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Suppose your patient has edema—
indicating that there’s enough fluid in
his body—but his vital signs and urine
output suggest that he’s hypovolemic.
What’s going on? He’s experiencing
third-spacing, a shifting of fluid into
interstitial spaces. Find out what
needs to be done to get that fluid
back where it belongs.
MARCIA BIXBY, RN, CS, CCRN, MS Critical Care Nurse Specialist • Beth Israel Deaconess Medical Center • Boston, Mass. Consultant for Critical Care Education • Randolph, Mass. The author has disclosed that she has no significant relationships with or financial interest in any commercial companies that pertain to this educational activity.
YOU’RE TAKING REPORT on John Miller, who had a colectomy 2 days ago because of a ruptured diverticulus. You learn that his heart rate has increased over the past 24 hours, yet his blood pressure has been gradually falling and he’s had marginal urine output (30 mL/hr). Mr. Miller weighs 4 kg more than before surgery, and he has generalized edema. The health care team has decided not to increase Mr. Miller’s maintenance intra- venous (I.V.) infusion of lactated Ringer’s solution. The nurse from the previous shift says not to worry: His fluid will “mobilize” and he’ll “make urine” soon. Not sure what she means by that, you head off to check out Mr. Miller’s condition for yourself. During your assessment, you find that Mr.
Miller has 2+ edema, warm skin, and palpa- ble peripheral pulses. His heart rate is 108 beats/min, his blood pressure is 110/64 mm Hg, and his urine output remains marginal at 30 mL/hr. Mr. Miller’s abdomen is firm and distended, with hypoactive bowel sounds. He says his pain is well controlled with his patient-controlled analgesia infu- sion. Mr. Miller’s edema indicates that he has enough fluid in his body. But his vital signs and urine output seem to tell a different tale—hypovolemia. How can you reconcile these differences?
Who’s on third?
Mr. Miller is experiencing third-spacing, which happens when fluid is trapped in the interstitial spaces. It can occur in the
42 Nursing made Incredibly Easy! September/October 2006
Where has all
Third-spacing:
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brain, lungs, abdomen, and extremities. Let’s look at the physiology of third-spacing and what you need to know to care for Mr. Miller. You may remember from your patho- physiology class that fluid moves from intravascular (inside the blood vessel) to extravascular (outside the blood vessel) spaces and from intracellular (inside the cell) to extracellular (outside the cell) spaces (see Fluids 101 ). Fluid is constantly on the move to maintain balance (see On the move ). Intravascular-to-extravascular movement of fluid occurs through diffusion, which is controlled by hydrostatic and capillary plas- ma oncotic pressures. Hydrostatic pressure is the pressure that fluid places on the wall of a blood vessel. If the vessel wall is strong, as with an artery,
September/October 2006 Nursing made Incredibly Easy! 43
the fluid gone?
On the move
Fluids are constantly on the move, seeking to keep the body in equilibrium. Here’s how they do it.
- Diffusion: This is passive movement of mol- ecules across a membrane from an area of higher concentration to an area of lower con- centration.
- Osmosis: Water moves through a selective- ly permeable membrane from an area of lower concentration of ions to an area of higher concentration of ions.
- Active transport: This is movement of mole- cules against a concentration as they move from an area of lower concentration to an area of higher concentration. The movement requires energy.
Quick guide to I.V. solutions
A solution is isotonic if its osmolarity falls within (or near) the normal range for serum (240 to 340 mOsm/L). A hypotonic solution has a lower osmolarity; a hypertonic solution, a higher osmolarity. This chart lists common examples of the three types of I.V. solutions and provides key considera- tions for administering them.
Solution Examples Nursing considerations Isotonic • Lactated Ringer’s • Because isotonic solutions expand the (275 mOsm/L) intravascular compartment, closely monitor the
- Ringer’s injection patient for signs of fluid overload, especially if (275 mOsm/L) he has hypertension or heart failure.
