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Fluid and Electrolyte Theory
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Fluid and Electrolyte Theory
Brittney Smith
The University of Akron
November 28, 2011
Tammy Smithson BSN, RN
8200:360:101
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Introduction
The purpose of this paper is to summarize the health status of a patient chosen from the
clinical setting. The patient’s medical history, current illness, and medication regimen will be
explained, but the primary focus is to describe present or potential fluid and electrolyte
imbalances and the impact of these imbalances on the patient’s health. The balance between
fluid and electrolytes is vital in order for the human body to operate appropriately, so
management of these elements is a key aspect of nursing care. In this patient’s case, the primary
fluid and electrolyte alterations, the pathophysiology behind these alterations, the expected and
actual signs and symptoms, the medical treatment and outcomes, and the nursing diagnoses,
interventions, and outcomes will be thoroughly discussed. The goal of care is to alleviate or
prevent any complications that could arise from the imbalances specific to this patient.
Clinical Description of Patient
SL is a sixty-three year old female admitted to the hospital with a diagnosis of diabetic
ketoacidosis and high blood sugar. This led to a diagnosis of new onset type one diabetes
mellitus. Pertinent medical history and comorbidities for this patient include hypertension,
gallbladder disease, arthritis, and gastroesophageal reflux disease (GERD). She has also
undergone a partial hysterectomy and a cholecystectomy. While in the hospital, her medication
regimen consisted of:
Heparin for deep vein thrombosis prophylaxis
Acetaminophen for pain
Priolosec to manage GERD
Zofran to manage nausea and vomiting
Nystatin (topical) for a persistent yeast infection
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Insulin Glargine (Lantus) to control hyperglycemia
Insulin Lispro (Humalog) to control hyperglycemia
Currently no medications are being used to treat SL’s hypertension, but during her hospital stay,
her blood pressures were often times in the normal range.
Fluid Alteration
SL presented to the hospital with fluid volume deficit related to diabetic ketoacidosis and
high blood sugar. Upon arrival SL’s blood sugar level was 306, and her hemoglobin A1C was
15.1% (normal range: 4.4%-6.4%). It was estimated that she had been living with an average
blood sugar of approximately 387 for at least three months. This hyperglycemic state causes
extracellular volume depletion due to osmotic diuresis, leading to fluid volume deficit, or
hypovolemia. Patients with uncontrolled diabetes have high sugar levels in the blood, which also
increase the blood sugar levels in kidney tubules. This elevated sugar level in the tubules attracts
water. The space inside the kidney tubules has a high glucose concentration, and the space
outside the tubules has a high water concentration. This causes water to move from outside the
tubules to inside the tubules. The fluid inside the tubules is expelled from the body causing
hypovolemia (LeMone & Burke, 2008). Even with constant intake of water, it was difficult for
SL to remain hydrated during the months prior to her admission to the hospital.
Pathophysiology
Fluid volume deficit is a decrease in intravascular, interstitial, or intracellular fluid in the
human body and can occur due to fluid loss, inadequate fluid intake, or malfunction of regulatory
mechanisms within the body (LeMone & Burke, 2008).
In SL’s case, the fluid volume deficit
is secondary to excessive fluid loss. Fluid volume deficit can develop slowly, as in this case, or
rapidly, as in a trauma. Loss of extracellular fluid volume leads to hypovolemia, decreased
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circulating blood volume. Fluid is drawn into the valculature from interstitial spaces. This is the
body’s effort to sustain perfusion. Eventually, depletion of fluid in the intracellular compartment
will occur. Hypovolemia stimulates regulatory mechanisms to maintain circulation (LeMone &
Burke, 2008). SL was drinking tremendous amounts of water due to the activation of her thirst
mechanism. This is an attempt by the body to increase perfusion and prevent cardiovascular
collapse.
Expected Signs and Symptoms
Fluid volume deficit impacts structures throughout the body. Signs and symptoms of
fluid volume deficit can be expected in the musculoskeletal, neurologic, integumentary, urinary,
and cardiovascular systems. The appearance of mucous membranes may also be an indicator of
this issue. Monitoring vital signs, lab values, and inputs and outputs can be imperative to the
diagnosis and treatment of fluid volume deficit.
