Running head: DUNBAR CASE STUDIES
Dunbar: Case Study Three and Four
Whitney L. Dunbar
Wright State University
Nursing 7201
June 30, 2013
Dr. Kristine Scordo
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Dunbar: Case Study Three and Four
Case Study Three
1. What is the differential diagnosis of this patient’s clinical deterioration and why?
There are many possible diagnoses that could be the reason for the patient’s clinical
deterioration. First, severe pneumonia should be considered since the patient’s chest x-ray
revealed a right lower lobe infiltrate on admission. The pneumonia could have been caused by
aspiration of gastric contents. An increased risk for aspiration pneumonia includes altered levels
of consciousness from head trauma and this patient was involved in a head-on collision mobile
accident and found poorly responsive at the accident scene. A large amount of gastric contents
that is aspirated can cause acute respiratory failure within an hour and progress to acute
respiratory distress syndrome (ARDS). This patient presents with a respiratory rate of 25 breaths
per minute, acute hypoxemic respiratory failure with a PO2 of 39 mm Hg, and these two signs
may present in patients with aspiration pneumonia. However, common clinical manifestations of
pneumonia include cough, fever, chest pain, and with or without sputum production, and the
patient does not exhibit these clinical manifestations (Longo et al., 2012; Papadakis, McPhee, &
Rabow, 2013).
Second, ARDS, non-cardiogenic pulmonary edema, should be considered since the
patient received massive fluid resuscitation due to trauma with multiple fractures and chest
trauma with a lung contusion. Also, the chest x-ray result did not display an enlarged heart,
signifying the patient had a normal cardiac size and the new chest x-ray displayed a diffuse
airspace pattern. Non-cardiac pulmonary edema due to fluid overload can cause an acute onset
of dyspnea, refractory hypoxia, and anxiety due to decreased lung compliance. This patient
presents with these symptoms. Patients may have crackles when auscultating lung fields and a
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pulmonary catheter wedge pressure less than 18 mm Hg, but it is not mentioned in the patient’s
assessment. Patients with ARDS have a PaO2/FiO2 less than 200 mm Hg and can be caused by
sepsis or aspiration. This patient’s PaO2/FiO2 ratio is 97.5 (Longo et al., 2012; Papadakis et al.,
2013).
Third, cardiogenic edema is a possible diagnosis for this patient due to the acute onset of
tachypnea, dyspnea, and anxiety. The patient’s history is unknown at this time and if he has left
ventricular dysfunction or valvular disease it can cause cardiogenic edema due to the massive
fluid resuscitation. Patients with cardiogenic shock may have crackles when auscultating lung
fields and an S3 when auscultating the heart. Cardiomegaly and perihilar bat-wing distribution of
infiltrate can appear on a chest x-ray. Patients with cardiogenic edema will improve hypoxemia
with high flow oxygen and their pulmonary catheter wedge pressure is greater than 18 mm Hg,
but this is not noted in the patients’ assessment (Longo et al., 2012; Papadakis et al., 2013).
Fourth, diffuse alveolar hemorrhage is another possible diagnosis due to the patient
having chest trauma and possibly experiencing a traumatic intubation. A patient may present
with hemoptysis, alveolar infiltrates on the chest x-ray, and dyspnea. If there is clearing of
diffuse lung infiltrates within two days then the diagnosis is probably diffuse alveolar
hemorrhage (Longo et al., 2012; Papadakis et al., 2013).
Fifth, fat embolism syndrome (FES) secondary to multiple fractures can be a differential
diagnosis for this patient. FES usually occurs within 12 to 72 hours of injury. A fat embolism
can be dislodged from long bone fractures and travel to the pulmonary circulation. This patient
has a high-risk for FES due to several pelvic fractures, an open fracture of the femur, and a
closed, displaced fracture of the left tibia. FES causes an acute onset of tachypnea and it is a
clinical manifestation that is found in over half of patients with FES. However, a chest x-ray of a
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patient with FES does not display bilateral infiltrates and this patient’s first chest x-ray displayed
a right lower lobe infiltrate and the latest chest x-ray displays diffuse airspace pattern. Also, a
petechial rash may be found on physical examination and usually resolves in five to seven days.
It is not stated that this patient manifests a petechial rash (Longo et al., 2012; Papadakis et al.,
2013).
Sixth, septic shock is another potential diagnosis for this patient. Septic shock can
develop acutely but it can develop and present differently in each patient. Symptoms of sepsis
include fever, chills, dyspnea, anxiety, or confusion. Respiratory alkalosis is an early sign of
septic shock and is present due to stimulus of the medullary respiratory center by endotoxins and
other inflammatory mediators. Also, the PO2 decreases early in the course of septic shock due to
ventilation-perfusion mismatching. The decrease in PO2 is a result of decreased pulmonary
compliance from an increase in alveolar epithelial injury and capillary permeability that causes
an increase in pulmonary water content. ARDS develops in approximately 50% of patients with
septic shock. Another manifestation of septic shock includes decreased peripheral vascular
resistance. Laboratory results that could indicate sepsis shock include leukocytosis and
leukopenia. Also, hypotension is another common clinical manifestation of septic shock. This
patient has many potential portals of entry for infection due to his fractures, had a chest tube
inserted, intubated, and had emergency surgery. This patient experiences anxiety, low PO2 of 39
mm Hg, and presents with respiratory alkalosis. However, it is not noted if the patient has a
fever, chills, any white blood cell count laboratory values, and a current blood pressure with the
dyspnea 12 hours post admission (Longo et al., 2012; Papadakis et al., 2013).
