An abdominal aortic aneurysm (AAA) refers to dilation of the abdominal aorta, with a diameter of more than 3cm. This is usually asymptomatic, however, it has the potential to rupture, leading to haemorrhage and rapid death.
Although the exact aetiology is unknown, it is largely believed to be due to atherosclerosis. Atherosclerotic plaques are thought to compress the aortic media, leading to ischaemia and wall weakening.
Anatomy:
Abdominal aorta is a continuation of the descendingthoracic aorta
Supplies all of the abdominal organs and its terminal branches supply the pelvis and lower limbs
Also supplies the undersurface of the diaphragm and parts of the abdominal wall
The abdominal aorta begins at T12 and ends at L4 - where it bifurcates into the right and left common iliac arteries
The normal diameter of the abdominal aorta is <2cm
Pathophysiology:
Atherosclerosis causes inflammation, which leads to infiltration by macrophages and deposition of immune complexes in the aortic wall - elastic depletion and smooth muscle loss = dilatation of aortic wall
Aneurysm can be juxta-renal (within 1cm of renal arteries), supra-renal (above renal arteries), and intra-renal (below renal arteries)
Can be saccular (spherical outpouching)
Most commonly fulsiform - diffuse and circumferential dilation
Risk factors:
Male sex (but women have a greater risk of rupture)
Smoking - most important risk factors
Family history
Increasing age
Hyperlipidaemia
History of atherosclerosis (PAD and coronary artery disease)
History of other aneurysm
Hypertension - also increases risk of rupture
COPD - elastin degradation
Connective tissue disorders
Diabetes appears to be a protective factor against the development of AAA.
Symptoms:
Usually asymptomatic and clinically well - most diagnosed due to screening programme or when AAA ruptures
If AAA ruptures - rapid onset abdominal, flank or back pain, shock and rapid loss of consciousness (usually with cardiac arrest)
Clinical exam:
Peripheral vascular exam
Expansible pulsatile central abdominal mass superior to the umbilicus (absence does not rule out AAA)
Signs of hyperlipidaemia - xanthelasma, corneal arcus
Abdominal scars
Features of Marfan syndrome - high arched palate, tall
No aneurysm found (less than 3 cm) - no further scans are required
Small AAA (3-4.4 cm) - placed under surveillance and repeat scan in 12 months
Medium AAA (4.5-5.4 cm) - placed under surveillance and repeat scan in 3 months
Large AAA (5.5 cm or more) - to be seen by vascular surgeon within 2 weeks
Also urgent referral if >4cm and rapidly growing (>1cm a year)
Conservative management of asymptomatic AAA:
If less than 5.5cm
Lifestyle advice - smoking cessation
Antiplatelet therapy - aspirin 75mg OD
Statins
Anti-hypertensives if BP >140mmHg
Surveillance (annually if 3-4.4cm, every 3 months if 4.5-5.4cm)
Surgical management:
If the aneurysm is ≥5.5cm in diameter or >4cm and rapidly growing (>1cm per year), the patient will need an elective surgical repair.
Antibiotic prophylaxis
VTE prophylaxis
Open aortic repair or endovascular aortic repair (EVAR)
Require 2 units of RBC cross-matched and cell salvage
EVAR:
For patients with more co-morbidities, women of any age and men >70 years
Lower perioperative mortality and decreased length of hospital stay
More prone to more longer-term complications than open repair so needs long term post surgical surveillance
Inserting a stent graft through the femoral arteries under radiological guidance - blood diverted through the graft instead of the aneurysm
Endoleaks is a common complication - blood flows outside the stent-graft
one, six, and 12 month post operative ultrasounds
Annual ultrasound following this
Open aortic repair:
Preferred in healthier patients and men <70 years
Grafting in open surgery lasts longer and has more up-front risks than EVAR
Done via laparotomy incision - aorta is clamped proximally and iliac arteries clamped distally. Removal of affected segment and replace with prosthetic graft.
Assessment and investigation of ruptured AAA:
Surgical emergency
Must be considered for anyone with abdominal/back pain and signs of shock
ABCDE assessment and urgent senior clinical review
Bedside aortic ultrasound
Bloods: G+S and cross match, coagulation, FBC
CT angiography is the definitive imaging modality - retroperitoneal haematoma and contrast extravasation
A stable patient with ruptured AAA has a better chance of survival with local anaesthetic EVAR compared to open surgery
CT angiography should not delay treatment of unstable patients - assess, scan and theatre within 30 minutes
Management of ruptured AAA:
IV access (and limited fluid resuscitation)
Analgesia
Antibiotic prophylaxis
Major haemorrhage protocol activation
Blood transfusion if Hb <100 g/L with intraoperative bleeding
Do not over correct the BP as this could exacerbate the rupture
Definitive treatment is an urgent surgical repair by either EVAR or open aortic repair
Ruptured AAA complications:
80% mortality rate
Abdominal compartment syndrome
Early postoperative complications:
Postoperative ileus - common
AKI - EVAR uses iodine contrast, clamping of renal arteries in open repair
Pseudoaneurysms - more common in EVAR following femoral artery puncture
Distal embolism resulting in acute limb ischaemia
Retrograde ejaculation - semen enters the bladder during ejaculation
Open surgery also has risks of chest infection, respiratory failure and MI
Late postoperative complications:
Aortic neck dilation
Graft infection - can lead to aortic fistula
Graft occlusion
Endoleak - following EVAR
Incisional hernia
Abdominal adhesions
Most AAA usually grow at a rate of 0.2-0.3cm per year. The risk of AAA rupture for aneurysms >5.5 cm is approximately 5% per year. However, the rupture risk depends on the size.
Do not give too many fluids if patient has ruptured AAA
will bleeding into retroperitoneal space but too much fluid can cause them to perforate and bleed into the peritoneal space - larger space for blood to collect