6. Dilatación focal mayor del 50%
del diámetro normal de la aorta
Dm de la Aorta > 3.0 cm
+ aorta infrarrenal
7. Prevalencia 4 a 9%
Aumenta con la edad (mas de 60 años)
Ruptura; 12 - 15 mil pacientes al año en USA
Crecen 2-3mm/ año
Dm de 5cm, el riesgo de ruptura es 5% año
Metcalfe D. Et al. The management of abdominal aortic aneurysms BMJ 2011
8. General: 80%
Pop de urgencia 48%
Qx electiva abierta 4.6%
Endovascular 1.2%
Metcalfe D. Et al. The management of abdominal aortic aneurysms BMJ2011
15. H:M 4: 1
-Mujeres mayor riesgo de ruptura. 40% mas riesgo de
morir
Tabaquismo: 7 veces mas riesgo
Edad: 25- 54 años: OR 0.15 --- 75 años OR 7.7
Caucásicos
Hipertensión
Historia familiar de AAA: 8 veces mas
Otra aneurisma ej. Iliaca, femoral, poplítea
Metcalfe D. Et al. The management of abdominal aortic aneurysms BMJ 2011
16. BMJ 2011
Riesgo de ruptura% Dm basal
<1 30 - 39 mm
1 40 - 49 mm
1-11 50 - 59 mm
10 - 22 60 - 69 mm
30 - 33 >70 mm
17.
18. Academic Emergency Medicine 2009
PREVALENCIA DE AAA EN PACIENTES ASINTOMATICOS DE
ALTO RIESGO QUE SE PRESENTAN A EM (n=140)
+50 AÑOS
TABAQUISMO
HISTORIA FAMILIAR DE AAA
8 de 140
Prevalencia:
5.7%
19. B. Hahn et al. Clinical Imaging. 2016:398–401
Retrospectivo
Más de 65 años con dolor abdominal Con Us o CT aorta previa
normal
Se les realizaba un segundo CT o US
606 pacientes
3 pacientes (0.5%) aneurisma Aorta: dm promedio 3.3 cm
Ninguno requirió intervención
20. Surgery for small asymptomatic abdominal aortic
aneurysms. Cochrane Database Syst Rev 2015;
21. Surgery for small asymptomatic abdominal aortic
aneurysms. Cochrane Database Syst Rev 2015;
• Vigilancia con US
• No diferencia entre Qx
temprana electiva vs
vigilancia
• *5.5 cm remitir a cirugia para
reparo electivo
25. HIPOTENSIÓN DE CAUSA NO
CLARA
PACIENTES > 65 AÑOS O Fx
RIESGO AAA
Dolor abdominal
Dolor dorsal o lumbar
Dolor en Flancos
Mareo
Vértigo
Síncope
Arresto cardiaco
European Heart Journal 2014
26. Paciente >65 años
o
Factores de riesgo
AAA
ESTABLE
US Aorta
urgencias
AAA
Estudio
Confirmatorio
TAC
NO AAA
Buscar OTRA
CAUSA dolor
INESTABLE
US Aorta
Urgencias
AAA
Cirugía
Inmediata
NO AAA
Buscar OTRA
CAUSA
HIPOTENSIÓN
50 ptes con AAA roto
25 con US al ingreso con tiempo de Dx 5,4 minutos y tiempo para Cx 12 minutos
25 con enfoque diagnóstico usual, tiempo de Dx: 83 minutos, Cx: 90 minutos
----------------------------------
Mortalidad en grupo de US inicial : 40 %
Mortalidad en grupo de enfoque convencional : 72
Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm. A true aneurysm is defined as a segmental, full-thickness dilation of a blood vessel that is 50 percent greater than the normal aortic diameter (figure 1) [1]. False aneurysms of the abdominal aorta can also occur but are much less common.
In most adults, an aortic diameter >3.0 cm is generally considered aneurysmal. Normal aortic diameter varies with age, gender, and body habitus, but the average diameter of the adult human infrarenal aorta is about 2.0 cm and typically less than 3.0 cm [1]. Thus, for the majority of patients, an infrarenal aorta with a maximum diameter ≥3.0 cm is aneurysmal [1-3].
