BACK TO BASICS

Abnormal Basic Metabolic Panel Findings:

Implications for Nursing
Protecting renal function and acid–base balance.

ABSTRACT
In this article, the second in a new series designed to improve acute care nurses’ understanding of labora-
tory abnormalities, the author continues her discussion of important values in the basic metabolic panel
(see Back to Basics, January, for a discussion of sodium and fluid balance). Here she addresses the electro-
lytes potassium and chloride as well as blood urea nitrogen and creatinine, four values that are best con-
sidered together because they both reflect and impact renal function as well as acid–base homeostasis.
Important etiology, clinical manifestations, and treatment concerns are also presented. Three case studies
are used to integrate select laboratory diagnostic tests with history and physical examination findings, al-
lowing nurses to develop a thorough, focused plan of care for electrolyte abnormalities and kidney disor-
ders commonly encountered in the medical–surgical setting.
Keywords: acute kidney injury, blood urea nitrogen, chloride, creatinine, fluid balance, hyperchloremia,
hyperkalemia, hypochloremia, hypokalemia, nursing care, potassium

A
62-year-old patient admitted from the ED sium. (For a basic understanding of potassium
with a diagnosis of acute hyperkalemia is physiology, see The Physiology of Potassium.1, 2)
transferred to your telemetry unit. The
patient has a history of type 2 diabetes and hyper- HYPERKALEMIA
tension; her medications include hydrochlorothiazide, Etiology. While there is some variation in the specific
lisinopril, and insulin. During handoff, the ED nurse value found in the literature and used in practice,
tells you the patient received 10 units of regular insulin hyperkalemia is often defined as a serum potassium
intravenously and 50 mL of 50% dextrose intrave- level greater than 5 mEq/L.2-4 Many potential factors
nously, and her serum potassium level has decreased can contribute to the development of hyperkalemia.
from 6.1 to 4.9 mEq/L. Once handoff is completed, Kidney disease. Acute and chronic kidney condi-
the patient tells you she’s “fixed” and wants to go home. tions can affect the ability of the kidneys to excrete
She discloses that she stopped taking her hydrochlo- potassium, resulting in hyperkalemia. Of note,
rothiazide three days earlier because she’d gone to a patients with chronic hyperkalemia usually adapt
wedding over the weekend and wanted to avoid fre- and may be able to tolerate higher potassium levels
quent trips to the bathroom; she insists she won’t without adverse effects.1
make that mistake again. (All cases in this article are Increased intake of potassium can result from a
composites based on my experience.) potassium-rich diet, use of potassium supplements,
How do you explain to the patient that she still and the administration of potassium-containing iv
requires monitoring and care? What do you now need solutions.1
to watch for, and in what ways can you advocate for Medications. Medications that inhibit aldosterone
her appropriate medical care? Although nurses review production or activity through the renin–angiotensin–
patient laboratory findings routinely, a thorough under- aldosterone system are commonly implicated in
standing of these findings in the context of patient his- the development of hyperkalemia. These include
tory and physical examination findings is essential in angiotensin-converting enzyme (ACE) inhibitors,
determining etiology, appropriate treatment, implica- angiotensin receptor blockers (ARBs), and aldosterone
tions for patient education, and ongoing nursing care. antagonists. Nonsteroidal antiinflammatory drugs
Before returning to this case study, let’s review (NSAIDs) can inhibit prostaglandin-mediated vasodi-
hyperkalemia and hypokalemia—or what happens lation in the kidney; the resulting decrease in renal
when patients have too much or too little potas- blood flow may inhibit kidney function and lead to

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 By Lydia A. Bertschi, DNP, APRN, ACNP-BC

