutes (Primarily Na)

1) Intravenous hypertonic saline solution (Sodium bicarbonate)
2) Near drowning in saltwater
3) Excess dietary Na' intake
4) Tube feedings (Excess intake of proteins; results in osmotic diuresis and diarrhea; much less common now)

d. Over secretion of aldosterone (Causes kidneys to reabsorb Na)

1) Primary hyperaldosteronism
2) Cushing syndrome

2. Clinical presentation (Cellular dehydration)

a. Neuromuscular (With severe hypernatremia; shrinkage of brain cells)

1) Apprehension, restlessness, lethargy
2) Coma, death (Cell shrinkage can result in cerebral hemorrhage)

b. Cardiovascular (Decreased intravascular volume; decreased cardiac output)

1) Postural hypotension
2) Tachycardia, weak pulses

c. Thirst (Occurs early: may be missed if you are caring for a patient who cannot communicate their thirst))

d. Hyperthermia

e. Dry mucous membranes (Including dry swollen tongue)

f. Weight loss

g. Decreased urine output

h. Tachypnea

i. Lab findings

1) Increased Hct (Secondary to hemoconcentration)
2) Increased serum electrolytes (Same reason)
3) Serum osmolality >295 mOsm/kg
4) Serum Na+ elevated (Usually)

3. Management

a. Treat underlying cause

b. Increase oral intake of water (If water deficit not too severe)

c. D5W infusion (Replace loss; increase renal perfusion; decrease Na+ reabsorption; replace slowly over 48 to 72 hours; too rapid can cause shifts; result in cellular edema and pulmonary edema)

d. Oral care (Important due to dry mucous membranes)

e. I and O, daily weight

f. Provide for patient safety (Potential for confusion and seizures)

III. Saline balance (Remember this is combination of Na+ and water)

A. Regulation

1. Aldosterone (Hormone secreted by adrenal gland; results in Na+ retention in renal tubules; also intestines, sweat and salivary glands)

Slide #3-2 (Renin-angiotensin-aldosterone system)

a. Stimulated by renin-angiotensin system
b. Response to low serum Na+ or low blood volume (Increases renin secretion; converts angiotensinogen to angiotensin I in liver; converted to angiotensin II in lungs; stimulates production of aldosterone; depresses renin secretion)

2. Atrial natriuretic hormone (Natrecor) (Also referred to as third factor; currently being studied to understand effects; increases renal excretion of Na+ and water by possibly varying mechanisms)

a. Increases glomerular filtration rate (GFR)
b. Inhibits reabsorption of Na+
c. Blocks aldosterone release (By inhibiting renin)
d. Inhibits release of ADH

3. Kidneys - control Na+ reabsorption

B. Saline excess (hypervolemia) (Isotonic imbalance; water and electrolytes increased in same proportion; secondary to increase in total body Na+ which leads to increase in TBW; serum Na+ normal; no swelling of cells)

1. Etiology

a. Excess intake
1) Excessive administration of isotonic solutions (LR and 0.9% NaCl; especially with patients with impaired regulatory mechanisms)
2) Increased dietary intake of NaCl
b. Compromised regulatory mechanisms
1) CRF, heart failure (HF), liver disease
2) Malnutrition
3) Hyperaldosteronism (Retention of Na+ and water in kidneys)
4) Excess steroid administration

2. Clinical presentation (Excess volume in intravascular space)

a. Respiratory
1) Dyspnea, cough, crackles
2) Pulmonary edema (if severe)
b. Cardiovascular
1) Bounding pulses
2) Neck vein distension
3) Hypertension
4) Increased right atrial pressure (RAP) and pulmonary artery wedge pressure (PAWP)
5) CHF (If severe or heart already compromised)
c. Weight gain (Over short period)
d. Distended abdomen (May develop ascites; when volume severe, fluid moves into body cavities)
e. Sweating
f.       Normal skin turgor
g. Edema (Increased hydrostatic pressure caused by increased volume; fluid moves into interstitial spaces)

3. Management (Primary focus is to treat causative condition)

a. Restrict intake of Na+ and fluids
b. Diuretics (Inhibit Na+ and water reabsorption)
c. I and O, daily weights (Caution not to cause fluid deficit with treatment)
d. Maintain skin integrity (Edematous tissue more prone to skin breakdown)

