abdominal aortic aneurysms.pptx GENERALSURGERY

ANEURYSMS

1. Abdominal aortic aneurysms Dr CHANDANA C

2. Anatomy Has 3 layers Tunica intima – consists of endothelium Tunica media – consists of smooth muscle surrounded by elastin, collagen and proteoglycans which are majorly responsible for the elastic properties of arteries Tunica adventitia – mainly collagen along with fibroblasts, immuno modulators cells and adrenergic nerves As we go above downwards from thoracic to abdominal aorta, there is a decrease in diameter, and content/lamellar layers of elastin and collagen

3. Definition Permanent localised focal dilatation of more than 50% of normal expected arterial diameter (measured as antero posterior or transverse diameter in a plane perpendicular to long axis of the artery ) After age 50 years, normal diameter of infra renal aorta is 1.5 cm in women (aorta is smaller in women which is clinically relevant in determining size threshold for intervention ) 1.7 cm in men Hence, an infrarenal aortic diameter of > 3 cm is considered an AAA even if asymptomatic At an age > 65 years, 1.7 % females and 5 % males have infra renal aortic diameter > 3 cm

4. Incidence AAA 9x more common then thoracic aortic aneuryms 30% of AAA are infra renal Predominantly in males showing 3 to 8 %. Being Male increases risk by roughly 6x Females – 0.5 to 1.5 % Incidence in females approaches that of males beyond 80 years age Incidence increases with age but an occur at any decade of life Smokers are 4 times more likely to develop AAA than non smokers and daily smoking intake is more relevant than number of years of smoking upto 30 % of patients with AAA report a family history

5. Who are at risk ? Predominantly males 65 years or older Smokers Hypertension Family history Out of diagnosed AAA 99% were Male and 94 % were white

6. Types of aneurysms True aneurysms - involve all 3 layers of the vessel wall False/ Pseudo aneurysms – focal defect in the artery with collection of blood in between tunica adventitia and peri arterial tissue “wall” is connective tissue formed in reaction to contained hematoma Causes – iatrogenic trauma or loss of anatomic integrity at site of surgical repair

7. Based on anatomy Fusiform aneurysms – smooth circumferential dilatation of arterial wall Saccular aneurysms – focal outpouching of arterial wall

8. Based on etiology Degenerative – Majority of aneurysms are degenerative in nature. Infectious – by haemaogenous seeding or spread from local infective focus Mostly saccular type. All saccular AAA must be evaluated for infective causes candida, aspergillus, mycotic, syphilitic aneurysms Mostly seen in IV drug abusers and immuno compromised patients Difficult to repair as grafts are usually contra indicated and repair is associated with difficult dissection due to inflammation but antibiotic impregnated grafts may be used Inherited – marfan syndrome, vascular type ehler danlos syndrome, familial aortic aneuryms and dissection and presence of family history of aneuryms

9. Based on site

10. Pathophysiology AAA are a result of failure of major structural proteins of aorta I.e elastin and collagen therefore they develop after degeneration of tunica media Proteolytic degeneration of connective tissue Inflammation and immune responses Biomechanical wall stress Molecular genetics Surgical specimens show Inflammation with infiltration by lymphocytes and macrophages Thinning of tunica media Marked loss of elastin

11. Elastin – principal lead bearing element of the aorta which is arranged in concentric layers to withstand arterial pressure. The content and number of elastin layers in the tunica media decreases from thoracic to infrarenal aorta. Hence, the increased incidence of infrarenal aortic aneuryms can be attributed to this Metalloproteinases – matrix metallo proteinases (MMPs) degrade aortic media by proteolytic process. MMPs and their inhibitors present in normal aortic tissue are responsible for vessel wall remodeling. Increased secretion and activity of MMPs and other proteases secreted by macrophages, lymphocytes and aortic smooth muscle cells is seen in aneurysmal tissue. They trigger proteolytic activity via cytokines (IL-1, IL-6, IL-8, TNF-alpha)

12. Atherosclerosis – may induce formation of AAAs by mechanical weakening of aortic wall with loss of elastic recoil, degenerative ischemic changes through obstruction of vasa vasorum Many patients with advanced atherosclerotic disease do not develop AAA and some with no atherosclerosis do. No causative association between the two has been currently established. Therefore atherosclerosis may represent a nonspecific secondary response to vessel wall injury that is induced by multiple factors. Molecular genetics – genetic predisposition has been studied

13. Risk factors Age > 65 Male gender Concurrent aneurysms Family history Smoking Hypertension Hyperlipidemia Female gender, black race and diabetes appear to be protective Males are more likely to present with concurrent aneurysms Females show a higher risk of rupture than males