When observing and assessing the mucous membranes of a person with fluid volume
deficit, it is expected that the membranes appear dry or sticky. A decrease in tongue size may be
evident as well. This is due to the lack of fluid in the interstitial and intracellular spaces
(LeMone & Burke, 2008). This is a partial cause of the symptoms seen in the integumentary
system, but vasoconstriction also plays a role. Vasoconstriction is a compensatory mechanism
activated to maintain circulation within the vasculature causing dry skin, pale, cold extremities,
and decreased skin turgor resulting in tenting of the skin (LeMone & Burke, 2008). Other
manifestations may also be seen.
When monitoring the urinary system of a patient with fluid volume deficit, a decrease in
urine output will be noted. Since the body has low fluids, antidiuretic hormone will be released
and the rennin-angiotensin-aldosterone system will be activated. These mechanisms promote
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sodium and water retention by the kidneys to increase fluid volume in the body, thereby
decreasing urine output. In severe fluid volume deficit, oliguria, which is a urine output of less
than 400cc in 24 hours, may occur (LeMone & Burke, 2008). Effects on other systems are
evident as well.
The musculoskeletal system will be very fatigued. The small amount of fluid that the
body has is moved to the vasculature to keep vital organs working, so little blood is reaching the
muscles. Since blood is not perfusing the muscles, oxygen is not able to travel to them, creating
a sense of fatigue. Therefore, activity intolerance may be a sign of fluid volume deficit easily
observable in a patient (LeMone & Burke, 2008). The effects of fluid volume deficit on the
neurologic system can be observed as well. An altered mental status, anxiety, decreased
alertness, and possible coma are common symptoms, especially with a severe deficit. In severe
cases, there is so little fluid circulating through the body that the brain is not being perfused
appropriately (LeMone & Burke, 2008). It is important to diagnose and treat this early, so that
the brain is not harmed.
Finally, and perhaps most importantly, major effects will be seen in the cardiovascular
system. The client is expected to have a low blood pressure and experience postural hypotension
due to the lack of fluid in the vascular system. Heart rate will increase due to activation of
mechanisms to compensate for low blood pressure and lack of blood flow to the body tissues.
The goal is to maintain circulation throughout the body. Increased time of capillary refill will be
present due to the decreased blood flow to the body’s extremities (LeMone & Burke, 2008). An
increased hemoglobin and hematocrit can also be expected due to the total blood volume being
decreased and the red blood cell count remaining unchanged (Leeuwen & Poelhuis-Leth, 2009).
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Though these are all expected symptoms of fluid volume deficit, actual symptoms expressed will
be different for every patient.
Actual Signs and Symptoms
SL’s actual signs and symptoms differ slightly from what is to be expected in a patient
with fluid volume deficit. She did complain of a dry mouth and raspy voice, and upon
observation, her mucous membranes appeared dry. Her skin was dry, but there was no evidence
of cold or pale extremities. When testing for skin turgor, there was no tenting. Also, as opposed
to what is expected, her urinary output is normal, if not high. This could be due to the polydipsia
that goes along with polyuria in uncontrolled diabetes mellitus. SL may have not actually
experienced extreme fluid volume deficit due to her excessive oral intake of fluids. She did
complain of overall body fatigue and weakness and was categorized as a high fall risk due to a
recent fall at home. This does match the expected symptoms of fluid volume deficit. She did not
exhibit any neurological symptoms associated with fluid volume deficit.
SL’s blood pressure ranged from 121-183 systolic and 55-101 diastolic. The diastolic
pressure of 55 is consistent with a fluid deficit diagnosis, but the other pressures are at or above
normal values. One of SL’s comorbidities is hypertension, so this could be a cause of the
unexpectedly high blood pressures. Her capillary refill was approximately three seconds, also
falling within the normal range. Her pulse ranged from 65-104. The value of 104 is slightly
tachycardic, but her average values were less than 100, which are considered normal.
Tachycardia is a compensatory mechanism to increase blood pressure, but since blood pressure is
not drastically decreased, a tachycardic rate is not expected.
Lab values for SL upon admission to the hospital showed a red blood cell count of 5.42
(normal: 4.1-5.1), a hemoglobin of 16.8 (normal: 12.3-15.3), and a hematocrit of 48.5 (normal:
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36-45). These are all elevated and expected of patients with fluid volume deficit. It seems from
assessment that SL may be in the beginning stages of fluid volume deficit. Her lab values are
indicative of this problem, along with her weakness, fatigue, and dry skin and mucous
membranes. Her body is experiencing dehydration, but her urinary output is high because she is
drinking large amounts of water to make up for it. This water is not going to the places it is
needed due to her high blood sugar, so even with a high urine output, dehydration of the body
and a fluid deficit is occurring.
