GNRS 588

Dr. Alomari

AZUSA PACIFIC UNIVERSITY

SCHOOL OF NURSING
GNRS 588: ADVANCED NURSING CARE FOR ADULTS
CARE MAP #: ____2_____
Care Map must be completed and submitted within one week of the date of care.

Student: Lauren Ratiani

Instructor: Professor Richards
Date of Care: February 27, 2015
Date of Submission: March 26, 2015

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GNRS 588
Dr. Alomari

ADMITTING DATA
Interview your patient or his/her family to obtain a complete health history. Do not just copy from the patients chart unless the patient
and family are not available.
Total 5.0 points (no point for initial, age, gender, or medical diagnoses).
Patients Initial
Age
Gender

Medical History
(0.5)

Surgical History (0.5)

Allergies/Reactions

Psychosocial History
(0.5)

DA
44
Male
Cardiovascular
Respiratory
Neurologic
Urinary
Digestive
Endocrine
Musculoskeletal

HTN
Pneumonia
Stroke
UTI
Ulcer
DM, DKA
Toe
amputation
Anemia
Shingles

MI
Pneumothorax
Parkinsons
ESRD
Diverticulosis
Hyperthyroidism
Obesity

Dysrhythmias
Asthma
Guillain-Barre
Renal insufficiency
Dysphasia
Hypothyroidism

Hema/Oncology
Cancer:
Infectious
Hepatitis
Integumentary
Subcutaneous Emphysema
Reproductive
Psychiatric
Depression Anxiety
Other
Glaucoma
Left toe amputation (wound VAC in place)
NKDA
Marital status
Single
Education level
High school
Social resources
Medi-Cal
Spiritual resources
Christian
Occupation
Unknown
Employment
Unknown
Smoking
Denies
Alcohol
Denies
Recreational Drugs
Denies

Meningitis

Hyperlipidemia HF
Respiratory Failure: ARDS
Encephalopathy IICP
ATN

PVD
ICH

STI

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GNRS 588
Dr. Alomari

History of Present
Illness
(1.0)
Chronological account
of patients current
illness with pertinent
+s and s included
and correct medical
terminology used.

OLDCART
Initial Symptom(s) at

3
Mr. DA is a 44-year old Hispanic male with a history of renal insufficiency, pneumonia, diabetes mellitus,
glaucoma, anemia, and is S/P amputation of left middle toe with wound-vac in place. He presented to RCH ER on
February 23, 2015 in the early morning with extreme shortness of breath and tachypnea. He had recently been treated at
an outside facility for pneumonia and had been experiencing SOB since discharge. Upon his arrival at RCH ER, MR.
DA was verbal with a GCS of 15. He was given 15L O2 via oxygen mask and ABGs were drawn, which revealed
significant refractory hypoxemia (pH 7.4, pCO2 29.8, pO2 50, HCO3 18). The patient was then sedated and intubated.
The patients labs revealed a WBC count of 30.8, glucose of 273, and BNP of 120.8, suggesting severe infection, DKA,
and CHF respectively. His platelet count was 456 and D-Dimer was >5250 suggesting coagulopathies as well. BUN (27)
and creatinine (3.0) were both high, indicating kidney dysfunction. The patient was afebrile and tachycardic with a pulse
of 110 bpm upon admission reaching 149 bpm just after intubation. CXRs and chest CT showed diffuse bilateral ARDS
and infiltrations suggestive of multifocal pneumonia. Mr. DA was diagnosed with acute hypoxic respiratory failure,
bilateral pneumonia, and severe ARDS. Doctors also noted acute renal failure, exacerbation of diabetes mellitus, and
possible congestive heart failure, which was later ruled out. The patient was closely monitored by RT and required
multiple ventilator adjustments.
Several hours after intubation, Mr. DAs SpO2 dropped to the mid 50s and required manual bagging at 100%
FiO2. He did not tolerate being switched back to the ventilator for several rounds. Eventually the patient tolerated the
ventilator on VC-plus and remained on the vent at 75% FiO2. The settings were later switched to bilevel mode with
100% FiO2 and a PEEP of 12. Large bilateral subcutaneous emphysema extending from the chest to the neck and left
orbital eye was then noted. Repeat CXR was done which showed diffuse subcutaneous emphysema with right
pneumothorax. A right chest tube was then placed. Mr. DA was later switched from bilevel mode to pressure control.
Prone positioning was recommended and Mr. DA was transferred to the ICU and placed in a rotoprone bed to
improve V/Q matching and oxygenation. He has since been treated with antibiotics, tamiflu, corticosteroids, insulin,
propofol, and fentanyl. On February 24 and 25, he remained in severe/extreme ARDS, but P/F ratio began to improve
(165) on the 25th. He was also diagnosed with ischemic ATN. He has therefore been kept in negative fluid balance with
good UOP and is allowed to stay hypertensive in order to ensure good renal perfusion. His blood glucose is being tightly
monitored and controlled with insulin and he is no longer in DKA. Today, on the 27th, he is still in ARDS but is
beginning to tolerate the supine position for longer intervals of time without oxygen desaturations. Leukocytosis, likely
due to steroids, has decreased. The plan for today is to obtain prone and supine ABGs to see if patient tolerates supine
position. He will be kept on airway pressure release ventilation (APRV) and will transition to a regular bed if supine
position is tolerated well.
Currently, Mr. DA has a temperature at or greater than 100.4F, pulse greater than 90 bpm, and a WBC count of
15.8. These factors meet the SIRS criteria. However, doctors have attributed these values to pneumonia and
corticosteroid treatment and he has not been diagnosed with SIRS or sepsis at this point.
Mr. DA had been experiencing shortness of breath since discharge from an outside facility where he was treated for
pneumonia. He was given antibiotics (Cipro and Augmentin) to treat the lung infection. Dyspnea progressively worsened

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Dr. Alomari

the time of admission

(in ED)
(1.0)
Medical Diagnosis
(Diagnoses)

Findings that
support/confirm the
medical diagnosis at
admission and during
your care
(1.0)

after discharge and was severe when he was admitted to the ER at RCH. 15 liters O2 on a BVM did not improve
saturations, so Mr. DA was sedated, intubated, and placed on a ventilator to improve oxygenation.
Severe Acute Respiratory Distress Syndrome (ARDS) related to pneumonia, with subcutaneous emphysema and right
pneumothorax; Acute Tubular Necrosis (ATN)
Physical Exam
2/23/15 Subcutaneous crepitation; crackles, rales,
rhonchi; barrel chest, tachypnea, dyspnea,
tachycardia (110-149 bpm); left orbital
subcutaneous emphysema; persistent
diminished lung volumes; extreme dyspnea
2/27/15 Scleredema, periorbital edema, right
upper chest and neck subcutaneous
emphysema, diminished breath sounds,
coarse crackles bilaterally after rotation from
prone to supine position.