C. Saline deficit (hypovolemia) (Isotonic imbalance; loss of ECF; electrolytes and osmolality within normal range)

1. Etiology

a. Inadequate intake (Anorexia, nausea, fatigue, swallowing problems, depression)
b. Loss of body fluids (Most common cause)
1) Hemorrhage
2) Loss from GI tract (Vomiting, diarrhea, GI suction, fistulas, drains)
3) Loss through skin (Severe sweating without fluid replacement; fever)
4) Draining wounds
5) Loss through kidney (Hyperglycemia; any other factor that causes diuresis)
c. Sequestration of fluids (Third spacing; fluid shifts from vascular space to area where exchange not easy; potential body spaces such as pleural, peritoneal, etc.; trapped in bowel by obstruction; interstitial space as with burns; inflamed tissue as with pancreatitis, peritonitis)

2. Clinical presentation

a. Cardiovascular
1) Postural hypotension (Low in all positions as deficit increases), tachycardia (Compensate for decreased volume)
2) Flat neck veins (Reflects decreased RAP)
3) Decreased filling pressures (Decreased RAP and PAW)
b. Renal
1) Decreased urinary output (Reflects inadequate renal perfusion; persistent fluid deficit can result in ARF)
2)            Increased specific gravity (Reflects kidneys response to reabsorb fluid in attempt to increase volume)
3)            Increased BUN (Best indicator of renal perfusion and GFR)
c. Decreased skin turgor, dry mucous membranes and tongue (Tongue actually becomes smaller with more furrows)
d. Rapid weight loss
e. Cold skin (Peripheral vasoconstriction)
f. Increased Hct
g. Altered level of consciousness (Decreased cerebral perfusion)

3. Management (Prevent by replacing losses as they occur)

a. Replacement of fluid
1) Increase oral intake (Best route if patient able to drink)
2) Isotonic IV fluids
a) May need fluid challenge (If oliguric, give initial bolus to see if kidneys able to respond to increased fluid; if not acute tubular necrosis [ATN] may have already developed)
b) Monitor response to fluid therapy (Filling pressures, lung sounds, urinary output, and BP closely to note early signs of fluid excess)
b. Identify cause and treat
c. I and O, daily weights
d. Frequent oral care

IV. Potassium 3.5-5.0 mEq/L (Major intracellular electrolyte; 98% is within cell)

A. Functions

1. Maintain osmotic pressure of ICF

2. Regulate neuromuscular excitability (Affects skeletal and cardiac muscle activity)

3. Acid base balance (K+ moves into cells when hydrogen ion moves out; the reverse is also true)

B. Regulation

1. Movement between intracellular and extracellular spaces

a. Acid base balance

1) Alkalosis can result in hypokalemia (In an attempt to raise the pH, H+ moves out of cells; since the cell wants to have electrical equilibrium, K+ moves in)
2) Acidosis can result in hyperkalemia (Conversely, in acidosis the H+ moves into cells in attempt to increase pH and K+ moves out)

b. Glucose and protein metabolism (Stimulates insulin release; promotes movement of K+ into cells)

c. Hormones

1) Insulin (Promotes movement of k+ into liver and muscle cells)
2) Epinephrine (Shift of K+ into cells: this occurs with both endogenous and exogenous epinephrine)

2. Excretion

a. Kidneys (Primary source for excretion; determined by K+ levels; pH; GFR; aldosterone - stimulates secretion of K) b.   Bowel and sweat glands (20%)

C. Hyperkalemia >5.5 mEq/L

1. Etiology (Rarely occurs with normal renal function)

a. Decreased excretion

1) Decreased aldosterone (Addison's disease; hypoaldosteronism)
2) Chronic or acute renal failure (Untreated), obstruction, NSAID's
3) K+ sparing diuretics, CEI's, ARB's
4) Saline depletion (Decreased renal perfusion; decreased GFR)

b. Release from cells

1) Destruction of cells (K+ released with cellular breakdown; catabolism, burns, trauma, sepsis, fever, cytotoxic agents)
2) Decreased insulin production (Hyperglycemia results in K+ movement out of cells into ECF)
3) Metabolic acidosis
4) 'Pseudo' hyperkalemia (tourniquet use for sampling; fist clenching, hemolysis of sample, marked thombocytosis, leukocytosis - in these latter cases elevated K is real, but only in blood tube)
5) Various medications (Beta blockers - interfere with entry of K+ into cells; digoxin at toxic levels will increase release from cells)

c. Increased intake (Rapid IV administration; blood transfusions; rare orally)

