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Splenic artery aneurysm

Splenic Artery Aneurysm (SAA): Comprehensive Disease Characteristics Research Report

2026-05-06
Falcon MONDO:0001856 Model: Edison Scientific Literature 50 citations

Splenic Artery Aneurysm (SAA): Comprehensive Disease Characteristics Research Report

Executive summary (current understanding)

Splenic artery aneurysm (SAA) is the most common visceral artery aneurysm and is often incidentally detected; despite a generally low rupture rate for true SAAs, rupture can be catastrophic, with particularly high maternal and fetal mortality in pregnancy. Contemporary expert guidance (SVS 2020; CIRSE 2024) recommends CTA-based diagnosis, aggressive management for pseudoaneurysms (treat regardless of size), and size-/risk-stratified treatment for true SAAs (treat ≥3 cm, symptomatic, enlarging, or in women of childbearing age). Endovascular therapy is generally preferred when anatomically feasible and is associated with lower perioperative morbidity and shorter length of stay, while open surgery remains crucial for rupture, hemodynamic instability, pregnancy-associated rupture, and distal/hilar anatomy. (chaer2020thesocietyfor pages 12-13, chaer2020thesocietyfor pages 13-15, rossi2024cirsestandardsof pages 1-3, hogendoorn2014openrepairendovascular pages 4-5, rinaldi2023endovascularandopen pages 1-3)