Diagnostic Tests
2/23/15 CXR- extensive patchy opacities; bilateral airspace
consolidation probably r/t pneumonia; pneumomediastinum,
pneumopericardium; old granulomatous disease; bibasilar
compressive atelectatic changes; repeat CXR showed right sided
pneumothorax and severe subcutaneous emphysema
2/23/15 Chest CT- extensive patchy bilateral airspace consolidation;
pneumomediastinum and pneumopericardium
2/23/15 ABGs- pH 7.4, pCO2 29.8, pO2 50, HCO3 18
2/23/15 Other labs- platelet count 456, D-Dimer >5250, BUN 27,
creatinine 3.0, WBC count 30.8, glucose 273, BNP 120.8,
2/26/15 CXR- severe bilateral lower neck and chest wall
emphysema, right worse than left; moderate bilateral perihilar
infiltrates noted
2/26/15 WBC count- 15.2
2/27/15 CXR- persistent moderately extensive bilateral pulmonary
infiltrates left greater than right; persistent extensive
subcutaneous emphysema throughout thorax, right greater than
left, extending to lower neck soft tissues; no significant interval
change
2/27/15 Labs- blood glucose 166-177, WBC count 15.8, BUN 64,
Creatinine 3.3
2/27/15 ABGs- pH 7.4, pCO2 26.8, pO2 73.3, HCO3 16.5

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GNRS 588
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HEAD-TO-TOE ASSESSMENT
Perform a head-to-toe assessment on your patient. Total 7.0 points.
General Status (0.5)

VS & Hemodynamics (1.0)

Neurologic & Pupils (0.5)

Head, Face, & Neck (0.5)

ENT (0.5)

Cardiovascular (1.0)

Pulmonary (1.0)

Gastrointestinal (0.5)

Patient is obese, sedated, and intubated with a GCS of 3, no eye opening, no verbal response, no motor response to
pain (E:1 V:1, M:1). Patient is in rotoprone bed, currently in supine position.
Time T(F) RR HR
ABP
MAP BS
CO CVP SVR PAP SpO2
ICP
EtCO2
0730 100.4 17 102 144/54
96
166 N/A N/A N/A
N/A
96
N/A
N/A
0945

101.6

16

100

176/75

94

176

N/A

N/A

N/A

N/A

94

N/A

N/A

1200

101.0

18

92

180/73

95

177

N/A

N/A

N/A

N/A

95

N/A

N/A

Sedated; pupils reactive 2:1.5 bilaterally; unable to assess mentation d/t sedation.
Head is normocephalic, skull symmetric.
Neck is supple. No palpable lymph nodes. Thyroid gland non-palpable. Subcutaneous crepitation palpated on
neck, shoulders, upper chest wall.
Eyes significant for scleredema and periorbital edema. Left orbital subcutaneous emphysema.
Ears equal size; no swelling or lesions.
Nose symmetric; nostrils patent; no swelling, discharge, or bleeding.
Lips, gums, and buccal mucosa pink and moist. Occasional blood-tinged sputum. 16 French oral gastric tube in
place: no residuals, placement confirmed with auscultation; 7.5 endotracheal tube in place: 21 cm at the lip
Sinus tachycardia at times; S1, S2 present; no extra heart sounds or murmurs.
Carotid artery smooth, no bruit; no JVD. Apical pulse bounding and palpable at 5th ICS, MCL; Capillary Refill: <
3 seconds. Non-pitting edema in all extremities; radial and pedal pulses present and bounding.
Triple lumen CVL at left IJ. Arterial line at left radial artery.
A/P diameter inappropriate r/t barrel chest; neck muscles supple. Chest expansion symmetric; diminished breath
sounds, coarse crackles bilaterally after rotation from prone to supine position. Chest tube in place, right upper
chest wall, set to suction at -20 mmHg, no air leak, no drainage since yesterday.
ET tube in place; respirations of 16 bpm on 40% FiO2 via ventilator (bilevel); pressure support of 15. ABGs
revealed compensated metabolic acidosis due to renal bicarbonate losses. Clear, thin pulmonary secretions.
Ventilator Mode
TV
RR
FiO2
PEEP
I: E Ratio
Bilevel
N/A
16
40%
High 30 cm/H2O,
5:1
Low 0 cm/H20
pH
PaO2
PaCO2
HCO3BE
SpO2
7.40
73.3 (L)
26.8 (L)
16.5 (L)
-6.9 (L)
95%
Abdomen symmetric bilaterally; soft, not distended. Bowel sounds active in all quadrants; oral-gastric tube in

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Dr. Alomari

Genitourinary (0.5)
Skin (wounds) (0.5)
Musculoskeletal (0.5)

place and clamped, patient NPO. Last bowel movement: 2/27/15.

16 Fr Foley inserted 2/23/15, draining clear yellow urine. Current output approximately 150 ml/hr.
Last I&O: Input: 1706 ml, Output: 910 ml, Balance: 796 ml.
Color slightly pale, warm to touch; no cyanosis; skin turgor good, tight on extremities r/t edema. Dressing on
coccyx to prevent pressure ulcers. Very high ulcer risk r/t rotoprone bed, position, immobility, and hyperglycemia.
Wound-vac on left middle toe.
Passive ROM in all joints; generalized weakness and paresis in all extremities r/t sedation. Non-ambulatory. High
fall-risk. Amputated left middle toe.

