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ABDOMINAL AORTIC
ANEURYSM
EPIGASTRIC LUMP
AN OVRVIEW
Dr.B.Selvaraj MS;Mch;FICS;
“Surgical Educator”
Malaysia
ABDOMINALAORTIC ANEURYSM
 Causes for Epigastric Lumps
 Epidemiology
 Risk factors
 Etiopathogenesis
 Natural history
 Clinical Features
 Investigations
 Treatment
 Complications
 Ruptured AAA
 Mindmap
 Treatment algorithm
OBJECTIVES
Causes For Epigastric Lumps
 Epigastric/Omental hernia
 Pancreatic tumor/Cyst including pseudocyst
 Gastric Carcinoma
 GIST- Gastro-Intestinal Stromal Tumors
 AAA- Abdominal Aortic Aneurysm
 Retroperitoneal Sarcoma
 Hepatomegaly
ABDOMINALAORTIC ANEURYSM
 Aneurysm—permanent focal dilation of an
artery to at least 1.5 times of its diameter
 A normal adult male has an aorta that is
approximately 2 cm in size (anything >3 cm is
considered abnormal).
 Arterial dilation less than 50% increase in
diameter is called vascular ectasia
 Diffuse enlargement of several arterial
segments that are 50% greater than the
normal diameter is called arteriomegaly
Epidemiology
 Abdominal aortic aneurysm (AAA) is the most
common type of aneurysm for which patients
present for treatment.
 Male/female ratio of 3:1
 Relative risk for first-degree relatives of
affected individuals is 11.6 times greater than
the general population.
 Those with known popliteal or femoral
aneurysms have a 50% likelihood of also
having an AAA.
ABDOMINALAORTIC ANEURYSM
Acquired factors:
 Cigarette smoking—strongest modifiable
risk factor
 Hypertension
 Age greater than 50 years old
 Heart transplant recipient
Risk Factors
Inherited factors:
 Connective tissue disorders—Marfan
syndrome, type IV Ehlers–Danlos
 First-degree relative with an AAA
Abdominal Aortic Aneurysm
 Causitive factors:
 Arterial wall degeneration from
atherosclerosis with concurrent loss of
elastin caused by proteolysis and
inflammation leads to a fusiform (spindle-
shaped) aneurysm.
 An infectious process in the arterial wall
leads to a mycotic aneurysm. Caused by
Salmonella or Staphylococcal infection
Etiopathogenesis
Pathology:
 Location:
 Infra renal 95%
 Juxtarenal- extends to renal arteries
 Supra renal-extends to Superior mesenteric
artery & coeliac axis
 Thoraco-abdominal
 10 to 20% involves iliac arteries
 40% are hypertensive
 30% are CAD patients
 4% femoral or popliteal aneurysms
Abdominal Aortic Aneurysm
GENERAL CONSIDERATIONS:
 Diameter is the strongest predictor of
rupture
 Increased size = increased rate of rupture
Laplace law—A larger radius increases wall
tension, which in turn increases the
risk for rupture of the aneurysmal wall.
 Average growth is 0.4 cm/year.
 Growth is often staggered, and an aneurysm
may be stable for one period and then grow
rapidly in another period.
NATURAL
HISTORY
STATISTICS:
 Risk of rupture is based on size
 Women have a higher rate of rupture at
smaller diameters.
 Renal artery involvement, chronic
obstructive pulmonary disease, and diastolic
hypertension also increase the rate of
rupture.
RISK OF RUPTURE BASED ON SIZE:
AAA Diameter (cm) Risk of Rupture per Year
<4= 0
4–5= 0.5–5
5–6= 3–15
6–7= 10–20
7–8= 20–40
>8 =30–50
Abdominal Aortic Aneurysm
SYMPTOMS:
 Most AAAs are asymptomatic
 Two-thirds of known AAAs are incidental
findings on imaging studies done for other
reasons
 Most common symptoms include new-onset
abdominal pain and low back pain. May also
present as flank, inguinal, or genital pain.
 Symptoms may be caused by compression of
surrounding structures— inferior vena
cava, ureter, duodenum.
 If ruptured AAA patient present with shock
Triad of severe abdominal pain, hypotension
and pulsatile abdominal mass.
CLINICAL
FEATURES
SIGNS:
 Presence of pulsatile mass on deep
palpation—larger than 5-cm aneurysm
palpable in up to 75% of patients
 In larger patients, it may be impossible to
detect AAAs regardless of diameter.
 Other pulses: It is important to evaluate
peripheral arteries for associated occlusive
disease (pulses and bruits) or additional
aneurysmal disease.