Table (click to expand)
Topic Key points Quantitative data Key sources
Disease definition / identifiers / synonyms Splenic artery aneurysm (SAA) is a dilation of the splenic artery; one review defines SAA as arterial dilation >50% of the normal splenic artery diameter. Distinguish true SAA from splenic artery pseudoaneurysm (SAP/SAPA), which has a much higher rupture risk. Common synonyms: splenic artery aneurysm, SAA, true splenic artery aneurysm; pseudoaneurysm terms: splenic artery pseudoaneurysm, SAP. “Giant” SAA is variably defined, most often ≥5 cm, sometimes >10 cm. Giant SAA definition used in literature: ≥5 cm in 62.5% of articles that specified a cutoff; >10 cm in 37.5%. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (rinaldi2024thedefinitiondiagnosis pages 1-2, rinaldi2024thedefinitiondiagnosis pages 4-6, rinaldi2024thedefinitiondiagnosis pages 7-9)
Epidemiology / frequency SAA is the most common visceral artery aneurysm. Population estimates vary by detection method; frequency has risen with modern imaging. SAAs account for ~60% of visceral/splanchnic aneurysms; reported incidence 0.09% at autopsy and 0.78% on angiography; one older clinical paper cites incidence <0.8%. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Sticco et al., Vascular 2016, DOI: 10.1177/1708538115613703, https://doi.org/10.1177/1708538115613703 (2016) (rinaldi2024thedefinitiondiagnosis pages 7-9, sticco2016acomparisonof pages 1-2)
Sex / age distribution Classic SAA is more common in women, especially multiparous women; giant SAA series show more balanced sex distribution. Diagnosis is usually in adulthood/midlife. Female predominance reported as ~4:1 for common SAA; giant SAA pooled review: 43 males / 39 females, median age 55.79 years. Obara et al., Surgery Today 2020, DOI: 10.1007/s00595-019-01898-3, https://doi.org/10.1007/s00595-019-01898-3 (2020); Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (obara2020currentmanagementstrategies pages 5-7, rinaldi2024thedefinitiondiagnosis pages 1-2)
Rupture risk and mortality True SAA rupture risk is generally low but clinically important because rupture can be catastrophic. Pseudoaneurysms rupture much more often and are treated regardless of size. Common true SAA rupture risk ~2–3%; older review cites ~3% in more recent series (historically ~10%). Pseudoaneurysm rupture risk reported 37–47%; SVS excerpt cites rupture 76.3% for pseudoaneurysm vs 3.1% for true aneurysm. Ruptured SAA mortality up to ~25% overall; older reports cite rupture mortality up to 30% or 36%. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Chaer et al., J Vasc Surg 2020, DOI: 10.1016/j.jvs.2020.01.039, https://doi.org/10.1016/j.jvs.2020.01.039 (2020); Obara et al., Surgery Today 2020, DOI: 10.1007/s00595-019-01898-3, https://doi.org/10.1007/s00595-019-01898-3 (2020); Dave et al., Ann Vasc Surg 2000, DOI: 10.1007/s100169910039, https://doi.org/10.1007/s100169910039 (2000) (rinaldi2024thedefinitiondiagnosis pages 7-9, chaer2020thesocietyfor pages 12-13, chaer2020thesocietyfor pages 13-15, obara2020currentmanagementstrategies pages 5-7, dave2000splenicarteryaneurysm pages 4-5, sticco2016acomparisonof pages 1-2)
Pregnancy-associated risk Pregnancy markedly increases rupture risk and is a major reason for aggressive treatment in women of childbearing age. Rupture often occurs in late pregnancy. Pregnancy accounts for ~20–50% of ruptures in older literature/SVS excerpt; maternal mortality ~70–80%; fetal mortality ~90–95%. Chaer et al., J Vasc Surg 2020, DOI: 10.1016/j.jvs.2020.01.039, https://doi.org/10.1016/j.jvs.2020.01.039 (2020); Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Dave et al., Ann Vasc Surg 2000, DOI: 10.1007/s100169910039, https://doi.org/10.1007/s100169910039 (2000) (chaer2020thesocietyfor pages 12-13, rinaldi2024thedefinitiondiagnosis pages 7-9, dave2000splenicarteryaneurysm pages 4-5)
Portal hypertension / liver transplant association Portal hypertension, cirrhosis, and liver transplantation are recurring associations and influence management because of higher rupture/growth concern. Older review: portal hypertension present in up to 24% of SAA patients; incidence in cirrhosis/portal hypertension 7–20%; 8–13% of liver-transplant candidates have SAA. Another review cites 20.5% in liver-transplant recipients. Dave et al., Ann Vasc Surg 2000, DOI: 10.1007/s100169910039, https://doi.org/10.1007/s100169910039 (2000); Obara et al., Surgery Today 2020, DOI: 10.1007/s00595-019-01898-3, https://doi.org/10.1007/s00595-019-01898-3 (2020) (dave2000splenicarteryaneurysm pages 4-5, obara2020currentmanagementstrategies pages 5-7, pratesi2024guidelinesonthe pages 51-53)