Seventh, transfusion-related acute lung injury (TRALI) can be a potential diagnosis for
this patient. A patient with TRALI may develop acute respiratory distress, signs of
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noncardiogenic pulmonary edema, and bilateral interstitial infiltrates on a chest x-ray during or
within six hours of a blood transfusion. When there is a trauma patient that receives more than
10 units of blood products within a 12 to 48 hour interval, it places them at risk for developing
ARDS. If a patient needs additional transfusions of blood products, each unit transfused
increases the patient’s risk for developing ARDS by 6%. This patient received eight units of
whole blood, five units of platelets, and eight units of fresh frozen plasma. This patient’s
respiratory status started to deteriorate 12 hours after admission and receiving the blood products
(Chaiwat et al., 2009; Longo et al., 2012).
2. What are the risk factors that put this patient at risk for ARDS? Provide rationale.
In general, the risk factors that can place a patient at risk for developing ARDS comprise
of sepsis (one-third of cases), traumatic brain injury, pulmonary contusion, TRALI, hypotension,
age more than 65 years old, fat embolism from long bone fractures, near drowning, chest injury,
pneumonia, pancreatitis, inhalation injury from harmful fumes or smoke, aspiration of stomach
contents, and ventilator-induced lung injury (VILI) (Bakowitz, Bruns, & McCunn, 2012; Longo
et al., 2012). The risk factors that this patient presents with include a pulmonary contusion, chest
injury, above the age of 65, TRALI, hypotension, long bone fractures, VILI, and he potentially
could have aspirated.
The chest x-ray of the patient reveals a pulmonary contusion and is a potential risk for
developing ARDS. Also, the patient presents with a flail chest on the right side and this suggests
the patient has a chest injury. Pulmonary contusions can develop over 24 hours after the initial
insult. Pulmonary contusions and chest injuries can lead to poor gas exchange from the edema
and hemorrhage of the lung parenchyma (Longo et al., 2012; Papadakis et al., 2013).
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In addition, the patient is 77 years old and places him at an increased risk for developing
ARDS. The elderly have an increased risk for developing ARDS because they have decreased
physiological reserves. Patients who are greater than 75 years of age have a 60% mortality rate
compared to patients who are younger than 45 years old with a 20% mortality rate (Longo et al.,
2012).
TRALI is another factor that increases the risk for developing ARDS. Patients develop
respiratory distress from non-cardiogenic pulmonary edema. Non-cardiogenic pulmonary is the
outcome from a transfusion of a donor plasma that includes high-titer anti-HLA antibodies that
connect with recipient leukocytes. The leukocytes collect in the pulmonary vasculature and
emancipate mediators that escalate capillary permeability (Longo et al., 2012). This patient
received 21 units of blood products.
Hypotension is a factor that places the patient at an increase risk for developing ARDS.
When a blood pressure is lower than 90/60 mm Hg, it is considered hypotension. This patient’s
blood pressure was 70/40 mm Hg at the scene and his hypotension was likely caused by blood
loss. When there is a decrease in blood flow to tissue, it leads to the bodies’ inability to clear
toxic metabolites. Furthermore, this can lead to shock as the body tries to enhance vital organ
perfusion to meet metabolic demands. The vital organs are the brain and heart (McKean, Ross,
Dressler, Brotman, & Ginsberg, 2012). Therefore, there could be decrease perfusion to the lungs
and could cause hypoxemia, hypercapnia, and possibly ARDS.
Long bone fractures place a patient at an increased risk for ARDS to evolve because of
FES. This patient has pelvic, femur, and left tibia fractures. A fat embolism can be dislocated
from long bone fractures and travel to the pulmonary circulation causing a decline in pulmonary
arterial blood movement to ventilated areas of the lung, rising dead space, and to pulmonary
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hypertension. Severe hypoxemia and hypercapnia resulting from a rise in pulmonary dead space
is conspicuous in early ARDS (Longo et al., 2012).
VILI can increase the patient’s risk of developing ARDS. This patient was intubated in
the emergency department. VILI results from repetitive alveolar over-distention and persistent
alveolar collapse. When there is differing lung compliance within the lung and there are efforts
to entirely inflate a consolidated lung, it may lead to over-distention and cause injury to more
“normal” parts of the lung. Also, high tidal volumes can increase alveolar damage. ARDS can
result from these two processes (Longo et al., 2012).
Aspiration of gastric contents increases a patient’s risk for developing ARDS. This
patient had a decreased level of consciousness and that increases the patient’s risk for aspirating.
The acid of gastric contents causes burns to the tracheobronchial tree that is involved in the
aspiration and leads to a parenchymal inflammatory reaction that involves the release of potent
cytokines and can lead to ARDS (Longo et al., 2012).
ARDS is usually related to a direct lung injury or an indirect lung injury. Pneumonia,
pulmonary contusion, and inhalation injury are examples of a direct lung injury. Severe sepsis,
transfusion, and pancreatitis are examples of indirect lung injury. Direct or indirect lung injury
disease states can lead to poor gas exchange, amplified pulmonary vascular resistance, and
reduced lung compliance. It is a result from direct injury to lung parenchyma, flooding of
protein rich material and cellular debris collecting in alveolar spaces, and loss of normal lung
structure and function. These changes in the pulmonary function are major activators of the
inflammatory pathways that can result in clinical deterioration and ARDS. The proinflammatory state is the essence of severe traumatic injuries. Therefore, there is an observed
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increase in frequency of developing ARDS in patients who had a traumatic injury (Bakowitz et
al., 2012; Longo et al., 2012).
3. What are specific considerations for managing an elderly trauma victim. Provide
rationale.
