Kembara Xtra - Medicine - Abdominal Aortic Aneurysm

Kembara Xtra - Medicine - Abdominal Aortic Aneurysm 
​Basic DESCRIPTION
True and false aneurysms exist in the world. All three vessel wall layers are involved in a genuine aneurysm. When the medial and intimal layers are torn, the dilated segment is surrounded by adventitia alone, and perhaps a perivascular clot, this results in false aneurysms or pseudoaneurysms. Due to inadequate support provided by the aneurysmal wall, rupture rates are typically higher in fake aneurysms.
The most frequent genuine arterial aneurysm is the abdominal aortic aneurysm (AAA). False abdominal aortic aneurysms are typically brought on by injury or illness.
● The infrarenal aorta typically has a diameter of 2.0 cm; an aortic diameter of 3.0 cm or greater is considered aneurysmal. AAA diameters in men are a good indicator of clinical outcomes. The aortic scaling index (ASI; diameter [cm]/body surface area [m2]) is more predictive of clinical events in women than the current definition of aneurysms, which is >3.0 cm.
cardiovascular, neurological, heme/lymphatic/immunologic system(s) affected
Synonym(s): AAA; aortic aneurysm
Aspects of Geriatrics
Age-related increases in surgical morbidity and mortality, rupture risk, and AAA prevalence.
Child Safety Considerations
Rare in children; may be brought on by congenital anomalies, connective tissue disorders, arteritides, or umbilical artery catheters

EPIDEMIOLOGY
​In wealthy nations, the prevalence of AAA is thought to be between 2 and 8%. Men experience age-related increases more so than women.
According to ultrasound research, 4-8% of elderly men have an occult AAA.
90% of AAA >4 cm are atherosclerotic disease-related, with the majority being infrarenally situated.
Male is more prevalent than female.
 Incidence

 Around 15,000 fatalities annually, ranking as the 15th highest cause of mortality in the United States.
0.4-0.67%, or 2.5 to 6.5 aneurysms per 1,000 patient-years, is the rate in Western populations.
The incidence of AAA is higher in older groups when stratified by age. For instance, if comparing men aged 65 to 74 years with men >85 years of age, the incidence rises from 55 to 298 per 100,000 patient-years.

Prevalence
With life expectancy rising in developed nations, the prevalence of AAA is anticipated to rise, but the decreased prevalence of smoking will have the opposite effect. Since the 1990s, the prevalence of AAA-associated mortality has decreased by 50%, most likely as a result of increased screening for AAA detection and early interventions.

PATHOPHYSIOLOGY AND ETIOLOGY
The structural elements of the aorta wall, elastin and collagen, are degraded abnormally, which results in AAAs.
Aortic aneurysms can be brought on by a variety of conditions, including vasculitis, infections, trauma, degenerative diseases, and inflammation. However, atherosclerosis serves as the catalyst for the vast majority of AAA, which are brought on by inflammation.
The aortic wall strength is decreased as a result of the degradation of elastin and collagen by B-cell and T-cell lymphocytes, macrophages, inflammatory cytokines, and matrix metalloproteinases, which also results in the ingrowth of new blood vessels and subsequent inflammation.
Although the majority of aortic aneurysms are brought on by the inflammatory or degenerative loss of elastin and collagen, infections, trauma, and connective tissue diseases can also cause elastin and collagen degradation, resulting in symptoms that are identical.
The most significant of these is on-going smoking. The normal trend of a AAA is progressive enlargement.

Genetics: There are familial aggregations where aneurysms appear early in life.

The mode of inheritance for familial abdominal aortic aneurysms is varied and polygenetic.
Thoracoabdominal aortic aneurysms are more frequently linked to monogenetic inheritance patterns like Marfan syndrome (fibrillin-1 defect), Ehlers-Danlos syndrome (type IV collagen defect), or Loeys-Dietz syndrome.
RISK ELEMENTS
Age, being a man, being Caucasian, having a family history, smoking, having hypertension (HTN), having high cholesterol, having atherosclerosis, having peripheral aneurysms, and being obese

DURATIONAL PREVENTION
Addressing risk factors for cardiovascular disease. Adhering to screening recommendations. American testing for the presence of AAA in male patients aged 65 to 75 who have ever smoked.