Other risk factors / associations Reported associations include multiparity, pancreatitis/pseudocysts, prior surgery, trauma, infection, and nonatherosclerotic arteriopathies such as segmental arterial mediolysis. Pseudoaneurysms are particularly linked to pancreatitis and local inflammatory/surgical injury. Giant SAA/SAP review: pancreatitis/pseudocysts present in 15.85% of pooled giant cases; giant pooled symptoms included pain in 59.76% and asymptomatic presentation in 17.07%. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Rinaldi et al., J Clin Med 2023, DOI: 10.3390/jcm12186085, https://doi.org/10.3390/jcm12186085 (2023) (rinaldi2024thedefinitiondiagnosis pages 4-6, rinaldi2024thedefinitiondiagnosis pages 9-10, rinaldi2023endovascularandopen pages 1-3)
Clinical presentation Most SAAs are asymptomatic and incidentally discovered, but symptomatic lesions usually present with abdominal or left upper quadrant/epigastric pain. Rupture can cause shock and hemoperitoneum. Older review: 80–95% asymptomatic. Giant pooled series: pain 59.76%, palpable mass 28.05%, asymptomatic 17.07%. Dave et al., Ann Vasc Surg 2000, DOI: 10.1007/s100169910039, https://doi.org/10.1007/s100169910039 (2000); Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (dave2000splenicarteryaneurysm pages 4-5, rinaldi2024thedefinitiondiagnosis pages 4-6, rinaldi2024thedefinitiondiagnosis pages 9-10)
Diagnostic imaging CTA is the preferred initial diagnostic test in most guidelines; MRA is preferred when iodinated contrast is contraindicated and is favored in pregnancy. Angiography is used when planning intervention or when noninvasive imaging is insufficient. Ultrasound/EcoColorDoppler can be first-line screening, but sensitivity for small SAA is limited. CT used in 80.49% of giant pooled cases; selective angiography 54.88%; EcoColorDoppler 45.12%; MRI 3.66%. SVS excerpt notes ultrasound has poor sensitivity for SAA <3 cm. Chaer et al., J Vasc Surg 2020, DOI: 10.1016/j.jvs.2020.01.039, https://doi.org/10.1016/j.jvs.2020.01.039 (2020); Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (chaer2020thesocietyfor pages 12-13, rinaldi2024thedefinitiondiagnosis pages 9-10, rinaldi2024thedefinitiondiagnosis pages 4-6)
SVS 2020 treatment thresholds Treat ruptured SAAs emergently; treat all splenic artery pseudoaneurysms regardless of size; treat all true SAAs in women of childbearing age regardless of size; treat true SAAs that are symptomatic, enlarging, or ≥3 cm. Observation is reasonable for small, stable, asymptomatic true SAAs in non-childbearing patients or those with limited life expectancy. Endovascular therapy is preferred initially when anatomically feasible; open surgery is favored for rupture, pregnancy-related rupture, or distal/hilar lesions. Thresholds: pseudoaneurysm any size; true SAA in women of childbearing age any size; true SAA ≥3 cm; interval growth >0.5 cm/year is an indication. Nonoperative series cited by SVS: mean observed size 2.1 cm, mean follow-up 75 months. Chaer et al., J Vasc Surg 2020, DOI: 10.1016/j.jvs.2020.01.039, https://doi.org/10.1016/j.jvs.2020.01.039 (2020) (chaer2020thesocietyfor pages 13-15, chaer2020thesocietyfor pages 12-13)
CIRSE 2024 thresholds / surveillance Intervene for any symptomatic VAA/VAPA; for SAA specifically, treat asymptomatic lesions ≥2 cm, especially if saccular/distal/favorable anatomy; treat any VAA growing ≥0.5 cm/year; treat VAPAs regardless of symptoms; treat any asymptomatic VAA in women of childbearing age. After endovascular therapy, CTA or MRA surveillance is recommended. Thresholds: SAA ≥2 cm; growth ≥0.5 cm/year. Surveillance after EVT: 3 months, 12 months, then yearly. Rossi et al., Cardiovasc Intervent Radiol 2024, DOI: 10.1007/s00270-023-03620-w, https://doi.org/10.1007/s00270-023-03620-w (2024) (rossi2024cirsestandardsof pages 1-3)
