Abdominal Aortic Aneurysm

Overview

• Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm.
• A true aneurysm is a segmental, full-thickness dilation of a blood vessel that is ≥50% greater than its normal diameter.
• False aneurysms of the abdominal aorta are rare, typically resulting from trauma or infection.
• An arterial aneurysm, in general, is defined as a permanent, localised dilation of a vessel to at least 150% of the normal adjacent arterial diameter.

Diameter Criteria

• In most adults, an aortic diameter >3.0 cm is considered aneurysmal.
• The normal infrarenal aortic diameter averages approximately 2.0 cm; 95% of adults have a diameter ≤3.0 cm.
• In males, absolute diameter is strongly predictive of clinical events.
• In females, an aortic size index (ASI = diameter [cm] / body surface area [m²]) is more predictive than absolute diameter.
• Classification by size:
  • Small: <4.0 cm
  • Medium: 4.0–5.5 cm
  • Large: >5.5 cm
  • Very large: ≥6.0 cm
• The natural history is progressive expansion, with growth rate influenced by initial diameter and modifiable risk factors, particularly smoking.

Aortoiliac Anatomy

• The abdominal aorta is retroperitoneal, extending from the diaphragmatic hiatus to the bifurcation at the fourth lumbar vertebra into the right and left common iliac arteries.
• Lies slightly left of the midline, with the inferior vena cava to its right.
• Branches from superior to inferior: inferior phrenic arteries, middle suprarenal arteries, coeliac axis, superior mesenteric artery, renal arteries, gonadal arteries, inferior mesenteric artery, common iliac arteries, middle sacral artery, and paired lumbar arteries (L1–L4).
• Common iliac arteries bifurcate into internal and external iliac arteries at the pelvic inlet:
  • Internal iliac: anterior and posterior divisions supply pelvic viscera and musculature.
  • External iliac: continues beneath the inguinal ligament as the common femoral artery.

AAA Classification by Relation to Renal/Visceral Arteries

• Most AAAs involve the segment between the renal and inferior mesenteric arteries. Around 5% involve renal or visceral arteries.
• Approximately 40% of AAAs coexist with iliac artery aneurysms.
• Thoracoabdominal aneurysms originate in the thoracic aorta and may extend to involve visceral or renal vessels.

Suprarenal aneurysm

• Involves the origins of one or more visceral arteries without extension into the thoracic aorta.

Pararenal aneurysm 

• Renal arteries arise from the aneurysmal segment, but the superior mesenteric artery region is unaffected.

Juxtarenal aneurysm

• Begins immediately distal to the renal artery origins; no normal segment exists between the renal arteries and aneurysm, but the renal artery origin itself is not aneurysmal.

Infrarenal aneurysm 

• Located distal to the renal arteries, with a normal aortic segment separating them.

Overview

• AAA is generally considered a degenerative condition of the aorta with a multifactorial origin.
• While intimal atherosclerosis is consistently present in AAA specimens, its role as the primary cause has been questioned.
• Aneurysm development can occur in the absence of significant lipid-related disease and shows distinct risk factor patterns compared with atherosclerosis.
• Proteolytic degradation of connective tissue within the aortic wall is a key pathological feature.
• Altered activity of tissue metalloproteinases reduces wall integrity and promotes progressive dilatation.

Smoking

• Most significant modifiable risk factor for AAA development and progression.
• Strongly linked to both the formation and expansion of aneurysms.
• Declining incidence of AAA in some populations, such as elderly Swedish men, is attributed to reduced smoking prevalence over recent decades.

Diabetes mellitus

• Appears to have a paradoxical protective effect against AAA development and growth.
• Mechanism for this protective association remains unclear.
• Despite the possible protective effect, patients with diabetes who undergo AAA repair have poorer operative and long-term survival.
• Increased cardiovascular comorbidity is the likely cause of worse postoperative outcomes.

Genetic predisposition

• Having a first-degree relative with AAA increases risk significantly.
• Familial prevalence is estimated between 15% and 25%.
• Evidence suggests the involvement of a single dominant gene with low penetrance that increases with age.
• An autoimmune basis has been proposed for inflammatory AAA.
• The DRB1 major histocompatibility locus has been associated with the inflammatory form of the disease.

Other medical conditions

• Chronic obstructive pulmonary disease (COPD) is associated with higher AAA risk.
• Coronary artery disease and hypertension are additional vascular risk factors.
• Previous aneurysms, including peripheral aneurysms, are often linked to AAA.