- 0.9% sodium chloride • Because the liver converts lactate to bicarbon- (308 mOsm/L) ate, don’t give lactated Ringer’s solution if the
- 5% dextrose in water patient’s pH exceeds 7.5. (D 5 W; 260 mOsm/L) • Avoid giving D 5 W to a patient at risk for
- 5% albumin increased intracranial pressure (ICP) because it (308 mOsm/L) acts like a hypotonic solution. (Although usually
- Hetastarch considered isotonic, D 5 W is actually isotonic (310 mOsm/L) only in the container. After administration, dex-
- Normosol (295 mOsm/L) trose is quickly metabolized, leaving only (295 mOsm/L) water—a hypotonic fluid.)
Hypotonic • 0.45% sodium chloride • Administer cautiously. Hypotonic solutions (154 mOsm/L) cause a fluid shift from blood vessels into cells.
- 0.33% sodium chloride This shift could cause cardiovascular collapse (103 mOsm/L) from intravascular fluid depletion and increased
- 2.5% dextrose in water ICP from fluid shift into brain cells. (126 mOsm/L) • Don’t give hypotonic solutions to patients at risk for increased ICP from stroke, head trauma, or neurosurgery.
- Don’t give hypotonic solutions to patient at risk for third-space fluid shifts (abnormal shifts into the interstitial space)—for example, patients with burns, trauma, or low serum protein levels from malnutrition or liver disease.
Hypertonic • 5% dextrose in 0.45% sodium • Because hypertonic solutions greatly expand chloride (406 mOsm/L) the intravascular space, administer them by I.V.
- 5% dextrose in 0.9% sodium pump and closely monitor the patient for circu- chloride (560 mOsm/L) latory overload.
- 5% dextrose in lactated • Hypertonic solutions pull fluid from the inter- Ringer’s (575 mOsm/L) stitial space, so don’t give them to a patient with
- 3% sodium chloride a condition that can cause cellular dehydration, (1,025 mOsm/L) such as diabetic ketoacidosis.
- 25% albumin • Don’t give hypertonic solutions to a patient (1,500 mOsm/L) with impaired heart or kidney function—his sys-
- 7.5% sodium chloride tem can’t handle the extra fluid. (2,400 mOsm/L)
September/October 2006 Nursing made Incredibly Easy! 45
46 Nursing made Incredibly Easy! September/October 2006
accumulates in the abdomen, the patient can develop edema of the bowel, which may result in intra-abdominal hyperten- sion or abdominal compartment syndrome if not reversed over the first 24 to 48 hours after surgery.
What’s going on inside
the cells?
Interstitial fluid trapping causes compres- sion of the microvasculature in the distal circulation. As the cells swell and com- press the capillaries around them, blood flow is further impaired, leading to hy- poperfusion and ischemia. Anaerobic me- tabolism kicks in (except in the brain cells) to sustain the cells until perfusion is re- stored. But when anaerobic metabolism eventually fails, the sodium/potas- sium pump inside the cell starts to fail too. Sodium and potassium switch places: Sodium moves into the intracellular space while potassium moves into the extracellular space. An increased level of intracellular sodium causes water to be pulled into the cell. The cell wall membrane stretches and releases cytokines and other mediators. Once released, mediators become active and create local inflammation, which further damages the cells. Mediators also get into the systemic cir- culation, where the blood gives them a ride to other parts of the body. This free ride can lead to systemic inflammatory response syndrome (SIRS). Organ failure may also occur, which leads to further inflammation and dysfunction, release of mediators, and progression to multiple organ dysfunction syndrome (MODS), which increases the incidence of mortality (see Mediators of SIRS and MODS ). Let’s hope Mr. Miller doesn’t go down this road!
Back to Mr. Miller
Now that you understand more about the fluid changes that occur with third-spacing, Mr. Miller’s vital signs aren’t surprising.