hyperkalemia.5 Many medications may contribute to

hyperkalemia, so consider consultation with a phar- The Physiology of Potassium
macist if a patient has or is at risk for hyperkalemia.
Endocrine disorders that result in inadequate aldo- Alterations in potassium balance are common in the acute care set-
sterone (the adrenal insufficiency seen in Addison’s ting and clinically relevant because of their potentially serious or
disease and in critical illness, for example) can result life-threatening consequences. Here are some important points to
in hyperkalemia.1 review in the physiology of potassium:
Acidosis. Hydrogen ions affect the shift of potas- • Potassium is a positively charged ion (cation) and is the major
sium between the intracellular and extracellular intracellular ion. For healthy cell functioning, it must be main-
spaces. Metabolic acidosis occurs when metabolic tained in higher concentration in the intracellular fluid relative
acids increase or are inadequately buffered in the body, to the extracellular fluid (ECF).
resulting in a decrease in pH.1 With certain types of • Potassium can combine with a negatively charged ion (anion)
metabolic acidosis, excess hydrogen ions diffuse into to form salts, such as potassium chloride and potassium phos-
cells for buffering. In order to maintain a balance in phate. In solution, ions dissociate. The concentration of ions in a
positively and negatively charged ions across cell mem- solution can be measured as the weight of the ions per unit of
branes, potassium ions will shift from the intracellular volume, such as milliequivalents per liter (mEq/L).
to the extracellular space, resulting in hyperkalemia.6 • Because cell membranes are semipermeable to water and sol-
Other factors can cause potassium to shift from the utes, potassium will diffuse along an electrochemical gradient;
intracellular space, where it’s found in higher con- that is, it will move into areas where the negative charge is greater
centrations, to the extracellular space. For example, and there are relatively fewer potassium ions until the concentra-
conditions such as hemolysis, tissue injury, and rhabdo- tions are equilibrated on both sides of the cell membrane. The
myolysis are associated with impaired cell membrane sodium–potassium–adenosine triphosphatase (Na+/K+-ATPase)
integrity and function. Without functional sodium– pump counters the passive diffusion of potassium. Energy from
potassium–adenosine triphosphatase (Na+/K+-ATPase) the hydrolysis of adenosine triphosphate molecules is required
pumps, potassium will diffuse passively from the intra- to power the Na+/K+-ATPase pump, moving potassium against
cellular fluid (ICF) to the extracellular fluid (ECF).1 its electrochemical gradient and, thereby, maintaining a higher
Clinical manifestations of hyperkalemia are pri- intracellular potassium concentration.1 See Figure 1.
marily related to a reduction in the transmembrane • The electrochemical gradient of potassium enables resting mem-
gradient of potassium and resting membrane poten- brane potential, a state in which the cell membrane is polarized
tial (RMP). In hyperkalemia, the potassium level in the but able to reverse polarity (depolarize) in response to a stimulus.
ECF is higher than it should be, so the membrane is A reversal in polarity results in an action potential, the cell-to-cell
less polarized (hypopolarized), and the cell interior signal that allows the nervous system to function and muscles to
becomes less negatively charged.2, 7 In hypopolarized contract.1 Alterations in the potassium gradient, therefore, primar-
cell membranes, RMP is closer to threshold, the point ily affect the excitability of muscle and nerve cells.2
at which a stimulus will result in an action potential. • Abnormal potassium concentrations in the ECF don’t arise only
Clinical manifestations in smooth muscle are, there- from an increase or decrease in total body potassium; they can
fore, mostly due to increased irritability (exaggerated also occur because of shifting of potassium between the intra-
responses to stimuli) and include gastrointestinal (GI) cellular and extracellular spaces. Failure or dysfunction of the
symptoms like abdominal cramping, nausea, vomiting, Na+/K+-ATPase pump or disruption of cell membrane integrity
and diarrhea. If hyperkalemia is severe enough, the cell will cause potassium to shift from the intracellular to the extra-
will remain hypopolarized even after an action potential, cellular space, resulting in hyperkalemia. Other conditions can
unable to repolarize and contract again. In skeletal cause the opposite; potassium shifting from the extracellular to
muscle, this severe hypopolarization would mani- the intracellular space would result in hypokalemia.1
fest as decreased deep tendon reflexes, weakness, and • When there is a normal dietary potassium intake, the body has a
even paralysis.2, 7 Manifestations in cardiac muscle are net positive balance of potassium, which must be continuously
more severe and potentially life-threatening because eliminated primarily by the kidneys and to a lesser degree by the
of changes in rhythm and conduction. On an elec- gastrointestinal system. Na+/K+-ATPase pumps in the distal tubule
trocardiogram (ECG), you may see peaked T waves, and collecting duct of the nephron are primarily responsible for
QRS complex widening, sinus bradycardia, junctional secreting potassium into the filtrate so it can be excreted in the urine.
rhythm, various heart blocks, and eventually, ventric- Aldosterone is an important hormone to regulate extracellular
ular fibrillation leading to asystole (see Unexpected volume. Aldosterone works by stimulating Na+/K+-ATPase pumps to
Laboratory Findings: Is It True Hyperkalemia?2). increase urinary excretion of potassium while reabsorbing sodium
Treatment of hyperkalemia may be needed emer- and water. Excessive elimination of potassium by the kidneys
gently because of potentially lethal changes in car- results in hypokalemia, and retention results in hyperkalemia.1
diac conduction, and often requires rapid nursing