Other 2024 guideline / review excerpts 2024 guidance excerpts broadly support emergency treatment for rupture and symptomatic lesions; observation for stable asymptomatic SAAs <3 cm; intervention for SAAs >3 cm. Some sources advocate treatment at ≥2 cm in pregnant/fertile patients with portal hypertension or those awaiting liver transplant. Usual cutoffs in 2024 excerpts: observe <3 cm if stable; treat >3 cm electively; lesions <2 cm often observed unless rapid growth. Pratesi et al. guideline excerpt (2024) (pratesi2024guidelinesonthe pages 51-53); Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (rinaldi2024thedefinitiondiagnosis pages 9-10)
Endovascular treatment Endovascular therapy is now generally first-line for elective anatomically suitable SAAs. Techniques include coil embolization, sac/parent-artery embolization, plugs, covered stents/stent-grafts, glue/Lipidol, thrombin, stent-assisted coiling. Advantages include shorter length of stay and lower perioperative morbidity; drawbacks include splenic infarction, post-embolization syndrome, and higher reintervention risk in rupture. Giant SAA pooled review: endovascular complication rate 23.08%, mean LOS 2.36 days, no recanalization during median follow-up 17.28 months. Stent-graft review: immediate technical/clinical success 90.2%, splenic infarction 4.9%, aneurysm exclusion 87.8%, no reinterventions. Wang 2024 cohort (63 pts): postembolization syndrome 10 pts; splenic infarction 7 pts; mean LOS 5.5 days; complete thrombosis in all at mean 17.2 months. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Borghese et al., J Clin Med 2024, DOI: 10.3390/jcm13102802, https://doi.org/10.3390/jcm13102802 (2024); Wang et al., CVIR Endovasc 2024, DOI: 10.1186/s42155-024-00427-9, https://doi.org/10.1186/s42155-024-00427-9 (2024) (rinaldi2024thedefinitiondiagnosis pages 1-2, rinaldi2024thedefinitiondiagnosis pages 6-7)
Open surgery Open repair remains important for ruptured SAAs, hemodynamic instability, pregnancy-associated rupture, and distal/hilar aneurysms where splenic preservation may not be feasible. Procedures include ligation, aneurysmectomy, splenectomy ± distal pancreatectomy, and selective reconstruction. Giant pooled review: open complication rate 14.89%, mean LOS 12.29 days. In nationwide inpatient comparison, open repair had higher cardiac (6.9% vs 2.3%), pulmonary (16.1% vs 8.9%), and SSI (5.1% vs 0.6%) complication rates and longer LOS (6 vs 4 days), with similar in-hospital mortality (3% both) compared with endovascular repair. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024); Sticco et al., Vascular 2016, DOI: 10.1177/1708538115613703, https://doi.org/10.1177/1708538115613703 (2016) (rinaldi2024thedefinitiondiagnosis pages 1-2, sticco2016acomparisonof pages 1-2)
Hybrid treatment Hybrid approaches are used selectively for anatomically complex giant lesions. Giant pooled review: hybrid used in 9/82 patients (10.98%), complication rate 22.22%, mean LOS 5 days. Rinaldi et al., J Clin Med 2024, DOI: 10.3390/jcm13195793, https://doi.org/10.3390/jcm13195793 (2024) (rinaldi2024thedefinitiondiagnosis pages 1-2, rinaldi2024thedefinitiondiagnosis pages 6-7)
Comparative outcomes: intact/elective SAA Comparative observational data generally favor endovascular repair for lower perioperative morbidity and shorter hospitalization, while open repair may offer fewer reinterventions/stronger primary technical success in some series. Nationwide inpatient study: LOS 4 vs 6 days (EVT vs open), similar mortality 3% each; lower cardiac/pulmonary/SSI complications with EVT. Mixed VAA/RAA series: LOS 7.2±6.9 vs 11.8±6.7 days in elective cases; primary technical success 79.3% EVT vs 100% open. Sticco et al., Vascular 2016, DOI: 10.1177/1708538115613703, https://doi.org/10.1177/1708538115613703 (2016); Wolk et al., Langenbecks Arch Surg 2021, DOI: 10.1007/s00423-021-02149-1, https://doi.org/10.1007/s00423-021-02149-1 (2021) (sticco2016acomparisonof pages 1-2)
Outcomes in ruptured SAA: open vs EVT For ruptured SAA, available evidence shows similar mortality between open and EVT overall, but EVT has substantially more reinterventions/conversions; open repair remains preferred in hemodynamic instability and pregnancy-related rupture. Systematic review of 350 ruptured SAA patients: overall mortality 10.6%; OSR 12.9% vs EVT 7.8% (p=0.84). Reinterventions after EVT 22.4% (37 total; many converted to laparotomy/splenectomy) vs 1.6% after OSR. Rinaldi et al., J Clin Med 2023, DOI: 10.3390/jcm12186085, https://doi.org/10.3390/jcm12186085 (2023) (rinaldi2023endovascularandopen pages 1-3)