14. Risk of rupture Most widely accepted risk factor is max cross sectional aneurysm diameter It said that risk of rupture is over estimated in most cases. In patients deemed medically unfit for repair, risk of death from non aneurysmal causes is higher than that of risk of rupture Life expectancy is also considered Rate of growth of aneurysm is also accepted > 5 mm in 6 months (or) > 1 cm per year has been widely accepted as an indication for repair independent of aneurysms size

15. AAA diameter (cm) Rupture risk ( %/yr ) < 4 4 - 5 0.5 - 5 5 - 6 3 - 15 6 - 7 10 - 20 7 - 8 20 - 40 Estimated Annual rupture risk

16. Diagnosis History – most unruptured AAA are asymptomatic Presents as – pain in the abdomen, chest or lower back different in character from usual abdominal or back pain Patient may feel pulsations in his abdomen or see a pulsatile mass in thin indiviuals Peripheral vascular disease if there is intra luminal thrombus Clinical examination - Dependent on aneurysm size ( < 5 cm aneurysm cannot be detected by routine clinical examination) Presents as a palpable pulsatile mass, mostly midline and supra umbilical. Aortic tortuosity can lead to lateral or infra umbilical position Majority of AAA missed if diagnosis is limited to physical examination

17. Ultrasound examination – most often incidentally found here. Investigation of choice for screening Provides excellent sensitivity and specificity Advantages Avoids complications associated with invasive tests, radiation, contrast media IOC for screening as multiple scans can be done Cost effective Disadvantages Not ideal for detecting rupture Cannot image all parts of aorta Not helpful in non fasting status of emergency patients Approx 50% of aneurysm ruptures are not detected by ultrasound imaging Diameter variations according to ultra sonographer

18. CT and CTA – provides excellent imaging with better diameter reproducibility than ultrasound. Advantages Investigation of choice for pre operative planning CTA with iodine contrast detects vessel calcification, thrombus, concurrent arterial occlusive disease Multiplanar and 3D reconstruction is possible which helps with operative planning Surrounding anatomy can be assessed Disadvantages Radiation Extensive radiation exposure with serial examination Contrast related complications

19. MRI and MRA – Advantages Not much advantage compared to CT or CTA provides dynamic images throughout cardiac cycel Disadvantages Does not detect wall calcification Gadolinium is used as contrast agent with renal complications Presence of metallic implants or foreign bodies

20. Screening Investigation of choice for screening is ultrasound According to practice guidelines by the clinical practice council of the society for vascular surgery One time screening of ALL MEN 65 years or older Men 55 years or older with a family history of AAA Women 65 years or older with either a family h/o AAA or a personal smoking history According to US Preventive services task force One time screening of men between 65 – 75 years with a personal smoking history Screening of women remains controversial

21. AAA shows a stronger association with women who have smoked than with men According to clinical practice council of the society for vascular surgery, once an AAA is detected < 2.6 cm No further screening recommended 2.6 – 2.9 cm Re examination at 5 years 3 – 3.4 cm Re examination at 3 years 3.5 – 4.4 cm Re examination at 12 months 4.5 – 5.4 cm Re examination at 6 months

22. Medical treatment Aim – to minimize rate of expansion or rupture To medically prepare the patient for potential repair NO medical therapy can prevent aortic aneurysm growth or rupture Stop smoking Controlling blood pressure Aspirin therapy – secondary preventive benefit where they minimised risk of concurrent cardiac or systemic complications Statins – useful in concurrent atherosclerotic disease

23. Pre operative evaluation Identification and management of medical comorbidities like coronary artery disease, renal insufficiency, peripheral arterial occlusive disease, diabetes, copd. CAD is the primary cause of mortality in patients undergoing AAA repair Hence, American College of Cardiology/ American Heart Association (ACC/AHA) guidelines for pre operative evaluation of patients undergoing non cardiac vascular surgery is used as a gold standard in pre operative workup of patients planned for AAA repair

24. patients are stratified according to presence or absence of symptomatic cardiac disease, presence of significant clinical risk factors, and the patients functional capacity( measured in mets) Resting ECG – not required for low risk surgery in patients with no symptoms or clinical risk factors. Routinely done in all patients undergoing high risk surgery Echocardiography – done in patients with symptoms or patients with clinical risk factors and the patients functional capacity Coronary angiography – symptomatic patients or evidence of active cardiac disease in non invasive testing