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action and multiple medications (see Table 12, 3, 7-10). eral, treatment is considered for serum potassium
The customary approaches to treatment have not levels greater than 6 mEq/L.3 Nurses should under-
changed much since the 1950s, and evaluating these stand how each treatment works and the important
treatments is limited by lack of standardization in patient safety considerations associated with medi-
definitions and lack of randomization in study cation administration. Patients treated for hyperka-
design.11 For ordering providers, individual patient lemia should have cardiac monitoring and adequate
factors should guide treatment approach, but in gen- iv access.2
Case 1: Out of balance. Let’s return now to the
case study at the beginning of the article. After set-
Figure 1. Active Transport of Sodium and Potassium tling your patient with hyperkalemia, you review
her laboratory findings and note the following:
sodium, 140 mEq/L; potassium, 6.1 mEq/L; chlo-

Na/K
ride, 105 mEq/L; carbon dioxide, 26 mEq/L; blood
Na+ + Extracellular fluid with high
concentration of Na+
urea nitrogen, 10 mg/dL; and creatinine, 0.9 mg/dL.
Na+ Na (For reference, see Normal Adult Laboratory Values.4)
+

+
Na+ Knowing the information discussed here so far, you
understand that the patient has acute hyperkalemia
primarily because she stopped taking a potassium-
Cell membrane wasting diuretic (hydrochlorothiazide) while con-
K+ K+
tinuing to take a potassium-sparing medication
K+
(lisinopril, which decreases release of aldosterone).
ATP You explain to her that although the insulin she was
given has shifted the potassium back into the cells

K/Na +
+
Intracellular fluid
with low concentration
of Na+ and high
for now, it’s still present in her body and her potas-
sium levels may increase again. Your plan of care
includes the following:
concentration of K+ • Monitor telemetry closely for ECG changes.
• Initiate hourly blood glucose monitoring for
hypoglycemia.
• Perform clinical assessment for signs and symp-
Potassium (K+) is the primary positively charged ion in intracellular fluid, and toms of hyperkalemia and hypoglycemia.
sodium (Na+) is the primary positively charged ion in extracellular fluid. When the • Discuss with the ordering provider the possible
concentration of either ion is altered, sodium or potassium is actively transported resumption of hydrochlorothiazide to begin
across the cell membrane via the sodium–potassium–adenosine triphosphatase removal of potassium from the body and con-
pump in order to regain the normal concentration gradient. Energy to drive firm timing of repeat laboratory assessment.
the pump is released by the hydrolysis of adenosine triphosphate (ATP). • Educate the patient on the potential dangers
of stopping any of her medications without
consultation.
Unexpected Laboratory Findings: Is It True
Hyperkalemia?2 HYPOKALEMIA
Etiology. Hypokalemia is defined as a serum potas-
• Nurses should investigate any new hyperkalemia. sium level of less than 3.5 mEq/L.4 As in hyperkale-
• If you note hyperkalemia, be sure to ask yourself whether the lab- mia, many potential factors can contribute to the
oratory value is accurate; it could be falsely elevated. (For example, development of hypokalemia, and its etiology is
if red cell lysis [hemolysis] occurs when drawing blood or process- conceptualized similarly1, 12:
ing the blood sample, potassium is released into the solution from • decreased potassium intake as a result of poor
the broken cells, resulting in an inaccurately high potassium level.) diet or npo (nil per os, or nothing by mouth)
• Hemolysis is more likely to occur if the tourniquet is left in place status
too long, the patient pumps her or his fist repeatedly, or there is • increased excretion (as the result of medications
a delay in processing the blood. or supplements, endocrine disorders like Cushing
• Along with the precaution of performing patient assessment for disease, or diarrhea)
signs and symptoms of hyperkalemia, the nurse who suspects a • shifting of potassium into cells (as the result of
falsely elevated potassium level should consider redrawing the alkalosis or high doses of insulin, for example)
specimen to verify accuracy. Loop and thiazide diuretics are the most common
causes of hypokalemia.5