2. Clinical presentation (Rapid onset increases potential for and severity of problems)

a. Cardiovascular (Major effects are on myocardium)

Slide #3-3 (ECG changes with hyperkalemia)

1) Decreased action potential (>6.5, occasionally less)
a) Tall tented symmetrical T waves
b) Shortened QT interval
2) Depressed intraventricular conduction (>8.0, occasionally less)
a) Widened QRS, prolonged PR
b) Low amplitude and widened P wave
3) Decreased automaticity (10-11.0, uh-oh)
a) P waves disappear
b) QRS merges with T to form sine wave
c) Asystole or ventricular fibrillation
4) Decreased strength of contraction (With profound hyperkalemia heart becomes dilated and flaccid; bradycardia, AV block)

b. Neuromuscular (Primarily peripheral; very little effect on CNS)

1) Numbness and tingling (Face, hands, tongue)
2) Muscle weakness (An early sign), flaccid paralysis (Ascending; starts with legs)
3) Apathy, confusion
4) Decreased deep tendon reflexes

c. GI (Smooth muscle hyperactivity)

1) Abdominal cramping
2) Nausea, vomiting, diarrhea
3) Hyperactive bowel sounds

3. Management (Goal is to treat cause, correct hyperkalemia, and prevent cardiac arrest)

a. Treat cause

b. Decrease intake (Use fresh blood; no supplements; decrease in diet)

c. Reduce production (Prevent skin breakdown or infection)

d. Promote excretion

1) Kayexalate/sorbitol (Exchange resin; exchanges K+ for Na+ in GI tract; slow so don't rely on in emergency situation)
2) Normal saline and diuretics (Increase renal flow, GFR, and Na+ excretion)

e. Increase movement into cells (Emergency management)

1) IV glucose and insulin IV (Insulin facilitates movement of K+ into cells; glucose prevents hypoglycemia; results in 30 min. and last about 4 - 6 hours: remember that this is a temporary measure and must be coupled with an intervention that will cause K+ to be eliminated from the body)
a) D50 bolus with 10-25 units of regular insulin IV (Some recommend 500 mL of 10% dextrose)
b) Check glucose and K+ every hour
2) Sodium bicarbonate (Shifts K+ back into cells; effects within few minutes, lasts about 2, hrs) - assess for fluid overload (Because of the Na+ load)

f. Antagonize effects on membrane (For immediate protection of myocardium; does not affect K+ level but protects heart) - Ca chloride (Cl) (10 mL of 10% over 2 - 3 minutes; may be repeated every 5 min.; effects within 1- 5 min.; last 30 - 60 min.; administer one of the above in conjunction)

g. Hemodialysis (Life threatening hyperkalemia)

D. Hypokalemia <3.5 mEq/L (Common imbalance)

1. Etiology

a. Intracellular shift (Total K+ may be normal, but there is increase in ICF level)

1) Alkalosis
2) Insulin
3) Hyperalimentation (Stimulates release of insulin; moves K+ into cells; need adequate amount of K+ when refeeding)
4) Tissue repair after trauma or burns

b. Inadequate intake (40 - 60 mEq/daily for normal replacement)

1) Anorexia, alcoholism
2) K+ free IVS

c. Increased loss (Most common cause)

1) GI
a) Vomiting, gastric suctioning (Actual loss as well as the resulting metabolic alkalosis, which encourages movement of K+ into cells)
b) Diarrhea, fistula, recent ileostomy (Large amounts of K+ in intestinal fluids)
c) Malabsorption
2) Stress (Release of aldosterone and epinephrine)
3) Excessive urinary loss
a) Diuretics (K+ losing), osmotic diuresis
b) Increased aldosterone (Occurs with cirrhosis, BF, malignant hypertension)
c) Renal tubular acidosis (Increases excretion of K) 4) Integument (Profuse perspiration in those acclimated to heat)

2. Clinical presentation (Symptoms not usually present unless < 3.0 mEq/L; can affect every system)

a. Cardiovascular

1) ECG changes (Correlate poorly with actual number)