Medical Interventions
The goal of medical interventions for SL is to control her blood glucose with insulin and
replace the excessive fluid loss by administering fluids intravenously and by mouth. Since SL
was alert and oriented, fluid replacement took place orally. Adults usually require eight to ten
liters of fluid in the first twelve hours to replace losses from polyuria (LeMone & Burke, 2008).
She was also given 0.9% Normal Saline at a rate of 50mL/hr intravenously. Insulin was
administered subcutaneously to bring blood glucose levels down. SL was given heparin
injections twice a day to prevent clotting of the slow-moving, viscous blood. She was put on a
carbohydrate controlled diet to control her blood glucose and prevent very high levels. Since this
is new onset diabetes, many disciplines, including a diabetes educator and a dietician, provided
consults to teach the patient how to avoid another episode of diabetic ketoacidosis and control
blood glucose levels.
Outcome of Medical Interventions
Upon leaving the hospital, SL’s weakness and fatigue had diminished. Her vital signs
were within normal limits, and her polyuria and polydipsia were no longer present. Her red
blood cells decreased from 5.42 to 4.2, her hemoglobin decreased from 16.8 to 13.4, and her
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hematorcrit decreased from 48.5 to 37.7. These lab values are all well within the normal ranges,
indicating that her hydration is appropriate for the body’s requirements. With continued control
of blood glucose levels and proper food and fluid intake, SL will likely avoid any further
incidences of fluid volume deficit.
Nursing Theory related to Fluid Alteration
Nursing Diagnosis 1
Diagnosis: Decreased peripheral tissue perfusion related to fluid volume deficit as
evidenced by dry skin and mucous membranes. The goal for SL is that she will demonstrate
adequate peripheral perfusion through palpable peripheral pulses, warm and dry skin, and
appropriate urine output by date of discharge from the hospital. Two nursing interventions for
SL include: 1. Administer intravenous and oral fluids as ordered to maintain adequate fluid
volume. 2. Monitor for signs and symptoms of fluid volume deficit including assessments of
urinary output, peripheral pulses, blood pressure, and heart rate (Ackley & Ladwig, 2008).
Implementing these interventions will help to prevent further complications.
The first intervention was successful. SL was administered 0.9% Normal Saline
intravenously as well as oral fluids to increase total fluid volume. She was also administered
subcutaneous insulin to bring her blood glucose levels within normal limits. This controlled the
osmotic diuresis that she was experiencing due to type one diabetes mellitus. The second
intervention was also successful. During the initial morning assessment, SL’s peripheral pulses
were palpated bilaterally, and they were palpabe +2 bilaterally. Her polyuria and polydipsia
decreased, and her urine output and thirst response were back to a normal level. Her blood
pressure and heart rate were within normal limits on the day of care with no tachycardia or
hypotension present.
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Nursing Diagnosis 2
Diagnosis: Risk for injury related to fluid volume deficit as evidenced by stated feelings
of weakness and fatigue and dizziness upon standing. The goals for SL is to remain free from
injury during the day of care. Two nursing interventions for SL include: 1. Anticipate times
during which client will need to use the restroom and assess for orthostatic hypotension and
assist with ambulation at these times. 2. Frequently check that side rails are up, that bed is in
the lowest position, and that wheels are locked (Ackley & Ladwig, 2008). In this situation, it is
extremely important to monitor the patient and assist with ambulation at all times.
The first intervention was successful. The patient was checked on frequently
(approximately every thirty minutes due to polyuria) and asked if she needed to use the restroom.
Upon standing, the client denied any dizziness and was assisted to and from the restroom.
Intervention two was also successful. Safety checks were performed every hour throughout the
day of care, and the side rails remained up and the bed locked and in the lowest position
throughout the day.
Electrolyte Alteration
SL is experiencing multiple electrolyte imbalances related to diabetic ketoacidosis, but
potassium and the resulting hypokalemia are the focus of this section. Upon admission to the
hospital, SL’s serum potassium level was 3.1 (normal: 3.4-5.1). Though hypokalemia can be
caused by many problems, in this case, the low potassium level is secondary to glucosuria and
osmotic diuresis. Excessive glucose in the urine causes osmotic diuresis, and potassium is
excreted in the urine with the glucose (LeMone & Burke, 2008). In SL’s case, acidosis caused
large amount of potassium to be released into the extracellular fluid, and osmotic diuresis along
with polyuria caused the potassium to be quickly expelled by the kidneys.
