Running Head: CASE STUDY NUR 7201 3&4
Case Study NUR 7201 3&4
Ashley Peczkowski
Wright State University
NUR 7201
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CASE STUDY NUR 7201 3&4
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Case Study NUR 7201
Case Study Three
Questions:
1.
What is the differential diagnosis of this patient’s clinical deterioration and why?
The differential diagnosis for the clinical deterioration presented is acute respiratory
distress syndrome (ARDS). The development of ARDS in a trauma victim usually results from
injury to the lung and heart. The most likely cause is massive blood transfusions, aspiration
pneumonia, nosocomial pneumonia, congestive heart failure, pulmonary contusion, or airway
hemorrhage (BMJ, 2011). The Berlin Definition developed by European Society of Intensive
Care Medicine, American Thoracic Society, and Society of Critical Care Medicine required
ARDS patients to have:
“A draft definition proposed three mutually exclusive categories of ARDS based on the
degree of hypoxemia: mild (200mmHg <PaO2/FIO2 ≤ 300 mm Hg), moderate (100 mm
Hg < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) and 4 ancillary
variables for severe ARDS: radiographic severity, respiratory system compliance (≤40
mL/cm H2O), positive end-expiratory pressure (≥10 cm H2O), and corrected expired
volume per minute (≥10 L/min)” (Caldwell et al., 2012, p. 2526).
Acute respiratory distress syndrome can present from any injury to the lung. Once an
injury has occurred inflammatory mediators create pulmonary vascular permeability allowing for
fluid accumulation. This increases the weight of the lung and minimizes aerated lung tissue
resulting in hypoxemia. There is an increased venous admixture, dead space, and decreased
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alveolar compliance from edema, inflammation, hemorrhage, or membrane damage (Caldwell el
al., 2012). Based on the patient’s trauma, he could have suffered an acute lung injury from any
one of the differentials. Aspiration pneumonia could have resulted from the traumatic collision
and impaired mentation. The acidic chyme of the stomach aspirated into the bronchioles,
damages the pulmonary parenchyma initiating endothelial deterioration and provides an optimal
medium for bacteria from the gut to propagate. Nosocomial pneumonia is always considered
when a patient has been in the OR or ICU for any period of time. This, however, is less likely
due to the sudden onset. The patient most likely suffered a major chest contusion from impact
into the steering wheel. This can cause a cardiac contusion increasing the risk for reduced cardiac
output; in combination with the massive fluid transfusions obtained during resuscitation, this can
lead to congestive heart failure, quickly manifesting into ARDS. Less likely is a pulmonary
contusion due to the localization generally seen in this type of injury. Typically pulmonary
contusion are unilateral; however if severe enough and bilateral, the hemorrhage can induce
ARDS. If bloody secretions are present then airway hemorrhage should be considered from
either traumatic intubation or traumatic bronchial damage. The most likely cause of ARDS for
this patient is autoimmune or non-autoimmune reaction from the massive blood transfusions
complicated by sustained hypotension (BMJ, 2011).
A massive blood transfusion is defined as the replacement of the patients total blood
volume within less than 24 hours. Massive blood transfusions are harmful to the body because it
displaces the body’s natural temperature, acid-base balance, biochemistry, and coagulation
factors. Because of this blood is warmed, electrolytes are replaced, bicarbonate is given, and
coagulation factors are given such as fresh frozen plasma (FFP), platelets, and cryoprecipitate.
Hypothermia from inadequate warming of the blood can cause impaired hemostasis, reduced
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metabolism, hypocalcaemia, metabolic acidosis, cardiac arrhythmias, and a shift to the left in the
oxyhemoglobin disassociation curve. Blood products contain citrate which binds to calcium
creating hypocalcaemia. This is mostly prevented by the body through hepatic metabolism but
becomes impaired if the patient becomes hypothermic. Hypocalcaemia causes hypotension,
reduced pulse pressure, flattened ST segments, prolonged QT intervals, and tetany. The citrate
contained in the blood products also causes acidosis from lactic acid production. This acidosis is
increased by hypotension and is often resolved by adequate fluid resuscitation. Finally the
administration of blood products results in a dilution coagulopathy. This causes further
hemorrhage from a disseminated intravascular coagulation (DIC). The reduced perfusion causes
the body to consume platelets and coagulation factors seen in DIC; this is avoided by aggressive
fluid resuscitation, replacement of clotting factors through FFP and cryoprecipitate
administration (Maxwell & Wilson, 2006).