Other

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GNRS 588
Dr. Alomari

PATHOPHYSIOLOGY
In your own words, describe the: (Total 6.0 points)
Pathophysiology of the admitting diagnosis (4.0 points):
Mr. D.A. was admitted to RCH for severe shortness of breath related to a recent pneumonia infection treated at an outside facility.
Pneumonia is the sixth leading cause of death in the United States due to infectious disease. It is an acute infection that causes inflammation of the
lung parenchyma, which causes the alveoli to fill with fluid, making them dysfunctional. Pneumonia can be caused by bacteria, fungi, viruses, or
protozoa. The specific cause of Mr. DAs pneumonia is unknown, so his physician started him on broad-spectrum antibiotics as well as Tamiflu to
combat a variety of possible causes including bacteria and viruses. He is also on corticosteroids to reduce pulmonary inflammation. Pneumonia is
confirmed by infiltrates on chest x-rays and crackles upon auscultation, both of which are present in Mr. DAs case.
Acute Respiratory Distress Syndrome (ARDS) has an abrupt onset. After an initial injury to the lung endothelium or epithelium occurs,
like pneumonia, mediators are released which increase vascular and alveolar permeability, leading to alveolar collapse. There is an accumulation
of fluid, surfactant is reduced, and gas exchange decreases. Surrounding alveoli are de-recruited by the alveoli initially filled with fluid, and also
collapse. This results in non-compliant alveoli and dysfunctional gas exchange. Once the alveoli become dysfunctional, unoxygenated blood
shunts past them and joins pulmonary venous circulation without being oxygenated. The lack of open alveoli causes refractory hypoxemia and
diffuse pulmonary infiltrates. These two criteria, along with no evidence of left atrial HTN or left ventricular dysfunction qualifies the diagnosis of
ARDS. Morbidity/mortality is greater than 60% once diagnosed with ARDS. Because of pneumonia, Mr. DAs alveoli were already insulted by
direct injury. Without proper or successful treatment and resolution of the initial infection, it progressed to ARDS making the alveoli completely
non-compliant for gas exchange. Even when placed on the ventilator, Mr. DAs oxygen saturation did not reach adequate levels because his
alveoli had collapsed making them unavailable for V/Q matching. His ventilator was eventually changed to bilevel settings with pressure control
in order to keep his alveoli open during inspiration and expiration to allow a longer window of ventilation. Mr. DA is currently in a rotoprone bed,
prone for six hours at a time followed by one hour supine. The position and oscillation that this bed provides for the patient facilitates drainage of
lung secretions and allows better ventilation of the dependent part of the lungs in order to increase oxygenation.
Mr. DA developed a right-sided pneumothorax related to stiff, noncompliant lungs from ARDS and high levels of ventilator support in
attempt to re-recruit and open alveoli to allow ventilation. A pneumothorax occurs when air gets trapped between the parietal and visceral pleura.
A pneumothorax can cause lung collapse due to a maldistribution of air pressure in the thoracic cavity. In this case, Mr. DA suffered from a
tension pneumothorax related to positive pressure mechanical ventilation with a high FiO2%. Air escaped the lung and entered the pleural space,
which then accumulated in the pleural cavity. Once there, the air cannot escape due to a higher intrapleural pressure versus alveolar pressure. This
can cause mediastinal shift, compressing the vena cava, and negatively impacting venous return preload, CO, and can lead to circulatory collapse.
Mr. DA had a chest tube placed in his right upper chest wall, which has allowed the trapped air to escape the pleural cavity and return its capacity
to normal. Excess trapped air was pushed into Mr. DAs subcutaneous tissue causing subcutaneous emphysema that extended into his anterior
thoracic, neck, and facial tissue. Crepitus can be palpated in these areas.
Mr. DA meets criteria for systemic inflammatory response syndrome (SIRS). He has a pulse greater than 90 bpm (102 bpm), a
temperature over 100.4F (101.6F), and a WBC count over 12 (15.8). Because he meets at least two out of four of the SIRS criteria and also has a

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source of infection (pneumonia), he is qualified for having sepsis. SIRS occurs when the bodys localized inflammatory process becomes
generalized and uncontrolled. The purpose of the inflammatory response is to move materials and the inflammatory immune response to the injury
to prevent foreign invasion or extension of injury. The initial inflammatory cells activate chemical mediators, whose goal is to contain the
infection. Mediators are released from endothelial cells, elicit the inflammation response, recruit WBCs to the area, and promote localized clotting
to contain the infection and promote healing. The many cellular mediators involved in this process increase vascular permeability, neutrophil
release, coagulation, and vasodilation. When acute infection or multiple traumas occur, systemic inflammation can occur as a result of massive
amounts of chemical mediators that are released in response to injury. Increased permeability and dilation of blood vessels in this state can cause a
reduction of blood pressure and hypoperfusion of tissues. This will eventually lead to tissue ischemia and organ failure due to lack of perfusion if
untreated.
Mr. DA is also experiencing a renal dysfunction called Acute Tubular Necrosis (ATN). Prolonged renal hypoperfusion due to septic shock
is a common cause of ATN. Acute Tubular Necrosis is the most common cause of acute renal failure or acute kidney injury. It can be the result of
a nephrotoxic injury, an ischemic injury, or because of pigmenturia. Physicians suspect that Mr. DAs ATN is the result of an ischemic injury and
are therefore allowing him to remain in a hypertensive state to ensure renal perfusion. Anything that leads to reduced renal perfusion can cause
ATN. The kidneys will send signals that they are not being perfused, which will in increase the sympathetic response and stimulate the RAAS
system resulting in severe constriction of the afferent arteriole, reducing glomerular blood flow. Cellular damage depends on the duration of
ischemia. Necrosis of renal tubular cells along with cast formation and a build-up of this debris in the renal tubules characterize ATN. ATN can
cause oliguria, however Mr. DA has adequate UOP at this point of approximately 150 ml per hour.
Now with acute renal failure and acute respiratory failure, Mr. DA is in multi-organ dysfunction syndrome as well (MODS). Pathologic
changes that are associated with MODS include uncontrolled systemic inflammation, tissue hypoxia, unregulated cell death, and microvascular
coagulopathy. With two organ systems now failing- pulmonary and renal- Mr. DA should be treated as a patient in severe sepsis with multiorgan
dysfunction syndrome (MODS).
(Baird & Bethel, 2011; Huether & McCance, 2012).
Correlation between medical/surgical history and admitting diagnosis (2.0 point):
Mr. DAs recent history of pneumonia is the direct cause of his ARDS. Whether his infection was not treated sufficiently or he simply did
not finish his prescribed antibiotics is unknown. The patients medical history of asthma made him more susceptible to pneumonia. His history of
diabetes mellitus has slowed or prevented his healing and has likely negatively impacted several of his other current disease processes. His recent
bout with DKA (hyperglycemic crisis, ketosis, acidosis) was most likely exacerbated by his lung infection: pneumonia caused his body to be in a
state of acute stress which increased blood glucose levels, further impaired insulin production, and raised his blood sugar levels even more.
Hyperglycemia impairs wound healing and also supplies a good breeding ground for infection. This could have prevented Mr. DAs pneumonia
from resolving and encouraged its progression into ARDS. Hyperglycemia negatively affects blood vessels and circulation, primarily the small
arterioles. Hyperglycemia is likely the primary factor that necessitated his toe amputation, caused his glaucoma, and damaged his kidney vessels,
contributing to ATN. Hyperglycemic crisis, ketosis, and acidosis can cause also hypovolemic shock due to dehydration and electrolyte imbalance.

