Running head: MCGUIRE CASE STUDIES THREE AND FOUR
Managing Common Acute and Emergent Adult Health Problems Case Studies Three and Four
Jamie McGuire BSN, RN
Wright State University
1
MCGUIRE CASE STUDY
2
Managing Common Acute and Emergent Adult Health Problems
Case Studies Three and Four
Case Three
1. What is the differential diagnosis of this patient’s clinical deterioration and why?
There are many potential differential diagnoses for this patient, for the purpose of this
assignment acute respiratory distress syndrome (ARDS), transfusion related acute lung injury
(TRALI), fluid overload, and or pneumonia should be considered.
ARDS is considered a form of hypoxic respiratory failure related to acute lung injury
(Foster, Mistry, Peddi, Sharma, 2010a). ARDS is believed to occur after some form of insult
triggers inflammatory response that promotes neutrophil accumulation within the
microcirculation of the lung (Saguil & Fargo, 2012). The neutrophils damage the vascular
endothelium and alveolar epithelium leading to pulmonary edema, hyaline membrane formation,
decreased lung compliance, and difficult air exchange (Saguil & Fargo, 2012). The end result of
this process is accumulation of inflammatory cells and protein rich edema fluid within the
alveolar space (Foster, Mistry, Peddi, Sharma, 2010a).
TRALI is a syndrome characterized by ARDS after transfusion of multiple blood
products (Santoso & Sachs, 2012). Much of the research of TRALI supports an antibody-antigen
interaction that causes neutrophil activation and release of cytotoxic agents which leads to
endothelial damage and capillary leak (Santoso & Sachs, 2012). The anti-human leukocyte
antigen or the antigranulocyte antibodies in the donor’s serum interact with the white blood cells
of the recipient and cause the disorder (Foster, Mistry, Peddi, Sharma, 2010a).
MCGUIRE CASE STUDY
Given the amount of fluids and blood products this patient required initially, he is at risk
of fluid overload. Patients that have suffered major trauma or infection are at risk to develop
multi-organ dysfunction due to the inflammatory mediators that effect circulation and lead to
tissue hypoxia and cell damage (Asehnoune, 2009). Attempt to regain adequate blood pressures
and perfusion can lead to fluid overload, pulmonary edema, and impaired gas exchange
(Asehnoune, 2009).
Pneumonia should be considered a differential diagnosis for this patient, whether due to
bacteria exposure or aspiration of gastric contents. Bacterial or viral pneumonia is considered
the leading cause of ARDS, followed by pneumonia caused by aspiration of gastric contents and
sepsis (Matthay, Ware, & Zimmerman, 2012).
2. What are the risk factors that put this patient at risk for ARDS? Provide rationale.
Common risk factors for ARDS that are also present with this patient are aspiration of
gastric contents, shock, infection, lung contusion, nonthoracic trauma, and multiple blood
transfusions (Papadakis & McPhee, 2013a). Patients with long or pelvic bone trauma are at risk
for fat embolism syndrome causing intravasation of fat in the pulmonary tree (Tzioupis, &
Giannoudis, 2011). If two or more of these factors coexist, the likeliness of developing ARDS is
increased (Matthay, Ware, & Zimmerman, 2012).
Environmental and genetic factors can also play a role in the development of ARDS,
further information of this patients’ history would be beneficial in determining his risk (Matthay,
Ware, & Zimmerman, 2012). Factors such as chronic alcohol use, past or present cigarette
smoke exposure, history of Legionella infections, and certain genomes such as PPFIA1
(Matthay, Ware, & Zimmerman, 2012).
3
MCGUIRE CASE STUDY
Research has demonstrated that trauma patients over the age of 65 years are at higher risk
for developing ARDS (Sarkar, 2009). These patients have been predicted to require greater
transfusion and fluid requirements, have lower mortality scores, and suffer higher morbidity
outcomes (Sarkar, 2009).
3. What are specific considerations for managing an elderly trauma victim? Provide
rationale.
The elderly trauma victim is associated with higher mortality and morbidity outcomes
due to physiological changes that occur with the normal aging process (Johnston, Rubenfeld, &
Hudson, 2003). These changes can be seen within the respiratory system of reduced elasticity or
airways and thoracic cage, increased alveolar collapse with tidal ventilation, stiffened rib cage,
and increased likelihood of fractures (Sarkar, 2009). Cardiovascular changes include reduced
arterial elastance, increased afterload, ventricular hypertrophy, reduced diastolic compliance,
need for higher end diastolic pressure to provide adequate stroke volume, and a number of other
changes that influence the hearts ability to compensate for stressors (Sarkar, 2009). Further age
influences include altered bone density, reduced lung capacities, reduction in brain size, altered
drug metabolism, and reduced muscle mass and strength (Sarkar, 2009).