For the purposes of this discussion:
●Small aneurysms have a diameter <4.0 cm
●Medium aneurysms have a diameter between 4.0 and 5.5 cm
●Large aneurysms have a diameter >5.5 cm
●Very large aneurysms have a diameter ≥6.0 cm
The natural history of AAA is one of progressive expansion, which is variable and depends upon aneurysm diameter and other factors, the most important of which is ongoing smokin
nd mortality after rup- ture exceeds 80%, accounting for 8000 deaths annually in the United Kingdom.5 w3 Elective surgical repair has anoperativemortalityof1-5%inthebestcentres,
Mortalidad general 80%
Mortalidad pop de urgencia 48%
Mortalidad qx electiva abierta 4.6%
Mortalidad qx endovascular 1.2%
●Small aneurysms have a diameter <4.0 cm
●Medium aneurysms have a diameter between 4.0 and 5.5 cm
●Large aneurysms have a diameter >5.5 cm
●Very large aneurysms have a diameter ≥6.0 cm
The natural history of AAA is one of progressive expansion, which is variable and depends upon aneurysm diameter and other factors, the most important of which is ongoing smokin
Abdominal aortic aneurysms (AAAs) are commonly described based on the relation to the renal arteries. Suprarenal AAA: The aneurysm involves the origins of one or more visceral arteries but does not extend into the chest.
Pararenal AAA: The renal arteries arise from the aneurysmal aorta but the aorta at the level of the superior mesenteric artery is not aneurysmal.
Juxtarenal AAA: The aneurysm originates just beyond the origins of the renal arteries. There is no segment of nonaneurysmal aorta distal to the renal arteries, but the aorta at the level of the renal arteries is not aneurysmal.
Infrarenal AAA: The aneurysm originates distal to the renal arteries. There is a segment of nonaneurysmal aorta that extends distal to the origins of the renal arteries.
Abdominal aortic aneurysm (AAA) most often affects the segment of aorta between the renal and inferior mesenteric arteries; approximately 5 percent involve the renal or visceral arteries. Up to 40 percent of AAAs are associated with iliac artery aneurysm
The Crawford classification of thoracoabdominal aortic aneurysm is based upon the extent of aortic involvement. Type I arises from above the sixth intercostal space, usually near the left subclavian artery, and extends to include the origins of the celiac axis and superior mesenteric arteries. Although the renal arteries can also be involved, the aneurysm does not extend into the infrarenal aortic segment.
Type II aneurysm also arises above the sixth intercostal space, and may include the ascending aorta, but extends distal to include the infrarenal aortic segment, often to the level of the aortic bifurcation.
Type III aneurysm arises in the distal half of the descending thoracic aorta, below the sixth intercostal space, and extends into the abdominal aorta.
Type IV aneurysm generally involves the entire abdominal aorta from the level of the diaphragm to the aortic bifurcation.
Type V aneurysm arises in the distal half of the descending thoracic aorta, below the sixth intercostal space, and extends into the abdominal aorta, but is limited to the visceral segment.
Adapted from: Safi HJ, Winnerkvist A, Miller CC 3rd, et al. Effect of extended cross-clamp time during thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 1998; 66:1204.
Population studies have shown associations between age and prevalence of AAA. One study of 4345 subjects found people aged 25-54 were signi cantly less likely (odds ratio 0.15, 95% con dence interval 0.07 to 0.32) to be diagnosed with an AAA than those aged over 75 (7.73, 1.89 to 31.73)
Although less commonly a ected, women with aneu- rysms have an increased risk of rupture.9 w1 w7 For this reason, women with aneurysms of smaller diameter (such as >5 cm) may be considered for operative intervention.10 Women also have a worse prognosis after aneurysm repair—one series of 8185 patients reported that women over 70 were 40% more likely to die postoperatively than men
Risk factors for the development of AAA — There is significant overlap between the risk factors that contribute to the development of AAA, and the risk factors that contribute to the expansion and rupture of AAA. However, the relative contribution of each risk factor to either the development or the expansion and/or rupture of AAA varies. Tobacco abuse appears to be the main modifiable risk factor for the development of AAA. Protective factors for the development of AAA include female gender, non-Caucasian race, diabetes, and moderate alcohol consumption. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Therapies to limit aortic expansion'.)