The considerations for managing an elderly trauma victim include physiologic changes of
aging, comorbidities, medications, common mechanisms of injury correlated to elderly trauma
victim, and specific features to the resuscitation of the elderly trauma victim. It is important to
know these considerations as a healthcare provider since the fifth leading cause of death in
patients over the age of 65 is trauma and it is predicted that 20% of the United States population
will be more than 64 years of age by 2050 compared to 12% today (Aschkenasy & Rothenhaus,
2006).
First, the physiologic changes of aging is a consideration for managing an elderly trauma
victim because the chances of dying after trauma rises by 6% for every one year increase in age
above 65. Aging is a normal and predictable process with irreversible changes of the different
organ systems over time and eventually death occurs. The typical outcome of aging is a loss of
functional reserve in most organ systems. Cardiac functional reserve decreases with age and
consists of a lower cardiac output, diminished cardiac reserve, and not as likely to tolerate
hemodynamic stress as well compared to a young adult. The electrical conducting system
displays aging by a diminished heart rate response to catecholamines. There can be a dampened
inotropic and chronotropic reaction to trauma in the elderly. For example, in young adults
compensatory tachycardia is typically seen as a response to hypovolemia or shock, but it is
absent in the elderly. With aging there are pulmonary changes that include a loss of elasticity in
the chest wall and lungs, diminished mechanical compliance, rise in standard work of breathing,
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lessening in mucociliary clearance, and a decline in the capability to clear the bronchial tree. As
a person ages there is a decrease in arterial oxygen tension that causes alveolar loss and
decreased diffusion capacity. Therefore, a standard PaO2 between 78 and 92 mm Hg can be
anticipated in a patient 80 years old. Also, with age the vital capacity, forced expiratory volume,
and functional reserve are altered and should be considered in the administration of ventilation.
There is a reduction in number of functioning nephrons and muscle mass with age and they cause
a decrease in creatinine clearance. Patients that have end-stage liver disease and cirrhosis have
an increase risk of mortality with a trauma due to risk of bleeding and uncontrolled hemorrhage.
End-stage renal disease places a patient involved in a trauma at a higher rate of mortality. Also,
age related changes in the brain include a 200-g reduction in brain weight, reduction in brain
size, distending of the bridging vessels around the surface of the brain, and a decrease in
cerebrovascular auto-regulation. There is an increase risk for fractures in the elderly trauma
victim due to bone demineralization. A decrease in defenses against microorganisms and loss of
temperature auto-regulation are age-related effects on the skin. In addition, glucose tolerance is
reduced with age and glycemic control is a vital goal in the critically ill trauma victim
(Aschkenasy & Rothenhaus, 2006).
Second, comorbidities are considerations in managing the elderly trauma victim. The
decrease in cardiac functional reserve previously mentioned can be disguised by heart failure and
enhance the decreased cardiac output. A heart block can additionally dull the rate reaction to
stress and coronary artery disease can become noticeable when there is demand ischemia during
the stress of trauma. An electrocardiogram is required in the initial work up of an elderly patient
due to an increased risk of developing an acute cardiac event. Patients who have osteoporosis
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have an increased incidence of fractures compared to patients of the same age without
osteoporosis (Aschkenasy & Rothenhaus, 2006).
Third, pre-existing medications are considerations in managing the elderly trauma victim.
Medications that are correlated with traumas in the elderly are psychotropic medications and
anti-hypertensive medications. Psychotropic medications include antidepressants, neuroleptics,
and sedatives. Anti-hypertensive medications consist of beta-blockers, calcium blockers, and
diuretics. Specifically, beta-blockers can diminish the patient’s compensatory hemodynamic
reaction to hemorrhage or volume depletion. If hemorrhage and ischemia have been ruled out
for the cause of a patient’s hypotension then the healthcare provider can consider
antihypertensive medications as a possible source. Other medications that have an increase use
in the elderly population include chronic therapy with oral warfarin, anticoagulants, aspirin, and
antiplatelet medications. When an elderly patient is taking warfarin it increases their risk for
major bleeding complications, for example, warfarin may exacerbate the result from a severe
head injury. The healthcare provider will need to assess treatment possibilities based on the
necessity for warfarin therapy and the need for immediate reversal, non-urgent reversal, simple
withdrawal from warfarin, or no adjustment in therapy when an elderly patient arrives to the
emergency department with an injury from a trauma (Aschkenasy & Rothenhaus, 2006).
Fourth, the mechanism of injury is a consideration in the management of the elderly
trauma victim. The leading causes of injuries for trauma patients above the age of 70 are due to
falls with 60.7% trailed by motor vehicle accidents with 21.5%. Other common causes of
injuries in an elderly trauma victim are pedestrians struck by automobiles, burns, accidental
hypothermia, and elder abuse and neglect. Each mechanism of injury is managed differently.
Specifically for motor vehicle collisions, it is thought that the elderly are put at a higher risk for
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being involved in motor vehicle accidents due to alterations in vision, reflexes, and balance and
cognition from the pathophysiology of aging and medical conditions. Conversely, the pattern of
injury for the elderly population in motor vehicle trauma looks comparable to the pattern of
injury for the younger patients excluding for an augmented frequency of sternal fractures due to
seatbelts in patients above the age of 65 (Aschkenasy & Rothenhaus, 2006).