The shift of fluid into the interstitial tis- sues decreased his intravascular circulat- ing volume. The baroreceptors in the aorta and carotid arches sensed the lower vol- ume and told the sympathetic nervous system (SNS) to get busy. The SNS did its job by causing release of epinephrine and norepinephrine, which lead to vasocon- striction of the peripheral vessels and an increasing heart rate. Let’s take a closer look at this process. Vasoconstriction shunts blood from the periphery to the major organs, which can compromise circulation to the extremities. Compromised circulation may lead to hypoxia, ischemia, and SIRS. You’ll want to keep a sharp eye on Mr. Miller’s perfusion: Check peripheral pulses, skin temperature and sensation, and capil- lary return on the hands and feet. An increased heart rate kicks up cardiac out- put so that the body’s oxygen requirements can be met. But the heart can only do so much. If myocardial oxygen demand keeps rising, the heart won’t be able to supply enough oxygen; myocardial ischemia or infarction may result. Be ready to respond quickly if Mr. Miller shows signs or symp- toms of myocardial ischemia, such as chest pain. Mr. Miller’s kidneys are doing their part to help out. When they sensed the decrease in glomerular filtration rate, which would hap- pen with his marginal urine output, they launched the renin-angiotensin-aldosterone system. This system causes peripheral vaso- constriction from the effects of angiotensin II and fluid retention from the release of aldos- terone. Antidiuretic hormone is also released in response to low circulatory volume, and it tells the kidneys to absorb more sodium from the tubules; this will also increase the absorption of water. The goal is to increase circulating volume, thereby boosting cardiac output and blood pressure. Without this compensatory mechanism, Mr. Miller’s blood pressure would be lower than it is right now.
This sodium and
potassium
switcheroo can
cause a lot of
trouble!
48 Nursing made Incredibly Easy! September/October 2006
How fluids affect cells: Hypertonic solutions
A hypertonic I.V. solution has a solute concentration
higher than the solute concentration of serum.
Infusing a hypertonic solution increases the solute
concentration of serum. Because the solute concen-
tration of serum is now different from the interstitial
fluid, osmosis occurs. Fluid is pulled from the cells
and the interstitial compartment into the blood ves-
sels.
Many patients receive hypertonic fluids postoper-
atively. The shift of fluid into the blood vessels
reduces the risk of edema, stabilizes blood pressure,
and regulates urine output.
Blood vessel
Shrunken cell
Great! This
hypertonic solution
will cause fluid to
flow from the cells
into the blood
vessels.
Gulp! This
hypertonic
stuff dries
me out.
Wanna try a
hypertonic I.V.
solution?
Yeah. I
could stand
to lose a
little fluid.
September/October 2006 Nursing made Incredibly Easy! 49
How fluids affect cells: Hypotonic solutions
A hypotonic I.V. solution is the opposite of a hyper-
tonic solution. It has a lower solute concentration
than serum. Infusion of a hypotonic solution causes
the solute concentration of serum to decrease.
Because the solute concentration of serum is now
different from the interstitial fluid, osmosis occurs.
This time, the fluid shift is in the opposite direction
than that of a hypertonic fluid. Fluid shifts out of the
blood vessels and into the cells and interstitial
spaces, where the solute concentration is higher.
Swollen cell
Blood vessel
Have you ever
had a hypotonic
solution?
Can’t say
I have.
Burp!
Great stuff.
But this fluid
shift has left me
a little bloated.
You should try one. A
hypotonic I.V. solution
hydrates cells while
reducing fluid in the
circulatory system.
pressure transducer and level the transduc- er to the iliac crest. Instill 50 mL of sterile 0.9% sodium chloride into the bladder, turn the stopcock or valve, and obtain the pres- sure measurement at end expiration. If the intra-abdominal pressure is more than 12 mm Hg, suspect that the patient has intra- abdominal hypertension (see Making the grade ). Elevated pressure in the abdomen indi- cates increased bowel edema. As the bowel edema progresses (as a result of cellular ischemia and hypoperfusion) and there’s more pressure in the abdomen, the blood return to the right side of the heart is im- paired; so is blood flow out of the left ven- tricle. The increased abdominal pressure can impair lung expansion as well, leading to respiratory distress. It can also exert pressure on the renal circulation, leading to renal dysfunction. Mr. Miller’s edema happened quickly because of his surgery, so his skin can’t keep pace with the swelling. That’s why his abdomen is firm. Rising pressure in the abdomen from third-spacing compresses the major blood vessels running through it, which causes the following problems: n in the vena cava , reduced preload (ve- nous return to the heart), leading to de- creased cardiac output, which results in decreased blood pressure n in the aorta and the iliac and femoral ar- teries , increased afterload (pressure in the peripheral circulation), further reducing cardiac output and blood pressure n in the renal vessels , impaired kidney function n in the spleen’s vasculature , impaired blood flow to the bowel, liver, and spleen. If the fluid shift isn’t corrected and pres- sure keeps rising, Mr. Miller will develop intra-abdominal hypertension or abdominal compartment syndrome. This situation results in a downward spiral of bowel ischemia and tissue death leading to necro- sis. So you’ll want to watch him closely for signs of intra-abdominal hypertension and
abdominal compartment syndrome: increas- ing abdominal girth or bladder pressure and increasing pain not controlled with the pre- vious medication dosing. Early suspicion of intra-abdominal hypertension or abdominal compartment syndrome will allow time for interventions to prevent or minimize tissue damage.