Advanced age and male gender — The incidence and prevalence are not significant in populations aged less than 60 years [6-9,19]. Aneurysms are rare in females less than 50 years of age. Compared with males, the prevalence of AAA in females is decreased four- to sixfold [10]. However, these figures may underestimate the true prevalence of aneurysm in females, since many of the prevalence studies defined aneurysm as having an aortic diameter ≥30 mm. This likely underestimates the true prevalence of aneurysm in females due to gender differences in body size [20].
Caucasian race — AAA occurs most frequently among non-Hispanic white Americans or Caucasians of European descent. The incidence is 10-fold lower in Asian populations, at 0.45 percent in Asian men over 65 years in age [21]. Among Black Americans, AAA occurred half as frequently as in their Caucasian counterparts [22]. The Life Line Screening cohort study also showed a reduced risk for the development of AAA among Hispanics (odds ratio [OR] 0.69), and confirmed the decreased risk of AAA among Asian-Americans and Black-Americans [23].
Family history — A genetic predisposition for the development of AAA has been suspected since the first report of three brothers who each underwent surgery for ruptured AAA [24]. Since this report, multiple other familial clusters have been identified, further suggesting a genetic predisposition [25,26]. Family history appears to increase the risk of the development of AAA by two- to fivefold [25,26]. These are variable with polygenetic inheritance patterns [27]. Syndromic monogenetic disorders, such as Marfan Syndrome (fibrillin-1 defect) or Ehlers-Danlos Syndrome type IV (abnormal type III procollagen) are more commonly associated with thoracoabdominal aortic aneurysms [28]. (See "Epidemiology, risk factors, pathogenesis and natural history of thoracic aortic aneurysm", section on 'Genetic predisposition'.)
Smoking — Tobacco smoking is the modifiable risk factor most strongly associated with the development of AAA. Among screened patients found to have small AAAs, 18 to 25 percent are current smokers [22,23,29]. Current smokers also initially present with larger aneurysms. The number of pack-years is positively associated with increased odds of AAA being found on screening [23,29]. Men who smoke over one pack per day also have a 15-fold increased risk of having a family member with AAA compared with age-matched males who do not smoke [30]. Smoking cessation decreases the subsequent odds of AAA being identified on screening, with the greatest benefit among those who have quit for more than 10 years. Unfortunately, the odds never returns to the baseline risk in nonsmokers, indicating that some degree of damage inflicted by tobacco use is permanent [23].
Presence of other large vessel aneurysms — Patients with other large vessel aneurysms (such as iliac, femoral, popliteal, or carotid artery aneurysms) have an increased risk for AAA. Patients with a femoral artery aneurysm are found to have a concomitant AAA 85 percent of the time. Subjects with popliteal aneurysms have a concomitant AAA 60 percent of the time [31,32]. Up to 25 percent of subjects have combined thoracic and abdominal aortic aneurysms [33,34]. Compared with men, more women have combined thoracic aortic aneurysms and AAA (48 versus 28 percent) [33].
Atherosclerotic risk factors — Systemic atherosclerosis is present concurrently with AAA in multiple studies corroborating the significant overlap in the risk factors between the two disease processes [22,23].
●Coronary artery disease is present in over 25 percent of individuals with AAA.
●Peripheral arterial disease is found in over 12 percent of those with AAA.
However, it is important to note that there are patients with aneurysmal disease with a low burden of peripheral artery disease (PAD). Moreover, the incidence of PAD is low in those with familial aortic aneurysm [35]. The pathophysiology responsible for AAA formation is felt to be distinct from atherosclerosis. (See 'Pathophysiology of AAA' below.)
With respect to the major risk factors associated with atherosclerosis, the role of male gender and tobacco use are discussed above. Hypertension and hyperlipidemia are frequently cited as etiologic risk factors for the development of AAA [22,23,36,37]. Intuitively, chronically elevated blood pressure would weaken the aortic wall, as would lipid-laden atherosclerotic plaques.
Other factors
●Obesity – There is inconsistency in the literature regarding the association of obesity with the presence of AAA [38-40]. If there is an association, it is mildly positive, increasing the odds of AAA by 22 percent in a large cohort from Australia [39]. Obesity may be more significant in conjunction with atherosclerotic disease, amplifying the odds of the development of AAA by twofold relative to nonobese atherosclerotic patients [40].