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Pathophysiology
Hypokalemia is an abnormally low serum potassium level and is usually a result of
excess potassium loss through the kidney or gastrointestinal tract (LeMone & Burke, 2008). In
SL’s case, potassium was lost primarily through the kidneys. When lost through these various
methods, potassium stores in the body are eventually depleted. Potassium loss is caused by a
shift of potassium from the intracellular to the extracellular space (Greenlee, Wingo,
McDonough, Youn, & Kone, 2009). With this shift, an exchange is made with hydrogen ions
that accumulate extracellularly in acidosis. This is the body’s attempt to return body fluids to a
normal pH. This state of hypokalemia can have a major impact on multiple body processes.
Expected Signs and Symptoms
Low potassium levels affect many parts of the body, but symptoms involving the
cardiovascular, musculoskeletal, and gastrointestinal system are highly anticipated. When
extracellular potassium decreases, the cell membrane becomes hyperpolarized. The cell is then
less responsive to exciting stimuli (LeMone & Burke, 2008). Stated in a different way, when
potassium levels are low, cells cannot repolarize and are incapable of firing repeatedly. Without
this rapid fire, muscles and nerves cannot function appropriately causing the associated muscle
weakness and cramping seen throughout the body (Palmer, 2010). This weakness and cramping
can then lead to paresthesia and diminished deep tendon reflexes in the extremities.
Hyperpolarization also causes decreased peristalsis in the gastrointestinal system, potentially
leading to bowel obstruction. Nausea, vomiting, and anorexia may be outcomes of decreased
peristalsis.
Since the heart is also a muscle, cardiovascular effects are expected. Dysrhythmias are
common, as well as changes on the electrocardiogram. These changes can include flattened or
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inverted T waves, U wave development, and a depressed ST segment (LeMone & Burke, 2008).
Symtpoms of the central nervous system may also manifest due to minimal transmission of nerve
impulses related to cell hyperpolarization. Symptoms may include confusion, lethargy, and
disorientation (LeMone & Burke, 2008). Serum potassium also has some control over insulin
release, so hypokalemia could potentially lead to glucose intolerance (Palmer, 2010). Though
these are all anticipated symptoms of hypokalemia, actual manifestation of these symptoms
differs with each patient.
Actual Signs and Symptoms
SL’s actual signs and symptoms differ from what is to be expected in a patient with
hypokalemia. She did complain of overall body fatigue and weakness and was categorized as a
high fall risk due to a recent fall at home. This is expected of a patient suffering from low
potassium levels, but she was able to move all extremities well and had strength and sensation in
each of them. Paresthesia was not noted and deep tendon reflexes were within normal limits. SL
did complain of nausea, possibly due to decreased peristalsis, but she was having regular bowel
movements indicating absence of a bowel obstruction. Her apical pulse was of regular rate and
rhythm, S1 and S2 were auscultated, and no murmurs were noted. An electrocardiogram was not
performed, so changes in T waves and the ST segment could not be seen. SL was alert and
oriented to person, place, and location, which does not indicate hyokalemia. She did however
present with glucose intolerance, with a blood glucose upon admission of 306. This however
seems more likely to be an effect of new onset type one diabetes mellitus rather than low
potassium levels. It seems much more likely that the diabetes caused the decrease in potassium
as opposed to the opposite.
Medical Interventions
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The goal of the medical interventions for SL in order to manage the state of hypokalemia
is to control her blood glucose with insulin. Insulin was administered subcutaneously to bring
blood glucose levels down. Insulin carries potassium back into the cell along with glucose
(LeMone & Burke, 2008). Since potassium is no longer moved into the extracellular fluid due to
metabolic acidosis after insulin injection, excessive amounts cannot reach the kidneys to be
excreted and potassium levels increase back to normal. Osmotic diuresis is no longer an issue
due to controlled sugars. SL was also put on a carbohydrate controlled diet to control her blood
glucose and prevent metabolic acidosis from occurring again. Since this is new onset diabetes
many disciplines, including a diabetes educator and a dietician, provided consults to teach the
patient how to avoid another episode of diabetic ketoacidosis and control blood glucose levels.