The effects of massive blood transfusion of the body are important to know for ARDS
because the pathology plays a crucial role in the development of pulmonary edema characteristic
of ARDS. Transfusion-related acute lung injury (TRALI) can result in ARDS and develops
during or within six hours of transfusion. The clinical features seen in ARDS from TRALI are
normal intracardiac pressures, bilateral pulmonary infiltrates, hypotension, fever, dyspnea,
cyanosis, and refractory hypoxemia (Maxwell & Wilson, 2006). Hypotension worsens ARDS by
increasing acidosis, hypoxemia, myocardial dysfunction, and reduces cardiac output and SvO2.
Respiratory acidosis is increased by higher CO2 production, increased dead space and decreased
minute ventilation (Russell & Walley, 1999). TRALI is caused by either immune or non-immune
reactions. Immune reactions are further characterized into hemolytic transfusion reaction, nonhemolytic febrile reactions, transfusion-associated graft versus host disease, and allergic
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reactions; non-immune reactions are divided into bacterial, viral, or prion. Immune TRALI
results from leukocyte antibodies from the donor blood attacking human leukocyte antigens and
human neutrophil alloantigen in the recipient causing lysis of the blood cells. In non-immune
TRALI, lipid products from the donor cell act as a trigger for lysis. Despite the cause, both types
of TRALI result in active neutrophil granulocytes to migrate to the pulmonary vasculature where
they become trapped. The neutrophils degrade, releasing oxygen free radicals and proteolytic
enzymes, which destroy surrounding endothelial cells. Destruction of the membrane results in
gaps where protein and exudate leak into the alveoli causing pulmonary edema (Maxwell
&Wilson, 2006).
2.
What are the risk factors that put this patient at risk for ARDS? Provide rationale.
This patient is placed at risk for developing ARDS due to his major trauma experience,
sustained hypotension, multiple transfusions, altered mentation, long bone fracture, and
advanced age (Antonelli et al., 2012). Major trauma is a risk factor for ARDS because injury
causes an initial increase in circulating neutrophils and increased pulmonary levels of
interleukin-8. This causes neutrophil infiltration into the pulmonary vasculature, which is
characteristic of ARDS development, resulting in organ damage (Dent, Pallister, & Topley,
2002). Sustained severe hypotension can cause ischemia, initiating an inflammatory response.
Inflammation in the lung increases alveolar-capillary permeability allowing albumin to leak into
the alveolar sacs (Antonelli et al., 2012). Multiple blood product transfusions increase the risk
for ARDS because the donor antibodies can react to the recipient antibodies causing activation of
inflammatory meditators again leading to ARDS (Dubois, Kambermont, Melot, Sardi, &
Vincent, 2007). Altered mental status reduces the ability of the patient to protect his airway
increasing his chance for aspiration pneumonia. Bone fractures of the leg can cause fat emboli to
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infiltrate the lungs resulting in a pulmonary embolism and shunting. Shunting is a characteristic
of ARDS (BMI, 2011). An advanced age is a controversial risk factor for developing ARDS.
There is a progressive increase in the associated risk until the age of 69 at which point the risk
decreases. Those individuals greater than 80 have the same chance of getting ARDS as does a 23
year old. This decline is thought to be related to older individuals having a reduced risk factor
lifestyle by not smoking or drinking and also because their traumas tend to be related to hip
fractures which can be quickly repaired, reducing morbidity (Effros, 2003). Because this patient
is older, received massive blood transfusions, sustained a bone fracture, has altered mental status,
and has sustained major trauma he is at greater risk for developing ARDS.
3.
What are specific considerations for managing an elderly trauma victim? Provide
rationale.