CONDITIONS OFTEN Associated with

 Tobacco usage, carotid artery atherosclerosis, heart failure, myocardial infarction (MI), lower extremity peripheral arterial disease, and
Thoracic aneurysm screening should also be taken into account.
20% of AAA patients also have a thoracic aneurysm.

DIAGNOSIS: Asymptomatic AAA (most cases); USPSTF advises males aged 65 to 75 who have smoked in the past to undergo a single abdominal ultrasound screening for a AAA.
– Based on a patient's preferences, personal or family history, and age range, selective screening for AAAs can be provided to nonsmoking men between the ages of 65 and 75.
- Abdominal ultrasound screening can be administered to women who have a first-degree relative with a AAA.

ALERT

 Symptomatic: A rupture of AAA is always suggested by the triad of shock, pulsatile mass, and abdominal discomfort, and prompt surgical assessment is advised (1)[A].
- Patients with hemodynamic stability (no shock since the rupture is confined) may have a CT abdomen with IV contrast for the assessment of a AAA.
- If AAA is evident, unstable patients who have an uncontained rupture have a targeted bedside ultrasound and surgical repair.
Non-standard presentations:
- Primary aortoenteric fistula: AAA eroding or rupturing into the duodenum
- Vena cava or left renal vein erosion/rupture resulting in an aortocaval fistula: 3-6%
- Inflammatory aneurysm: surrounded by a thick inflammatory rind; may result in weight loss, chronic abdominal pain, and an elevated ESR. Viscera may be tightly adhered nearby.

HISTORY: Back, flank, or abdominal pain; AAA risk factors; hypotension if presenting in an emergency; discovered on regular screening if presenting in an outpatient setting.

PHYSICAL EXAMINATION – Pulsatile supraumbilical mass – Sensitivity varied according to abdominal circumference and aneurysm size in one research. But when the girth was less than 100 cm, the sensitivity was 100% of aneurysms larger than 5.0 cm. Between 23% and 68% and 75% and 91%, respectively, were the ranges for sensitivity and specificity.
Lower extremities ischemia related to embolization of mural thrombus - Vertebral body erosion, gastric outlet obstruction, ureteral obstruction - Rupture results in tachycardia, hypotension, signs of shock and anemia, and maybe a flank contusion (Grey Turner sign).

Other abdominal masses and other back or abdominal pain reasons, such as peptic ulcer disease, renal colic, diverticulitis, appendicitis, incarcerated hernias, intestinal obstructions, GI hemorrhages, arthritis, metastatic disease, and MI, are differential diagnoses.

DETECTION & INTERPRETATION OF DIAGNOSIS
Initial examinations (lab, imaging)
If AAA rupture is suspected, comprehensive blood chemistry (chemistries, PT/INR, PTT, type and cross), and ECG should be performed.
The best test for an asymptomatic AAA is ultrasound, which is the easiest and least expensive diagnostic method with high sensitivity (94-100%) and specificity (98-100%). 

Monitoring asymptomatic aneurysms
2.6 to 2.9 cm: Screen every five years.
3.0 to 3.9 cm: Screen every three years.
- Every six to twelve months, screen for 4.0 to 5.4 cm.
If a symptomatic AAA is suspected, CT scans are the preferable preoperative examination (care with IV contrast in renal failure).
MRI/MRA can visualize AAA, although it is frequently impractical in life-threatening circumstances.
Aortography does not specify the aneurysm's exterior diameters.
If there are calcifications, abdominal x-rays can be diagnostic but are not the preferred diagnostic method.

Tests in the Future & Special Considerations
Prior to elective AAA repair, evaluation for coronary artery disease is necessary. This includes stress testing, echocardiography, and, if necessary, an ECG.

If AAA was found anywhere, a complete examination of the aorta, including the thoracic aorta and aortic valve, is advised.


Procedures for Diagnosis/Other ALERT
Use your clinical judgment: Despite a negative CT scan, patients with known AAA who exhibit abdomen or back pain symptoms may be experiencing a rupture.

GENERAL TREATMENT MEASURES
Treating HTN, dyslipidemia, diabetes mellitus, and smoking are ways to reduce atherosclerotic risk factors.
Smoking is the most significant predictor of AAA outcome and is related with a 0.35 mm/year AAA growth rate, which is twice as fast as AAA growth in nonsmokers.