These changes lead to higher mortality and morbidity rates. Increased awareness among
providers in the care of elderly trauma patients can influence the overall outcome and mortality
and morbidity rates (Sarkar, 2009). Utilization of invasive hemodynamic monitoring combined
with early and aggressive treatment survival rates can be improved (Sarkar, 2009).
4
MCGUIRE CASE STUDY
4. How would you manage this patient’s hypoxemia? Provide rationale.
This patient needs sedation and continued lung-protective ventilation (Marino, 2007).
According to the ARDSnet protocol, he should receive gradual increase in PEEP and FiO2 to
obtain PaO2 of 55 mmHg. Based on the National Heart, Lung, and Blood Institute’s ARDS
Network protocol, mechanical ventilation would be adjusted for goal oxygen saturation of 8895%, plateau pressures of 30 cm H20 or less, and a pH of 7.30 – 7.45, with permissive
hypercapnia with a pH greater than or equal to 7.15 being accepted (Saguil & Fargo, 2012).
Higher positive end expiratory pressures (PEEP) and lower tidal volumes have been associated
with improved mortality outcomes (Saguil & Fargo, 2012). The ARDSnet protocol has a set
oxygenation goal of a PaO2 of 55-80 mmHg or SpO2 of 88-95%. A minimum of 5 cm H2O
PEEP is recommended in combination with incremental FiO2 to obtain this goal (Saguil &
Fargo, 2012). PEEP of 12 – 15 cm H2O is likely to be needed in the initial treatment of ARDS
(Saguil & Fargo, 2012). The FiO2 should be decreased to less than 60% as soon as possible to
avoid oxygen toxicity (Papadakis & McPhee, 2013a). Recommended tidal volumes of 6ml/kg of
predicted body weight should be achieved within two hours of initiating ARDSnet protocol
(Saguil & Fargo, 2012).
Lower tidal volumes have demonstrated a 9% reduction in mortality rates when the
plateau pressures were less than 30 cm H20 (Marino, 2007). Lower tidal volumes are needed
due to the markedly reduced functional volumes of the lungs in effort to prevent volutrauma
(Marino, 2007). When lower tidal volumes are being utilized there is an increased collapse of
the terminal airways at the end of expiration and the beginning of inspiration, thus the need for
PEEP (Marino, 2007). PEEP functions as a stent to keep airways open allowing an increase in
diffusion time and the ability to reduce the fraction of oxygen delivered (Marino, 2007).
5
MCGUIRE CASE STUDY
According to the ARDSnet protocol, placing patients in the prone position can help to
improve oxygenation among those diagnosed with ARDS. This should be used in caution and
given this patient’s injuries would not be an acceptable treatment modality.
5. What are the problems associated with PEEP?
Complications can occur with the use of PEEP. If the lung is not recruitable due to noncompliance issues, the lung can become over distended and lead to barotrauma, pneumothorax,
or pneumomediastinum (Marino, 2007). This response can be measured by the PaO2/FiO2 ratio;
recruitable lung will be reflected by an increase in the ratio in the presence of PEEP, whereas
non-recruitable lung will demonstrate a decrease in the ratio (Marino, 2007). Cardiac
complications include a decrease in cardiac output by reduction of venous return, reduced
ventricular compliance, and cardiac constraint by hyper-inflated lungs (Marino, 2007).
Sudden disruption of PEEP should be avoided. This can result in collapse of distal lung
units, worsening of shunt, and potentially life threatening hypoxemia (Foster, Mistry, Peddi,
Sharma, 2010a). PEEP should be weaned in 3-5 cm H2O increments while monitoring
oxygenation closely (Foster, Mistry, Peddi, Sharma, 2010a).
6. What is the mortality rate associated with ARDS?
Associated mortality rates vary among ARDS cases from 30% - 90% pending the
underlying cause, genetic influence, environmental factors, and the patient’s co-morbidities
(Papadakis & McPhee, 2013a). Research indicates a correlation of CT scan findings as mortality
outcome predictor tool, for example findings of greater than 80% lung involvement
demonstrated significant increase in mortality (Chung et al., 2011). Scoring systems such as
APACHE II and severity of illness scoring tools are useful in predicting mortality outcomes
6
MCGUIRE CASE STUDY
among individuals (Chung et al., 2011). Key patient indicators such as the severity of
oxygenation, degree of dead space ventilation, severity of infection, and promptness or
aggressiveness of treatment are all considered in the predicted mortality rate among individuals
(Chung et al., 2011).
7
MCGUIRE CASE STUDY
Case Four
A 62 year old white male presents in the Emergency Department with complaints of fever
for 3 days with generalized malaise, joint pains, and mid-sternal chest pain that seems to become
more intense with inspiration. He has a recent history of STEMI and underwent stent placement
one week ago, DMII – controlled, hyperlipidemia, and HTN.