Table: This table summarizes high-yield, evidence-supported facts on splenic artery aneurysm, including epidemiology, major risk factors, imaging, guideline thresholds, and treatment outcomes. It is designed as a compact reference for disease knowledge-base curation and clinical/research synthesis.

1. Disease information

1.1 Overview / definition

1.2 Key identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

  • Data gap in retrieved corpus: The provided full-text/guideline excerpts did not include explicit OMIM/Orphanet/MeSH/ICD-10/ICD-11/MONDO identifiers. This report therefore cannot cite authoritative codes from the current evidence set.

1.3 Synonyms / alternative names

1.4 Evidence provenance (individual patients vs aggregated resources)

Most available evidence for SAA derives from aggregated disease-level sources such as guidelines, systematic reviews/meta-analyses, and retrospective series; the rarity and heterogeneity of SAA limit randomized evidence. (marone2023currentdebatesin pages 1-4, hogendoorn2014openrepairendovascular pages 4-5)

2. Etiology

2.1 Disease causal factors (mechanistic)

SAA is a multifactorial vascular disease driven by arterial wall vulnerability and hemodynamic stress.

2.2 Risk factors (clinical associations)

2.3 Protective factors

  • Data gap: No protective genetic variants or environmental protective factors were identified in the retrieved evidence. One 2024 guideline excerpt notes debate on whether arterial wall calcification is protective, but does not resolve it with quantitative evidence in the excerpt. (pratesi2024guidelinesonthe pages 51-53)

2.4 Gene–environment interactions

  • Data gap: No gene–environment interaction studies were present in the retrieved corpus.

3. Phenotypes

3.1 Core clinical phenotypes (with suggested HPO terms)

A. Asymptomatic/incidental detection (common in non-giant SAAs) * Older review: 80–95% asymptomatic and incidentally found. (dave2000splenicarteryaneurysm pages 4-5) * Giant series differs: only 17.07% asymptomatic. (rinaldi2024thedefinitiondiagnosis pages 4-6) * Suggested HPO: Asymptomatic (HP:0000007).

B. Abdominal pain (most common symptom in giant lesions) * Giant pooled review: pain in 59.76% (left upper quadrant/epigastric common). (rinaldi2024thedefinitiondiagnosis pages 4-6) * Suggested HPO: Abdominal pain (HP:0002027); Left upper quadrant abdominal pain (HP:0025404, if used);

C. Palpable abdominal mass (giant lesions) * Giant pooled review: palpable mass 28.05%. (rinaldi2024thedefinitiondiagnosis pages 4-6) * Suggested HPO: Abdominal mass (HP:0003270).

D. Rupture phenotype: hemorrhage and shock * Ruptured SAA commonly presents with severe abdominal pain, hypotension/hemorrhagic shock, anemia/coagulopathy; emergent CTA used for diagnosis. (rinaldi2023endovascularandopen pages 1-3) * Suggested HPO: Hemorrhagic shock (HP:0001919); Hypotension (HP:0002615); Anemia (HP:0001903).

3.2 Temporal phenotype notes

3.3 Quality of life impact

4. Genetic / molecular information

4.1 Causal genes / pathogenic variants

4.2 Syndromic/associative conditions (non-exhaustive, from retrieved evidence)

Kaya et al. list associated conditions including collagen vascular disease, arteritis, medial fibrodysplasia, and alpha-1 antitrypsin deficiency, but do not provide gene/variant-level data in the excerpt. (kaya2016prevalenceandpredictive pages 5-6)

4.3 Epigenetics / omics

  • Data gap: No epigenomic, transcriptomic, proteomic, or metabolomic signatures were identified in the retrieved corpus.

