Abdominal Aortic Aneurysm

Definition
Also known as AAA, pronounced "triple-a" is a localized permanent dilatation of the abdominal aorta wall (all 3 layers) exceeding the normal diameter by more than 50 percent, and is the most common form of aortic aneurysm.

Types of AAA
Shape

• Saccular- Resembles small sac
• Fusiform- Narrow cylinder

Location

• 80% infrarenal
• The remainder: suprarenal  +/- thoracic aorta

Anatomy

Enters abdomen @ T12- With azygous vein and thoracic duct

Branches:

• Unpaired branches: Coeliac axis, Superior mesenteric artery, Inferior mesenteric artery
• Paired branches: Inferior phrenics, Adrenals, Renals, Gonadals, Lumbar x 4

Bifurcates into Common Iliacs below umbilicus @ L4

Epidemiology
M > F = 4 : 1
9th  most common cause of  death in males > 55
1% of men 55-64 have AAA

Aetiology
Atherosclerosis: media  degeneration
Trauma
Inflammatory: P.A.N.
Infective: syphillis, fungal
Genetic : Ehlers Danlos,  Marfans, Polycystic kidney disease, Tuberous sclerosis
Cigarette smoking: >90% of pti

Pathophysiology

• Aortic medial degeneration
• Data suggest major role for matrix metalloproteinases and their inhibitors
• Gradual and/or sporadic expansion of aneurysm and accumulation of mural thrombus
• Aneurysms tend to expand over time. (Laplace law: T (wall tension) = pressure × radius. Wall tension directly related to BP and the radius of the artery. When wall tension exceeds wall tensile strength, rupture occurs.
• Average small AAA (<5.5 cm) grows at a rate of 2.6–3.2 mm/year. Larger aneurysms grew at a faster rate, as did increased tobacco use, but otherwise no identifiable risk factors to assess which small AAAs will advance to require further intervention

Associations
Family history++  :

• Familial aggregations exist: Aneurysms may develop at an earlier age

• The frequency of AAA in 1st-degree relatives is 15–19% compared with 1–3%
• family  members should be  screened: 25% chance of  having AAA

DM
HTN
CAD
COPD
Hyperlipidaemia

Presentation

Asymptomatic (70%)	Incidental finding on : Exam; PFA (calcifications); US Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass  .
Pain	back, loin, groin, iliac  fossa
Thrombus	Thrombus/emboli to lower  limbs. Atheroemboli from small AAAs produce livedo reticularis of the feet or blue toe syndrome
Compression	Pressure on other structures -Mass effect, eg :Ureteric obstruction =  renal failure, duodenum, IVC
Fistula	Aorto-caval or  duodenal
Rupture	Emergency Signs Triad: Abdominal/back pain Pulsatile mass Hypotension Prognosis 50% of ruptured AAA will  die before reaching hospital Of the 50% that survive to  surgery half of these will die Types Retroperitoneal (80%) Contained in  retroperitoneum Tamponade effect Classic triad Intraperitoneal (20%) Collapse Higher MR Risk of rupture in 5 years Normal aorta diameter is  2cm Aorta diameter Risk of rupture <5.5cm 10% 5.5cm 25% 6 – 7cm 30 – 40% >7cm 75% Why do patients survive rupture? Tamponade in  retroperitoneum Vasoconstriction of non  essential circulatory beds Prothrombic state effect Drop in BP.   NB: careful with IVF in  rupture: may effect the  above mechanisms

Investigation

Screening	Recommended 1-time ultrasound for AAA in men 65–75 who have ever smoked. Men >60 years old who are siblings or offspring of patients with AAA should undergo physical exam and ultrasound screening
FBC	Assess transfusion requirements and the possibility of infection
Blood chemistries	Ascertain the integrity of renal and hepatic function to best manage the patient postoperatively and to assess operative risk
Crossmatch	Type and crossmatch blood Prepare for the possibility of transfusion, including clotting factors and platelets
Urinalysis	Because synthetic material is used in the intervention, assess and eliminate potential foci of infection preoperatively.
ABG	determine operative risk and postoperative care.
CXR	preliminary assessment of the status of the heart and lungs.
Abdominal US	determination of aneurysm presence, size, and extent.
CT/MRI	define the anatomy
Angiography	criterion standard for the diagnosis of AAA indicated in the presence of associated renal or visceral involvement, peripheral occlusive disease, or aneurysmal disease.essential with any renal abnormality (eg, horseshoe kidney, pelvic kidney)
Others	PFT, ECG, Stress test

Management

Conservative	smoking cessation. Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm)
Medication	No medical therapy Blood pressure and lipids should however be treated like in any atherosclerotic condition
Surgery	Indications for repair: Rupture/leaking Symptomatic > 5.5cm Rapid growth : >0.5 cm per  annum Distal emboli