Connective tissue disorders

• Marfan syndrome, Ehlers-Danlos syndrome, and other collagen-vascular diseases are rare but important causes.

Infective (mycotic) aneurysms

• Account for fewer than 5% of AAA cases.
• Usually caused by haematogenous spread of infection.
• Gram-positive organisms are the most frequent pathogens.
• Cause direct invasion of the intima and media, leading to abscess formation and aneurysmal dilatation.

Uncommon causes

• Cystic medial necrosis.
• Arteritis.
• Trauma.
• Anastomotic disruption producing pseudoaneurysms.

Medication-related risk

• Fluoroquinolone antibiotics have been linked to increased risk of aortic aneurysm.
• The US FDA warns against prescribing these drugs to at-risk patients, including those with vascular disease, hypertension, genetic connective tissue disorders, or advanced age.

Risk Factors for Rupture

• Aneurysm diameter is one of the strongest predictors of rupture.
• Most AAAs enlarge at an average rate of 0.2–0.8 mm per year before rupture.
• Haemodynamic factors contribute to rupture, with high wall stress areas often corresponding to rupture sites.
• Computer modelling suggests aneurysm volume may be a more accurate predictor of rupture risk than diameter alone.
• Rupture occurs when wall stress exceeds the tensile strength of the vessel.
• Wall tension, calculated using Laplace’s law (P × R / W), is a sensitive predictor of rupture risk.
• Acute blood pressure control is recommended in hypertensive patients with AAA to reduce wall stress.

General

• AAAs result from progressive destruction of the aortic wall’s major structural proteins, elastin and collagen.
• The initiating trigger is unclear, but a combination of genetic predisposition, biochemical processes, and haemodynamic stress is implicated.
• Degeneration primarily affects the media, causing loss of smooth muscle cells, thinning of the wall, and dilatation of the vessel lumen.
• Approximately 90% of AAAs occur in the infrarenal aorta, where medial thinning and intimal thickening are more pronounced compared with the thoracic aorta.
• Histological findings include loss of elastin and collagen in the media and adventitia, smooth muscle cell depletion, lymphocyte and macrophage infiltration, and adventitial neovascularisation.

Proteolytic degradation of aortic wall connective tissue

• Driven by matrix metalloproteinases (MMPs) and other proteases secreted by macrophages and aortic smooth muscle cells into the extracellular matrix.
• MMPs normally regulate vessel-wall remodelling, but in AAA there is an imbalance favouring proteolysis, with increased enzyme activity and reduced inhibitor activity.
• Excessive breakdown of elastin and collagen weakens the aortic wall, leading to dilatation and predisposition to rupture.
• Certain MMP gene polymorphisms (e.g., MMP-2, MMP-3, MMP-13, and MMP-9 in some patient groups) are associated with increased AAA risk and may have future prognostic value.

Inflammation and immune responses

• Aneurysm walls demonstrate chronic adventitial and medial infiltration by macrophages and lymphocytes.
• These cells release cytokines (e.g., IL-1, IL-6, IL-8, TNF-α) that activate proteases, further promoting elastin and collagen degradation.
• Immunoglobulin G deposition within the aortic wall supports an autoimmune component to AAA formation.
• Autoantigens, such as collagen-associated microfibrils, have been identified in aneurysm tissue; possible infectious triggers (e.g., Chlamydia pneumoniae, Treponema pallidum) have been investigated but without definitive causal proof.
• Oxidative stress and reactive oxygen species may also contribute to the inflammatory cascade.

Biomechanical wall stress

• The elastin-to-collagen ratio declines progressively along the aorta, with the infrarenal segment having lower elastin content, predisposing it to dilation.
• Collagen degradation reduces tensile strength, increasing rupture risk.
• Increased wall stress is influenced by altered haemodynamics, MMP-9 upregulation, disturbed blood flow patterns, and relative hypoxia in the distal aorta.
• These biomechanical factors act synergistically with structural degradation to accelerate aneurysm expansion.

Molecular genetics

• Family and twin studies confirm strong heritability, suggesting a polygenic aetiology rather than a single causative mutation.
• Genome-wide association studies have identified multiple risk loci, some unique to AAA and others shared with different cardiovascular diseases.
• Gene expression profiling demonstrates upregulation of pathways linked to extracellular matrix breakdown and inflammation, and downregulation of protective or stabilising processes.

Atherosclerosis

• Frequently coexists with AAA but is unlikely to be the primary cause.
• May contribute to aneurysm formation by mechanically weakening the aortic wall and promoting degenerative ischaemic changes via obstruction of the vasa vasorum.
• Many individuals with advanced atherosclerosis do not develop AAA, and some patients without significant atherosclerosis do, indicating a more complex interplay of factors.