Specific considerations for managing an elderly trauma victim are vast. There is a
significant increase in length of hospital stay in patients over the age of 45. This increase is due
to increased risk for complications and reduced healing capacity; however, there was a decline in
length of stay over the age of 74 most likely due to increased mortality. There is a decrease in
baseline functioning status and an increase in pre-existing medical conditions that can complicate
recovery. It is well documented that there is a decreased reserve for stress response in the elderly
as well. Respiratory system declines with age as the result of a four percent decrease of alveolar
surface production per decade after 30 years of age. This reduces gas exchange of 0.5% each
year. Reduced lung capacity coupled with flailed chest/ rib fractures greatly increases morbidity
from atelectasis, pneumonia, ventilator dependence, and overall mortality. Renal failure
increases with age due to sclerosis of glomeruli by 10% per decade after 40 (Adams et al., 2011).
One of the biggest problems with elderly trauma is development of skin issues such as pressure
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ulcers. This is due to skin atrophy, decreased tissue water, increase subcutaneous fat, and
tonicity. These combined with increased immobility results in higher pressure ulcer formation.
Cardiovascular co-morbidities are high in elderly population increasing the risk for many
complications. Elderly cannot sustain hypotension without end-organ damage and increased
mortality as a result of atherosclerosis and reduced baroreceptor activation. A hypercoagulability
state from surgery and increased stasis make developing a deep venous thrombosis a significant
risk factor. This risk is further increased with immobility and medications. Urinary tract
infections peak at age 75 to 84 but overall infections decrease after age 65. This is thought to be
because elderly do not mount a typical immune response and immune response time can be
greatly delayed. This can result in an elderly patient becoming septic before laboratory values
show leukocytosis or increased sed rate. Lastly this patient has under gone a major trauma
causing his body to mount an inflammatory response; a secondary hit or response is initiated
when surgery is performed. The second hit in elderly can overcome the normal process resulting
in a dysfunctional immune response leading to multisystem organ failure (Adams et al., 2011).
4.
How would you manage this patient’s hypoxemia? Provide rationale.
The first step for treating hypoxia in this patient is making sure there is no sign of
equipment failure. Equipment failure is one of the most common causes of respiratory
complications in a vented patient. For immediate and temporary effect the FiO2 should be
increased to 100%. This should not be done for long periods of time due to oxygen toxicity
complications. Oxygen stats should be maintained above 88% with the lowest FiO2 percentage
needed to obtain goal (Mahajan, 2005). FiO2 should not go above 60%; this reduces the risk for
oxygen toxicity. A mode of volume limited or pressure limited is used to allow for stable airway
pressure or stable tidal volume. These modes require the patient to be completely sedated and
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have a neuromuscular blockade on board. The ARMA trail showed that by using lower tidal
volumes (six ml/kg), mortality was lower and the patient had more ventilator-free days than
those in the comparison group who had large tidal volumes (12ml/kg). The tidal volume should
be based on six to eight ml/kg of ideal body weight based on height. Based on research the tidal
volume should be adjusted from a total of 90ml to six ml per kg of ideal body weight. Lower
tidal volumes (based on six ml/kg vs 12ml/kg) require permissive hypercapnic ventilation by
creating alveolar hypoventilation to obtain a lower alveolar pressure. Acidosis is common in
permissive hypercapnic ventilation and can be reduced by increasing the minute ventilation.
Respirations must be high enough to reduce acidosis but low enough to prevent auto-PEEP
which can cause alveolar distention and barotrauma. If this increase is difficult to obtain then
PEEP should be initiated. Low tidal volumes and applied PEEP are called open lung ventilation
strategy. The theory is the lower tidal volumes will reduce alveolar distention while the applied
PEEP will maximize alveolar recruitment and minimize atelectasis (Hyzy & Siegel, 2010). The
optimal PEEP for an ARDS patient is > five cmH20. This higher PEEP allows for a reduction in
air trapping and helps clear secretions (Mahajan, 2005). A high PEEP does not require pressurevolume curves so a neuromuscular blockade may not be needed. Other benefits are the higher
PEEP is thought to open collapsed alveolar, reduce alveolar distention by distributing the tidal
volume to more open alveolar, further reduce atelectasis, and increase oxygenation. Higher
PEEP should only be used in those patients with a lot of recruitable lung since the mechanism of
effect works on that principle. Those with low recruitable lung volume have an increased risk for
barotrauma. Other treatments include prone position and nitric oxide. Endotracheal suctioning is
one of the most important steps in preventing ventilator associated pneumonia which can
increase morality in ARDS patients (Hyzy & Siegel, 2010).