 In ruptured AAA features of shock
Abdominal Aortic Aneurysm
Plain AXR:
 Calcific rim (“eggshell”) or large soft-tissue
shadow is often visible projecting anterior to
the spine.
INVESTIGATIONS
B-MODE ULTRASOUND:
 Screening imaging test of choice because of ease of
use and most cost effective
 Can evaluate blood flow in renal and visceral arteries
 Because of presence of gas couldn’t pick up
suprarenal AAA.
Abdominal Aortic Aneurysm
CECT SCAN:
 Can provide accurate characterization of entire
aorta—gold standard for preoperative planning
and diagnosis of a ruptured AAA
 Permits assessment of diameter, length, wall
thickness, and thrombus
 3D reconstruction used for endograft evaluation
and planning
INVESTIGATIONS
MRI SCAN:
 May have a role in patients in whom intravenous
contrast is contraindicated
 No role in ruptured patients, given the length of
time needed to complete the examination
Abdominal Aortic Aneurysm
AORTOGRAPHY:
 Poor study for diagnosis or assessment of size,
because mural thrombus within AAA can obscure
actual aneurysm sac size
 Expensive and invasive
 Being replaced by CT and MRI angiograms that
provide noninvasive three-dimensional images
 Provides information regarding associated
vascular lesions for renal arteries and distal runoff
 Indications for aortography—evidence of accessory
renal arteries, horseshoe kidneys, mesenteric
ischemia, and peripheral arterial occlusive disease
INVESTIGATIONS
DSA: CT Angiogram
Abdominal Aortic Aneurysm
OPEN REPAIR:
 Uses a synthetic (Dacron) graft to
repair aneurysm.
 Long midline incision
(laparotomy).
 Aorta clamped below renal
arteries where possible to prevent
renal ischaemia.
 Graft can be straight if iliac
arteries not involved or bifurcated
if iliac arteries involved.
 3-7% mortality
TREATMEN
T
Abdominal Aortic Aneurysm
Endovascular aneurysm repair (EVAR):
 Insertion of a stent over aneurysmal
segment
 Small groin incisions (may be vertical or
transverse)
 Does not require cross clamping of aorta
 Procedure carried out under direct
radiological guidance.
 Uses high doses of nephrotoxic contrast.
 Reduced early mortality.
 High early re-intervention rate if
endoleak occurs.
 Requires lifelong surveillance post-op for
endoleak.
TREATMEN
T
Abdominal Aortic Aneurysm
EARLY:
 Death
 Haemorrhage- uncontrolled vessels or anastomotic
breakdown
 Myocardial ischaemia- 20% of patients
 Cardiac arrhythmias.
 Cardiac failure
 Bowel ischaemia- characterized by abdominal
pain, and bloody diarrhoea. Urgent laparotomy if
evidence of peritonitis
 Abdominal compartment syndrome
 Atelectasis, ARDS, RTI
 Endoleak (EVAR)
 Renal dysfunction- pre-existing renal disease,
nephrotoxic contrast/antibiotics, prolonged
hypotension/ dehydration, use of NSAIDs
 Limb ischemia
COMPLICATIONS
LATE:
 Graft infection- usually needs to be removed.
 Graft limb occlusion- within 30 days, may present
with acute ischaemic limb.
 Aortoenteric fistula
 Endoleak (EVAR)
 Impaired sexual function
 Endoleak: An endoleak is persistent blood flow
into an aneurysmal sac after EVAR is performed.
Type I Leak at attachment sites of graft
Type II Filling of aneurysmal sac by collateral vessels (IMA,
Lumbar)
Type III Leak through defect in graft
Type IV Leak through fabric of graft due to porosity
Type V Expansion of aneurysm sac without evidence of leak
on imaging
Abdominal Aortic Aneurysm
Clinical Features:
 Presentation may be delayed if rupture is
contained within retroperitoneal space.
 A contained leak may initially be
haemodynamically stable but can proceed rapidly
to rupture.
 Longstanding leak causing aortoenteric fistula can
present with high output cardiac failure and GI
bleed.
 Sudden onset abdominal/back/flank pain.
 Sudden collapse with hypotension.
 May have a history of AAA under surveillance.