Overall

• The prevalence of abdominal aortic aneurysm (AAA) varies with region, sex, age, and ethnicity, with large-scale screening programmes providing the most accurate estimates.
• In resource-abundant countries, overall prevalence ranges between 2% and 8%, with higher rates in men (4–8% in those over 50 years) compared with women (1–1.3%).
• Screening data from the United States suggest approximately one million people have an AAA, and prevalence increases with age in both sexes, though more sharply in men.
• Ultrasound-based population screening has shown that 4–8% of older men have an occult AAA.
• The prevalence in the UK National Health Service (NHS) screening programme during its first five years (2009–2013) was 1.34% for men screened in their 65th year.
• For the screening year 2019–2020, of 291,904 eligible men invited for their first AAA scan, 76.1% attended, with a detection rate of 0.92%. Among 8,340 self-referred men aged over 65, 88.9% attended screening, with a higher detection rate of 3.8%.
• Among women, pooled data from multiple screening studies show prevalence exceeding 1% in those over 70 years, with higher rates in smokers (>1% in ever-smokers and >2% in current smokers).
• The prevalence in men increases by roughly 6% per decade of life.
• Prevalence is lower in Asian populations but can approach Western rates when adjusted for cardiovascular risk factors. In the UK, AAA is more common in white British and particularly white Irish men compared with black or Asian men.

Trends in mortality and rupture

• In the 2010s, deaths from ruptured AAA in the United States were estimated at around 7,000 per year.
• AAA-related mortality has fallen by nearly 50% since the early 1990s.
• In the UK, mortality in men over 65 years declined from 65.9 to 44.6 per 100,000 between 1997 and 2009, and admissions for ruptured AAA fell from 18.6 to 13.5 per 100,000 across all age groups.
• These declines are attributed to reduced smoking prevalence, increased elective AAA repairs in older patients, and the impact of national screening programmes.
• Data from the UK screening programme in 2019–2020 reported 30 ruptured AAAs in men with previously detected aneurysms, 25 of which were fatal.

Risk factors associated with aneurysmal disease

• Older age.
• Male sex.
• Cigarette smoking (most important modifiable risk factor).
• Positive family history of AAA.
• Other large artery aneurysms (e.g., iliac, femoral, popliteal).
• Atherosclerosis.
• Hypertension.

General

• The medical history is central to assessing a patient’s risk for developing AAA and, if an aneurysm is already present, estimating the potential for rupture.
• Risk factors to elicit include cigarette smoking, family history of AAA, older age, male sex for prevalence, female sex for rupture risk, and connective tissue disorders (e.g., Marfan, Ehlers-Danlos).
• History should document whether a diagnosis of AAA has been made previously, with review of prior imaging to record maximal aortic diameter and calculate expansion rate (cm/year). An expansion rate >0.5 cm/year increases rupture risk.
• Ask about prior AAA repair:
  • Open repair may result in later anastomotic failure or pseudoaneurysm.
  • Endovascular repair may be complicated by endoleak, which can re-pressurise the aneurysm sac and lead to rupture.
• Only 20–30% of patients presenting with rupture have a known prior history of AAA.

Symptoms of intact AAA

• Most AAAs are asymptomatic and discovered incidentally or via screening.
• When symptomatic, pain is the most common manifestation, typically in the abdomen, back, or flank; less often in pelvis, groin, or thigh.
• Pain ay be due to:
  • Rapid expansion (>0.5 cm/year).
  • Compression/erosion into adjacent structures (spine, inferior vena cava).
  • Inflammatory or infected aneurysm, often with constitutional symptoms (fever, weight loss).
• Local compression can cause gastrointestinal or urinary symptoms, venous thrombosis, or back pain from vertebral erosion.
• Atheroembolism from mural thrombus may cause distal manifestations such as livedo reticularis or blue toe syndrome.
• Patients may report awareness of an abdominal pulse or mass.

Pain characteristic

• Location correlates with aneurysm position: proximal aneurysms → upper abdominal/back pain; distal aneurysms → lower abdominal/pelvic pain or radiculopathy.
• Pain is typically unaffected by movement or position.
• Onset may be gradual and vague in nonruptured AAA, or sudden and severe with rupture.