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What are the problems associated with PEEP?
Lower PEEP is shown to provide little benefit whereas too much PEEP can cause
distention, high pressures, and reduced pressure gradient. An increase in PEEP can cause the
already open alveolar to expand to the point of rupture. The resulting damage is called
barotrauma. The high pressure also causes collapsing of the surrounding blood vessels and
reduces cardiac preload resulting in hypotension. This collapse further causes dead space and
unnecessary increased work of breathing. The increased intrathoracic pressure reduces the
pressure gradient of the blood flow, lowering right atrial preload, right ventricle output and
finally cardiac output (Mahajan, 2005).
6.
What is the mortality rate associated with ARDS?
The current average mortality rate associated with ARDS is at 40%. This is much better
than in previous years when the mortality rate was at 70%. The dramatic improvement in the
mortality rate is due to better awareness of ARDS, understanding of the disease process, quicker
diagnosis and treatment, and improved ventilator care/ changes needed for ARDS (The ARDS
Foundation, 2013). If using the Berlin definition and stages of mild, moderate, and severe then
the outcomes of morality were: Mild 27%, 95% confidence interval (CI), 24%-30%; Moderate
32%, 95% CI, 29%-34%, And severe 45%, 95% CI 42%-48% with P<.001. By using the Berlin
definition there was a more accurate predictor of mortality (area under the receiver operating
curve of 0.577; 95% CI, 0/561-0.593) allowing for better care, research, and planning of service
provided. Through stricter definitions and further studies into ARDS it may be possible to further
reduce mortality rates (Caldwell et al., 2012).
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Case Study Four: Abdominal Aortic Aneurysm
Abdominal Aortic Aneurysm
A 54 year old white man presents to the emergency department (ED) c/o right flank pain
for one hour. Upon questioning the patient he tells you he developed a sudden onset of pain one
hour ago that has progressively gotten worse in his right flank and mid-back. He describes the
pain as being a sharp, constant, tearing pain that is worse with movement and cannot be relieved.
The patient states “I think I have another kidney stone”. He is diaphoretic, restless, pale, and
grimacing. His history includes hypertension (HTN), hypercholesterolemia, kidney stones,
alcoholism (three beers a day), and a one pack a day smoker for 35 years. His triage vital signs
are blood pressure (BP) in the right arm of 167/92, pulse 89, temperature 98.9 oral, respirations
24, oxygen saturation at 95% on room air. Stat urinalysis, complete blood count, basic metabolic
panel, and a CT renal stone protocol (abdominal/pelvis without contrast) are ordered. Upon
arrival back to his room the radiologist calls the ED physician to inform them of the findings of
an abdominal aortic aneurysm (AAA) seven centimeters (cm) in diameter. The patient now
appears very pale and states his pain has changed to a tearing feeling in between his shoulder
blades. Two large bore IVs are established and vitals are retaken. The patients vitals are now
pulse 115, respirations 26, BP in the right arm are 110/75, and in the left are at 89/58. The patient
is then transferred immediately to the operating room.
Questions:
1) What is your differential diagnosis? Explain.
2) What are the risk factors for developing an AAA?
CASE STUDY NUR 7201 3&4
3) What is the treatment for stable AAA and for unstable AAA?
4) What are the complications for AAA surgery?
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Questions:
1) What is your differential diagnosis? Explain.
The differential diagnosis for this patient is an abdominal aortic aneurysm (AAA),
myocardial infarction (MI), renal calculi, bowel diseases, and arterial diseases. These
differentials vary by gender, comorbidities, and physical findings. Because AAA can present
with severe and sometimes nonspecific abdominal pain; pancreatitis, bowel obstruction,
diverticulitis, inflammatory bowel disease, appendicitis, gastrointestinal hemorrhage, gastric
ulcer disease, splenic artery ischemia, and cholelithiasis should all be considered. For women the
diagnosis of MI, irritable bowel disease (IBS), and ovarian torsion are considered. Ripping back
pain is a classic sign of AAA but back pain can also be sharp or achy. For patients that present
with different types of back pain the differential diagnoses to consider may include
musculoskeletal pain and, if hematuria is present, renal calculi or pyelonephritis (BMJ, 2013;
Brewster et al., 2009).