Fifth, there are specific features to the resuscitation of the elderly trauma victim and is a
consideration in the management of the patient’s care. The features include pre-hospital care,
triage, initial resuscitation, patterns of injury, central nervous system, spine, rib fractures and
other thoracic injuries, abdominal trauma, and musculoskeletal system. The pre-hospital aspect
focuses on the elderly’s social environment and home situation. It is to assess if the living
environment is safe for the patient. Triage includes standard trauma criteria for patients older
than 55 years old as a vital factor of trauma center preference in wounded patients. Standard
protocols direct the initial resuscitations of the elderly trauma victim. An arterial blood gas
should be drawn since it can display an increased base deficit or a high serum lactate
concentration. These two laboratory values are indicators of hidden hypovolemia or forthcoming
shock. There are distinctive patterns of injury in the elderly trauma victim and that information
should help the healthcare provider diagnose injuries and define severity of illness. Central
nervous system includes the suggestion of using computer tomography for the elderly due to
increase risk for intracranial hemorrhage. The spine includes the elderly trauma victim having a
radiograph of the cervical spine implemented due to the increased possibility of cervical spine
fractures. A chest radiograph should be executed because mortality rate increases as the number
of fractured ribs increase. Abdominal trauma includes executing abdominal computer
tomography in an elderly trauma victim to assess for spleen or liver injury. The musculoskeletal
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system feature consists of the healthcare provider in the emergency department to assess and
implement tests for hip, vertebral, and pelvic fractures since these fractures are more commonly
seen in the elderly trauma victim (Aschkenasy & Rothenhaus, 2006).
4. How would you manage this patient’s hypoxemia? Provide rationale.
There are a few different interventions that can be implemented to manage this patient’s
hypoxemia. There are five general principles when providing care to patients with ARDS. The
principles consist of recognizing and treating the primary medical and surgical conditions,
reducing procedures and their complications, venous thromboembolism, gastrointestinal
bleeding, aspiration, excessive sedation, and central venous catheter infections prophylaxis,
quick identification of nosocromial infections, and providing adequate nutrition. This patients’
underlying condition is trauma and was intubated and mechanically ventilated due to his
respiratory failure. Initially, the FiO2 should be set at 100% (Longo et al., 2012). The healthcare
provider should try to reduce the FiO2 to less than 60% as quickly as possible to prevent oxygen
toxicity. The FiO2 should be titrated with an oxygenation goal of the PaO2 between 55 to 80 mm
Hg or a SpO2 between 88 to 95%. Next, the patient’s predicted body weight (PBW) should be
calculated and the selection of ventilator mode. The initial ventilator mode can be assistcontrolled with a set tidal volume but may need to be altered depending on the patient’s
condition. Also, the initial set ventilator setting is to achieve a tidal volume of 8 mL/kg PBW
and then decrease tidal volume by 1 mL/kg at interval of less than or equal to two hours until
tidal volume is 6 mL/kg PBW (National Heart, Lung, and Blood Institute’s (NHLBI) ARDS
Network, 2008). Conventional methods to mechanical ventilation set tidal volumes of 10 to 15
mL/kg PBW but it can cause volutrama in patients with ARDS. A randomized control trial was
implemented to compare the mortality rate and number of days without ventilator use from day
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one to day 28 between 6 mL/kg and 12 mL/kg tidal volumes PBW in 861 mechanically
ventilated adult patients with ARDS. The mortality rate was decreased by 22% and there was an
increase in the number of ventilator-free days in the group of patients treated with 6 mL/kg PBW
tidal volumes compared to the group of patients being treated with 12mL/kg tidal volumes PBW
(ARDS Network, 2000). Therefore, this patient’s tidal volume should be increased to 8 mL/kg
PBW from the initial tidal volume set of 90 mL. Positive end expiratory pressure (PEEP) is used
to improve oxygenation through alveolar recruitment and the minimal amount of PEEP is set at 5
cm H2O. PEEP is used to reduce the amount of FiO2 and raise PaO2. Therefore, the healthcare
provider can increase PEEP while trying to titrate down FiO2 administration to the goal of 60%
and obtain a PaO2 between 55 to 80 mm Hg. The ideal PEEP is 12 to 15 mm Hg in ARDS
patients for alveolar recruitment and PEEP should be titrated up in slight increments (Longo et
al., 2012). The patient’s airway pressure rose from 20 to 60 cm H2O. The plateau pressure goal
is less than or equal to 30 cm H2O. Elevated plateau pressures and PEEP can cause barotrauma
and hypotension (Saguil & Fargo, 2012). Pressure control ventilation with inverse ratio can be
implemented to improve oxygenation by an increase in mean airway pressure and decrease peak
pressures. This kind of ventilation extends inspiratory time so that it is longer than expiratory
time. Other strategies in mechanical ventilation to improve oxygenation in the ARDS patients
include high-frequency ventilation, airway pressure release ventilation, partial liquid ventilation,
inhaled nitric oxide, extracorporeal membrane oxygenation, and prone-position ventilation
(Bakowitz et al., 2012; Longo et al., 2012). Also, the primary respiratory rate is set to near
baseline minute ventilation and does not exceed 35 breaths per minute. The pH goal for patients
with ARDS is 7.30 to 7.45. The healthcare provider can modify the tidal volume and respiratory
rate to attain pH and plateau pressure goals (NHLBI ARDS Network, 2008).
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5. What are the problems associated with PEEP?
There are a few problems related to PEEP. First, when there is too much PEEP it can
lead to increased stretching of the alveoli and bronchi. This causes a rise in dead space
ventilation and a decline in lung compliance. Both outcomes can escalate the work of breathing.
Also, a rise in pulmonary vascular resistance and right ventricular afterload can be the result of
over-distention of normal alveoli due to compression of the alveolar capillaries. Second, there is
a high frequency of barotrauma witnessed with excessive amounts of PEEP. The levels of PEEP
are usually more than 20 cm H2O. A pneumomediastinum can occur when there is disruption of
alveoli and high levels of PEEP. The air from the mediastinum can rupture and produce a
pneumothorax, pneumopericardium, pneumoperitoneum, pneumoretroperitoneum, or
subcutaneous emphysema. Additional risk factors for barotrauma besides an increase in PEEP
include underlying lung disease, stacking of breaths, tidal volumes more than 10-15 mL/kg, and
young age. Third, hypotension is associated with PEEP due to a decrease in cardiac output due
to an increase in mean airway pressure, increase in mean intrathoracic pressure, and a decrease in
venous return to the heart. Fourth, a rise in PEEP can delay blood drainage from the brain and
blood return to the heart and might cause a rise in intracranial pressure in patients who have
reduced ventricular compliance. Therefore, the amount of PEEP should be wisely selected to
balance oxygenation requirements versus possible adverse outcomes on intracranial pressure
with patients who are being mechanically ventilated for ARDS and who have confirmation of
increased intracranial pressure (Butterworth, Mackey, & Wasnick, 2013).