5. Environmental information

5.1 Environmental, lifestyle, occupational

  • Not specifically characterized for SAA in the retrieved evidence.

5.2 Infectious agents

  • Infection is cited as a potential cause of pseudoaneurysm via arterial wall injury in the 2024 systematic review (as part of SAP etiology), but no organism-specific data are provided. (rinaldi2024thedefinitiondiagnosis pages 7-9)

6. Mechanism / pathophysiology

6.1 Mechanistic causal chains (upstream → downstream)

A. Portal hypertension-associated true SAA 1. Chronic liver disease → portal hypertension → hyperdynamic splanchnic circulation and increased splenic venous flow (“splenic hyperkinetic state”). (dave2000splenicarteryaneurysm pages 4-5) 2. Hyperkinetic splenic arterial flow increases arterial diameter and wall tension (Laplace law) → progressive wall degeneration → aneurysm formation and increased rupture susceptibility. (kobori1997splenicarteryaneurysms pages 3-4, dave2000splenicarteryaneurysm pages 4-5) 3. Clinical manifestation: incidental aneurysm or rupture with hemoperitoneum/shock. (dave2000splenicarteryaneurysm pages 4-5, rinaldi2023endovascularandopen pages 1-3)

B. Pregnancy-associated SAA rupture risk 1. Pregnancy → elevated estrogen/progesterone/relaxin and other hormonal mediators → structural weakening (fragmented internal elastic lamina, subendothelial thickening) and altered elastin integrity. (rinaldi2024thedefinitiondiagnosis pages 7-9, dave2000splenicarteryaneurysm pages 4-5) 2. Concurrent late-pregnancy hemodynamic stress (increased blood volume/cardiac output, increased BP) → increased wall stress → rupture risk. (rinaldi2024thedefinitiondiagnosis pages 7-9)

C. Pancreatitis-associated splenic artery pseudoaneurysm (SAP) 1. Acute/chronic pancreatitis or pseudocyst → enzymatic/inflammatory injury to arterial wall or focal disruption → pseudoaneurysm formation. (rinaldi2024thedefinitiondiagnosis pages 7-9, uy2017vasculardiseasesof pages 4-5) 2. Clinical manifestation: hemorrhage, GI bleeding (e.g., hemosuccus pancreaticus), hemodynamic instability. (obara2020currentmanagementstrategies pages 5-7)

D. Segmental arterial mediolysis (SAM) leading to SAA 1. SAM: segmental medial lysis with smooth muscle loss → gaps/dissecting hematoma → aneurysmal dilation. (lohr2013rapidprogressionof pages 2-3) 2. Superimposed hemodynamic stress (BP surges; portal hypertension increasing inflow) → expansion/rupture. (lohr2013rapidprogressionof pages 2-3, imai2005berrysplenicartery pages 4-5)

6.2 Suggested ontology terms

7. Anatomical structures affected

7.1 Primary anatomy (with suggested UBERON terms)

7.2 Tissue/cell and subcellular

8. Temporal development

8.1 Onset

8.2 Progression

  • Many small, stable true SAAs show minimal growth in observed cohorts; SVS excerpt summarizes mean observed size ~2.1 cm with mean follow-up 75 months in a nonoperative Mayo Clinic series. (chaer2020thesocietyfor pages 12-13)

8.3 Critical periods

9. Inheritance and population

9.1 Epidemiology (general population)

9.2 Portal hypertension / cirrhosis / transplant populations

  • Liver transplant candidates/recipients: Kóbori et al. (1997) found SAA in 45/337 (13%) liver transplant patients; incidence 16% among those with portal hypertension and 0% without portal hypertension (p<0.001), with higher incidence in adults (17%) vs children (4%). (kobori1997splenicarteryaneurysms pages 2-3)
  • Cirrhosis cohort: Kaya et al. (2016) found SAA in 27/171 (15.7%) cirrhosis patients on four-phase CT; most were distal (74%), solitary (88.8%), and small (mean diameter 11.66 mm). (kaya2016prevalenceandpredictive pages 1-2)

9.3 Sex ratio / age distribution

9.4 Inheritance

  • No Mendelian inheritance pattern is supported by the retrieved evidence for isolated SAA.