A MI can be ruled out by obtaining an electrocardiograph (ECG) which are absent of new
ischemic changes. ST segment changes can be seen only if the dissection causes obstruction of
the coronary ostium causing myocardial ischemia or infarction (Braverman, 2013). Renal calculi
are considered if hematuria is present in a urinalysis with or without evidence of crystals or
infection. Further tests such as a renal ultrasound or stone protocol CT will show a normal aorta
diameter and renal or ureteral calculi. Bowel diseases such as diverticulitis, IBS, inflammatory
bowel diseases, appendicitis, cholelithiasis, or gastrointestinal hemorrhage can be ruled out with
a variety of tests such as a positive guaiac stool, the presents of leukocytosis, endoscopic
evaluation with biopsy, and a CT scan with the presents of a normal aorta and/or inflammatory
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bowel process. Ovarian torsion is ruled out by the presents to a twisted and swollen ovary on
abdominal ultrasound. Lastly arterial diseases such as splenic artery ischemia or bowel infarction
are ruled out by an angiography which demonstrates vascular occlusion in the spleen or bowel.
Leukocytosis, acidosis, increased amylase, and increased phosphatase are also seen (BMJ, 2013).
By obtaining a detailed history and physical, a complete blood count (CBC), a basic metabolic
panel (BMP), a liver function panel (LFTs), urinalysis (UA), and appropriate imaging, most of
the differential diagnosis can be ruled out.
An AAA is defined as dilation or widening of the abdominal aorta diameter of 3.0cm or
more. This set range is obtained by being more than two standard deviation above the mean
width in both men and women (Nossuli & Tsapatsaris, 2012). The normal dimension of the
infrarenal abdominal aorta is about two cm anteroposterior and is up to 10% smaller in women.
Therefore any width of three cm and above is considered to be aneurysmal and two to three cm is
considered ectatic (Desjardins et al., 2012). An important differentiation of an aneurysm from a
dissection is that an aneurysm involves bulging of all layers of the aorta and a dissection creates
a false lumen or intimal flap (Nossuli & Tsapatsaris, 2012). Clinical signs and symptoms
indicative of an AAA are ripping or tearing pain in between the shoulder blades; different BPs in
arms, pulsatile abdominal mass, “wheeling” murmur, hypotension, tachycardia, syncope, or
orthopnea (Bonin, Davey, Kuhn, Langlois, & Rowland, 2000). When chief complaints, history,
and physical are suspicious for AAA then the best test to perform is a bedside ultrasonography.
This tests is preferred because of the ability to perform the test quickly, it is non-invasive, cheap,
and has sensitivity and specificity close to 100%. (Fraedrich et al., 2011). Obesity and internal
bowel gas can inhibit evaluation of an AAA with ultrasound; in which case an abdominal CT is
used for evaluation. An abdominal CT with contrast is preferred because it can outline the
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dissecting aorta and show false aneurysms; however if a patient has chronic kidney disease then
an abdominal CT without contrast is preferred. A creatinine must always be checked first before
contrast is given to reduce the incidence of contrast induced nephropathy (Nossuli & Tsapatsaris,
2012).
2) What are the risk factors for developing an AAA?
The development of AAA is complex and multifactorial. Pathology of AAA development is
caused by a weakening of the media lumen as the result of atherosclerosis. Other factors that
have been indicated are: Endovascular proteases, which cause degradation of the elastic lamellae
in the aorta; increased levels of matrix metallopreoteinases 2, 9, and 14; cathepsin S and K, and
increased levels of MMP-9, all of which are known to decrease after repair. The weakening of
the lumen and the buildup of arthrosclerosis causes an inflammatory response releasing
interleukin-6 and C-reactive protein further damaging the media lumen. There is also a large
genetic component in up to 28% of patients with a first degree family history of AAA
development (Nossuli & Tsapatsaris, 2012).
Although atherosclerosis and genetic mutation are indicated in the pathology of AAA
development and are an important risk factor, smoking has been the greatest risk factor
identified. By smoking we inhale carbon monoxide which damages the smooth endothelial layers
creating a ridged area for plaque to accumulate resulting in atherosclerosis. Nicotine further
injuries the vascular system by increasing the release of epinephrine into the body which causes
the body to release fat into the blood stream for energy. Because there is no increased muscular
demand for the fat released, it circulates until it attaches to the damaged endothelium and plaque.