Slide #3-4 (ECG changes with hypokalemia)

a) Increased automaticity - ventricular ectopy
b) Prolonged action potential
i. ST segment depression
ii. T waves inverted with progressive flattening
iii. U waves (As become larger and positioned on T, looks like prolonged QT)

2) Hypotension (Decreased peripheral resistance)

b. Respiratory

1) Hypoventilation (Hypoventilation and hypotension are late signs)

2) Paralysis

c. Neuromuscular (Primarily affects skeletal muscles, mostly in legs)

1) Muscle weakness/cramping, tender muscles

2) Parasthesias

d. GI

1) Nausea, vomiting, anorexia

2) Abdominal distension (Smooth muscle weakness), paralytic ileus (Decreased bowel motility)

e. Endocrine

1) Hyperglycemia (Suppresses insulin release; slightly elevated glucose)

2) Metabolic alkalosis

f. Renal (Prolonged hypokalemia causes decreased ability to concentrate urine)

1) Polyuria, nocturia

2) Increased H+ excretion

3. Management (Be aware of high risk patients)

a. Thorough assessment (Most significant aspect of management)

1) Apnea

2) Cardiac dysrhythmias (Ventricular ectopy very common)

3) Characteristic abdomen and bowel sounds

4) Monitor acid base balance

b. Replace K+

1) Oral supplements or increased dietary intake when possible (Allows to rise slowly so can equilibrate with intracellular level)

2) IV (Never IM or IV bolus)

a) Standard dose 40 mEq over 4 hours (Total amount needed depends on level of K)
b) If giving >10- 20 mEq/hr, start cardiac monitoring
c) Monitor IV site (Very irritating to vessels)
d) Ensure adequate renal function (To prevent hyperkalemia)

V. Calcium 8.5 - 10.5 mg/dL (Imbalance of Ca++ common in acutely ill)

A. Functions

1. Bone formation and metabolism (99% located in skeletal system; 1% exchanges rapidly with serum Ca++)

2. Neural transmission and function

3. Initiates skeletal and cardiac muscle contraction

4. Coagulation (Coenzyme in coagulation cascade; activates complement)

5. Regulation of enzyme system (Activates enzymes in many chemical reactions)

6. Maintains functional integrity of cell membrane

B. Regulation

1. Excretion/Absorption of Ca++ (Normally 150 - 200 mg excreted daily)

a. Kidneys primary route/small amount in feces
b. Parathyroid hormone (PTH) (Decreased ECF levels cause stimulation)
1) Causes renal reabsorption
2) Absorption from GI tract
c. Calcitonin - decreases renal and intestinal absorption (Produced by thyroid gland in response to increased ECF)
d. Calcitrol (Metabolite of vitamin D) - increases Ca ++ reabsorption from intestine (Main purpose is to increase availability of Ca++ and phosphate for bone formation; prevent hypocalcemia)

2. Effect of albumin on serum Ca++

a. Most serum Ca++ is bound to albumin (1% of Ca++ is not in the bone; of that about 40% is bound to plasma proteins; only the Ca++ which is not bound is physiologically active and is referred to as ionized Ca++; need to be able to directly measure ionized Ca++; need to be aware of how albumin affects serum level)
b. In non-critically ill patient with normal pH, 1 gram per deciliter (G/dL) change in albumin results in 0.8 mg/dL change in Ca++.       Change in acid base balance changes relationship
1) Alkalosis
a) More Ca++ bound to protein-ionized decreased (Total serum unchanged)
b) Symptoms of hypocalcemia
2) Acidosis
a) Less Ca ++ bound to protein
b) Ionized Ca ++ increased (Even with low serum levels; signs of hypocalcemia rare)

C. Hypercalcemia >10.5 mg/dL (Can have mortality rate as high as 50%)

1. Etiology

a. Increased reabsorption from bone

1) Malignancy (98% have malignancy, parathyroidism or thiazide diuretic use)
2) Hyperparathyroidism (Increase in. PTH causes increase release of Ca++ from bone)
3) Immobilization (Rate of bone resorption > bone formation)

b. Increased absorption from GI tract (Increased Ca++ intake; milk and Ca++ containing antacids)

c. Decreased excretion

1) Acute or chronic renal failure
2) Increased renal reabsorption (Thiazide diuretics; increased PTH; large doses of vitamin D)