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GNRS 588
Dr. Alomari

DIAGNOSTIC TESTS
Include all diagnostic tests and ECG strip.
Remember, a diagnostic test is any kind of medical test performed to aid in the diagnosis or detection of disease (i.e. laboratory tests, radiology
tests, biopsies, endoscopies, etc.).
Total 6.0 points
Test

Results

Normal Range

Patient-Specific Etiology

Chest CT

Extensive patchy
bilateral airspace
consolidation;
pneumomediastinum
and
pneumopericardium

Normal bony
structure and
normal lung
tissue; normal
size and shape
of heart

Chest CT indicates infiltration of the

lungs caused by pneumonia and
progression to ARDS. Air is also
noted in the mediastinal and
pericardial cavities related to
ineffective gas exchange due to
atelectasis; air has escaped the lungs
and entered these cavities.

CXR

2/23/15: Extensive
patchy opacities;
bilateral airspace
consolidation r/t
pneumonia;
pneumomediastinum,
pneumopericardium;
old granulomatous
disease; bibasilar
compressive
atelectatic changes;
repeat CXR showed
right sided

Normal bony
structure and
normal lung
tissue; normal
size and shape
of heart

Initial CXR revealed lung

consolidation and infiltrations r/t
pneumonia as well as air in the
mediastinal cavity and within the
pericardium. It also showed
atelectatic changes, r/t alveoli
collapse c/b alveoli filling with fluid
and derecruiting adjacent alveoli.
Repeat CXR showed pneumothorax
and subcutaneous emphysema caused
by positive pressure ventilation and
air escaping the parenchyma and
entering the pleural cavity.

Nursing Implications
- If patient is conscious, explain procedure to
patient. CT scanner is circular, with a
doughnut-like opening. The scanner revolves
around the area to be examined and clicking
noises will be heard from the scanner as the
radiologist or technician observes from a
control room. The test is not painful.
- Obtain history of allergies to seafood, iodine,
and contrast dye if contrast is to be used
during the test.
- Observe for S/S of allergic reaction to dye if
dye is used.
- Describe x-ray procedure to client and/or
family, explaining that it takes from 10-15
minutes.
- Encourage family to ask questions

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WBC

pneumothorax and
severe subcutaneous
emphysema
2/26/15: severe
bilateral lower neck
and chest wall
emphysema, right
worse than left;
moderate bilateral
perihilar infiltrates
noted
2/27/15: no changes
noted
30,800 uL at
admission to ER;
15, 800 uL 2/27/15

4000-11000 uL

Blood
Glucose

60-110 mg/dL

177 mg/dL

BUN

27 mg/dL at
admission to ER,
64 mg/dL 2/27/15

5-25 mg/dL

Elevated WBC count indicates

infection. Mr. DAs initial infection is
pneumonia and has progressed to
ARDS. His WBC count was
extremely elevated at admission,
reflecting significant acute infection
and possible progression into sepsis.
Increased blood glucose (BG)
represents hyperglycemia and is
significant in patients like Mr. DA,
who has DM and is also in a state of
acute stress. Hyperglycemia can be
exacerbated during illness and/or
stress and can further impact the
bodys defensive processes. Mr. DA
is currently resolving a case of DKA.
Urea is formed as an end product of
protein metabolism and is excreted by
the kidneys. Elevated BUN is
indicative of dehydration, prerenal
failure, or renal failure. Patientspecific etiology likely related to

- Notify HCP if any changes in clients

condition such as fever, increased pulse rate,
respiration rate, leukocytosis
- Administer prescribed antibiotics in a timely
manner and teach patient and family the
importance of finishing prescribed antibiotics
to prevent bacterial resistance.
- Obtain a history regarding the clients
glucose testing method, including past
glucose testing results.
- Discuss the procedure with the client/family
and answer any questions concerning the
meter.
- Test the clients BS regularly and tightly
control hyperglycemia with insulin.
- Repeat CBC with glucose levels.
- Report urinary output less than 25 ml/hr or
600 ml/day. Urea is excreted by the kidneys,
and with decreased urine output, urea
accumulates in the blood.
- Check vital signs: fast pulse, decreased BP
and increased respiration could indicate

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1
1
chronic diabetic hyperglycemia and
current state of illness
(ARDS/pneumonia).

Creatinine

3.0 mg/dL at
admission to ER, 3.3
mg/dL 2/27/15

0.5-1.5 mg/dL

ABGs

pH: 7.4; PaCO2:

26.8; PaO2: 73.3;
HCO3: 16.5;
2/27/15

pH: 7.35-7.45;
PaCO2: 35-45
mmHg; PaO2:
75-100; HCO3:
24-28 mEq/L

Creatinine is a by-product of muscle

catabolisim. It is filtered by the
glomeruli and excreted in urine. It is a
sensitive and specific indicator of
renal disease, rising later than BUN,
and is not affected by diet or fluid
intake. An increased level can
indicate acute or chronic renal failure.
Mr. DAs increased creatinine reflects
his current diagnosis of ATN.
ABGs assess disturbances of acidbase balance caused by respiratory
and/or metabolic disorders. Because
of his extreme SOB, Mr. DAs ABGs
were drawn revealing severe hypoxia.
His current ABGs reveal metabolic
acidosis due to renal bicarbonate
losses.

dehydration leading to shock.

- Determine the hydration status of the client.
Elevated BUN may be attributed to
hemoconcentration.
- Relate the elevated creatinine levels to
clinical problems. Serum creatinine may be
low in clients with small muscle mass, in
amputees, and in clients with muscle disease.
- Monitor I&Os; monitor output in 24 hrs:
less than 600 mL/24 hrs can indicate renal
insufficiency.
- Compare BUN and creatinine levels. If both
are increased the problem is most likely
kidney disease.
- Assess for signs of metabolic acidosis, such
as Kussmauls breathing, flushed skin,
restlessness, confusion, decreased
bicarbonate value of less than 24
- Check for respiratory compensatory
mechanism with metabolic acidosis (PaCO2
< 35 mmHg)
- Monitor respiration rate, oxygen saturation,
urine output, and serial ABGs (Kee, 2014).