6. What is the mortality rate associated with ARDS?
The in-hospital mortality rate associated with ARDS is approximately 34% to 55%. It is
suggested that the frequency of ARDS is around 64 cases per 100,000 person-years. Also, it is
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estimated that 16.1% of all patients requiring mechanical ventilation progress to acquiring acute
lung injury or ARDS. Risk factors associated with a higher mortality rate for ARDS comprises
of advanced age, deteriorating multi-organ dysfunction, existence of pulmonary and nonpulmonary coexisting medical conditions, an elevated acute physiology and chronic health
evaluation (APACHE) II score, and acidosis (Saguil & Fargo, 2012).
Case Study Four
Chief Complaint: “I have been peeing less and my swelling in my feet and ankles are worse.”
History of Present Illness: This is a 77-year old Caucasian male who had a kidney transplant in
2008 from a living unrelated donor who presents to the transplant clinic for evaluation of
decrease urination and increase swelling in feet and ankles. The decrease in urination started two
months ago. He used to urinate a moderate amount four or five times a day and now it is only a
small to moderate amount twice a day. Reports his urine is now a dark yellow. Patient states
there are no aggravating or relieving factors for his decreased urination. Him and his wife both
have noticed that his ankles and feet have become more swollen in the last month and that he has
been having a harder time putting his shoes on his feet. The swelling in his ankles and feet are
worse at night and he finds relief by raising his feet while sitting in his recliner. Reports that he
has gained five pounds in the last month. He states that he typically drinks four to five glasses of
water a day and his fluid intake has not changed in the last two months.
He received hemodialysis for 16 months prior to the kidney transplant and had an AV
fistula placed in his right upper arm. Hypertension was thought to cause his chronic kidney
disease. He developed an acute rejection three months following his kidney transplant and the
episode was reversed with treatment. Him and his wife both report that the patient takes all of
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his immunosuppressive medications every day and has not missed a dose in the last month.
Patient was last seen at the transplant clinic three months ago.
Past Medical History:
Hypertension (HTN), Type II diabetes mellitus (DM),
Hyperlipidemia, skin cancer, anemia, and End-Stage kidney
disease with hemodialysis M, W, F
Surgical History:
Kidney transplant from living unrelated donor in 2008 and right
upper arm AV fistula placed in 2007
Family History:
Father- HTN, Mother- HTN, DM, and peripheral vascular disease
Social History:
Lives with wife. 3 living children, all in good health
No cigarette, alcohol, or illicit drug use
Retired police officer
Served in the Army for 20 years, Agent Orange exposure in
Vietnam
Medications:
Furesemide 20 mg tablet, one tablet by mouth (PO) twice a day
Insulin, Aspart, human 100 unit/mL, inject 20 units subcutaneous
(SC) before breakfast and inject 6 units SC with lunch and
inject 18 units SC before supper plus correction
Insulin, Glargine human 100 unit/mL, inject 20 units SC daily at
night
Losartan 50 mg tablet, take one tablet PO daily
Metoprolol tartrate 100 mg tablet, take one and one half tablet PO
twice a day
Simvastatin 20 mg tablet, take one tablet PO daily at night
Sirolimus 1 mg tablet, take two tablets PO daily
Tacrolimus 1 mg tablet, take one tablet PO twice a day
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Aspirin 81 mg tablet, take one tablet PO daily
Allergies:
No known allergies
Review of Systems:
General health:
Overall good health except reports a five-pound weight gain in last
month. Denies fatigue, fever, chills, or night sweats.
Skin:
Denies rash or skin color changes, pruritis, bruising, or new
lesions.
HEENT:
Denies headache, blurred vision, tinnitus, epistaxis, glaucoma,
cataract, sore throat, earaches, hearing loss, or nasal discharge.
Neck:
Denies neck pain, stiffness, decreased range of motion or swollen
glands.
Respiratory:
Denies cough, productive sputum, chest pain with breathing,
shortness of breath, wheezing.
Cardiac:
Reports swelling in feet and ankles. Denies palpitations, chest
pain, irregular heartbeat, dyspnea on exertion, orthopnea.
GI:
Denies decrease in appetite, food intolerance, nausea, vomiting,
dysphagia, diarrhea, constipation, or abdominal pain. Last
bowel movement this morning.
GU:
Reports decrease in frequency of urination and amount of urine.
Urine is dark yellow. Denies pain on urination, blood in urine,
urgency, hesitancy, nocturia, or straining.
Musculoskeletal:
Denies muscle or joint pain. Denies weakness. No decrease range
of motion.
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Neurological:
18
Denies confusion or memory problems, poor coordination, history
of seizure, or sensory changes.
Physical Exam:
Vitals:
T. 97.5 P 67, B/P 152/69, R 18, Wt. 234.5 lbs
General:
Alert, pleasant, obese white male in no distress.
Skin:
Warm, dry, and intact. No cyanosis.
HEENT:
Normocephalic. PERRL. EOMI. No nystagmus. Conjunctiva clear
and sclera white. Nares patent mucosa pink without lesions. Oral
mucosa pink and moist. Throat without lesions, erythema, or
exudates. Tongue midline. Good dentition.