2. Clinical presentation (Primarily result of decreased neuromuscular excitability)

a. Cardiovascular (Exerts positive isotropic affect)

Slide #3-S (ECG changes with hypercalcemia)
1) ECG changes
a) Shortened QT interval
b) Flat inverted T wave
c) Dysrhythmias (With severe excess >18 mg/dL - cardiac arrest)
2) Hypertension

b. Neuromuscular

1) Weakness, fatigue, lethargy
2) Diminished deep tendon reflexes
3) Drowsiness to coma (Degree of behavior change corresponds with level and rapidity at which it increased; slow rise results in fewer symptoms)
4)            Psychotic manifestations (With higher levels)

c. GI (Decreased GI motility)

1) Nausea, vomiting
2) Increased thirst (Secondary to dehydration)
3) Anorexia, constipation
4) Pancreatitis (With acute hypercalcemic crisis)

d. Renal (Impairs ability to concentrate urine)

1) Polyuria, polydipsia, nocturia (May cause acute renal failure)
2) Renal calculi (Result of excess Ca++ in kidneys)

3. Management (Correct underlying cause)

a. Intake and output (Because of impact on kidneys important to monitor function)

b. Neuromuscular assessment

c. Reduce serum Ca++ level (Increase excretion; decrease absorption from intestines)

1) Increase oral fluids (Most are volume depleted fluids essential; when not emergent can simply increase fluid intake)
2) Normal saline plus diuretics when volume replete (When emergent, NS at 300 - 500 cc/hr until intravascular volume restored; assess for fluid overload; continue saline infusion to enhance renal perfusion; increase excretion and prevent renal calculi; may also result in loss of K+ and Mg + so monitor)
3) Dialysis if severe
4) Administration of sodium bicarbonate (Promotes Ca++ excretion; decreases ionized Ca++)
5) Glucocorticoids (Blocks absorption in intestine and bone resorption)

d. Decrease release of bone Ca++

1) Calcitonin (Blocks bone resorption; temporarily decreases serum levels; effective within 2 hours; other drugs used include mithramycin and EDTA)
2) Oral phosphate (Given with low serum phosphate and adequate renal function: consider reciprocal relationship)
3)  Diphosphanates (Slow bone turnover)
4) Frequent ambulation (If not possible, then active or passive range of motion)

D. Hypocalcemia < 8.5 mg/dL

1. Etiology

a. Decreased absorption

1) Small bowel resection
2) Crohn's disease
3) Biliary obstruction
4) Alcoholism

b. Increased excretion

1) Diuretics
2) Chronic renal failure (Results in hyperphosphatemia; results in reciprocal decrease in Ca++)
3) Overuse of antacids or laxatives (Phosphate containing)

c. Decrease in ionized Ca++­

1) Blood transfusions (Citrate combines with Ca++; seen with rapid, multiple infusions; increased risk with shock or liver failure)
2) Alkalosis
3) Hypoparathyroidism (Primary or surgical; thyroidectomy; radical neck dissection for first 24-48 hrs secondary to decreased blood supply in area)
4) Pancreatitis (Increase in fatty acids to bind with Ca++)
5) Hypomagnesemia (Decreases PTH release; in end organ failure results in resistance to PTH)

2. Clinical presentation (Dependent of severity, duration and rate of rise)

a. Cardiovascular

Slide #3-6 (ECG changes with hypocalcemia)

1) ECG changes
a) Prolonged QT interval and ST segment
b) T wave inversion
2) Hypotension

b. Neuromuscular (Increased neural excitability; spontaneous firing of sensory and motor fibers in peripheral nerves)

1) Tingling around mouth, hands and feet
2) Muscle spasms/tetany (To check for tetany, evaluate for the following signs)
a) Chvostek's sign (Tap finger on facial nerve in front of ear and below temporal bone; causes spastic contraction of muscle and lip twitch if tetany present)
b) Trousseau's sign (Inflate BB cuff on arm > patient's systolic pressure; leave inflated and observe for carpal spasms; unable to open hand)
3)  Seizures (With severe hypocalcemia)
4) Irritability, delusions/hallucinations

c. Respiratory

1) Labored shallow breathing
2) Bronchospasm (Wheezing and stridor) - airway obstruction (Secondary to laryngospasm) - arrest

d. GI (Smooth muscle hyperactivity)