 Pulsatile abdominal mass is not always palpable
 Triad of severe abdominal pain, hypotension and
pulsatile abdominal mass
RUPTURED
Management:
 Airway
 Breathing (give 15L 100% O2 via non-rebreather
mask)
 Circulation (Wide bore IV Access X2, give IV
Fluids)
 Do not aggressively hydrate: Allow permissive
hypotension to avoid worsening a rupture
 Analgesia
 Alert vascular surgeon, anaesthetist, theatre, ICU
 Gain consent for surgery
 If not a candidate for surgery: analgesia &
palliative care
 If a candidate for open/endovascular repair:
Urgent transfer to theatre
 ICU care post-op
ABDOMINALAORTIC ANEURYSM
Mindmap
ABDOMINALAORTIC ANEURYSM
Treatment Algorithm
UNRUPTURED RUPTURED
Peripheral Arterial Diseases(PAD)

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ABDOMINAL AORTIC ANEURYSM- EPIGASTRIC LUMPS- Abdominal Lumps.pptx

  • 1. ABDOMINAL AORTIC ANEURYSM EPIGASTRIC LUMP AN OVRVIEW Dr.B.Selvaraj MS;Mch;FICS; “Surgical Educator” Malaysia
  • 2. ABDOMINALAORTIC ANEURYSM  Causes for Epigastric Lumps  Epidemiology  Risk factors  Etiopathogenesis  Natural history  Clinical Features  Investigations  Treatment  Complications  Ruptured AAA  Mindmap  Treatment algorithm OBJECTIVES
  • 3. Causes For Epigastric Lumps  Epigastric/Omental hernia  Pancreatic tumor/Cyst including pseudocyst  Gastric Carcinoma  GIST- Gastro-Intestinal Stromal Tumors  AAA- Abdominal Aortic Aneurysm  Retroperitoneal Sarcoma  Hepatomegaly
  • 4. ABDOMINALAORTIC ANEURYSM  Aneurysm—permanent focal dilation of an artery to at least 1.5 times of its diameter  A normal adult male has an aorta that is approximately 2 cm in size (anything >3 cm is considered abnormal).  Arterial dilation less than 50% increase in diameter is called vascular ectasia  Diffuse enlargement of several arterial segments that are 50% greater than the normal diameter is called arteriomegaly Epidemiology  Abdominal aortic aneurysm (AAA) is the most common type of aneurysm for which patients present for treatment.  Male/female ratio of 3:1  Relative risk for first-degree relatives of affected individuals is 11.6 times greater than the general population.  Those with known popliteal or femoral aneurysms have a 50% likelihood of also having an AAA.
  • 5. ABDOMINALAORTIC ANEURYSM Acquired factors:  Cigarette smoking—strongest modifiable risk factor  Hypertension  Age greater than 50 years old  Heart transplant recipient Risk Factors Inherited factors:  Connective tissue disorders—Marfan syndrome, type IV Ehlers–Danlos  First-degree relative with an AAA
  • 6. Abdominal Aortic Aneurysm  Causitive factors:  Arterial wall degeneration from atherosclerosis with concurrent loss of elastin caused by proteolysis and inflammation leads to a fusiform (spindle- shaped) aneurysm.  An infectious process in the arterial wall leads to a mycotic aneurysm. Caused by Salmonella or Staphylococcal infection Etiopathogenesis Pathology:  Location:  Infra renal 95%  Juxtarenal- extends to renal arteries  Supra renal-extends to Superior mesenteric artery & coeliac axis  Thoraco-abdominal  10 to 20% involves iliac arteries  40% are hypertensive  30% are CAD patients  4% femoral or popliteal aneurysms
  • 7. Abdominal Aortic Aneurysm GENERAL CONSIDERATIONS:  Diameter is the strongest predictor of rupture  Increased size = increased rate of rupture Laplace law—A larger radius increases wall tension, which in turn increases the risk for rupture of the aneurysmal wall.  Average growth is 0.4 cm/year.  Growth is often staggered, and an aneurysm may be stable for one period and then grow rapidly in another period. NATURAL HISTORY STATISTICS:  Risk of rupture is based on size  Women have a higher rate of rupture at smaller diameters.  Renal artery involvement, chronic obstructive pulmonary disease, and diastolic hypertension also increase the rate of rupture. RISK OF RUPTURE BASED ON SIZE: AAA Diameter (cm) Risk of Rupture per Year <4= 0 4–5= 0.5–5 5–6= 3–15 6–7= 10–20 7–8= 20–40 >8 =30–50
  • 8. Abdominal Aortic Aneurysm SYMPTOMS:  Most AAAs are asymptomatic  Two-thirds of known AAAs are incidental findings on imaging studies done for other reasons  Most common symptoms include new-onset abdominal pain and low back pain. May also present as flank, inguinal, or genital pain.  Symptoms may be caused by compression of surrounding structures— inferior vena cava, ureter, duodenum.  If ruptured AAA patient present with shock Triad of severe abdominal pain, hypotension and pulsatile abdominal mass. CLINICAL FEATURES SIGNS:  Presence of pulsatile mass on deep palpation—larger than 5-cm aneurysm palpable in up to 75% of patients  In larger patients, it may be impossible to detect AAAs regardless of diameter.  Other pulses: It is important to evaluate peripheral arteries for associated occlusive disease (pulses and bruits) or additional aneurysmal disease.  In ruptured AAA features of shock
  • 9. Abdominal Aortic Aneurysm Plain AXR:  Calcific rim (“eggshell”) or large soft-tissue shadow is often visible projecting anterior to the spine. INVESTIGATIONS B-MODE ULTRASOUND:  Screening imaging test of choice because of ease of use and most cost effective  Can evaluate blood flow in renal and visceral arteries  Because of presence of gas couldn’t pick up suprarenal AAA.