Neck:
Smooth movement with full range of motion. No carotid bruits.
No lymphadenopathy or JVD. Trachea midline.
Respiratory:
Anteroposterior to transverse diameter one to two. Chest
excursion and respiratory effort equal, unlabored, and
symmetrical. No rhonchi, crackles, wheezes, or rub.
Cardiac:
S1 and S2 regular without murmur, clicks, rubs, or gallops.
Abdomen:
Well-approximated seven inch scar on RLQ without erythema or
drainage. Transplant kidney palpated in RLQ with mild
tenderness. No organomegaly otherwise. Round and obese. BS x4.
No costovertebral tenderness.
GU:
Bladder palpated in suprapubic region without tenderness.
Musculoskeletal:
Muscle strength in all limbs 5/5. Smooth full range of motion
of joints without crepitus.
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Neuro:
19
Oriented to person, place, and time. Smooth and coordinated gait.
Remote and recent memory intact.
Extremities:
2+ pitting edema up to lower knees BLE. Good capillary refill
BLE. Right upper arm with AV fistula that has bruit and thrill. No
tenderness or erythema in BUE/BLE. No femoral bruit. 2+ pulses
in brachial and radial, 1+ pulses in dorsalis pedis and posterior
tibial. No clubbing or cyanosis.
Data:
Laboratory values from
last clinic visit
(3 months ago):
Trough Tacroli blood level: 6.1 ng/mL; Trough Sirolim blood
level: 6.6 ng/mL
Serum NA mEq/L: 141; K: 4.6 mEq/L; Cl 108 mEq/L;
CO2 mEq/L; BUN: 22 mg/dL; HbA1c 7.2%
WBC: 7.0 mm3; RBC: 4.35 mm3; Hgb: 10.3 g/dL; Hct: 34.7%;
PLT: 194 mm3
Urine: Creatinine, U: 106 mg/dL; Protein, U: 300 mg/dL and has
increased over the last four clinic visits
Serum Creatinine: 2.70 mg/dL and has gradually increased from
1.13 mg/dL in last two years; eGFR: 26 mL/min and has gradually
decreased from 78 mL/min in last two years
LDL-C: 98 mg/dL; Triglycerides: 139 mg/dL
Questions
1. What are the differential diagnoses? Explain.
The differential diagnoses for this patient include chronic allograft injury (CAI)
secondary to chronic rejection of the renal transplant, drug toxicity secondary to calcineurin
inhibitors (CNI), glomerulonephritis, nephrosclerosis, transplant renal artery stenosis (TRAS),
BK virus nephropathy or ureter obstruction (Chapman, O’Connell, & Nankivell, 2005; Sijpkens,
Joosten, & Paul, 2003). The first five diagnoses will be discussed.
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First, CAI secondary to chronic rejection of the renal transplant is a potential diagnosis
for this patient. Chronic rejection is an alloantigen-dependent immune reaction eventually
causing CAI. Chronic rejection is depicted by system HTN, vasculopathy, glomerulopathy, and
chronic tubulointerstitial nephritis. Chronic rejection clinically displays as CAI. CAI is a
clinical syndrome that appears past three months post-transplantation and is illustrated by a
gradual rising plasma creatinine concentration. It is associated with an increase in proteinuria
and typically these patients with chronic rejection excrete between one to two grams of protein a
day. Elevated blood pressure is a manifestation that is commonly found in renal transplant
recipients and the frequency is currently at 80%. Other manifestations include anemia, swelling
of feet and ankles, secondary hyperparathyroidism, and acidosis (Kidney Disease Improving
Global Outcomes (KDIGO), 2009; Sijpkens et al., 2003). This patients laboratory values display
a gradual increase in serum creatinine from 1.13 mg/dL to 2.70 mg/dL over two years,
proteinuria with a urine protein level 300 mg/dL, and displaying anemia with a red blood cell
count of 4.35 mm3 and a hemoglobin of 10.3 g/dL. Also, his blood pressure is elevated at 152/69
mm Hg. A renal allograft biopsy will need to be implemented to make this diagnosis.
Second, drug toxicity secondary to CNI is another potential diagnosis for this patient.
CNI nephrotoxicity is a major and dose-limiting side effect of both cyclosporine and tacrolimus.
CNI nephrotoxicity can happen even in those patients with trough-levels preserved at the
presently standard levels. Clinical manifestations consist of an elevated blood urea nitrogen
(BUN) level, acidosis, fluid overload, HTN, decrease in urine output, or blood, pus, or uric acid
crystals present in the urine. Gum hyperplagia, hypertichosis, gout, and tremor are additional
adverse outcomes of CNI toxicity (Naesens, Kuypers, & Sarwal, 2009; Sijpkens et al., 2003).
The therapeutic range for the whole blood tacrolimus trough is 5 to 15 ng/mL (Lexi-Comp, Inc.,
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2013). This patient’s last whole blood trough level of tacrolimus is 6.1 ng/mL. This patient has
a slightly elevated BUN at 22 mg/dL, fluid overload exhibited by feet and ankle swelling, HTN,
decrease in urine output. None of the other symptoms or signs are present in this patient.
Third, glomerulonephritis is another possible diagnosis for this patient. Inflammatory
glomerular lesions are observed from a pathology view. Clinical manifestations include HTN,
edema, decrease urine output, and abnormal urinary sediment. Serum creatinine can rise over
days to months depending on the rapidity of the underlying process. Urine studies reveal
evidence of hematuria, proteinuria, red cell casts, and white cells (Longo et al., 2012). This
patient has HTN, edema in feet and ankles, decrease urine output, and an increased serum
creatinine level. However, he denies blood in his urine and further studies would be needed to
make this diagnosis.