1) Diarrhea, nausea, vomiting (Increased motility)
2) Abdominal cramps
3) Paralytic ileus (Tetany)

e. Bleeding (Lack of Ca++ necessary for coagulation cascade)

f. Pathological fractures

g. Chronic changes

1) Dry, scaling skin
2) Brittle nails
3) Dry, shedding hair

3. Management (When symptomatic with acute crises, considered medical emergency)

a. Identify cause and treat

b. Replace Ca'+

1) Oral intake of 1-2 gm daily (If not symptomatic)
2) IV administration - 20 mL of 10% Ca++ gluconate over 10 min
a) D5W if diluting (NS can worsen hypocalcemia) and administer slowly (do not exceed 2 mL/min; can cause bradycardia, hypotension and cardiac arrest)
b) Observe site for extravasation (Very irritating to veins, especially Ca chloride)
c) Cardiac monitoring

c. Provide for patient safety (Confusion and seizures)

d. Minimize external stimuli

e. Monitor airway (For bronchospasm)

VI. Magnesium 1.3 - 2.1 mEq/L (Second most abundant in intracellular compartment)

A. Functions

1. Activates several intracellular enzyme reactions

2. Affects protein and carbohydrate metabolism

3. Affects neuromuscular irritability and contractility (By acting directly on myoneural junction)

4. Produces peripheral vasodilation

5. Influences transport of Na+ and K+ across cell membrane

6. Structural element of bone

7. Influences secretion of parathyroid hormone

B. Regulation (67% is in bones; 1% extracellular; remainder in muscle and soft tissue; regulation not well understood)

1. Absorption - primarily in ileum and jejunum (Daily requirements 18 - 30 mEq

2. Excretion - kidneys are primary route (Reabsorbed in Loop of Henle; any factor which impacts GFR will affect Mg ++ excretion)

a. PTH (Decreases excretion)

b. Extracellular volume (Increased ECF promotes excretion; decreased inhibits excretion)

3. Exchange between bone and ECF

C. Hypermagnesemia > 2.1 mEq/L

1. Etiology

a. Decreased excretion - renal failure (Most common cause of hypermagnesemia)

b. Increased intake

1) Antacids or laxatives (Those containing Mg ++)
2) Hemodialysis (Hard water contains Mg++; dialysate may also contain too much Mg++)
3) Excess administration (Primarily in treatment of eclampsia)

c. Extracellular volume deficit (Adrenal insufficiency or diuretic abuse)

d. Acidosis (Primarily diabetic ketoacidosiis; release of cellular Mg ++ caused by catabolism)

e. Endocrine related (Addison's disease; hypothyroidism; hyperparathyroidism)

2. Clinical presentation

a. Cardiovascular

1) ECG changes
a) Prolonged PR, QRS and QT intervals
b) Sinus bradycardia
c) Heart block and cardiac arrest (15 - 20 mEq/L)
2) Hypotension (Peripheral vasodilation at 3 - 5 mEq/L)
3)       Flushed, warm skin

b. Neuromuscular

1) Drowsiness, lethargy (Coma at ~10 - 15 mEq/L)
2) Decreased deep tendon reflexes (Note loss of patellar reflex at ~7 -10 mEq/L)
3) Muscle weakness to flaccid paralysis

c. Depressed respirations (~10 mEq/L) - respiratory arrest (Paralysis at ~10 - 15 mEq/L)

3. Management (Most effective treatment is prevention)

a. Identify source and treat

b. Decrease intake (May be only treatment necessary if DTR's still present)

c. Increase excretion

1) Fluids and diuretics (Enhance GFR)
2) Mg++ free dialysate

d. Ca ++ administration (Emergency measure used in presence of respiratory depression or impaired cardiac conduction; Ca++ is direct antagonist to Mg ++; give 10 - 20 cc of 10% Calcium gluconate iv over 10 min)

e. Assessment of at risk patients

1) Hypotension
2) Shallow respirations with apnea
3) Level of consciousness
4) Patellar reflexes