Symptoms of ruptured AAA

• Classic triad (severe pain, pulsatile abdominal mass, hypotension) present in only ~50% of ruptures.
• Pain distribution varies: abdominal, back, flank, groin, or thigh; can be associated with syncope or nausea.
• Posterior wall rupture often initially contained in the retroperitoneum, causing focal pain that may subside before re-rupture.
• Anterior wall rupture may lead quickly to free intraperitoneal haemorrhage and profound shock.
• Transient hypotension, temporary loss of consciousness, cyanosis, mottling, tachycardia, and altered mental status may occur.
• Many patients die before reaching hospital (~65%).

Other acute presentations

• Limb ischaemia from thromboembolism of aneurysm contents, which may present as acute painful, pulseless limb or blue toe syndrome.
• Rarely, acute thrombosis of the aneurysm can cause bilateral limb ischaemia or spinal cord ischaemia.
• Arteriovenous fistula from rupture into the vena cava or iliac vein may present with heart failure, leg swelling, haematuria, or abdominal bruit.
• Aortoduodenal fistula can cause a herald gastrointestinal bleed followed by catastrophic haemorrhage.

Chronic and less common manifestations

• Inflammatory AAA: abdominal pain, weight loss, raised inflammatory markers, ureteric obstruction; lower rupture risk than standard AAA.
• Infected (mycotic) aneurysm: fever, malaise, chronic abdominal discomfort.
• Disseminated intravascular coagulation from large or extensive aneurysms, leading to bleeding or thrombosis.
• Myocardial infarction related to acute blood loss in up to 25% of ruptures.
• Groin pain or acute groin hernia due to sudden rise in intra-abdominal pressure.

General

• Most clinically significant AAAs can be palpated on abdominal examination, but detection depends on aneurysm size, patient body habitus, and examiner experience.
• Palpation should be performed with the patient supine, between the xiphoid process and umbilicus, to identify a widened aortic pulse; palpation is safe and has never been shown to precipitate rupture.
• Sensitivity of palpation increases with aneurysm size and decreases with increasing abdominal girth:
  • ~29% sensitivity for AAA 3.0–3.9 cm,
  • ~50%for AAA 4.0–4.9 cm,
  • ~76–100% for AAA ≥5.0 cm in patients with waist <100 cm.
• In obese patients or those with an abdominal girth >100 cm, detection rates are significantly lower (~53%).
• A pulsatile abdominal mass is virtually diagnostic but is found in fewer than 50% of all AAA cases and in up to 62% of ruptured AAA cases.
• An abdominal bruit may be heard, but it is non-specific; thrills may occur with aortocaval fistulae.
• Overlying normal structures (pancreas, stomach) or a tortuous, prominent but normal-sized aorta may mimic AAA.
• Palpation should be supplemented with imaging for confirmation due to the potential for false positives and negatives.

Additional abdominal signs

• Abdominal tenderness may occur, especially with inflammatory or infected aneurysms, but is not always present.
• Abdominal distension is common in ruptured AAA.
• Ecchymosis may indicate retroperitoneal haemorrhage:
  • Grey-Turner sign (flank),
  • Cullen sign (periumbilical),
  • Fox’s sign (proximal thigh),
  • Bryant’s sign (scrotal).
     These are not specific and may be seen in other intra-abdominal or retroperitoneal pathologies.

Vascular examination

• Peripheral pulses (femoral, popliteal, pedal) should be palpated to detect associated aneurysms or occlusive disease; popliteal aneurysms coexist with AAA in 25–50% of cases.
• Asymmetric upper limb pulses or significant differences in blood pressure between arms (>30 mmHg) may suggest proximal aortic or subclavian artery disease.
• Carotid bruits may indicate concomitant carotid stenosis.
• If pulses are not easily palpable, handheld Doppler can assist localisation and facilitate monitoring.
• Signs of distal embolisation (e.g., ischaemic toes, mottling, blue toe syndrome) may indicate thromboembolic complications from AAA.

Systemic findings in rupture

• Vital signs may be normal initially if rupture is contained, especially with posterior wall involvement.
• Hypotension, tachycardia, cyanosis, mottling, and altered mental status can develop rapidly with anterior wall rupture or haemodynamic decompensation.
• Fever may occur with infected AAA.

General Principles

• Many AAAs are asymptomatic and undiagnosed until rupture or detection through screening.
• A definitive diagnosis is made by imaging confirmation of focal aortic dilation >1.5 times normal diameter, or intraoperative findings.
• Imaging is not always required before surgery in unstable patients with known AAA and classic rupture symptoms; intraoperative diagnosis is acceptable in these cases.
• Abdominal ultrasound and CT scan are the primary diagnostic modalities. MRI is less commonly used but may have a role in specific scenarios such as contrast allergy or post-repair complications.
• Conventional arteriography is less accurate for diameter assessment as it only shows luminal flow and may miss mural thrombus.