Surgery

Workup	2 situations: emergency or elective Emergency Repair Work-up Elective AAA work up If haemodynamically  stable : CT If haemodynamically  unstable:OT Routine bloods: FBC, INR,  U/E A.C.T. A = Anaesthesist (contact) C = Crossmatch 10 u T = Theatre If < 5.5cm , risk of  operation >  risk of rupture Annual surveillance : US or  CT Routine bloods + Group x- match 4u Heart: ECG/Echo/Angiogram Lungs: CXR/PFTs CT : to examine Extent of aneurysm  (infra/supra renal) Type ( fusiform/saccular) Is it suitable for  endovascular repair? 2 types Open repair Endovascular repair (EVAR)
Open repair	Situation Elective : 5 – 8% Emergency symptomatic:  10 – 20% Rupture : 50% Media Aneurysm with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis. Procedure Midline laparotomy For proximal infrarenal control, first identify the left renal vein. Division of the left renal vein is usually required to clamp above the renal arteries. the inferior mesenteric artery is sacrificed divide the ligaments to the left lateral segment of the liver and then retract the segment. The crura of the diaphragm are separated the aorta is bluntly dissected Aorta cross-clamped :  causing huge back pressure  on heart and lower limb  ischaemia Sac opened, Dacron graft  inset Aortic sac closed over  prosthetic graft to prevent  infection Post-op Fluid shifts are common Fluid requirements may be high in the first 12 hours, depending on the amount of blood loss Monitor for intensive care unit Do ECG, CXR Prophylactic antibiotics (eg, cefazolin at 1 g) for 24 hours. 1-2 weeks for suture or skin staple removal, then yearly thereafter. Complications Death - 1.8-5% if elective and 50% if ruptured Cardiac: MI, CCF,  arryhthmias Lung: atelectasis, Pneumonia (5%), ARDS Bowel ischaemia : as IMA is  ligated (1% elective, 15-20% if ruptured) Distal emboli: ischaemic  limb, trash foot Incisional hernia - 10-20% Aorto-duodenal fistula ARF Anastomotic breakdown Anterior spinal syndrome  (spinal arteries) Paraplegia Incontinence Pain and temp loss Proprioception normal Erectile dysfunction and retrograde ejaculation (<30%) Graft infection Staph aureus/epidermidis Rx: remove graft and  perform bilateral axillo- bifem graft
EVAR	Advantages less invasive than open surgery, has a lower surgical morbidity and mortality rate, and reduces the length of post-operative stay in hospital. Disadvantages Cost (stent-grafts and their delivery system are very expensive, plus the cost of any adjunctive procedures), the need for life-long follow-up imaging, History The world's first EVAR was performed in 1987 by Nicholas Volodos in Kiev, Soviet Union relative CI Young patients < 60   -? Long term patencyAortic neck < 1.5cm Mural thrombus in proximal neck Severe iliac disease with strictures Angle between neck of aorta and aneurysm >60° Renal insufficiency Large  patent lumbar vessels Media EVAR Graft Procedures Stent deployed via femoral  arteries No need to cross clamp  aorta Can de done under regional  anaesthesia Post-op ICU for 2 days Disharge after 5 days regular scans every 6-12 months or so for the rest of your life Complications Systemic Myocardial infarction, congestive heart failure, arrhythmias, respiratory failure, renal failure, distal emboli Post implantation syndrome     -↑T°, ↑WCC, ↑ESR, ↑CRP Procedure related Dissection, malpositioning, renal failure, thromboembolizaton, ischemic colitis, groinhematoma, wound infection Device related Graft infection, migration, detachment, rupture, stenosis, kinking, Endoleaks An endoleak is a leak into the aneurysm sac after endovascular repair. 5 types Failure of proximal or distal  seal Filling of sac via collaterals  (IMA etc) Breach in graft material Increased porosity of graft Endotension: ↑  graft size  without visible leak

Complications
Nonoperative:Rupture, dissection, thromboembolization
Elective operative (conventional) :Death 2–8%; All cardiac 10–12% (MI 2–8%)
Pulmonary 5–10%; renal 5–7%; wound infection >5%; colon ischemia 1%; spinal cord ischemia <1%

Prognosis
Annual risk of rupture:

• <4 cm diameter: ~0%
• 4–4.9 cm: ~1%
• 5–5.9 cm: ~11%
• 6–6.9 cm: ~26%
• >;7 cm: ~32%

Patients with AAAs measuring 5.5 cm or larger should undergo repair, as should all patients with symptomatic AAA.
Only ~18% of patients with ruptured AAA survive.
Although there is a 5:1 ratio of AAA between males to females, women have a higher mortality and morbidity associated with AAA, regardless of open or endovascular repair