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Table 1. Common Emergency Treatments for Hyperkalemia
Treatment Mechanism of Action Nursing Implications
Cardiac cell membrane stabilization
Calcium While calcium doesn’t affect serum con- Monitor the ECG for resolution of
centration of potassium, it’s an important hyperkalemic effects within 5 minutes
component of emergency treatment of of calcium administration. If ECG
hyperkalemia. changes do not resolve, contact the
Calcium stabilizes the cell membrane of ordering provider to ask about calcium
cardiac muscle cells by increasing the readministration.
transmembrane voltage gradient, which If calcium is administered as calcium
in cardiac muscle will normalize ECG chloride, central IV access is preferred
findings and reduce the risk of lethal owing to risk of tissue necrosis if extrav-
arrhythmias.2 asation occurs. Calcium gluconate is
safer for peripheral IV administration.2
Monitor for hypotension and bradycar-
dia. Do not mix with sodium bicarbonate
as this may cause a precipitate to form.
Use caution if a patient is on digoxin.8
Intracellular shift of potassium
Insulin and dextrose Insulin indirectly triggers the Na+/K+- Providers often use a standard dose of 10
ATPase pump to shift sodium out of the units OF IV insulin along with 25 g or 50 g of
cell and pump potassium in, decreasing IV dextrose, but the ideal dose may vary
the extracellular concentration of potas- based on patient factors (such as lower
sium. The onset of potassium shifting is baseline blood glucose, kidney disease,
rapid (within 15 minutes of administra- low body weight, female sex). Therefore,
tion), and can lower potassium levels by patients are at risk for hypoglycemia after
0.6–1.2 mEq/L.3 insulin administration for hyperkalemia.3, 9
Dextrose is given to counter the hypogly- Insulin is a temporizing measure, shift-
cemic effects of insulin administration. ing potassium into body cells temporar-
ily and reducing serum potassium.
When the effect wears off, hyperkalemia
may return.
Nurses should monitor for hypoglyce-
mia and recurrent hyperkalemia, along
with associated signs and symptoms.
Consider recommending hourly blood
glucose monitoring for 4–6 hours after
treatment with insulin and dextrose,
and if hypoglycemia develops, proac-
tively request doses of additional dex-
trose as needed.3, 9
β-agonists (albuterol, β-agonists such as nebulized albuterol Monitor for side effects, including
for example) stimulate the Na+/K+-ATPase pump, shift- tachycardia, tremors, and anxiety.
ing more potassium to the cell and, Although β-agonists may be given
thereby, reducing serum concentration.2 intravenously, they are more likely to
result in adverse effects when adminis-
tered by this route.7
Patients already on β-blockers may
receive less therapeutic benefit.2
Because β-agonists work by shifting
potassium, the hyperkalemia may recur
when the effects wear off.2