Fourth, nephrosclerosis is a potential diagnosis for this patient. Typically, the kidney
transplant recipient has a long period between receiving the transplant and diagnosis of CAI. A
diagnosis can be potentially made when the patient also has HTN, smokes tobacco, older donor
age, hyperlipidemia, and peripheral artery disease. Nephrosclerosis is depicted histologically
(Sijpkens et al., 2003). It has been five years since he received his transplant and he has a history
of HTN and hyperlipidemia. He is not a smoker, unknown older donor age, no diagnosis of
peripheral artery disease, and no renal biopsy of the transplant kidney has been implemented.
Fifth, TRAS is another possible diagnosis for this patient. TRAS occurs with
atherosclerotic occlusive disease or fibromuscular dysplasia. TRAS is a cause for post-transplant
HTN and can result in graft dysfunction. The most common appearances of HTN develop as a
recent onset or as refractory HTN at any time post-transplant. Pulmonary edema can occur if the
blood pressure is not well controlled and an audible bruit on the affected side may be auscultated
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during the physical examination. Also, the diagnosis of TRAS should be considered when a
patient is started on an angiotensin-converting enzyme inhibitor (ACEI) and develops acute
kidney injury. Risk factors consist of chronic kidney disease, DM, tobacco use, and HTN.
Serum BUN and creatinine will rise (Longo et al., 2012). This patient has a history of HTN,
DM, and chronic kidney disease. His serum creatinine has risen but it has been gradually.
However, his HTN is not a new onset or refractory, not a tobacco user, he is not taking an ACEI
currently, and he does not have pulmonary edema. Further testing needs to be implemented to
make a diagnosis of TRAS.
2. What are ten risk factors associated with chronic rejection in renal transplantation?
Provide rationale.
There are several risk factors associated with chronic rejection in renal transplantation.
First, acute rejection episodes are the most vital risk factor for chronic rejection. Patients who
have repeated rejection episodes have lower graft survival rates compared to patients who had no
or only one acute rejection episode. If an acute rejection episode occurs in the first three months
it may not effect chronic rejection but if an acute rejection episodes happens after three to six
months it presents the greatest risk for chronic rejection. Second, age is another factor. Patients
who receive a kidney transplant at a young age are more likely to have the occurrence of chronic
rejection due to forgetting to take immunosuppressive medications and young age is correlated
with a moderately high state of immune responsiveness to alloantigens. Third, race is another
factor associated with chronic rejection. African Americans have more acute rejection episodes
due to differences in immunological responsiveness. Fourth, sensitization is another risk factor
for chronic rejection. Pregnancy, blood transfusions, and failed transplants can stimulate
antibodies against human leukocyte antigens (HLA) and the presence of anti-HLA antibodies
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before or after transplantation is correlated with chronic rejection. Fifth, HLA matching is
another risk factor for chronic rejection of the kidney transplant. Key histocompatibility
complex particles of the graft are the principle foci of the immune reaction post-transplantation.
HLA-matched grafts have a projected half-life of 12.4 years compared to 8.6 years for HLAmismatched grafts. Sixth, peritransplantation injury is another factor for chronic rejection.
Examples of peritransplantation injury include donor factors, for example, brain death and
ischemia/reperfusion injury, and these injuries trigger an inflammatory cascade with upregulation of cytokines, adhesion and HLA-DR particles. This leads to an increase in graft
immunogenicity and to more early acute rejection episodes. Also, it may cause delay graft
function and require the recipient of the kidney transplant to receive dialysis for the first week
after transplantation. Delay graft function has a small increased risk for chronic rejection.
Seventh, inadequate immunosuppression is another risk factor for a patient to develop chronic
rejection. A low serum drug level and fluctuating oral bioavailability of immunosuppressant
medications in the early post-transplant phase are linked with increased rates of chronic
rejection. Typically, patients have a lower graft rate survival of five years after transplantation
when they do not comply and consistently take their immunosuppressive medications. Eighth,
renal function is another factor for chronic rejection. A decrease in glomerular filtration rate
between six and 12 months has been correlated with the incidence of chronic rejection following
12 months. Also, an elevation of the serum creatinine level at six and 12 months can be
associated with chronic rejection. Ninth, HTN is a risk factor for chronic rejection of the kidney
transplant. HTN can stimulate arteriosclerosis within the kidney blood vessels and glomerular
HTN. This can lead to an increase in glomerular permeability and subsequently augment protein
trafficking. The degree of depreciation of graft function is related to diastolic blood pressure.
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The graft survival of patients with HTN is lower compared to patients without HTN. Tenth,
hyperlipidemia is a risk factor for chronic rejection of the kidney transplant. Between 70 to 80
percent of transplant patients have elevated cholesterol levels and patients with
hypercholesterolemia at six months, one and two years have an increased risk for graft
dysfunction or death-censored graft loss. Additional risk factors include donor age, donor
source, proteinuria, genetic polymorphisms, DM, female sex, and smoking (Chapman et al.,
2005; KDIGO, 2009; Sijpkens et al., 2003).
3. What are the routine screening tests that should be ordered for a patient that received a
kidney transplant more than 12 months ago and why?