Nicotine also causes internal vascularization which supplies oxygen and nutrients to the plaques
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and hardens arteries causing them to be less compliant. The increased pressure against a noncompliant wall further damages the endothelium until the weakened aorta media lumen breaks
causing dilatation. There is a correlation between the number of years smoking and an increase
in the risk factor. The opposite is also true with number of years since smoking cessation
equaling a decrease in the risk of AAA development compared to those who continue to smoke.
Other risk factors include white, male, family history, HTN, hypercholesterolemia, and age.
Negative risk factors include diabetes and African American or Asian descent. Diabetes is
thought to lower the risk of AAA because it protects the aorta by causing negative remodeling
(EGorova et al., 2010; Nossuli & Tsapatsaris, 2012).
There are similar risk factors for expansion of an AAA and rupture. Expansion includes
smoking but also increased age, cardiac disease, previous stroke, and cardiac or renal transplant.
Rupture of an AAA are similar in that they include not only smoking, HTN, and cardiac and
renal transplant but also other risk factors such as women, decreased FEV1, critical wall stress,
and a large initial AAA diameter. Any AAA can enlarge and rupture at any time but some risk
factors are known to carry an increased risk. One of the leading and most consistent risk factors
for all three groups is smoking. The risk of AAA with smoking is increased for current smokers,
longer pack years, and higher cigarette quantity. The risk is decreased if the patient quits
smoking (EGorova et al., 2010). Age causes structural changes that include a decreased collagen
to elastin ration in vessels, making them vulnerable to dissection especially in increased turbulent
blood flow (Darioli, Depairon, Glauser, & Mazzolai, 2013). Men have larger-diameter aortas
with more age dependent increase in diameter associated with compensatory increase in wall
thickness to reduce circumferential wall stress. Therefore the taller height (elongated aorta) and a
stiffer abdominal aorta make male gender a risk factor (Norman & Powell, 2007). Because of
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this it is recommended that men who are smokers over the age of 65 to 75 should have an
abdominal ultrasound screening. The highest incidence for AAA development occurs within the
fifth and seventh decade of life (Darioli, Depairon, Glauser, & Mazzolai, 2013).
Hypercholesterolemia, HTN, cardiac disease, previous stroke, critical wall stress, and cardiac or
renal transplant all affect the lumen, weakening the collagen, and makes the integrity of the
media lumen wall susceptible to breaks. A decreased FEV1 is indicative of having COPD. This
is a controversial risk factor in that COPD its self does not cause an increased risk for AAA but
chronic steroid use caused accelerated elastin degradation and COPD is associated with
increased morbidity and mortality (Brewster et al., 2009). Also there are some associations that
COPD patients lack alpha-one antitrypsin activity that are known to inhibit elastases weakening
the aortic wall (Nossuli & Tsapatsaris, 2012). Women are at higher risk for rupturing but studies
have shown that routine screening in women is not beneficial. Men tend to have slower growing
AAA while women tend to have rapid dissection (Halpern & Starr, 2013). Women have shorter
and more angulated aortic necks then men causing a higher pressure system. Smoking causes
greater vessel stiffening than in men leading to rupture versus dilation. Women are also protected
from AAA development by endogenous estrogen. Estrogen reduces the aortic collagen: elastin
ratio making the aorta more pliable. In females there are less destruction of the aorta media, less
infiltrating macrophages, and lower levels of matrix metalloproteinase-9. This protection is lost
after menopause and estrogen supplements do not produce protective effects (Norman & Powell,
2007).
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3) What is the treatment for stable AAA and for unstable AAA?