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Table 1. Continued
Treatment Mechanism of Action Nursing Implications
Sodium bicarbonate Sodium bicarbonate, typically given as a A temporary measure, sodium bicarbon-
bolus to treat hyperkalemia, is thought to ate may be less effective if the patient
indirectly stimulate the Na+/K+-ATPase doesn’t also have metabolic acidosis.
pump, shifting more potassium into the Monitor for effect, as well as for return of
cell. This effect may be more pronounced hyperkalemia.2
if the patient also has metabolic acidosis.2 Sodium bicarbonate may cause hyper-
There are limited data supporting the use natremia and volume overload, which
of sodium bicarbonate for hyperkalemia.8 could be problematic in patients with
congestive heart failure.7 Monitor for
signs of volume overload.
Potassium removal from the body
Potassium-wasting Loop diuretics affect a cotransporter in The patient must have adequate renal
diuretics (loop diuret- the thick ascending limb of the loop of function and be producing urine for
ics, such as furose- Henle that is responsible for reabsorption diuretics to be effective. If the patient
mide, for example) of a large proportion of filtered sodium becomes volume depleted from
and chloride. When blocked, more the diuretics, urine production will
sodium is delivered to the distal tubule decrease, and potassium excretion
and Na+/K+-ATPase pumps are stimulated, may not be adequate. Nurses should
resulting in more potassium excretion.7, 8 closely monitor urine output and
monitor for signs and symptoms of
hypovolemia. Consider contacting
the ordering provider for IV fluids as
needed.2
Sodium polystyrene Sodium polystyrene sulfonate is a potas- Although sorbitol is added to sodium
sulfonate (Kalexate sium exchange resin that is not absorbed polystyrene sulfonate to act as a lax-
and others) from the bowel. In the large intestine, it ative and move the resin through the
binds to potassium, thereby trapping it in GI tract quickly, there is still the risk
the bowel lumen.8 Its onset of action of constipation, bowel obstruction,
(about 2 hours) is slower than that of colonic necrosis, and perforation.2, 7
other treatments, but it eliminates potas- Notify the ordering provider if the
sium from the body rather than shifting it patient does not have a bowel move-
into cells.2 ment, as this could indicate GI compli-
cations.
Note: Patiromer (Veltassa) and sodium
ziconium cyclosilicate (Lokelma), both
recently approved by the FDA, also
act in the bowel lumen to bind potas-
sium. While neither medication seems
to have the major adverse GI effects
reported with sodium polystyrene
sulfonate,8 they are not approved
for emergency treatment of acute
hyperkalemia owing to delayed onset
of action.10
Hemodialysis Although it requires specialized vascular Unlikely to be initiated outside of a
access, hemodialysis is the most effective high-acuity setting; patients with
way to remove potassium from the body, preexisting dialysis access sites may
as it is both rapid and permanent.2 be started on this treatment in a
medical–surgical setting.
ECG = electrocardiogram; FDA = Food and Drug Administration; GI = gastrointestinal; Na+/K+-ATPase = sodium–potassium–adenosine triphosphatase.