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ECG STRIP

HR
92 bpm

Rhythm
Regular

P wave
SA (on
monitor)
Interpretation: Normal sinus rhythm
(see attached strip)

PR
0.12

QRS
0.08

P:Q ratio
1:1

ST segment
0.10

T-wave
0.14

Q-T
0.28

Ectopy
None noted

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GNRS 588
Dr. Alomari

1
3

SIX SCHEDULED MEDICATIONS AND IV FLUIDS

Include all scheduled medications and the PRN if administered. Total 6.0 points.
Medication (Name, Dose, And Route): fentanyl citrate (Sublimaze) 1000 mcg/100 ml IV as dir PRN pain, currently @ 200 mcg (20 ml)/hr
Classification
Opioid analgesic
Mechanism of Action
Binds to opiate receptors in CNS, altering the response to and perception of pain. Produces CNS
depression. Metabolized mostly by liver; ~ 2-4 hr half-life in adults.
Patient-Specific Indication
Decreases pain and supplements in anesthesia
Side Effects and Adverse Effects
Confusion, postoperative depression and drowsiness, blurred vision, bronchospasm, respiratory
depression, arrhythmias, bradycardia, hypotension, biliary spasm, N/V, facial itching, skeletal and
thoracic muscle rigidity c/rapid IV infusion, apnea, laryngospasm
Nursing Implications
Initial rate: 25 mcg/hr
Titrate by: 25 mcg/hr q 30 min
Maximum rate: 200 mcg/hr
Goal: Ramsay 4
- Intermittent infusion: may be diluted in D5W or 0.9% NaCl. Up to 50 mcg/ml.
- Monitor respiratory rate and BP frequently throughout therapy. Report significant changes
immediately. Respiratory depressant effects of fentanyl may last longer than the analgesic
effects. Initial doses of other opioids should be reduced by 25-33% of usual recommended
dose.
- Assess fall risk and implement fall prevention strategies.
- Symptoms of toxicity include respiratory depression, hypotension, arrhythmias, bradycardia,
asystole. Atropine may be used to treat bradycardia. Mechanical ventilation may be required to
treat respiratory depression. Narcan can be used to reverse respiratory depression or coma.
Patient/family Education
- Educate family that this medication is to decrease pain and also supplements in anesthesia.
- Medication causes dizziness and drowsiness.
- Caution patient to change positions slowly to minimize orthostatic hypotention after weaned
off of drug for at least 24 hours after completion of medication (Deglin, Vallerand 2015).
Medication (Name, Dose, And Route): diprivan (Propofol) 100mg/100 ml IV as dir PRN, currently @ 40 mcg/kg/min
Classification
General anesthetics
Mechanism of Action
Short-acting hypnotic. MOA is unknown. Produces amnesia. Has no analgesic properties. Crosses BBB
well. Metabolized by liver. Half life of 3-12 hrs (Blood-brain equilibration half-life 2.9 min).
Patient-Specific Indication
Induction and maintenance of anesthesia; sedation of intubated, mechanically ventilated patient in ICU
Side Effects and Adverse Effects
Bradycardia, hypotension, burning, pain, stinging at IV site, dizziness, headache, apnea, cough, HTN,
abdominal cramping, N/V, flushing, cold/numb/tingling IV site, discoloration or urine (green), fever,

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Nursing Implications

Patient/family Education

involuntary muscle movement, perioperative myoclonia, propofol infusion syndrome.

Initial rate: 5 mcg/kg/min
Titrate by: 5 mcg/kg/min q 15 min
Maximum rate: 50 mcg/kg/min Goal: Ramsay 4
- Additive CNS and respiratory depression w/ETOH, antihistamines, opioids analgesics, and
sedative/hypnotics. Decreased dosage may be required. Dose is titrated to patient response.
- Propofol has no effect on pain threshold. Adequate analgesia should always be used when
propofol is used as an adjunct to surgical procedures
- Discard after 12 hr if administered directly from vial or after 6 hr if transferred to syringe or
other catheter.
- Aseptic technique is essential: solution is capable of rapid growth of bacterial contaminants.
- Intermittent/continuous infusion: administer undiluted. Allow 3-5 minutes btwn dose
adjustments to allow for and assess clinical effects. 10 mg/ml. Rate based on patients weight.
- Assess respiratory status, pulse, BP continuously throughout therapy. Frequently causes apnea
lasting > 60 sec. Maintain patent airway and adequate ventilation. Propofol should be used only
by individuals with endotracheal intubation.
- Assess level of sedation and level of consciousness throughout and following administration.
- When using for ICU sedation, wake-up and assessment of CNS function should be done daily
during maintenance to determine minimum dose required for sedation. Maintain a light level of
sedation during these assessments; do not discontinue. Abrupt discontinuation may cause rapid
awakening with anxiety, agitation, and resistance to mechanical ventilation
- Monitor for propofol infusion syndrome (severe metabolic acidosis, hyperkalemia, lipemia,
rhabdomyolysis, hepatomegaly, cardiac and renal failure).
- Inform family that this medication is for sedation and will decrease the patients mental recall
of procedures and events during medication administration.
- Teach family that when patients are on this medication, it is necessary for them to be on
mechanical ventilation since it depresses the respiratory drive.
- After patient is awake, advise patient to request assistance with ambulation and transfer and to
avoid driving or other activities requiring alertness for a minimum of 24 hours following
administration (Deglin, Vallerand 2015).

Medication (Name, Dose, And Route): piperacillin- tazobactam (Zosyn) 3.375 gm/100ml dextrose 5%/H20 q8h IV
Classification
Anti-infective; extended spectrum penicillin
Mechanism of Action
Death of susceptible bacteria.
Piperacillin: Binds to bacterial cell wall membrane, causing cell death. Spectrum is extended compared

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Patient-Specific Indication
Side Effects and Adverse Effects

Nursing Implications

Patient/family Education

1
5
with other PCNs
Tazobactam: Inhibits beta-lactamase, an enzyme that can destroy penicillins.
Pneumonia
Confusion, dizziness, headache, insomnia, lethargy, seizures, diarrhea, constipation, drug-induced
hepatitis, nausea, vomiting, pseudomembranous colitis, interstitial nephritis, urticaria, SJS, toxic
epidermal necrolysis, bleeding, leucopenia, neutropenia, thrombocytopenia, pain, phlebitis at IV site,
anaphylaxis and serum sickness, superinfection, fever. .
- Assess patient for infection (VS, sputum, urine, stool, WBC) at beginning of and during
therapy.
- Obtain a history before initiating therapy to determine previous use of and reactions to
penicillins or cephalosporins.
- Obtain specimens for culture and sensitivity prior to initiating therapy. First dose may be given
before receiving results.
- Observe patient for signs and symptoms of anaphylaxis. Discontinue drug and notify HCP
immediately if these occur. Keep epinephrine, and antihistamine, and resuscitation equipment
close by in the event of anaphylactic reaction.
- Evaluate renal and hepatic function, CBC, serum potassium, and bleeding times prior to and
routinely during therapy.
- Advise patient and/or family to report rash and signs of superinfection (black furry overgrowth
on tongue, loose or foul-smelling stools) and allergy.
- Caution patient to notify health care professional if fever and diarrhea occur, especially if stool
contains blood, pus, or mucus. May occur up to several weeks after discontinuation of
medication.
- Teach patient and family the importance of finishing prescribed antibiotics to prevent creating
resistance (Deglin, Vallerand 2015)