While in the emergency room a 12-lead ECG was completed that demonstrated sinus
rhythm with ST elevation and T wave inversion in most leads. His CXR demonstrates blunted
costophrenic angles and suggestive of cardiomegaly. Upon assessment his lungs are clear with
decreased air movement bilateral bases and poor effort. He has distant S1 S2 with high pitched,
scratchy cardiac friction rub. He has 1+ pitting edema to bilateral lower extremities. Labs
include CBC with WBC of 15.5, HGB 12.4, PTL 180; normal renal panel, HbA1c 5.8%, ESR
88, troponin 2.4, and BNP 88. Blood and urine cultures have been sent to the lab with results
pending. He is currently on ASA, Plavix, Glucophage, Zocor, Lopressor, Lisinopril, and has a
supply of Nitroglycerin sublingual tabs. He has been taking Tylenol for his pain. He is alert and
oriented but unable to recall his doses of medications. Current VS BP 115/65, HR 72, RR 18,
Temp 100.9. He was placed on 2L O2 upon presentation and saturating 97%.
Questions:
1. What is differential diagnosis for this patient? Provide three with rationale.
Further acute coronary syndrome is a possibility for this patient. Studies demonstrate the
highest risk for progression of a myocardial infarction in the first two months post original insult
(Foster, Mistry, Peddi, Sharma, 2010b). It is estimated that 20-30% of patients will experience
8
MCGUIRE CASE STUDY
recurrent angina (Foster, Mistry, Peddi, Sharma, 2010b). Re-infarction is indicated by
recurrence of pain and ST-elevation on the ECG (Papadakis & McPhee, 2013b).
Dressler’s syndrome presents as a pericarditis-like illness usually occurring one to eight
weeks after a myocardial infarction (MI) or cardiac intervention (Foster, Mistry, Peddi, Sharma,
2010b). This syndrome is characterized by pleuritic chest pain, low grade fever, abnormal chest
x-ray, and the presence of pericardial and or pleural effusions (Wessman & Stafford, 2006). The
pathophysiology of Dressler’s syndrome involves auto-antibodies that target antigens exposed
after a form of damage to cardiac tissues (Wessman & Stafford, 2006).
Acute pericarditis typically occurs 24-96 hours after MI and can be seen in approximately
10-15% of patients (Foster, Mistry, Peddi, Sharma, 2010b). The associated chest pain is pleuritic
and may have some relief when the patient is sitting upright (Foster, Mistry, Peddi, Sharma,
2010b). A friction rub may be auscultated and presence of diffuse ST changes on the ECG can
be indicative of pericarditis (Foster, Mistry, Peddi, Sharma, 2010b).
2. What further work up is needed to determine the most likely diagnosis for this
patient?
The basic workup for a patient with these symptoms and history would include a 2D
echocardiogram, CRP, Serial cardiac enzymes to be compared to previous levels, and repeat
ECG and CXR (Foster, Mistry, Peddi, Sharma, 2010b). Research has demonstrated clinical
findings that support a diagnosis of Dressler’s syndrome include fever (56%), pericardial friction
rub (32%), pleuritic chest pain (54%), globular cardiac silhouette with new pleural effusion on
CXR, new or increased tachycardia and ST-T elevations on the ECG (24%), pericardial effusion
(89%) on 2D-echocardiogram, and elevated ESR/CRP levels (74%) (Imazio et. al., 2011).
Repeat ECG and serial CK-MB should be monitored to assess for new ischemic changes and if
9
MCGUIRE CASE STUDY
suggestive of such changes, repeat angiography should be performed (Foster, Mistry, Peddi,
Sharma, 2010b).
3. Explain the recommended treatment plan for Dressler’s Syndrome.
Treatment of Dressler’s syndrome is similar to that of pericarditis. The European Society
of Cardiology recommends Ibuprofen at 400-800mg every six to eight hours with a gradual
tapering of the total daily dose by 400-800mg each week over a period of three to four weeks as
first line treatment or Aspirin 650mg – 800mg every six to eight hours with a gradual tapering of
the total daily dose by 650-800mg each week over a period of three to four weeks (Seferovic et.
al., 2013). If the syndrome is associated with an acute MI then Ibuprofen should be avoided due
to the effects on scar formation (Foster, Mistry, Peddi, Sharma, 2010b).
If the first line treatment option fails, use of glucocorticoids (prednisone 1mg/kg/day)
may be useful in refractory symptoms but should not be used within four weeks of acute MI
(Foster, Mistry, Peddi, Sharma, 2010b). Colchicine can also be used for recurrent symptoms,
this may create diarrhea or gastrointestinal symptoms (Foster, Mistry, Peddi, Sharma, 2010b).