Laboratory Studies and Biomarkers

• Most patients presenting with acute abdominal symptoms undergo initial laboratory testing, including full blood count, electrolytes, urea, and creatinine.
• Patients presenting in shock require additional urgent studies: liver function tests, coagulation profile, fibrinogen, fibrin split products, arterial blood gases, lactate, cardiac enzymes, and toxicology screen.
• Anaemia and metabolic acidosis may suggest acute blood loss in ruptured AAA.
• Leukocytosis may indicate aortic infection or inflammation, particularly if accompanied by systemic features such as fever or weight loss.
• In suspected inflammatory or infected AAA, further tests such as blood cultures and ESR can help differentiate these from typical aneurysms. ESR may be markedly raised in inflammatory AAA.
• Coagulation tests are usually normal in ruptured AAA, but some patients develop coagulopathy or disseminated intravascular coagulation, particularly with large or thoracoabdominal aneurysms.
• In asymptomatic individuals, there are no definitive laboratory markers for AAA detection or progression. Elevated hemostatic markers (e.g., fibrinogen, D-dimer, thrombin–antithrombin III complex) are non-specific but correlate with aneurysm presence and diameter.
• D-dimer levels have a strong correlation with aneurysm size and have been used for serial monitoring in known AAA cases.
• Myeloperoxidase and D-dimer levels combined may help predict rapid disease progression.
• Other studied markers include elevated homocysteine, pro–brain natriuretic peptide (BNP), interleukin-6, and matrix metalloproteinase-9.
• In large cohort studies, elevated levels of multiple biomarkers (including WBC count, fibrinogen, D-dimer, troponin T, NT-proBNP, and high-sensitivity CRP) were associated with higher AAA incidence, particularly in smokers.

General Principles

• Many AAAs are asymptomatic and undiagnosed until rupture or detection through screening.
• A definitive diagnosis is made by imaging confirmation of focal aortic dilation >1.5 times normal diameter, or intraoperative findings.
• Imaging is not always required before surgery in unstable patients with known AAA and classic rupture symptoms; intraoperative diagnosis is acceptable in these cases.
• Abdominal ultrasound and CT scan are the primary diagnostic modalities. MRI is less commonly used but may have a role in specific scenarios such as contrast allergy or post-repair complications.
• Conventional arteriography is less accurate for diameter assessment as it only shows luminal flow and may miss mural thrombus.

Imaging in Asymptomatic Patients

• Abdominal ultrasound is the preferred first-line modality for suspected AAA in asymptomatic patients based on risk factors or incidental findings.
• Advantages: non-invasive, inexpensive, high sensitivity (98%) and specificity (99%), cost-effective for detecting small aneurysms.
• Examination should include suprarenal to infrarenal aorta and iliac arteries.
• Limitations include dependence on operator skill, patient body habitus, and interference from bowel gas. In 1–2% of cases, the aorta is inadequately visualised, necessitating further imaging (usually CT).
• Measurement technique variations (outer-to-outer, inner-to-inner, leading-edge) can cause discrepancies; SVS guidelines recommend outer wall measurement perpendicular to the aortic path on CT.

Imaging in Symptomatic Patients

• Choice of imaging depends on haemodynamic status.
• In unstable patients with suspected ruptured AAA, immediate intervention without imaging may be necessary, but bedside ultrasound can rapidly confirm diagnosis.
• In stable symptomatic patients, urgent contrast-enhanced CT is preferred for anatomical assessment, rupture confirmation, and EVAR planning. Non-contrast CT may be used if there is risk of contrast-induced nephropathy.
• CT advantages include better assessment of rupture versus non-rupture, identification of suprarenal aneurysms, and evaluation of other abdominal pathology.
• CT findings suggestive of rupture: retroperitoneal haematoma, indistinct aortic wall, retroperitoneal stranding, loss of fat plane, and contrast extravasation.
• Signs of impending rupture: crescent sign, aortic blebs, aortic draping over vertebrae, wall irregularity, calcification breaks, and focal high attenuation within mural thrombus.

Specific Imaging Considerations

• Features suggesting embolic source from AAA on CT include irregular luminal surface, multiple lumens, thrombus heterogeneity, calcification within thrombus, and fissures.
• Infected AAA on CT: saccular or multilobulated morphology, periaortic soft tissue inflammation, intramural/perivascular air, or fluid collection.
• Inflammatory AAA on CT: thick periaortic inflammatory rind (≥1 cm), indistinct retroperitoneal tissue planes, enhancement with contrast, fibrosis, and adherence to adjacent structures; absence of periaortic air or fluid supports non-infective nature.