What’s next?
Mr. Miller’s vital signs are slightly abnor- mal but stable, so he seems to be tolerat- ing the fluid shifting. Over the next sev- eral hours (up to 48 hours), the fluid shift will be resolved or he will continue to de- velop bowel edema and, eventually, is- chemia. During this time, closely monitor Mr. Miller’s vital signs, urine output, and periph- eral perfusion. Report any changes to the health care provider. Here are other areas to keep tabs on: n Mental status. Is Mr. Miller responsive and able to communicate and answer questions appropriately? If not, his blood pressure isn’t high enough for adequate perfusion. n Ventilation/perfusion status. Can he maintain adequate ventilation to support his oxygen needs? Does he have crackles? Is his oxygen saturation greater than 97% on room air, or does he need supplemen-
September/October 2006 Nursing made Incredibly Easy! 51
Making the grade
A patient’s intra-abdominal pressure (IAP) determines if he has intra- abdominal hypertension. In a consensus statement, the World Society of Abdominal Compartment Syndrome defines intra-abdominal hyperten- sion as “sustained or repeated pathologic elevation of IAP $ 12 mm Hg.” There are four grades of intra-abdominal hypertension, according to this group:
- Grade I: IAP of 12 to 15 mm Hg
- Grade II: IAP of 16 to 20 mm Hg
- Grade III: IAP of 21 to 25 mm Hg
- Grade IV: IAP of > 25 mm Hg. The higher the number, the more severe the condition and the greater the risk of complications.
tal oxygen therapy? n Hematocrit and hemoglobin. Rising hematocrit and hemoglobin levels indicate hemoconcentration of serum due to fluid shifting to the interstitial space; decreases in these values may indicate bleeding— unless Mr. Miller’s had several liters of fluid replacement solution, causing a dilu- tional effect. n Serum electrolytes. Increased sodium may occur with hemoconcentration. Potas- sium may rise due to intracellular shifting or if Mr. Miller is developing renal dys- function. Elevated blood urea nitrogen (BUN) and creatinine levels may be due to hemoconcen-
tration, but a rising creatinine with a normal BUN level may signal intrarenal dysfunction. Lactate is produced as a byproduct of anaerobic metabolism. In patients who’ve had bowel surgery, an elevated lactate level may indicate bowel ischemia—unless the patient has liver dysfunction or failure and received several liters of lactated Ringer’s solution for fluid resuscitation. The lactate in lactated Ringer’s solution is converted to bicarbonate in a healthy liver. But in a dys- functional or diseased liver, lactate isn’t con- verted; it remains in the blood. n Abdominal pressure. Measure abdomi- nal girth or bladder pressure at least every 4 to 8 hours while Mr. Miller’s vital signs are abnormal and his urine output is low. n Fluid resuscitation. You’ll continue to
give Mr. Miller a maintenance I.V. infusion of isotonic fluid, as well as in- termittent boluses of a colloid, such as albumin. Albumin will pull fluid from the interstitial space into the in- travascular space. If the kidneys can’t get rid of the extra fluid on their own, a small dose of a loop diuretic like furosemide (Lasix) can help. Remem- ber, colloid fluids are plasma pro- teins, so their higher molecular structures allow you to give less volume to support Mr. Miller’s blood pressure. If his hemoglobin is low, infusing blood products, such as packed red blood cells, as needed will help increase oxygen-carrying capacity, as well as increase intravascular oncotic pressure and pull fluid from the interstitial space.
What if…?