4. What does the current research support in prevention of Dressler’s syndrome?
Current research demonstrates promising outcomes in the use of colchicine as a
preventative agent for postpericardiotomy or Dressler’s syndromes (Imazio et. al., 2013). The
COPPS trial has demonstrated promising outcomes among patients given colchicine 30 days post
cardiac surgery and further trials are being studied to evaluate the benefits of adding colchicine 3
days prior to a planned cardiac procedure (Imazio et. al., 2013). Further studies are needed to
expand the patient population to include those of acute MI. Colchicine demonstrates anti-
10
MCGUIRE CASE STUDY
inflammatory properties that work to effectively reduce the auto-immune inflammatory response
(King, 2010).
Colchicine is indicated for adjunctive therapy with first line treatment agent for
autoimmune associated and recurrent pericarditis (Imazio & Adler, 2012). Recommended length
of treatment is three months for acute pericarditis and 6-12 months for recurrent cases (Imazio &
Adler, 2012). The course of treatment should be continued until symptoms resolve and the CRP
has normalized, then slowly tapered off (Imazio & Adler, 2012).
11
MCGUIRE CASE STUDY
12
References:
Asehnoune, K. (2009). Resuscitation volume and multiple organ dysfunction
syndrome. Journal Of Organ Dysfunction, 5(2), 91-100.
doi:10.1080/17471060701324301
Chung, J. H., Kradin, R. L., Greene, R. E., Shepard, J. O., & Digumarthy, S. R. (2011).
CT predictors of mortality in pathology confirmed ARDS. European Radiology,
21(4), 730-737. doi:10.1007/s00330-010-1979-0
Foster, C., Mistry, N., Peddi, P., & Sharma, S., (2010a). Acute Respiratory Distress
Syndrome. The Washington Manual of Medical Therapeutics. (33rd Ed.), St.
Louis: Missouri, Lippincott, Williams, & Wilkins, p 249-264.
Foster, C., Mistry, N., Peddi, P., & Sharma, S., (2010b). Acute Coronary Syndrome.
The Washington Manual of Medical Therapeutics. (33rd Ed.), St. Louis: Missouri,
Lippincott, Williams, & Wilkins, p 112-154.
Imazio, M. & Adler, Y. (2012). Treatment with aspirin, NSAID, corticosteroids, and
colchicine in acute and recurrent pericarditis. Heart Failure Reviews, published
online 6/2012, doi:10.1007/s10741-012-9328-9.
Imazio, M., et. al., (2011). Contemporary features, risk factors, and prognosis of postpericardiotomy syndrome. American Journal of Cardiology 108(8): 1183-1187.
doi: 10.1016/j.amjcard.2011.06.025
MCGUIRE CASE STUDY
Imazio, M., et. al., (2013). Rationale and design of the COPPS-2 trial: A randomized,
placebo-controlled, multicenter study on the use of colchicine for the primary
prevention of postpericardiotomy syndrome, postoperative effusions, and
postoperative atrial fibrillation. American Heart Journal, 166(1), p 13-19.
Johnston, C. J., Rubenfeld, G. D., & Hudson, L. D. (2003). Effect of age on the
development of ards in trauma patient. Chest, 124(2), 653.
King, A. (2010). COPPS trial heralds new indication for colchicine. Nature Reviews
Cardiology, 7(11), 600-601.
Marino, P. (2007). Acute respiratory distress syndrome. The ICU Book. (3rd ed.)
Philadelphia: Lippincott, Williams, & Wilkins, p. 419-433
Matthay, M. A., Ware, L. B., & Zimmerman, G. A. (2012). The acute respiratory distress
syndrome. Journal Of Clinical Investigation, 122(8), 2731-2740.
doi:10.1172/JCI60331
Papadakis, M., & McPhee, S., (2013a). Acute respiratory distress syndrome. Current
Medical Diagnosis & Treatment. (52nd ed.) McGraw Hill Companies, p 322-323.
Papadakis, M., & McPhee, S., (2013b). Heart disease. Current Medical Diagnosis &
Treatment. (52nd ed.) McGraw Hill Companies, p 369-371.
Santoso, S. S., & Sachs, U. J. (2012). New insights in mechanisms of transfusion-related
acute lung injury. ISBT Science Series, 7(1), 124-128. doi:10.1111/j.17512824.2012.01579.x
13
MCGUIRE CASE STUDY
Sarkar, S. N. (2009). Major trauma in the elderly. Trauma, 11(3), 157-161.
Seferovic, P., et. al., (2013). Pericardial syndromes: An update after the ESC guidelines
2004. Heart Failure Reviews, 18(3) p 255-266.
Tzioupis, C., & Giannoudis, P. (2011). Fat embolism syndrome: What have we learned
over the years?. Trauma, 13(4), 259-281. doi:10.1177/1460408610396026
Wessman, D. E., & Stafford, C. M. (2006). The Postcardiac injury syndrome: Case
report and review of the literature. Southern Medical Journal, 99(3), 309-314.
14