Diverticulitis

• Severe constipation and localised abdominal pain, typically in the left lower quadrant.
• May present with fever; abdominal or perirectal ‘fullness’ can be detected on examination; no pulsatile abdominal mass.
• Leukocytosis may be present.
• CT scan: normal-calibre aorta, diverticula, pericolic fat inflammation, bowel wall thickening (>4 mm), or peridiverticular abscess.

Ureteric Colic (Nephrolithiasis)

• Severe flank pain radiating to the groin, often with nausea, vomiting, haematuria, dysuria, frequency, or urgency.
• Men >55 years with ureteric colic should be considered to have a leaking/ruptured AAA until excluded.
• Urinalysis: blood, crystals, or infection.
• Ultrasound/CT scan: normal-calibre aorta, ureteral or renal stones.

Irritable Bowel Syndrome (IBS)

• Intermittent abdominal discomfort, often lasting 2–4 days, with bloating, altered stool frequency, and abnormal defecation.
• Common in women aged 20–40 years.
• Examination is usually normal but may reveal poorly localised abdominal tenderness; patients may appear anxious.
• Imaging: normal-calibre aorta.

Inflammatory Bowel Disease (Crohn’s disease, ulcerative colitis)

• Crampy, often left-sided abdominal pain; diarrhoea (bloody or non-bloody), urgency, and tenesmus.
• May have extra-intestinal manifestations, mucocutaneous lesions, or perianal fistulae/fissures.
• Examination: abnormal bowel sounds, palpable mass, tenderness.
• Anaemia common.
• Imaging: normal-calibre aorta.
• Endoscopy with biopsy: diagnostic mucosal lesions.

Appendicitis

• Periumbilical pain migrating to the right lower quadrant, often with nausea, vomiting, and anorexia.
• Fever and right lower quadrant tenderness on examination.
• Leukocytosis and sterile pyuria may be present.
• Ultrasound/CT scan: normal-calibre aorta, inflamed appendix, or perforation.

Ovarian Torsion

• Sudden, continuous lower abdominal pain with nausea and vomiting; possible fever.
• Adnexal mass may be palpable.
• Leukocytosis may occur.
• Ultrasound: normal-calibre aorta, reduced or absent adnexal blood flow.

Gastrointestinal Haemorrhage

• May mimic ruptured AAA if presenting with haemorrhagic shock.
• History of GI bleed, haematemesis, melaena, or haematochezia; risk factors for peptic ulcer disease or malignancy.
• Rectal examination: gross blood; nasogastric aspiration may return coffee-ground material.
• Stool: guaiac positive.
• Endoscopy: source of bleeding, mucosal ulceration, polyps, or tumour.
• Imaging: normal-calibre aorta.

Mesenteric Artery Aneurysms or Acute Occlusion

• Acute embolic/thrombotic splanchnic vessel occlusion: severe mid-abdominal pain, nausea, vomiting, explosive diarrhoea; minimal early findings.
• Most splanchnic aneurysms are asymptomatic until rupture.
• Labs: leukocytosis, haemoconcentration, systemic acidosis; elevated amylase, inorganic phosphorus, creatine phosphokinase, alkaline phosphatase if bowel infarction present.
• Angiography: diagnostic and may be therapeutic.
• Ultrasound/CT scan: normal-calibre aorta; identifies splanchnic artery aneurysms.

Other Possible Differentials

• Acute gastritis.
• Urinary tract infection or cystitis (especially in females).
• Gallstones (cholelithiasis).
• Large- or small-bowel obstruction.
• Myocardial infarction.
• Peptic ulcer disease.
• Mesenteric ischaemia.
• Pyelonephritis.

Ruptured AAA

• Discuss suspected ruptured AAA cases immediately with a regional vascular service for urgent surgical repair if bedside ultrasound confirms an AAA, is inconclusive, or unavailable. Do not delay treatment for imaging.
• Initiate hypotensive resuscitation if the patient is conscious. The European Society for Vascular Surgery (ESVS) recommends preoperative systolic blood pressure (SBP) 70–90 mmHg; the Royal College of Emergency Medicine suggests 90–120 mmHg while awaiting vascular input.
• Use blood products in a fresh frozen plasma:red blood cell ratio close to 1:1 if available.
• Transfer to the receiving centre within 30 minutes of acceptance by the vascular service.
• Immediate supportive care: supplemental oxygen, large-bore intravenous access, arterial line, urinary catheter.