10. Diagnostics

10.1 Imaging (core diagnostic modality)

SVS 2020 (key points from excerpt): * CTA recommended as initial diagnostic tool for SAA (thin sections if available). (chaer2020thesocietyfor pages 12-13) * MRA recommended when iodinated contrast is contraindicated; arteriography reserved for unclear noninvasive results or when planning endovascular therapy. (chaer2020thesocietyfor pages 12-13) * Ultrasound has poor sensitivity for SAA <3 cm in SVS excerpt. (chaer2020thesocietyfor pages 12-13)

Giant SAA/SAP imaging patterns (2024 systematic review): CT used in 80.49%, angiography in 54.88%, EcoColorDoppler in 45.12%, MRI rarely (3.66%). (rinaldi2024thedefinitiondiagnosis pages 4-6)

10.2 Laboratory / biomarkers

  • No specific laboratory biomarkers for diagnosis were identified in the retrieved corpus.

10.3 Differential diagnosis

  • Not systematically enumerated in the retrieved excerpts; pseudoaneurysm vs true aneurysm distinction is clinically crucial because pseudoaneurysm rupture risk is much higher. (chaer2020thesocietyfor pages 13-15)

10.4 Screening

11. Outcome / prognosis

11.1 Natural history and rupture outcomes

11.2 Pregnancy-related prognosis

11.3 Prognostic factors

12. Treatment

12.1 Guideline-driven treatment thresholds (expert consensus)

SVS 2020 (Journal of Vascular Surgery; published Jul 2020; DOI: 10.1016/j.jvs.2020.01.039): * Treat ruptured SAA emergently. (chaer2020thesocietyfor pages 12-13) * Treat splenic artery pseudoaneurysms of any size (high rupture risk). (chaer2020thesocietyfor pages 12-13) * Treat all true SAAs in women of childbearing age regardless of size. (chaer2020thesocietyfor pages 12-13) * Treat true SAAs ≥3 cm, those with growth, or those that are symptomatic. (chaer2020thesocietyfor pages 12-13) * Observation suggested for small (<3 cm), stable, asymptomatic true SAAs or patients with limited life expectancy. (chaer2020thesocietyfor pages 12-13)

CIRSE Standards of Practice (Cardiovascular and Interventional Radiology; Nov 2024; DOI: 10.1007/s00270-023-03620-w): * Treat any symptomatic VAA/VAPA; treat SAA ≥2 cm (particularly saccular/distal/favorable anatomy); treat lesions growing ≥0.5 cm/year; treat VAPAs regardless of symptoms; treat asymptomatic VAAs in women of child-bearing age. (rossi2024cirsestandardsof pages 1-3) * Post-endovascular surveillance suggested with CTA/MRA at 3 months, 12 months, then yearly. (rossi2024cirsestandardsof pages 1-3)

Guideline-collision commentary (May 2023; DOI: 10.3390/jcm12093267): * Notes discrepancies across ESVS vs SVS thresholds (e.g., SVS 3 cm threshold for SAA) and differences in surveillance intervals (SVS annual imaging vs ESVS every 2–3 years for small asymptomatic aneurysms). (marone2023currentdebatesin pages 1-4)

12.2 Endovascular treatment (current applications / real-world implementation)

MAXO suggestions (non-exhaustive): * Endovascular embolization procedure; stent-graft placement; aneurysm repair (endovascular). (chaer2020thesocietyfor pages 13-15, rossi2024cirsestandardsof pages 1-3)

12.3 Open surgery

MAXO suggestions: * Aneurysmectomy; arterial ligation; splenectomy; distal pancreatectomy (for select hilar lesions). (rinaldi2024thedefinitiondiagnosis pages 6-7, chaer2020thesocietyfor pages 13-15)

12.4 Treatment outcomes in ruptured SAA

13. Prevention

13.1 Primary prevention

  • No established primary prevention interventions were identified in the retrieved evidence; prevention focuses on risk recognition (pregnancy/portal hypertension) and addressing modifiable contributors to pancreatitis/trauma when applicable.