●Diet and alcohol consumption – Data regarding moderate alcohol consumption are inconsistent, with several studies citing a moderate protective effect (hazard ratio [HR] 0.57 to 0.80) [41]. Conversely, with higher levels of alcohol intake (≥30 grams/day; ≥2 drinks/day) there appears to be an increased risk of AAA [30]. This decreased risk of AAA with modest alcohol intake seemed to be most pronounced with beer and wine; however, larger studies are required to corroborate these findings.
Fruit and vegetable consumption appears to be mildly associated with less AAA development [23,42]. The Lifeline Registry in the United States showed that individuals who adhered to a diet of fruit and nuts ≥3 servings/week decreased their odds of developing AAA by approximately 10 percent [23]. The effect appears stronger with higher fruit intake. Among a Swedish cohort of 80,426 participants, a higher consumption of fruits (>2 servings/day) was associated with a 25 percent decreased risk of AAA relative to those with lower fruit intake (0.7 servings/day) [42].
Parámetro asociado a ruptura es el dm basal del aneurisma. Riesgo de ruptura a 12 meses
Main results
For this update, four trials with a combined total of 3314 participants fulfilled the inclusion criteria. Two trials compared surveillance
with immediate open repair; two trials compared sur veillance with immediate endovascular repair. Overall, the risk of bias within
the included studies was low and the quality of the evidence high. The four trials showed an early survival benefit in the sur veil lance
group (due to 30-day operative mortality with surgery) but no significant differences in long-term survival (adjusted HR 0.88, 95%
confidence interval (CI) 0.75 to 1.02, mean f ol low-up 10 years; HR 1.21, 95% CI 0.95 to 1.54, mean follow-up 4.9 years; HR 0.76,
95% CI 0.30 to 1.93, median follow-up 32.4 months; HR 1.01, 95% CI 0.49 to 2.07, me an follow-up 20 months). A pooled analysis
of participant-level data from two trials (with a maximum follow-up of seven to eight years) showed no statistically significant difference
in survival between immediate open repair and surveillance (propensity score-adjusted HR 0.99; 95% CI 0.83 to 1.18), and that this
lack of treatment effect did not vary by AAA diameter (P = 0.39) or participant age (P = 0.61). The meta-analysis of mortality at one
year for the endovascular trials likewise showed no significant association (RR at one year 1.15, 95% CI 0.60 to 2.17). Quality-of-life
results among trials were conflicting.
Main results
For this update, four trials with a combined total of 3314 participants fulfilled the inclusion criteria. Two trials compared surveillance
with immediate open repair; two trials compared sur veillance with immediate endovascular repair. Overall, the risk of bias within
the included studies was low and the quality of the evidence high. The four trials showed an early survival benefit in the sur veil lance
group (due to 30-day operative mortality with surgery) but no significant differences in long-term survival (adjusted HR 0.88, 95%
confidence interval (CI) 0.75 to 1.02, mean f ol low-up 10 years; HR 1.21, 95% CI 0.95 to 1.54, mean follow-up 4.9 years; HR 0.76,
95% CI 0.30 to 1.93, median follow-up 32.4 months; HR 1.01, 95% CI 0.49 to 2.07, me an follow-up 20 months). A pooled analysis
of participant-level data from two trials (with a maximum follow-up of seven to eight years) showed no statistically significant difference
in survival between immediate open repair and surveillance (propensity score-adjusted HR 0.99; 95% CI 0.83 to 1.18), and that this
lack of treatment effect did not vary by AAA diameter (P = 0.39) or participant age (P = 0.61). The meta-analysis of mortality at one
year for the endovascular trials likewise showed no significant association (RR at one year 1.15, 95% CI 0.60 to 2.17). Quality-of-life
results among trials were conflicting.