Symptomatic Unruptured AAA

• Urgently consult a vascular service.
• Urgent surgical repair is indicated regardless of size; pain may indicate impending rupture.
• EVAR is widely used; a short delay to optimise the patient is possible, with ICU monitoring.

Asymptomatic AAA (Incidental or Screen-detected)

• UK referral:
  • Seen within 2 weeks if ≥5.5 cm.
  • Seen within 12 weeks if 3.0–5.4 cm.
• Surgical repair is generally advised for:
  • ≥5.5 cm (men); in some countries ≥5 cm (women).
  • 4.0 cm with growth >1 cm/year.
• Consider anatomy, comorbidities, life expectancy, and patient preference.
• Conservative management with ultrasound surveillance and risk factor modification if below threshold.
• Smoking cessation is essential; also control blood pressure, lipids, and manage cardiovascular risk factors.

Surveillance (UK NICE guidance)

• Ultrasound annually if 3.0–4.4 cm.
• Every 3 months if 4.5–5.4 cm.

Surgical Repair

Indications

• Ruptured or symptomatic AAA; asymptomatic AAA meeting size/growth thresholds.

EVAR

• Preferred for ruptured infrarenal AAA in most, especially men >70 years and all women; advantages include lower perioperative mortality and shorter hospital stay. Long-term surveillance required.

Open Repair

• Preferred if EVAR unsuitable, in men <70 years, or with connective tissue disorders.

Complex AAA

• Consider fenestrated EVAR (FEVAR) or branched EVAR for juxtarenal/suprarenal aneurysms in high-volume centres.

Perioperative Care

• Optimise comorbidities, give antibiotic prophylaxis, provide VTE prophylaxis, and avoid starting beta-blockers de novo. Continue single antiplatelet therapy; manage anticoagulation per perioperative protocols. 
• Start statin ≥4 weeks preoperatively if possible.

Infectious AAA

• Early diagnosis, urgent antibiotics, and surgical repair (open or EVAR depending on suitability).
• Extended antibiotic therapy (4–6 weeks to lifelong) tailored to pathogen and immune status.

Inflammatory AAA

• High-dose corticosteroids plus surgery; tamoxifen use reported but unproven benefit over steroids alone.
• Preoperative ureteric stenting may help prevent injury.

Ruptured AAA

• The prognosis is extremely poor; over 50% of patients die before reaching hospital.
• Survivors face high morbidity, with mortality influenced by factors such as preoperative cardiac arrest, age >80 years, female sex, massive blood loss, and ongoing transfusion requirements.
• The most important determinant of survival in rupture is rapid achievement of proximal aortic control.

Elective Repair

• Prognosis following elective repair is generally good to excellent.
• Long-term survival is primarily determined by coexisting conditions such as chronic obstructive pulmonary disease, ischaemic heart disease, and peripheral vascular disease.
• Approximately 70% of patients survive for 5 years post-repair.

Natural History

• AAAs typically enlarge gradually, and rupture risk rises with increasing diameter.
• Most ruptures occur before patients reach surgery.
• Repair is usually delayed until the predicted rupture risk exceeds estimated operative mortality.

Outcomes After Open Repair

• Late graft-related complications are uncommon (0.4%–2.3%).
• Five-year survival after intact aneurysm repair averages 60%–75%.

Outcomes After Endovascular Aneurysm Repair (EVAR)

• Patients are more likely to experience delayed complications and require re-intervention compared with open repair.
• Late survival may be lower in EVAR-treated patients with intact AAA compared with those undergoing open repair.

Risk Factors for Poor Postoperative Outcome

• Low skeletal muscle mass is significantly associated with higher morbidity after AAA repair.
• In elderly patients, postoperative quality of life declines initially—mental health recovery often takes 4–6 weeks, and physical recovery 1–3 months—regardless of surgical technique.
• Quality of life generally returns to baseline and remains stable long-term, supporting surgical intervention even in older individuals.

Renal Dysfunction

• Acute kidney injury (AKI) is one of the more common complications following AAA repair, whether by open surgery or EVAR.
• In open repair, AKI is typically transient, whereas after EVAR—particularly when suprarenal fixation is used—it is often more severe and multifactorial in origin.
• Patients who develop AKI after EVAR face increased medium-term morbidity and mortality.
• Risk reduction strategies include limiting contrast dose, avoiding nephrotoxic agents, ensuring adequate hydration, and preserving large accessory renal arteries.
• Smaller trials suggest potential benefit from mannitol, antioxidants, an extraperitoneal surgical approach, or human atrial natriuretic peptide, but high-quality multicentre studies are needed.