If the health care provider suspects bowel ischemia or necrosis, he may order a kidney-ureter-bladder (KUB) X-ray and computed tomography (CT) scan. A KUB image will show the extent of bowel edema and any “free” air, which would indicate bowel perforation. A CT scan detects worsening bowel edema, lack of adequate perfusion, or hematomas formed from bleeding. A patient whose vital signs are deteriorat- ing and who has decreasing urine output and increasing abdominal girth or bladder pressure readings will likely return to the operating room; he may have a perforated bowel that needs to be repaired. If the bowel
52 Nursing made Incredibly Easy! September/October 2006
Listen, I know
things are
shifting right
now, but give
it some time
to resolve.
did you
know?
Why does fluid fol- low a protein like albumin? Protein is a large molecule with a negative charge. It attracts the most abundant extracellular fluid ion—sodium— which has a posi- tive charge. You probably remem- ber that water fol- lows sodium. So, sodium follows protein, and water follows sodium..
54 Nursing made Incredibly Easy! September/October 2006
1. Third-spacing refers to fluid trapped in the a. intravascular spaces. b. interstitial spaces. c. intracellular spaces. 2. Third-spacing typically occurs in the extremities, ab- domen, and a. lungs. b. liver. c. kidneys. 3. In third-spacing, fluid in the body moves from the a. intravascular spaces to the extravascular spaces. b. extravascular spaces to the intracellular spaces. c. extracellular spaces to the extravascular spaces. 4. Hydrostatic pressure primarily affects the a. lymph system. b. veins. c. capillaries. 5. Loss of albumin or protein can cause a. increased cardiac output. b. decreased oncotic pressure. c. decreased hydrostatic pressure. 6. Ascites is caused by a. a low albumin level and fluid accumulation in the peri- toneum. b. decreased plasma proteins in the peritoneum. c. excess fluid in the intracellular spaces of the liver. 7. Hypertonic I.V. fluids are used as therapy because they a. pull fluid from intravascular space into interstitial space. b. replace lost proteins. c. increase circulating volume. 8. Normally, the body’s fluid is distributed as a. 75% intracellular and 25% extracellular. b. 60% extracellular and 40% intracellular. c. 20% intracellular and 80% extracellular. 9. Albumin is effective in treating third-spacing because it a. decreases oncotic pressure. b. attracts sodium and water. c. increases hydrostatic pressure. 10. How does third-spacing relate to systemic inflamma- tory response syndrome (SIRS)? a. Swollen cells of interstitial edema release mediators. b. Histamine release causes capillary vasoconstriction. c. Bradykinin release inhibits the coagulation cascade. 11. Decreased intravascular circulating volume leads to a. vasoconstriction and increased heart rate. b. vasodilation and decreased heart rate. c. vasodilation and increased blood pressure. 12. Compression of the vena cava from abdominal third- spacing can cause a. increased blood pressure. b. decreased cardiac output. c. increased preload. 13. Which lab finding may indicate postoperative bowel ischemia? a. increased sodium b. increased blood urea nitrogen c. increased lactate 14. Five percent dextrose in 1 ⁄ 2 normal saline is classified as a. isotonic. b. hypotonic. c. hypertonic. 15. Patients receiving hypertonic I.V. solutions should be monitored for which adverse effect? a. circulatory overload b. increased peripheral edema c. decreased intravascular volume 16. Signs of abdominal compartment syndrome include each of the following except a. increased abdominal girth. b. decreased bladder pressure. c. increased pain levels. 17. Rising hemoglobin and hema- tocrit in a postoperative patient probably result from a. acute bleeding. b. fluid shifts to inter- stitial space. c. compensation for hypoxemia.
Third-spacing: Where has all the fluid gone?
GENERAL PURPOSE: To provide the registered professional nurse with an overview of the pathophysiology, signs and symptoms, and nursing care of a patient who is experiencing third-spacing of fluids. LEARNING OBJECTIVES: After reading this article and taking this test, you should be able to: 1. Describe the pathophysiology and complications of third-spacing. 2. Identify nursing as- sessments, monitoring, and interventions for patients with third-spacing.
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Go to the next page for the CE Enrollment Form.
Ready to shift
into test-taking
mode?
September/October 2006 Nursing made Incredibly Easy! 55
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Third-spacing: Where has all the fluid gone? (page 42) B. Test Answers: Darken one circle for your answer to each question. a b c
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Acute pancreatitis: Inflammation gone wild (page 18) B. Test Answers: Darken one circle for your answer to each question.
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