Main results
For this update, four trials with a combined total of 3314 participants fulfilled the inclusion criteria. Two trials compared surveillance
with immediate open repair; two trials compared sur veillance with immediate endovascular repair. Overall, the risk of bias within
the included studies was low and the quality of the evidence high. The four trials showed an early survival benefit in the sur veil lance
group (due to 30-day operative mortality with surgery) but no significant differences in long-term survival (adjusted HR 0.88, 95%
confidence interval (CI) 0.75 to 1.02, mean f ol low-up 10 years; HR 1.21, 95% CI 0.95 to 1.54, mean follow-up 4.9 years; HR 0.76,
95% CI 0.30 to 1.93, median follow-up 32.4 months; HR 1.01, 95% CI 0.49 to 2.07, me an follow-up 20 months). A pooled analysis
of participant-level data from two trials (with a maximum follow-up of seven to eight years) showed no statistically significant difference
in survival between immediate open repair and surveillance (propensity score-adjusted HR 0.99; 95% CI 0.83 to 1.18), and that this
lack of treatment effect did not vary by AAA diameter (P = 0.39) or participant age (P = 0.61). The meta-analysis of mortality at one
year for the endovascular trials likewise showed no significant association (RR at one year 1.15, 95% CI 0.60 to 2.17). Quality-of-life
results among trials were conflicting.
squema de los grandes vasos abdominales. TC: tronco celíaco, la primera rama de la aorta abdominal, que al poco de su nacimiento se bifurca en la arteria hepática (AH) que discurre hacia la derecha del paciente, y la arteria esplénica (AE), que se dirige a la izquierda, en dirección al bazo. La segunda rama de la aorta abdominal es la arteria mesentérica superior (AMS), que al poco de nacer se dirige caudalmente paralela a la aorta, formando un espacio entra ellas, la llamada pinza aorto-mesentérica, por donde discurre transversalmente la vena renal izquierda (VRI) en su recorrido hacia la cava inferior. Las arterias renales nacen de la cara lateral de la aorta; la arteria renal derecha (ARD) se dirige hacia el riñón derecho pasando por detrás de la cava, mientras que la arteria renal izquierda (ARI) se dirige al riñón izquierdo directamente. La VRI aboca la cara lateral de la vena cava inferior, previamente ha pasado por la pinza aorto-mesentérica en su camino procedente del riñón izquierdo; y la vena renal derecha (VRD) viene del riñón correspondiente abocando en la cara lateral derecha de la cava directamente
Corte transversal a nivel de epigastrio medio al nivel de la salida de la primera rama de la aorta abdominal, el tronco celíaco. Podemos observar cómo al poco de su salida el tronco celíaco se divide en la arteria esplénica (que discurre hacia la izquierda del paciente, en dirección al bazo) y la arteria hepática (que se dirige a la derecha del paciente, para formar parte junto con la vena porta y el colédoco de la tríada portal), esta bifurcación es la típica imagen de la «gaviota».
Corte longitudinal paramedial izquierdo, en el que podemos ver, usando el lóbulo hepático izquierdo (LHI) como ventana, una imagen tubular anecogénica, que apoya sobre los cuerpos vertebrales, que en la imagen in vivo es pulsátil, y se corresponde con la aorta. De su cara ventral nacen en primer lugar el tronco celíaco y a continuación la arteria mesentérica superior, que al poco de su nacimiento discurre paralela a la aorta, formando así la pinza aortomesentérica. A su vez en este corte también se puede apreciar el páncreas y parte del intestino delgado proximal.
B. Corte transversal a nivel de epigastrio inferior, justo en la zona de la pinza aorto-mesentérica, que se forma por el espacio que existe entre la arteria mesentérica superior y la aorta, y por la que discurre la vena renal izquierda en su recorrido hacia la vena cava inferior, que se encuentra a la derecha de la columna vertebral. También podemos ver en esta imagen el páncreas (cabeza, istmo, cuerpo y cola), un corte de través de la arteria mesentérica superior (rodeada de un halo hiperecogénico, lo que la hace resaltar más) y el nacimiento de la arteria renal derecha, que se dirige hacia el riñón derecho, pero pasando por detrás de la cava inferior.
Measure aorta in short axis in AP diameter from outer wall to outer wall
Pitfall: Thrombus within aorta may be confused with aortic wall
Thrombus typically forms anterior and lateral within the aorta
Measure from anterior to posterior aorta walls (including the thrombus)
Do not limit measurement to open lumen (underestimates aneurysm)
Aorta diameter >3 cm is consistent with aneurysm
Aorta diameter >5.5 cm meets criteria for elective repair
Aorta diameter >7-8 cm is at high risk of rupture