13.2 Secondary prevention (surveillance)

14. Other species / natural disease

  • Data gap: No veterinary or non-human natural disease evidence was identified in the retrieved corpus.

15. Model organisms

  • Data gap: No model organism systems specific to SAA were identified in the retrieved corpus.

Recent developments and expert analysis (2023–2024 emphasis)

  1. Guideline harmonization and persistent evidence gaps (2023): A 2023 expert commentary highlights how rarity and heterogeneity impede high-level evidence and lead to threshold/surveillance disagreements across SVS vs ESVS, emphasizing the need for careful individualized decision-making. (marone2023currentdebatesin pages 1-4)
  2. Endovascular standardization (2024): CIRSE’s 2024 standards codify endovascular indications, device options, and structured post-procedure surveillance schedules, reflecting the central role of interventional radiology in contemporary care. (rossi2024cirsestandardsof pages 1-3)
  3. Refined characterization of giant SAA/SAP (2024): The 2024 systematic review quantifies presentation patterns, imaging choices (CT predominance), and comparative LOS/complication rates across open/endovascular/hybrid approaches for giant lesions, while underscoring inconsistent “giant” definitions. (rinaldi2024thedefinitiondiagnosis pages 1-2, rinaldi2024thedefinitiondiagnosis pages 4-6)

Clinical trials / research in progress

  • NCT07053605 (ClinicalTrials.gov; first posted 2025-07-08; recruiting): single-group interventional study of laparoscopic resection of SAA with spleen preservation; estimated enrollment 10; start 2025-06-23; primary completion 2027-06-30; primary outcomes emphasize immune function markers (C3/C4, immunoglobulins, lymphocyte subsets) across follow-up timepoints. URL: https://clinicaltrials.gov/study/NCT07053605 (NCT07053605 chunk 1)
  • NCT01387828 (ClinicalTrials.gov; posted 2011; completed): randomized parallel trial comparing open vs laparoscopic splenic aneurysm repair; enrollment 29; start Jan 2001; completion Apr 2011; primary outcome postoperative morbidity (Dindo–Clavien). URL: https://clinicaltrials.gov/study/NCT01387828 (NCT01387828 chunk 1)

Key limitations of this report (evidence availability)

  • Formal MeSH/ICD/ICD-11/MONDO/OMIM/Orphanet identifiers were not present in the retrieved full-text excerpts; therefore, codes are not provided with citations.
  • Genetic variant-level evidence, multi-omics profiling, model organism data, and validated QoL metrics were not found in the retrieved evidence set; the literature here is predominantly clinical and procedural.
  • The report necessarily integrates older landmark sources (e.g., 1997–2000) for portal-hypertension/pregnancy epidemiology because those specific quantitative observations are widely cited and remain foundational; they are contextualized by 2020–2024 guideline syntheses.

References

  1. (chaer2020thesocietyfor pages 12-13): Rabih A. Chaer, Christopher J. Abularrage, Dawn M. Coleman, Mohammad H. Eslami, Vikram S. Kashyap, Caron Rockman, and M. Hassan Murad. The society for vascular surgery clinical practice guidelines on the management of visceral aneurysms. Journal of Vascular Surgery, 72:3S-39S, Jul 2020. URL: https://doi.org/10.1016/j.jvs.2020.01.039, doi:10.1016/j.jvs.2020.01.039. This article has 660 citations and is from a domain leading peer-reviewed journal.

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