D. Hypomagnesemia <1.3 mEq/L (Common in critically ill; undiagnosed frequently)

1. Etiology

a. Decreased intake

1) Prolonged malnutrition (Alcoholism most common cause) 2) Prolonged IV therapy or TPN (Containing inadequate amounts of Mg+)

b. Decreased absorption

1) Problems with lower GI tract (Steatorrhea; inflammation)
2) Resection of bowel
3) Pancreatitis (Can result in malabsorption)
4) Malabsorption syndrome

c. Increased excretion

1) GI tract
a) NG suctioning (Prolonged)
b) Diarrhea, fistulas (More of a problem then gastric loss; intestinal fluid rich in Mg++)
2) Kidneys
a) Hypercalcemia
b) Volume expansion (Anything that increases intravascular volume; hyperaldosteronism one factor)
c) Diuretic therapy (Loop diuretics)
d) Osmotic diuresis (Caused by mannitol, urea or glucose)
e) Renal disease (anything that impacts reabsorption)
3) Other factors
a) Citrate in blood (Binds with Mg++)
b) Hypothermia
c) Burns (Lost with debridement) d) Sepsis

2. Clinical presentation (Mg++ < 1 mEq/L)

a. Cardiovascular

1) ECG changes
a) Prolonged PR and QT intervals
b) Widened QRS
c) T wave inversion, ST segment depression
d) Dysrhythmias (PVC's; SVT; V fib)
e) Increased risk for digoxin toxicity
2) Cold, painful hands and feet (Secondary to vasomotor changes)

b. Neuromuscular (Similar to hypocalcemia; result from increased neuromuscular excitability)

1) Seizures (Generalized or focal)
2) Confusion (Common), hallucinations, ataxia, depression
3) Hyperreflexia
4) Muscle tremors and weakness, tetany
5) Positive Chvostek's and Trousseau's sign
6) Laryngeal stridor
7) Nystagmus

3. Management

a. Increase intake

1) Dietary (Mild deficiency can be corrected by diet)
2) IV or deep IM (When symptomatic or cause is malabsorption; controversial use of Mg ++ with cardiac dysrhythmias and myocardial infarction)
a) IV - 1-2 g MgS04 over 15 min. (Use 20% concentration or less)
b) Assess renal function (Kidneys responsible for elimination; if impaired, monitor blood levels closely)
c) Monitor deep tendon reflexes (Depressed reflexes indicates Mg ++ too high)
d) Mg++ in TPN (Mg++ driven into cells with refeeding so assure adequate Mg ++ in TPN)

b.   Seizure precautions (When hypomagnesemia is severe)

c. Monitor airway (Laryngeal stridor)

d. Decrease excretion (Identify cause and tireat)

 

Case Studies

A 65-year-old male with chronic alcoholism is brought into the critical care unit following after prolonged seizure activity. The following are present on admission:

BP=108/60, Temp=38, HR=120, RR=16

Serum: Na+=130 mEq/L            ABG's: pH=7.05, PC02=15, p02 80, HC03=4

K+=8.9 mEq/L, BUN=48 mEq/L, Creatinine 3.0 mg/dL

Urine: Na+ 45 mEq/L, Osmolality=600 mOsm/L

1. What factors are contributing to his hyperkalemia?

Cellular breakdown secondary to seizures,  impaired renal function, and possibly metabolic acidosis.

2. On admission his ECG shows sine waves. What would be the appropriate intervention and why?

CaCl - protect myocardium from effects of K+; NaHC03 - obvious metabolic acidosis, shift K+ back into cells; could also give glucose and insulin if others not effective; possibly start exchange resin (kayexalate) to promote removal of K+, and/or dialysis.

A 46-year-old female is admitted to the CCU with viral encephalitis. VS are stable on admission. She does complain of a severe headache and has had periods of mild confusion over past 24 hours. Labs on admission include the following:

Serum: Na+=140 mEq/L,  K+=3.8 mEq/L, Osmolality=282 mOsm/kg

Creatinine=0.9 mg/dL, Hct=38.0%,  Urine: Osmolality=300 mOsm/kg

For the first 24 hours after admission she remained stable. Urine output averaged > 50ml/hr. Today you note that she is showing increased confusion. She is also hyperventilating. Her urine output has decreased over the past 12 hours to < 30 ML/hr. Weight is up 2 kg with no change in intake. Labs are obtained and the results are:

Serum Na+: 124 mEq/L,   K+ 3.5 mEq/L,  Serum Osmolality  260 mOsm/kg 

Urine Osmolality 1050 mOsm/kg,

1. Discuss her current fluid status.

Serum osmolality is low with a low Na+ indicating relative water excess; urine osmolality is high indicating very concentrated urine.