Depending on the size of the AAA the treatment options vary. Among those at risk or an
AAA has been identified, the treatment option of choice is conservative management. Once the
AAA has been identified and is greater than three centimeters, repeat ultrasounds are needed to
monitor growth. Abdominal aortic aneurysms that are three to 3.9 cm should have an ultrasound
every three years. Every two years for those that is four to 4.4cm and every year for those that
are 4.5 to 5.4cm (Brewster et al., 2009). Yearly based monitoring is based on the observation that
AAA grow approximately 0.2-0.3 cm per year (Fraedrich et al., 2011). Surgery is indicated for
those aneurysms at 5.5cm or large in males. These recommendations come from previous studies
that demonstrated that risk of rupture per person-years was zero percent for AAA with a
diameter of four cm or less. The percentage increased to one percent for AAA four to 4.99cm in
diameter; 11% for AAA five to 5.99 cm diameter; and 25% for AAA six to 6.99cm diameter per
person-years. Also studied was the rate of expansion of the AAA overtime increased the risk of
rupture (Norman & Powell, 2007). The Multicenter Aneurysm Screening Study (MASS)
demonstrated that screening in men over the age of 60 with a sibling or offspring with an AAA
or one time screening of men age 65 to 75 who have ever smoked reduced AAA related
mortality and all-cause mortality. This is now the recommendation by the American Heart
Association and American College of Physicians along with some other organizations. Women
are not included in the screening guidelines because women have lower prevalence of the disease
and are not considered high risk. Smoking cessation is the most important treatment option for
both conservative and surgical intervention. Both lipid control and BP control are also essential
for management. Studies have suggested that there are some protective effects when ACE
inhibitors, beta blockers, and statins are all used as pharmacological treatment (Brewster et al.,
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2009; Darioli, Depairon, Glauser, & Mazzolai, 2013). The recommendation of beta blockers is a
class IIb recommendation only because it was shown to reduce the rate of expansion in only one
trial. The development of a mural thrombus is associated with AAA however anticoagulation is
not recommended because the risk of bleeding is far more superior to risk of embolism (Norman
& Powell, 2007). Although statins and Ace inhibitors are known endothelium protectors and are
recommended for treatment, a large and carefully conducted study (name not mentioned) did not
demonstrate a reduced growth rate (Fraedrich et al., 2011). Reduced heart rate and blood
pressure control of a systolic blood pressure less than 130 is essential in management of a stable
AAA.
A dissecting AAA is a medical emergency with a high mortality rate. Intense
hemodynamic monitoring is indicated and the placement of an art-line is the preferred method.
In absence of hypotension, initial therapy is directed at first lowering the heart rate and then
secondly reducing the blood pressure. A reduced cardiac contractility and systemic arterial
pressure in turn reduces aortic wall stress and shearing. This is achieved by administration of an
IV beta-blocker such as esmolol, metoprolol, or propranolol. The target heart rate is 60 beat per
minute or less. Beta-blockers alone cannot reduce the systemic atrial pressure enough and
therefore sodium nitroprusside should be continuously infused to reach a target systolic blood
pressure of 120 or less. For acute and rapid reduction of the blood pressure labetalol can be used.
Other therapies are verapamil, diltiazem, and enalaprilat. Vasodilators are contraindicated
because they increase hydraulic shearing and cause dissection widening. Blood transfusion is
commonly necessary and emergent surgical repair is required (Creager & Loscalzo, 2012).
Surgical treatment of an AAA involves two different forms: open repair and
endovascular repair. Because to the risky nature of these surgeries careful consideration for risk
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and benefits, size of native aorta, co-morbidities, and quality of life should be taken (Cikrit et al.,
2009). The indications for repair are: 5.2cm in women only; 5.5cm in all genders; eight
centimeters requires custom endograft and open urgent open repair is recommended; and greater
than nine centimeters requires in-patient management and immediate repair. Statin therapy
should be initiated one month prior to surgery and continued indefinitely to reduce the risk of
cardiovascular morbidity. Beta-blockers are indicated only in high cardiac risk patients and only
if they can be started one month prior to surgery. If beta-blockers are started less than one month
prior to surgery there was a higher risk of hypotension and bradycardia complications during
surgery and thus should be avoided. Low dose aspirin was also shown to reduce cardiac
complications and did not increase risk of hemorrhage. Current guidelines now indicated that
AAA patients should be started on low dose aspirin and remain on aspirin perioperatively. Blood
pressure control, usually with an ACE inhibitor, is essential beginning at the time of diagnosis
and also post-surgery. The current guidelines recommend a cardiac risk assessment on all
patients with a preoperative ECG. Patients undergoing open repair and who have cardiac risk
factors should have a stress echo or myocardial perfusion scan prior. Endovascular aortic repair
(EVAR) patients with cardiac risk factors should have a transthoracic echocardiogram and either
a stress test or myocardial perfusion scan prior (Fraedrich et al., 2011).