Medication (Name, Dose, And Route): methylprednisolone (Solumedrol) 60 mg q 12 h IV

Classification
Corticosteroids, immunosuppressant agents
Mechanism of Action
Suppresses inflammation and the normal immune response. Has numerous intense metabolic effects.
Suppresses adrenal fxn at chronic doses of 4 mg/day.
Patient-Specific Indication
Acute respiratory distress syndrome (ARDS): suppression of inflammation and modification of the
normal immune response
Side Effects and Adverse Effects
HA, IICP, depression, euphoria, personality changes, restlessness, cataracts, increased IOP, HTN,
peptic ulceration, anorexia, N/V, acne, decreased wound healing, echymoses, fragility, hirsutism,

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Patient/family Education

petechiae, adrenal suppression, hyperglycemia, fluid retention, hypokalemia, thromboembolism, weight

gain/loss, muscle wasting, osteoporosis, avascular necrosis of joints, muscle pain, cushingoid
appearance, susceptibility to infection.
- Reconstitute with provided solution; max of 125 mg/ml. May be diluted further in D5W, NS.
- Give over 3-15 minutes
- Assess involved systems before and periodically during therapy. Auscultate lung sounds and
note any changes.
- Assess patient for signs of adrenal insufficiency (hypotension, weight loss, weakness, N/V,
anorexia, lethargy, confusion, restlessness) before and periodically during therapy.
- Monitory I&O ratios and daily weights. Obwerve for peripheral edema, steady weight gain,
rales/crackles, or dyspnea. Notify HCP if these occur.
- Monitor serum electrolytes and glucose. May cause hyperglycemia, especially in persons with
diabetes. May cause hypokalemia. May decrease WBC counts.
- Teach patient and family that during periods of stress, such as surgery, patients may require
supplemental systemic corticosteroids.
- Teach patient and family that stopping the medication suddenly may result in adrenal
insufficiency. It is important to titrate doses down after hospitalization as directed by HCP.
- Teach patient and family that glucocorticoids cause immunosuppression and may mask
symptoms of infection. Instruct to avoid others with known contagious illnesses and to report
possible infections immediately.
- Review side effects with patient and family. Instruct patient to inform HCP promptly if
abdominal pain or tarry stools occur. Also report unusual swelling, weight gain, tiredness, bone
pain, bruising, non-healing sores, visual disturbances, or behavioral changes.
- Explain need for continued medical follow-up to assess effectiveness and possible side effects
of medication. Periodic lab tests and eye exams may be needed (Deglin, Vallerand 2015)

Medication (Name, Dose, And Route): insulin detemir (Levemir) 55 units BID SQ
Classification
Antidiabetics, hormones, pancreatics
Mechanism of Action
Lower blood glucose by stimulating glucose uptake in skeletal muscle and fat and by inhibiting hepatic
glucose production. Additionally inhibit lipolysis and proteolysis; enhance protein synthesis.
Patient-Specific Indication
Diabetes mellitus and concurrent corticosteroid use: controls hyperglycemia in diabetic patients.
Side Effects and Adverse Effects
Hypoglycemia, lipodystrophy, pruritis, erythema, swelling, allergic reactions (anaphylaxis).
Nursing Implications
- Do not confuse levemir with lovenox.
- Use only insulin syringes to draw up dose. The unit markings on the insulin syringe must match

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7

Patient/family Education

the insulins units/ml. Prior to withdrawing dose, rotate vial between palms to ensure uniform
solution. Do not shake.
Administer SC; rotate injection sites. Do not administer if cloudy, discolored, or unusually
viscous.
Clarify ambiguous orders and check type, dose, and expiration date with other licensed nurse
before administering.
Not for IV administration or use with insulin pumps.
Assess patient for S/S of hypoglycemia (anxiety; restlessness; tingling in hands, feet, lips, or
tongue; chills; cold sweats; confusion; difficulty in concentration, etc) and hyperglycemia
(confusion, drowsiness, flushed/dry skin, fruit-like breath odor, rapid/deep breathing, polyuria,
N/V, unusual thirst) periodically during therapy.
Monitor body weight changes.
Monitor blood glucose levels every 6 hrs during therapy and more frequently during
ketoacidosis and times of stress.
Instruct patient and family on proper technique for administration. Include type of insulin,
equipment, storage, and place to discard syringes. Discuss importance of not changing brands
and selection and rotation of injection sites.
Explain to pt that this medication controls hyperglycemia but does not cure diabetes. Therapy is
long term.
Instruct pt on proper testing of serum glucose and ketones (to be carefully monitored during
times of stress or illness).
Emphasize importance of compliance with nutritional guidelines and regular exercise as
directed by HCP (Deglin, Vallerand 2015).

Medication (Name, Dose, And Route): oseltamivir (Tamiflu) 30 mg BID NG

Classification
Antivirals; neuraminidase inhibitors
Mechanism of Action
Inhibits the enzyme neuraminidase, which may alter virus particle aggregation and release. Reduces
duration or prevents flu-related symptoms.
Patient-Specific Indication
Pneumonia; possible viral infection
Side Effects and Adverse Effects
Seizures, abnormal behavior, agitation, confusion, delirium, hallucinations, insomnia, nightmares,
vertigo, bronchitis, N/V.
Nursing Implications
- Treatment should be started as soon as possible from the first sign of flu symptoms within 2
days of exposure.
- If oral suspension is not available, capsules may be opened and mixed with flavored foods or
liquids.

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-

Patient/family Education

Monitor influenza symptoms (sudden onset of fever, cough, HA, fatigue). Additional
supportive treatment may be indicated to treat symptoms.
Take missed doses as soon as remembered unless within 2 hrs of next dose. Do not double
doses.
Caution patient that oseltamivir should not be shared with anyone, even if they have the same
symptoms.
Advise patient that oseltamivir is not a substitute for a flu shot. Patients should receive annual
flu shot according to immunization guidelines.
Advise pt to report behavioral changes (hallucinations, delirium, and abnormal behavior)
(Deglin, Vallerand 2015).