2. How would you explain the changes seen with her assessment?

Presumably SIADH initiated by inflammatory condition of brain; ADH causes retention of water; with SIADH urine osmolality is high; serum osmolality is low; serum Na+ is low; this would account for her decreased output; hyponatremia and water excess would account for confusion and sudden weight gain.

3. What would be the appropriate intervention for her fluid imbalance?

Water restriction; hypertonic (3-5%) saline to increase Na+; diuretic to increase free water loss.

4. Why is it essential to replace Na+ slowly?

Rapid replacement of Na+ can cause intracellular dehydration. Hypertonic extracellular fluid pulls free water out of cells which shrink.

A 74-year-old male is admitted to the surgical floor in preparation for surgery for metastatic bone CA. He is also known to have a history of diabetes mellitus. He states his blood sugar has really been tough to manage for about the past 3 days. In his assessment: you note flat neck veins and dry mucous membranes. Vital signs on admission include:

lying BP=130/68, HR=98

sitting BP 120/68, HR=112

standing BP 108/60, HR=122

During his history he tells you he has been voiding large amounts for about the past 48 hours. Lab findings obtained on admission include:

Serum: Na+ 135 mEq/L, Glucose=300 mg/dL, Mg++=1.0 mEq/L, Serum Osmolality=275 m0sm/kg, Ca ++=11.5 mEq/L

1. What does this information indicate in regards to his fluid status?

Physical findings indicate fluid deficit; normal Na+ and osmolality would indicate saline deficit.

2. What would be possible cause for this imbalance and the changes in output he described? Glucose of 300 could result in an osmotic diuresis resulting in large loss of water in urine (osmotic diuresis).

3. Discuss his electrolyte balance and possible causes?

Na+ normal; Mg++ is low which could be combination of loss through diuresis as well as in response to hypercalcemia; Ca++ is high most likely secondary to mobilization from bone resulting from cancer.

4. What aspects of his assessment would be important given his electrolytes?

ECG changes; dysrhythmias; diminished deep tendon reflexes (elev. Ca++); LOC changes; seizures; laryngeal stridor.

Study Questions

1. JS, a 34-year-old male alcoholic, was in an MVA and sustained multiple injuries. He has received 8 units of whole blood over past 24 hours. His ECG is now showing T wave inversion with a prolonged QT interval and ST segment. What would you expect to find in relationship to his electrolytes and why?

Ca++ may be quite decreased which would account for ECG changes. Multiple transfusions over a short period of time can cause decreased ionized Ca++. The citrate binds with the Ca++. He is also an alcoholic, which may mean hypomagnesemia, and liver dysfunction which may also increase risk.

What other clinical changes would you want to monitor JS for in relation to his Ca++?

Hypotension, tetany, positive Chvostek's sign and Trousseau's sign, seizures, bronchospasm and possibly obstruction leading to arrest, lack of bowel sounds indicating paralytic ileus, bleeding.

2. TM, a 28-year-old female, has been receiving chemotherapy for hepatic carcinoma. She is admitted to the critical care unit with recent onset of confusion and lethargy. Oxygenation status is normal. BP is 80/50. Laboratory results are as follows:

Na=131 mEq/L, Hgb=13 G/dL

K+=3.7 mEq/L, Hct=41

Glucose=124 mg/dL, Total protein=3.1 G/dL

These findings are most consistent with which of the following?

a. Decreased hydrostatic pressure secondary to hyponatremia

b. Increased colloidal oncotic pressure secondary to increased protein in vascular space

c. Increased hydrostatic pressure secondary to hypervolemia

d. Decreased colloidal oncotic pressure secondary to low protein

Correct answer: d

3. A 65-year-old male comes to the critical care unit with a history of compulsive water drinking. He is hyperventilating and is confused. Would you expect his Na+ to be increased or decreased and why?

He most likely has water excess relative to sodium, causing a dilution of ECF, resulting in a decreased serum Na+. With saline excess, water and electrolytes are increased in the same proportion, TBW is increased along with sodium, and serum Na+ concentration is normal. Except with impaired kidney function, one needs to drink a whole lot of water to reduce sodium concentration (typically 15+ liters!).