Outcome of Medical Interventions
Upon leaving the hospital, SL’s weakness and fatigue had diminished as well as her
nausea. Her vital signs were within normal limits, and her polyuria and polydipsia were no
longer present. Her serum potassium increased from 3.1 to 3.6, which is well within the normal
range, indicating that the amount of potassium is appropriate for the body’s requirements. With
continued control of blood glucose levels and proper food and fluid intake, SL will likely avoid
any further incidences of hypokalemia.
Nursing Theory related to Electrolyte Imbalance
Nursing Diagnosis 1
Diagnosis: Risk for falls related to muscle weakness and hypokalemia. The goal for SL
is to remain free from falls during her hospital stay. Two nursing interventions for SL include: 1.
Using a “high-fall risk” armband to alert staff of the increased assistance needed with mobility
by the client. 2. Placing the patient in a room near the nursing station to allow more frequent
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checks (Ackley & Ladwig, 2008). Falling could lead to more serious issues, so it is important to
initiate these interventions as soon as possible.
The first intervention was successful. SL wore her “high-fall risk” armband throughout
the entire length of her stay. This notified staff members of the extra assistance needed while
walking to the restroom, ambulating in the hallway, etc. The second intervention was successful
as well. SL was placed in the room closest to the nursing station and in the bed closest to the
door in her semi-private room in order to allow frequent checks by the nursing staff. The client
was checked on approximately every thirty minutes and helped to the bathroom as necessary.
Because of these interventions, the patient remained free of falls during her entire
hospitalization.
Nursing Diagnosis 2
Diagnosis: Risk for decreased cardiac tissue perfusion related to hypokalemia. The goal
for SL is to remain free of arrhythmias, tachycardia, and bradycardia throughout her hospital
stay. Two nursing interventions for SL include: 1. Monitor for chest, neck, and jaw pain,
shortness of breath, diaphoresis, nausea, and vomiting. 2. Provide client teaching related to risk
factors for decreased cardiac tissue perfusion, in this case, hypertension, diabetes mellitus, and
the female gender (Ackley & Ladwig, 2008). Teaching is a very important part of nursing.
Patients need to be able to identify signs and symptoms of health issues when at home.
The first intervention was successful. SL was told to inform a healthcare professional if
she was feeling any of these symptoms associated with decreased cardiac perfusion. Though
some nausea was present at admission into the hospital, no cardiac issues were noted, and this
symptom decreased as treatment took place. Before being discharged home, SL was taught
about the risk factors she possesses related to decreased cardiac perfusion. Both comorbidities
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and gender increase her risk of decreased cardiac perfusion and possible heart attack. She
demonstrated understanding by repeating the stated risk factors. These interventions will help
SL identify any cardiovascular issues early and obtain prompt treatment.
Conclusion
Fluid and electrolyte balance is of primary importance in maintaining body function.
Even slight imbalances can cause severe cardiovascular, musculoskeletal, neurological, and
urinary problems, as seen in the case of SL. Through careful observation and assessment, nurses
are able to notice signs and symptoms of fluid and electrolyte disorders early. Therefore,
medical and nursing interventions can be started before body wide effects and system failure
occur. Monitoring fluid and electrolyte imbalance is a primary aspect of nursing care and when
done vigilantly, can prevent many associated complications.
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Referneces
Ackley, B. & Ladwig, G. (2008). Nursing diagnosis handbook: An evidence based guide to
planning care (9th ed.). St. Louis: Mosby.
Greenlee, M., Wingo, C., McDonough, A., Youn, J., & Kone, B. (2009). Narrative review:
evolving concepts in potassium homeostasis and hypokalemia. Annals of Internal
Medicine, 150(9), 619-625.
LeMone, P. & Burke, K. (2008). Medical surgical nursing: Critical thinking
in client care (4th ed.). Upper Saddle River, NJ: Pearson Education.
Palmer, B. (2010). A physiologic-based approach to the evaluation of a patient
with hypokalemia. American Journal of Kidney Diseases, 56(6), 1184-1190.
Van Leeuwen, A. & Poelhuis-Leth, D. (2009). Davis’s comprehensive handbook of laboratory
and diagnostic tests with nursing implications (3rd ed.). Philadelphia: F. A. Davis
Company.