Additional Medications:
0.9% sodium chloride 1000 ml IV q 13H20m @ 75 mls/hr
acetaminophen 650 mg PR q 4 hr PRN when temperature is greater than 101F/38.3C
chlorhexidine gluconate 15 ml BID in oral cavity
mupirocin (Bactroban) 1 applic BID in nares
dextrose/water 25 ml as dir PRN IV if BS < 70 and NPO or unconscious (infuse @ 3ml/min)
famotidine (Pepcid) 20 mg QD IV (administer at a rate of 10 mg/min over at least 2 min to avoid hypotension)
insulin (Humulin R) drip per sliding scale below; 250 units/247.5 ml NS as dir (D/C on date of care; switched to levemir SQ)

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9

SYNTHESIS, CRITICAL THINKING, AND PRIORITIZING

Provide a synopsis of your patients hospitalization story. Briefly highlight the acute physiological and psychological alterations and the
needs of your patient. Total 3.0 Points.
Mr. DA is a 44-year old Hispanic male with a history of pneumonia, asthma, diabetes mellitus, renal insufficiency, glaucoma, anemia, and
is S/P toe amputation. He was admitted to RCH ICU via the ER when he presented with extreme dyspnea and refractory hypoxemia. After a recent
discharge from an outside facility, Mr. DAs pneumonia and dyspnea continued to worsen. Upon arrival to the ER, pneumonia was confirmed via
CXR, ABGs were drawn revealing severe hypoxemia, and the patient was intubated. He was diagnosed with ARDS when his PaO2 saturations
remained as low as 50% while intubated and ventilated at high rates. The patient was started on broad-spectrum antibiotics, corticosteroids,
propofol, and fentanyl and was moved to the ICU. He developed a pneumothorax and subcutaneous emphysema, for which a chest tube was
placed. He is currently in a rotoprone bed to increase V/Q matching.
Physiological alterations and needs:
Mr. DA requires mechanical ventilation to oxygenate his blood despite his collapsed and noncompliant alveoli due to ARDS. Being on a
mechanical ventilator puts Mr. DA at risk for acquiring other pneumonias, therefore ventilator-associated pneumonia (VAP) protocol, including
oral care every 4 hours and H2 blocker medication, must be followed. He is sedated with propofol and fentanyl to decrease oxygen consumption
and to prevent him from competing with the ventilator. He is in a rotoprone bed to keep him prone and oscillating six hours at a time followed by
one hour supine, in order to improve ventilation and V/Q matching. The rotoprone bed facilitates drainage of pulmonary secretions and allows
better ventilation of dependent parts of the lungs in order to increase oxygenation. Risk factors related to use of the rotoprone bed include risk for
periorbital and scleredema, corneal abrasions, and skin breakdown. Therefore, this patient requires special attention to skin breakdown and eye
care. Because of his prolonged bedrest and time spent in the prone position, he requires heel protectors, preventative bandages on his coccyx, and
frequent skin breakdown checks in order to prevent the formation of ulcers. Mr. DAs body is recovering from an acute and debilitating event,
therefore he needs rest and hydration in order to heal.
Psychological alterations and needs: Mr. D.A. is currently sedated. However, he was admitted because of an exacerbation and progression of
pneumonia into ARDS. He lacks knowledge regarding his own healthcare and needs education and teaching about self-care and preventative
measures including dietary, exercise, and diabetes control. He requires additional knowledge regarding controlling his asthma, diabetes in order to
prevent future complications like amputations, glaucoma, kidney failure, pneumonia, and ARDS.

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Based on your analysis, list the needs of your patient in each of the following areas. Total 7.0 Points (1 point per area).
Basic Care and Comfort
Sedation, pain medication, oral care
Health Promotion and Education
Medication and disease process teaching once weaned off sedation; teaching family
Physiological Needs (high priority)
Ventilation support, sedation, positional drainage of lung secretions and increased V/Q matching
Physiological Needs (low priority)
Ulcer prevention, VAP prevention protocol (oral care Q4hrs)
Psychological Needs
Medication and disease process teaching once weaned off sedation; teaching family; support of family;
spiritual support of family at bedside
Pharmacological Considerations
Sedation, anti-infective, and pain medications
Safety and Infection Control
Continual monitoring and prevention of injury; double checks when turning rotaprone bed
Synthesize the patient needs and generate nursing diagnoses. Total 5.0 Points (1 point per diagnosis).
Two High Priority Nursing Diagnoses:
1.
Impaired gas exchange and ineffective airway clearance R/T ARDS and altered level of consciousness secondary to sedation AEB patchy
opacities, bilateral airspace consolidation, compressive atelectatic changes, pneumothorax on CXR; and ventilator settings on bilevel
mode 16/40%/high peep 30/low peep 0/PS 15 and with O2 desaturations to <90% when turned from prone to supine position in
rotoprone bed.
2.
Ineffective renal tissue perfusion R/T acute ischemic renal injury secondary to SIRS/Sepsis and uncontrolled DM AEB increasing BUN
(27 mg/dL) and creatinine (3.3 mg/dL) levels.
Two Medium Priority Nursing Diagnoses (at least one of them should be spiritual or psychosocial diagnosis):
1.
Noncompliance R/T evidence of development of complications and health conditions AEB progression of pneumonia to ARDS as well
as microvascular complications secondary to uncontrolled DM (toe amputation, glaucoma, renal injury).
2.
Self-care deficit/knowledge deficit R/T uncontrolled diabetes mellitus AEB hyperglycemia, kidney injury, glaucoma, and recently
amputated toe.
One Low Priority Nursing Diagnosis:
1.
Risk for impaired skin integrity R/T position in rotoprone bed in combination with hyperglycemia AEB facial swelling, scleredema,
periorbital edema, preventative wound care bandage on coccyx, heel protectors, and frequent skin checks as well as BG readings up to
177 and recent toe amputation.
(Ackley & Ladwig, 2014; Baird & Bethel, 2011)