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 Clinical manifestations of hypokalemia are also
related to alterations in action potentials.1 Hypo- Normal Adult Laboratory Values4
kalemia hyperpolarizes cell membranes because the
potassium gradient between the ICF and ECF is Sodium: 135–145 mEq/L
increased. Hyperpolarized cells become less respon- Potassium: 3.5–5 mEq/L
sive to stimuli. Manifestations are due to slowing of Chloride: 98–106 mEq/L
action potentials: constipation and ileus (smooth Carbon dioxide: 23–30 mEq/L
muscle), and weakness and paralysis (skeletal mus- Blood urea nitrogen: 10–20 mg/dL
cle). Effects to cardiac muscle are likely the most dan- Creatinine: 0.5–1.1 mg/dL (in women)
gerous and mediated by a different process. At very 0.6–1.2 mg/dL (in men)
low potassium concentrations, cardiac muscle cells
are hypopolarized because of effects to potassium Note: Normal laboratory values may vary slightly, both in the literature and in practice, depend-
ing on the laboratory or health care facility.
conductance. Hypokalemia is commonly associated
with ectopic beats (premature atrial and ventricular
contractions, for example) and tachyarrhythmias.1
Treatment of hypokalemia is accomplished mal saline, however, contains one molecule of
through oral and iv potassium administration, sodium for every molecule of chloride, both in a con-
although the oral route is safer and preferred when centration of 154 mEq/L. Normal saline solution has
appropriate (generally, when serum potassium is higher levels of chloride than are normally present in
2.5 mEq/L or greater).12 Safety concerns with iv the body, so administering large volumes of normal
potassium administration include phlebitis and saline may cause hyperchloremia and hyperchlor-
ECG changes because of the potential onset of emic metabolic acidosis.13
hyperkalemia. When administering iv potassium, Normal saline–induced hyperchloremia may also
be mindful of patients’ renal function and do not lead to a decrease in renal blood flow and glomer-
administer at rates faster than those specified in ular filtration rate (GFR), as well as to decreased
hospital- and unit-approved guidelines.5 Discuss renal cortical perfusion.10 Research on the clinical
with the ordering provider whether the patient impact of these physiological alterations has focused
receiving iv potassium should have telemetry on critically ill patients. Retrospective studies have
monitoring, and consider that patients with severely shown conflicting findings. Oh and colleagues stud-
low potassium may need intermediate or critical ied patients with intracranial hemorrhage who were
nursing care and more frequent laboratory moni- treated with craniotomy and found that hyperchlor-
toring (see Association Between Hypokalemia and emic acidosis was associated with increased risk of
Hypomagnesemia1, 12). acute kidney injury, but hyperchloremia alone was
not.17 In contrast, Yessayan and colleagues stud-
HYPERCHLOREMIA ied critically ill patients with sepsis and found an
As in hypernatremia, hyperchloremia can occur increased risk of acute kidney injury in patients with
from water loss; as water is lost, the concentrations hyperchloremia.18 In an earlier study, Oh and col-
of sodium and chloride increase. Common causes leagues examined perioperative surgical ICU patients
of water loss include excessive sweating, fever, and and found no association between hyperchloremia
inadequate water intake, and these etiologies are and acute kidney injury, except possibly in patients
treated through replacement of free water.13 A net
gain in chloride may also cause hyperchloremia.14
Metabolic acidosis is linked to hyperchloremia; as
chloride levels rise, bicarbonate levels and pH tend Association Between Hypokalemia and
to decrease (see The Physiology of Chloride1, 13, 15, 16). Hypomagnesemia
For example, severe diarrhea results in the loss of
bicarbonate-rich fluids and the reabsorption of chlo- • When magnesium is low, the kidneys increase excretion of
ride; patients who have diarrhea may develop hyper- potassium.
chloremia and hyperchloremic metabolic acidosis.13 • Both hypokalemia and hypomagnesemia contribute to cardi-
Although chloride abnormalities tend to follow ac dysrhythmias, so when you notice signs of ectopy on your
sodium abnormalities, administration of iv normal patient’s electrocardiogram, be sure to discuss checking and
saline disproportionately increases serum chloride treating both electrolyte deficiencies with the ordering provider.1
concentration.13 Normal serum sodium levels range • If hypomagnesemia is not addressed, it may not be possible to
from 135 to 145 mEq/L, whereas normal serum resolve hypokalemia even with potassium supplementation.12
chloride levels range from 98 to 106 mEq/L.4 Nor-

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pilot study by Magee and colleagues found that