Abdominal Compartment Syndrome (ACS)

• A serious early complication after repair of ruptured AAA, with reported incidence ranging from ~6–9% in registry data to 20–34% in single-centre reports.
• ACS can occur after both open repair and EVAR, and is strongly associated with increased perioperative mortality.
• It should be suspected in any patient whose condition fails to improve postoperatively; decompressive laparotomy is the definitive treatment.

Gastrointestinal Complications

• Ileus affects roughly 11% of patients after open repair; intestinal obstruction and colitis are less common (~1% each).
• Clinically significant bowel ischaemia, including colonic ischaemia, occurs in up to 10% of cases after ruptured AAA surgery.
• Causes include compromised blood flow through the inferior mesenteric or hypogastric arteries; risk exists in both open and endovascular repair, though severe necrosis requiring colectomy is rare in EVAR.
• If suspected, flexible sigmoidoscopy can confirm the diagnosis. Management involves hydration, bowel rest, antibiotics, and, if needed, surgical resection.

Endoleak

• A complication unique to EVAR, affecting about 24% of patients.
• Classified as:
  • Type I: Leak at graft attachment sites; requires immediate correction—options include balloon remodelling, proximal cuff placement, fenestrated or branched extension, or open conversion.
  • Type II: Retrograde flow from branch vessels; often self-resolving, but treat if aneurysm sac enlarges ≥10 mm.
  • Type III: Fabric defect or graft component separation; requires stent graft extension.
  • Type IV: Leak through graft wall porosity; rare and self-limiting with modern devices.
  • Type V (Endotension): Raised sac pressure without visible leak; intervention considered if sac expansion occurs.

Sexual Dysfunction

• Autonomic nerve injury during open repair and reduced pelvic perfusion from either open or endovascular repair can lead to erectile dysfunction or retrograde ejaculation.
• Internal iliac artery occlusion during EVAR is a recognised cause, with bilateral occlusion posing higher risk.
• Reported incidence of new erectile dysfunction ranges from 20–83% in the first postoperative year after open repair and ≤14% after EVAR with unilateral occlusion.
• Specialist referral is recommended for persistent and distressing dysfunction.

Spinal Cord Ischaemia

• Rare after elective EVAR (~0.21%) but more frequent following emergency EVAR for ruptured AAA (up to ~11%).
• Risk factors include prolonged procedures, challenging anatomy, and extensive vessel manipulation.
• Management involves early detection, cerebrospinal fluid drainage, and corticosteroids, though many patients have incomplete or no neurological recovery.

Graft-Related Issues

Anastomotic Pseudoaneurysm

• Para-anastomotic aneurysms occur in ~10% after aortic bypass grafting; femoral pseudoaneurysms may reach 20% at 10 years after aortobifemoral reconstruction. Infection should be excluded; non-infectious cases can be managed endovascularly.

Aortic Neck Dilation

• Present in nearly a quarter of EVAR patients during follow-up, and associated with endoleak, migration, and re-intervention.

Graft Limb Occlusion

• Long-term incidence is ~2.6–3.0% after open repair and up to 7.2% after EVAR; kinking increases risk.

Graft Infection

• Rare (<0.2% within 2 years) but life-threatening; best managed with surgical graft removal.

Obstructive Complications

Ureteric Obstruction

• Most often linked to inflammatory perianeurysmal fibrosis, particularly in inflammatory AAA; can involve the inferior vena cava.

Functional Gastric Outlet Obstruction

• Results from duodenal compression between the aneurysm and superior mesenteric artery.

Limb Ischaemia and Amputation

• Amputation due to limb ischaemia is uncommon (0.1% at 30 days after open repair).
• Any sudden onset or worsening of limb ischaemia warrants urgent investigation for graft occlusion or kinking.

Distal Embolisation

• Occurs in 3–29% of cases, most often presenting as blue toe syndrome; severe events (5% incidence) may cause limb-threatening ischaemia or muscle necrosis.

Abdominal Wall Hernia

• Common after open repair, with postoperative incisional hernia rates of 11–37%.
• Mesh reinforcement at the time of closure reduces risk.

Post-implantation Syndrome

• An inflammatory response occurring in the first 10 days after EVAR, with fever, malaise, and back pain.
• Linked to increased early cardiovascular events, but no evidence of long-term survival impact.

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