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1

NURSING DIAGNOSIS
Total 25.0 Points
Nursing Diagnosis I:
Impaired gas exchange and ineffective airway clearance R/T ARDS and altered level of consciousness secondary to sedation AEB patchy
opacities, bilateral airspace consolidation, compressive atelectatic changes, pneumothorax on CXR; and ventilator settings on bilevel
mode 16/40%/high peep 30/low peep 0/PS 15 and with O2 desaturations to <90% when turned from prone to supine position in rotoprone
bed.
* Relevant Assessment: Patient sedated and intubated. Does not tolerate turning from prone to supine position. Lung sounds: diminished; coarse
crackles when turned from prone to supine position.
* Relevant Diagnostic Tests: CXR revealed patchy opacities, bilateral airspace consolidation, compressive atelectatic changes, pneumothorax,
subcutaneous emphysema
* Relevant Medications and Therapies: mechanical ventilation @ bilevel mode 16/40%/high peep 30/low peep 0/PS 15 via ET tube; prone
positioning in rotoprone bed; solumedrol, abx, Tamiflu, sedation
* Expected Outcomes: By the time of discharge from the ICU, this patient will have adequate gas exchange without ventilator support as
evidenced by appropriate mental status and orientation, SpO2 > 94%, respiratory rate 12-20 breaths per minute with normal depth and pattern; and
absence of adventitious breath sounds. By the end of next shift, this patient will maintain O2 saturations above 94% when in supine positions.
* Nursing Interventions with Rationales:
- Assess patients respiratory rate, depth, and rhythm. Auscultate lung fields for breath sounds every 1-2 hours and as needed. Auscultate
upper chest over artificial airway to assess for leaks. Monitor for abnormal respiratory patterns. Be alert to IICP. The presence of crackles
and wheezes may alert the nurse to airway obstruction, which may lead to exacerbate existing hypoxia.
- Monitor oxygen saturation continuously using pulse oximetry. Correlate arterial oxygen saturation blood gas results with pulse oximetry.
An oxygen saturation less than 90% or a partial pressure of oxygen of less than 80 mmHg indicates significant oxygenation problems.
Pulse oximetry is useful for tracking and/or adjusting supplemental oxygen therapy.
- Monitor serial ABG values. Be alert to levels indicative of hypoxemia (PaO2 < 80 mmHg) and to PaCO2 > 35 mmHg (levels higher than
this may increase ICP).
- Observe for cyanosis of the skin; especially note color of tongue and oral mucous membranes. Central cyanosis of the tongue and oral
mucosa is indicative of serious hypoxia and is a medical emergency.
- Assist with turning every 2 hours to promote lung drainage, expansion, and alveolar perfusion. Raise HOB 30 degrees to enhance gas
exchange and decrease risk of aspiration of oral, nasal, and gastric secretions. Evidence shows that a mechanically ventilated client has a
decreased incidence of VAP if client is placed in a 30- to 40- degree semi-recumbent position as opposed to supine position.
- Assess ventilator for proper functioning and parameter settings, including FiO2, tidal volume, rate, mode, peak inspiratory pressure, and
temperature of inspired gases. Ensure connections are tight and alarms are set. Assessing the ventilator for proper function and the
patients response to therapy is most often a collaborative effort between nursing and respiratory therapist (Ackley & Ladwig, 2014;
Baird & Bethel, 2011).
* Evaluation: Goal not yet met. Patient still dependent on mechanical ventilation on bipap mode. However, pt is starting to tolerate turning supine
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Nursing Diagnosis II:

Ineffective renal tissue perfusion R/T acute ischemic renal injury secondary to SIRS/Sepsis and uncontrolled DM AEB increasing BUN
(27 mg/dL) and creatinine (3.3) mg/dL levels .
* Relevant Assessment: UOP adequate at ~150 ml/hr; not oliguric
* Relevant Diagnostic Tests: BUN 27; Cr 3.3
* Relevant Medications and Therapies: Permissive HTN to allow perfusion to kidneys (BP currently at 180/73); monitor I&Os, no diureses at this
time per MD to avoid further renal insult
* Expected Outcomes: Patient will maintain adequate UOP at a minimum of 30 mL/hr and BUN and Cr will decrease to normal limits (5-25
mg/dL and 0.5-1.5 mg/dL, respectively) by time of discharge from ICU.
* Nursing Interventions with Rationales:
- Measure intake and output on a regular basis. Calculate fluid balance. Oliguria and/or anuria are generally associated with onset of acute
renal failure but up to 60% of clients can be in renal failure with almost normal urine output (nonoliguric acute renal failure). Urine
output shoul be 0.5 mL/kg/hr.
- Assess client for Hx of risk factors for decreased renal perfusion, which can result in renal insufficiency, renal artery stenosis, and acute
renal failure. Intrinsic/intrarenal: There is structural damage to the kidney, something directly toxic to the kidney. Causes include
hypertension, diabetes, glomerulonephritis, kidney infection, lupus, nephrotoxic drugs, IV contrast.
- Assess for sighs of dehydration. Dehydration may cause decreased renal perfusion and lead to renal failure.
- Monitor vital signs carefully. Especially note new onset of HTN from onset of kidney dysfunction or decreased MAP. Chronic HTN can
lead to atherosclerosis, the most common cause of renal artery stenosis. Hypotension may lead to poor renal perfusion and ARF.
- Utilize continuous cardiac monitoring as needed. Monitor for dysrhythymias d/t possible increased serum potassium and phosphorus, or
low hemoglobin due to poor kidney function.
- Listen to lung sound, noting presence of adventitious lung sounds. Crackles or rales are signs of fluid overlad due to acute or chronic
renal failure (Ackley & Ladwig, 2014; Baird & Bethel, 2011).
* Evaluation: Goal not yet met. Patient is still attaining an adequate output of approximately 125 ml/hr, but has not yet had BUN and Cr labs
return to be within normal limits.

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REFERENCES

Ackley, B. J., & Ladwig, G. B. (2014). Nursing Diagnosis Handbook: An evidence-based guide to planning care (10th ed.). Maryland Heights,
Mo: Mosby Elsevier.
Baird, M. S. & Bethel, S. (2011). Manual of critical care nursing: Nursing interventions and collaborative management (6th edition). St. Louis,
MO: Elsevier.
Chernecky, C. C. & B. J. Berger (2004). Laboratory tests & diagnostic procedures. Philadelphia, PA, Saunders.
Deglin, Pharm D, J. H., & Vallerand, PhD, Rn, FAAN, A. H. (Ed.). (2015). Davis' Drug Guide for Nurses (13th ed.). F.A. Davis Co.
Dirksen, S. R. (2011). Clinical companion to Medical-surgical nursing: Assessment and management of clinical problems (8th ed.). St. Louis,
Mo: Elsevier/Mosby.
Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed). Upper Saddle River, NJ., Pearson Education Inc.
S. E. Huether & McCance, K. L. (2012). Pathophysiology: The biologic basis for disease in adults and children. Maryland Heights, Mo., Mosby
Elsevier.
Potter, P. A., A. G. Perry, et al. (2009). Fundamentals of nursing. St. Louis, Mo., Mosby Elsevier.

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