The Physiology of Chloride patients who received medications with normal
saline as the diluent were more likely to experience
Chloride (an anion), like sodium (a cation), is important for maintain- hyperchloremia than patients whose medications
ing the solute concentration (tonicity) of the extracellular fluid (ECF) were diluted in 5% dextrose water.22 Van Regen-
and, therefore, the balance of volume in the intracellular and extra- mortel and colleagues also found that maintenance
cellular spaces. The concentrations of chloride and sodium are higher iv fluids and fluid used to dilute medications had a
in the ECF compared with the intracellular fluid (ICF). The kidneys’ more significant impact on sodium and chloride
regulation of sodium, chloride, and water balance is tightly controlled intake than any resuscitation fluids given as iv
to maintain volume of the ICF and ECF. Therefore, increases and boluses.23 Nurses should monitor intake from all
decreases of sodium, chloride, or water volume tend to go hand in iv sources, consider how use of normal saline to
hand, and dyschloremia isn’t usually a primary problem.13, 15 Sodium dilute medications may affect serum chloride levels,
and chloride levels and volume status are important in the activation and advocate the avoidance of excessive iv fluid
of the renin–angiotensin–aldosterone system. Once aldosterone is administration when appropriate.
produced, its main effect is to increase reabsorption of sodium.
Both chloride and water will follow the sodium; the anion (chloride) HYPOCHLOREMIA
follows the cation (sodium), and the water moves by osmosis.1, 15 Compared with hyperchloremia, fewer scenarios
Chloride also plays a major role in acid–base balance because involve clinically significant hypochloremia. Certain
it has an inverse relationship with a key acid buffer, bicarbonate, conditions (such as water intoxication and syndrome
which can form a loose, reversible bond with hydrogen ions, of inappropriate [excessive] antidiuretic hormone)
thereby minimizing changes in pH.16 Hyperchloremia tends to cause proportionate decreases in sodium and chlo-
result in a decrease in bicarbonate; as bicarbonate levels decrease, ride. Disproportionate loss of chloride may occur in
fewer hydrogen ions are buffered and metabolic acidosis results.1 upper GI fluid losses (those caused by excessive vom-
iting or nasogastric suctioning, for example) due to
loss of hydrochloric acid in stomach acid.15 Certain
diuretics, including loop and thiazide diuretics, also
with preexisting, moderate-to-severe chronic kidney cause disproportionate loss of chloride, which may
disease.19 cause hypochloremic alkalosis. As with hyperchlor-
Prospective studies have also shown conflicting emia, clinical manifestations tend to derive from the
findings. Commereuc and colleagues conducted a primary disorder, such as hyponatremia, changes in
post hoc analysis of a randomized trial that com- volume status, or alkalosis.14
pared normal saline with 3% saline in fluid resus-
citation.20 When examining hyperchloremia, the BLOOD UREA NITROGEN AND CREATININE
researchers found an increased risk of metabolic Blood urea nitrogen (BUN) and creatinine are
acidosis but not of acute kidney injury or 28-day important markers of kidney function, for both
mortality. Semler and colleagues conducted a cluster acute and chronic conditions. Both are end products
randomized trial comparing normal saline with bal- of muscle metabolism, with creatinine exclusively
anced crystalloid solutions.21 (The electrolyte con- and BUN primarily excreted by the kidney. Normal
centrations in balanced crystalloid solutions, such creatinine levels range from 0.5 to 1.2 mg/dL (depend-
as lactated Ringer’s solution, are more similar than ing on the patient’s sex), and normal BUN levels
normal saline is to human physiological norms, range from 10 to 20 mg/dL.4 Tests for both markers
including a lower chloride concentration.) In this provide information about glomerular filtration, and
study, balanced crystalloid solutions reduced the they are fairly reliable, as long as there is a constant
risk of hyperchloremia, metabolic acidosis, and state of muscle breakdown. BUN is slightly less spe-
major adverse kidney events in 30 days. cific to kidney function than creatinine because it can
Given the somewhat conflicting research on the be influenced by other factors, namely, fluid volume
medical implications of hyperchloremia in critically status, protein catabolism (breakdown), and dietary
ill patients, further research is needed to determine protein intake. A BUN–creatinine ratio of 10:1 to 20:1
the nursing implications in treating hyperchloremia is considered normal; a ratio greater than 20:1 is con-
in the medical–surgical setting. Although patients sidered elevated and likely due to a prerenal condi-
in this setting are less likely to receive large vol- tion, in which blood flow to the kidney is lower than
umes of normal saline than patients in the critical normal. For example, if the BUN level increases out
care setting, nurses should be aware of the cumula- of proportion to the creatinine level, the patient may
tive effects of fluids used to dilute antibiotics and be dehydrated. If BUN and creatinine increase in pro-
other iv medications. A prospective, sequential portion to each other, the patient may be experiencing