There are several routine screening tests that should be ordered for a patient that received
a kidney transplant more than 12 months ago. An annual urine total protein and/or urine albumin
should be ordered to screen for proteinuria since it is an early and sensitive marker of kidney
damage in chronic kidney disease and it is associated with chronic rejection. A serum creatinine
should be ordered every two to three months, however, the health care provider can order a renal
function panel if they also want to monitor other electrolytes. The measurement of serum
creatinine can detect acute changes of kidney function and monitor for CAI. These tests are
obtained to detect CAI early and allow time to diagnose the etiology and provide treatment that
may improve results. A complete blood cell count is ordered to monitor any signs of infection or
anemia. A fasting lipid profile is obtained annually since hyperlipidemia is a risk factor for
chronic rejection. The healthcare provider needs to screen for tobacco use at every clinical visit
since it is a risk factor for developing chronic rejection. Also, the healthcare provider needs to
screen for DM by obtaining a fasting blood glucose, glucose tolerance test, or a hemoglobin A1c
since DM is a risk factor for developing chronic rejection. Also, if the healthcare provider is
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suspecting CAI, then a renal ultrasound should be ordered since many of the causes of CAI can
be diagnosed by ultrasound. These causes of CAI include arterial occlusion, venous thrombosis,
urinary obstruction, a urine leak, compressing perinephric hematoma and arteriovenous fistula
from a kidney biopsy (KDIGO, 2009).
4. What are the indications for a kidney allograft biopsy? What is chronic allograft
nephropathy and its relationship to chronic rejection?
There are five indications for a kidney allograft biopsy (KAB). First, a KAB is
recommended when there is a persistent, inexplicable rise in the serum creatinine. Second, when
the serum creatinine does not return to the patients baseline following treatment of acute
rejection. Third, when a patient has delayed graft function a KAB is suggested to be
implemented every seven to days. Fourth, when the projected kidney function is not attained
within the first month or two after receiving the kidney transplant. Fifth, when there is a new
onset of proteinuria or unexplained proteinuria of greater than or equal to three grams in 24 hours
(KDIGO, 2009).
Chronic allograft nephropathy (CAN) is diagnosed by histological changes and signifies
the last common pathway of CAI. As noted earlier CAI clinically manifests chronic rejection.
CAN is characterized by widespread interstitial fibrosis and tubular atrophy within the kidney
and CAN is reproducible in small biopsy samples. Also, the Banff classification of renal
transplant pathology is the grading system for diagnosing CAN. The grading of CAN ranges
from I (minor changes) to grade III (severe changes) based on the severity of tubular atrophy (ct0
to ct3) and interstitial fibrosis (ci0 to ci3). For example, if this patient has CAN grade III then he
could have ci3/ct3, ci2/ct3, or ci3/ct2. Other characteristics of CAN are arteriosclerosis and
glomerulosclerosis. The relationship between chronic rejection and CAN is that chronic
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rejection can cause CAN. When chronic transplant glomerulopathy or transplant vasculopathy is
present with no other causes of CAN, this supports the diagnosis of chronic rejection. For
differential diagnosis purposes, if a patient has CNI toxicity, the renal biopsy will display fibrosis
and tubular atrophy with nodular arteriolar hyalinosis (Chapman et al., 2005; KDIGO, 2009;
Sijpkens et al., 2003).
5. The patient’s renal biopsy results display ci2/ct3 with transplant glomerulopathy. How
would you manage this patient’s chronic rejection of his kidney transplant? Explain
rationale.
There will need to be preventative and therapeutic strategies implemented to manage this
patient’s chronic rejection of his kidney transplant. It should be known that there is no
established treatment for chronic rejection and this is generally due to the occurrence of
irreversible injury at the time of diagnosis. One of the preventative measures is that the patient
should avoid all nephrotoxic drugs, for example, ibuprofen. The patient should not start smoking
since smoking is a risk factor for chronic rejection (Chapman et al, 2005). Also, the patient
should decrease his protein intake and not eat red meat because the derivatives of protein
breakdown can accumulate in the blood and increase the workload of the kidneys. In addition,
the patient should check his blood pressure every morning, daytime, and nighttime. The patient
should make journal entries of his blood pressures in order for the healthcare provider to better
assess his HTN. The therapeutic strategy begins with the continuation of both
immunosuppressive agents since the patient’s biopsy did not display CNI toxicity (arteriolar
hyalinosis and striped fibrosis) and both of his blood trough levels were in therapeutic range.
Since the patient has unspecified tubular atrophy and interstitial fibrosis confirmation, the
appropriate medical treatment would be to control the patient’s blood pressure, proteinuria, DM,
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and hyperlipidemia in order to delay progression of chronic rejection (European Association of
Urology, 2010). The patient’s blood pressure is elevated at 152/69 mm Hg and the goal for
patients with renal disease, DM, and proteinuria is a blood pressure less than 130/80 mmHg.
The healthcare provider could increase the furosemide to 40 mg tablet PO twice a day to help
lower the blood pressure and decrease the patient’s bilateral pitting edema. The patient should
have a follow-up appointment in a week to assess his pitting edema and to check his blood
pressure. If the patient does not have hypotension, the healthcare provider could increase
losartan to 50 mg tablets PO twice a day since angiotensin II receptor antagonists are associated
with reducing proteinuria in clinical transplantation. This patient is currently receiving insulin
aspart and insulin glargine to manage his DM. His current hemoglobin A1c is 7.2% and the goal
for managing DM in kidney transplant patients is a hemoglobin A1c of 7.0% to 7.5%. Therefore,
there is no need to adjust his insulin regimen. This patient has a medical history of
hyperlipidemia and is currently taking simvastatin 20 mg PO daily at night. The goal for lowdensity lipoprotein is less than 100 mg/dL and the goal for triglycerides is less than 150 mg/dL
for patients with kidney transplants. The patients calculated low-density lipoprotein is 98 mg/dL
and his triglycerides are 139 mg/dL. Therefore, there is no need to adjust his simvastatin
medication (KDIGO, 2009; Lexi-Comp, Inc., 2013). A nurse in Ohio with a CTP may prescribe
furosemide and losartan (Ohio Board of Nursing, 2013).
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