Rapid bedside ultrasonography, proper IV access, adequate resuscitation, type and cross for multiple units, and fast vascular surgery consultation are all necessary for emergency therapy in unstable or symptomatic patients.

Elective repair and risk factor reduction are less urgent treatments for AAA and rupture prevention.


MEDICATION
According to theory, -blockers, aspirin, and statins slow the growth of AAAs by reducing shear wall stress, inflammation, and the risk of an intraluminal mural thrombus. However, there are RCT and metaanalysis trials that are in dispute. It is advised to use them in individuals with coronary artery disease or its counterparts to prevent mortality because concurrent atherosclerosis frequently serves as a triggering factor in AAAs.
The use of ACE inhibitors has not been proven to prevent the growth of AAA, however studies do suggest a lower incidence of rupture.
Doxycycline and roxithromycin, which were originally thought to lessen wall inflammation, have not been demonstrated to have any effect on AAA.

SURGICAL AND OTHER PROCEDURE

The following suggestions are currently being made:
5.5 cm in diameter is the minimum for repair in the "average" patient in elective surgery.
- Low-risk patients who are younger and have a longer life expectancy could favor early repair.
Saccular aneurysms ought to be taken into account for elective repair.
- Women or AAA at high risk of rupture: At 4.5 to 5.0 cm, think about elective repair.
Consider delaying repair in patients at high risk.
For open elective repairs, the perioperative mortality rate is 5%.
High risk of rupture - Expansion of more than 0.5 cm per year - Severe COPD / steroids
- Family history; numerous relatives - HTN if not properly managed - Non-fusiform shape.
Patients at high risk for elective repair
- Age >75 years, COPD, chronic kidney disease with a Cr >1.75, and suprarenal clamp site are risk factors for open repair.
– Coronary artery disease is the main factor in early death following AAA repair, and open AAA treatment has a significantly higher risk than endovascular AAA repair.

In the RCT IMPROVE trial, patients with ruptured AAA who received endovascular surgery compared to open repair experienced a similar 30-day death rate (35.4% vs. 37.4%); at 1-year follow-up, all-cause mortality was similar in both groups (41.1% vs. 45.1%).
Even though it's difficult to measure, perioperative morbidity rates for EVAR are lower, indicating that this procedure is preferable in patients with a ruptured AAA who have poor prognostic indicators for an open repair, such as SBP 80 mm Hg, age >80, Cr >1.3 on admission, ischemic heart disease, female sex, and hemoglobin 9.0 on admission.
Aortic necks longer than 32 mm and ruptured AAAs with aortic neck length less than 7 mm are contraindications to AAA endovascular repair. Due to anatomical restrictions, an open AAA repair is carried out on these individuals.

CONSIDERATIONS FOR ADMISSION, INPATIENT, AND NURSING S
After repair, there is a 4-12% risk of developing abdominal compartment syndrome; this is typically related to massive fluid resuscitation
CONTINUAL CARE
SUCCESSIVE RECOMMENDATIONS

patient observation

 Five years following an open repair, a CT scan may be performed to check for any late aortic dilatation or pseudoaneurysm.
Follow-up imaging needs to be patient-specific. An evaluation of the endograft using a CT scan can be done if renal function has returned to normal following surgery.
Postoperatively, aggressive risk factor adjustment is always advised. 

Low-fat, low-salt, and caffeine-free diet; optimal nutrition before surgical repair

EDUCATION OF PATIENTS
Aerobic exercise, quitting smoking, and proactive management of atherosclerotic risk factors like HTN

PROGNOSIS
Disorder that naturally progresses at a rate of 0.3 to 0.4 cm per year. Fast expansion is defined as >0.6 cm/year, and it has to be assessed for surgical management.
The risk of rupture rises with aneurysm diameter >5.5 cm or a rapid rate of expansion (>0.5 cm over 6 months), ongoing cigarette usage, female sex, recent surgery, uncontrolled high blood pressure, and aneurysm couture.


COMPLICATIONS
Complications include MI, respiratory failure, and acute renal injury in the early stages of both elective and urgent AAA repair, albeit the latter has a greater incidence.
Ischemic bowel and abdominal compartment syndrome typically develop after a ruptured open AAA repair because of the significant blood loss, prolonged procedure, and magnitude of fluid resuscitation. Late complications like aortic graft infection, aortoenteric fistula, and graft occlusion have similar rates between emergent and elective repair.