Repair is indicated for patients with an AAA greater than 5.5cm, expanding greater than
one centimeter per year, symptomatic, or those with signs and symptoms of rupture. A
preoperative screening is needed because those with coronary artery disease, chronic kidney
disease, chronic lung disease, and liver cirrhosis with portal hypertension have a tripled risk for
complications. Decision for open repair versus EVAR remains unclear however the AAC/AHA
guidelines currently recommend open repair for low or average risk patients and EVAR for high
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risk patients and considered in low or average risk (Nossuli & Tsapatsaris, 2012). Overall the
open repair option is mainly used in younger less at risk patients or in emergent situations such
as AAA rupture. This procedure involves placing an incision between the breastbone and the
pubic bone and clamping off the aorta for repair. Fast and accurate surgical repair is needed
because blood flow to the abdomen and lower portion of the body is stopped when the aorta is
clamped. Once the procedure is complete recovery is long and involves an extended stay in the
ICU. Endovascular repair is the preferred method and is used for older at risk adults (Cikrit et al.,
2009). It is important to note that females have smaller femoral arteries making endovascular
repair typically not an option (Norman & Powell, 2007). This procedure is indicated only if a
stent-able portion of the AAA is enlarged. It is done by placing a custom made graft through the
femoral artery vessel and into the expanding aneurysm. The advantages are a decreased ICU
stay, less general hospital stay, and quicker return to normal activity. Disadvantages include
more frequent monitoring and further procedures. There is no difference in post-surgical
mortality rate between the two procedures (Cikrit et al., 2009).
4) What are the complications for AAA surgery?
Complications from AAA surgery are similar for both types with certain variations. Open
repair is most likely to result in bleeding during surgery and post op. Because the aorta is
clamped during surgery there is a significant risk for limb ischemia, embolism, and kidney
damage. Because of the anterior approach, bowel injuries can occur along with a high infection
risk and spinal cord damage (Brewster et al, 2009; Cikrit et al., 2009). Infection is a complication
that can be reduced by administering a single prophylactic antibiotic of either first or second
generation cephalosporins, penicillin β-lactamase inhibitor or aminoglycosides. This reduces the
risk for early graft infection and wound infection (Fraedrich et al., 2011).Up to 60% of open
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repair patients can develop severe complications such as MI, pneumonia, and acute renal failure.
The highest rates of complications are as follows: wound complication 3.3%, arrhythmias three
percent, pneumonia three percent, intestinal obstruction and ischemia two percent, renal
insufficiency 1.7%and MI 1.4%. Congestive heart failure, ARDS, pulmonary embolism, sepsis,
stroke, retroperitoneal bleeding, and amputation had a one percent or less rate of complication
(Fraedrich et al., 2011). The endovascular repair has similar complications but is mainly caused
by technical failure, local vascular injury, device or procedure complication and medical
complications. These risk are kidney damage, groin infection, groin hematoma, bleeding intra
and post op, endovascular leaking, spinal cord injury, limb ischemia, and damage to surrounding
vessels or organs (Brewster et al, 2009; Cikrit et al., 2009). Technical failure is rare and only
caused 3.8% to be converted to open. Most complications arise from groin and wound injuries.
Other complications are inexperience with closure device system, limb ischemia from occlusion
or thrombosis, and inappropriate stent graft sizing. A rare phenomenon called post implantation
syndrome can be seen. This presents with fever, malaise, back or abdominal pain, transient rise
in C-reactive protein levels, and leukocytosis. Treatment includes observation and aspirin. There
is a five times greater risk of need for intervention within the first 30 days with EVAR. The most
common cause for re-intervention was related to the development of endoleak. An endoleak is a
condition where the blood flows outside the sent graft but within the aneurysm sac. Benefits of
EVAR are reduced procedure time, blood loss, transfusion requirement, and duration of
mechanical ventilation, hospital stay, and ICU stay. Compared to open repair there is a two
percent less likely rate for the development of complications (Fraedrich et al., 2011).
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