  • 10. Abdominal Aortic Aneurysm CECT SCAN:  Can provide accurate characterization of entire aorta—gold standard for preoperative planning and diagnosis of a ruptured AAA  Permits assessment of diameter, length, wall thickness, and thrombus  3D reconstruction used for endograft evaluation and planning INVESTIGATIONS MRI SCAN:  May have a role in patients in whom intravenous contrast is contraindicated  No role in ruptured patients, given the length of time needed to complete the examination
  • 11. Abdominal Aortic Aneurysm AORTOGRAPHY:  Poor study for diagnosis or assessment of size, because mural thrombus within AAA can obscure actual aneurysm sac size  Expensive and invasive  Being replaced by CT and MRI angiograms that provide noninvasive three-dimensional images  Provides information regarding associated vascular lesions for renal arteries and distal runoff  Indications for aortography—evidence of accessory renal arteries, horseshoe kidneys, mesenteric ischemia, and peripheral arterial occlusive disease INVESTIGATIONS DSA: CT Angiogram
  • 12. Abdominal Aortic Aneurysm OPEN REPAIR:  Uses a synthetic (Dacron) graft to repair aneurysm.  Long midline incision (laparotomy).  Aorta clamped below renal arteries where possible to prevent renal ischaemia.  Graft can be straight if iliac arteries not involved or bifurcated if iliac arteries involved.  3-7% mortality TREATMEN T
  • 13. Abdominal Aortic Aneurysm Endovascular aneurysm repair (EVAR):  Insertion of a stent over aneurysmal segment  Small groin incisions (may be vertical or transverse)  Does not require cross clamping of aorta  Procedure carried out under direct radiological guidance.  Uses high doses of nephrotoxic contrast.  Reduced early mortality.  High early re-intervention rate if endoleak occurs.  Requires lifelong surveillance post-op for endoleak. TREATMEN T
  • 14. Abdominal Aortic Aneurysm EARLY:  Death  Haemorrhage- uncontrolled vessels or anastomotic breakdown  Myocardial ischaemia- 20% of patients  Cardiac arrhythmias.  Cardiac failure  Bowel ischaemia- characterized by abdominal pain, and bloody diarrhoea. Urgent laparotomy if evidence of peritonitis  Abdominal compartment syndrome  Atelectasis, ARDS, RTI  Endoleak (EVAR)  Renal dysfunction- pre-existing renal disease, nephrotoxic contrast/antibiotics, prolonged hypotension/ dehydration, use of NSAIDs  Limb ischemia COMPLICATIONS LATE:  Graft infection- usually needs to be removed.  Graft limb occlusion- within 30 days, may present with acute ischaemic limb.  Aortoenteric fistula  Endoleak (EVAR)  Impaired sexual function  Endoleak: An endoleak is persistent blood flow into an aneurysmal sac after EVAR is performed. Type I Leak at attachment sites of graft Type II Filling of aneurysmal sac by collateral vessels (IMA, Lumbar) Type III Leak through defect in graft Type IV Leak through fabric of graft due to porosity Type V Expansion of aneurysm sac without evidence of leak on imaging
  • 15. Abdominal Aortic Aneurysm Clinical Features:  Presentation may be delayed if rupture is contained within retroperitoneal space.  A contained leak may initially be haemodynamically stable but can proceed rapidly to rupture.  Longstanding leak causing aortoenteric fistula can present with high output cardiac failure and GI bleed.  Sudden onset abdominal/back/flank pain.  Sudden collapse with hypotension.  May have a history of AAA under surveillance.  Pulsatile abdominal mass is not always palpable  Triad of severe abdominal pain, hypotension and pulsatile abdominal mass RUPTURED Management:  Airway  Breathing (give 15L 100% O2 via non-rebreather mask)  Circulation (Wide bore IV Access X2, give IV Fluids)  Do not aggressively hydrate: Allow permissive hypotension to avoid worsening a rupture  Analgesia  Alert vascular surgeon, anaesthetist, theatre, ICU  Gain consent for surgery  If not a candidate for surgery: analgesia & palliative care  If a candidate for open/endovascular repair: Urgent transfer to theatre  ICU care post-op