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direct or intrarenal kidney damage. Of note, GI bleed- sodium, 138 mEq/L; potassium, 2.9 mEq/L; chlo-
ing may also cause a disproportionate increase in BUN.4 ride, 102 mEq/L; carbon dioxide, 28 mEq/L; BUN,
Many acutely ill patients are at increased risk for 38 mg/dL; and creatinine, 1.2 mg/dL. You note an
acute kidney injury. Creatinine level and urine out- office appointment from about a week ago, at
put are considered together to diagnose acute kid- which time the patient’s daily furosemide dose was
ney injury. Creatinine is not a perfect measure, as it increased from 20 to 60 mg. The patient’s heart rate
may lag behind changes in kidney function and can is 104 beats per minute, and his blood pressure is
be affected by other factors (for example, the creati- 92/62 mmHg. You recognize approximately eight
nine level may appear lower than it really is in a premature ventricular contractions (PVCs) per min-
patient with a fluid overload, and creatinine pro- ute on the patient’s ECG. On physical examination,
duction naturally decreases during acute illness).10 the patient’s mucus membranes are dry, his skin tur-
Before treatment can begin, providers need to gor is poor, and his lung sounds are clear.
determine the cause of acute kidney injury. Looking Being a discerning nurse, you recognize an impor-
at the timeline of events and patient history is impor- tant pattern in the laboratory findings when they’re
tant, but additional tests may also be ordered to help considered in the context of history and examination
determine the type (prerenal, intrarenal, or postrenal) findings. The increased dose of furosemide caused
and specific etiology of the kidney injury as well as excessive potassium and volume loss. The patient is
any associated complications, such as metabolic aci- weak, dizzy, tachycardic, and borderline hypotensive
dosis and hyperkalemia.10 because of the combined effects of hypokalemia and
To help with prevention, nurses need to keep a hypovolemia and is experiencing palpitations and
careful record of intake and output and be attentive PVCs due to hypokalemia. The BUN–creatinine ratio
to patient signs and ordered treatments that increase of 32:1 (note that in laboratory reports, this ratio
the risk of acute kidney injury. Many medications is often expressed as a single number—in this case,
have the potential to be nephrotoxic; common cul- 32), dry mucous membranes, and poor skin turgor
prits include certain antibiotics, NSAIDs, iodinated also support your conclusion that the patient is dehy-
contrast material, ACE inhibitors, and ARBs. Also drated. The other medications for blood pressure
be mindful that many medications require dosage (metoprolol and losartan) have worsened the hemo-
adjustments based on renal function. If you note an dynamic effects of hypovolemia.
increase in creatinine, consider consultation with a A focused plan of care emerges based on your
pharmacist or the ordering provider before medica- ability to integrate all this information:
tion administration. • Carefully administer iv fluids as ordered, while
Treatment for acute kidney injury targets any or monitoring for signs of volume overload (given
all of the three major renal functions: maintaining the patient’s history of heart failure).
potassium balance, acid–base balance, and fluid vol- • Administer potassium as ordered, ensuring a safe
ume homeostasis. Emergent treatment of hyperkale- rate of administration if given intravenously; con-
mia was discussed earlier. Treatment of metabolic duct appropriate clinical and laboratory monitor-
acidosis may be attempted with administration of ing for evidence of hyperkalemia; and advocate
sodium bicarbonate, and diuretics may be effective for telemetry monitoring during treatment.
to treat fluid volume overload if the kidneys are still • Obtain frequent vital signs, including assessment of
able to produce urine. However, temporizing mea- postural hypotension, and institute fall precautions.
sures may not be enough. In some situations, renal • Discuss checking the magnesium level with the
replacement therapies such as hemodialysis may be ordering provider. (Furosemide causes urinary
initiated, and the patient may be transferred to a magnesium losses, and hypomagnesemia wors-
higher-acuity setting.10 ens hypokalemia and cardiac dysrhythmias.)
In the treatment of chronic conditions, creatinine Case 3: Radiology overload. You are caring for a
levels are important in estimating GFR. Estimated 71-year-old patient whose chief complaint is two
GFR is helpful when evaluating and staging chronic days of abdominal pain, nausea, and poor oral
kidney disease, provided the patient’s creatinine intake, who presented to the hospital yesterday and
trend remains more or less steady.24 underwent computed tomographic scanning with
Case 2: Diuretics and the elderly: proceed with iodinated contrast material. The patient is more
caution. An 86-year-old man with chronic heart alert this morning but complains of increased
failure presents with palpitations, dizziness, and abdominal pain and weakness. Due to continued
weakness due to acute hypokalemia. In a review of nausea, she’s still not eating or drinking. She isn’t
home medications, you note furosemide, metopro- on telemetry, but you note the following vital signs:
lol, and losartan. Laboratory findings include heart rate, 52 beats per minute; respiratory rate,

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 BACK TO BASICS

26 breaths per minute; and blood pressure, 88/50 Lydia A. Bertschi is an assistant professor at Illinois Wesleyan
mmHg. She has not voided since the previous eve- University School of Nursing in Bloomington, IL. Contact author:
ning. Morning laboratory findings include sodium, lbertsch@[Link]. The author has disclosed no potential conflicts
of interest, financial or otherwise.
142 mEq/L; potassium, 6.5 mEq/L; chloride,
108 mEq/L; carbon dioxide, 22 mEq/L; BUN REFERENCES
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