25. Adjunctive medical therapy beta blockers, statins, aspirin – recommended use peri operatively in titration with intra operative heart rate and blood pressure according to ACC/AHA focused update on perioperative beta blockade Copd is associated with increased risk of post operative complications and need for ventilator support which must be informed to the patient. Anti coagulants – Vitamin k antagonists must be stopped 5 to 7 days before surgery with bridging anti coagulation with heparin Intra operative renal protection – adequate hydration with sodium bicarbonate or normal saline, perioperative discontinuation of ACE inhibitors and immediate post operative resumption, use of anti oxidants (mannitol, ascorbic acid, vitamin e, n acetyl cysteine, allopurinol) but mainstay in Preventing renal complications is adept surgery with reduced ischemic time and clamping

26. Pre operative workup Blood investigations like cbc, blood chemistries, coagulation studies Pulmonary assessment – pfts, abg Assessment of cardiac status according to ACC/AHA guidleines for mon cardiac vascular surgery Chest radiographs- evidence of infection, thoracic aortic disease, malignant disease Ct imaging – careful evaluation of pre operative imaging for anatomical variations like retro aortic renal vein, variant ivc, horse shoe kidney which can lead to disasters if not appreciated beforehand Ct imaging for vascular calcifications which allows surgeon to assess for feasibility of clamping at various levels.

27. Surgical treatment Recommended for aortic aneurysms with max diameter > 5.5 cm > 5 mm growth in 6 months > 1 cm growth in 1 year Aneurysms of saccular type more than fusiform Females recommended repair at smaller aneurysm sizes due to increased risk of rupture and rapid growth in size associated with female gender Factors like body build, bmi, BSA, can also be considered

28. Surgical repair

29. ADVANTAGES NO DIFFERENCE DISADVANTAGES Under local, spinal or epidural anaesthesia No improvement of quality of life beyond 3months Higher rates of graft related complications Shorter post operative stay avg. 5 days No improvement of survival beyond 2 years Higher rates if need of re intervention Lower 30 day mortality (1.54% vs 4.8%) No significant difference in overall mortality rate Expensive EVAR VS OPEN REPAIR In younger patients, open repair may be a better long term solution if surgically fit Requires frequent ling term follow up

30. Open surgical repair of AAA AAA is permanently eliminated as the entire diseased segment is replaced by a graft Hence risk if rupture or recurrence no longer exists No need of long term surveillance (CT every 5 years) Permits surgeon to assess all surrounding structures Circulatory integrity of colon can be assessed Approach to the operative field is based on technical considerations of both approaches and the surgeons experience and preference

31. Trans peritoneal approach

32. Retro peritoneal approach Disadvantages Increased incidence of persistent postoperative pain, flank wall laxity and hernias Right renal and right iliac arteries not satisfactorily exposed Advantages Fewer postoperative pulmonary complications and postoperative ileus Greater access to visceral segment of aorta which allows full access to decide placement of proximal clamp Allows thoracic extension without division of diaphragm Variety of approaches to juxtarenal, pararenal and para visceral aorta

33. Post operative management Admitted to an ICU Continuous cardio pulmonary monitoring Adequate pain control – epidural analgesia or patient controlled analgesia Adequate oxygenation and resuscitation Heart rate control Prophylaxis for DVT Early mobilization and nutrition Follow up with CT every 5 years

34. Post operative complications Post operative MI DVT Anastamotic and para anastamotic aneurysms Colon ischemia, spinal cord ischemia Renal failure Injury to lungs due to ischemia and reperfusion Abdominal compartment syndrome Lower limb compartment syndrome

35. Endovascular repair (EVAR) According to a study published by agency for healthcare research and quality – “EVAR has shorter length of stay, lower 30 day mortality and morbidity but does not improve quality of life beyond 3 months or survival beyond 2 years” Early morbidity and mortality I.e 0.5 % and 1.54 % respectively with EVAR versus 3 % and 4 % respectively with open repair are seen but a higher rate for re intervention is seen with EVAR No significant difference in overall mortality rate several anatomical considerations dictate patient suitability for EVAR like anatomy of aneurysm neck, condition of iliac arteries

36. Procedure can be performed under local, spinal or epidural anaesthesia The graft typically comprises of 2 components, both inserted on catheters under flouroscopic guidance Main body of the graft – stents the aorta and common iliac artery Contralateral limb – stents contralateral common iliac artery

37. Follow up Recommended that contrast CT surveillance be conducted at intervals of 1 month, 6 months, 1 year, and then annually after graft implantation Accumulated lifetime radiation exposure must be considered as it also includes pre operative investigations Hence, advent of color doppler and contrast enhanced duplex ultrasound has occurred Implnatable sensor technology into the repaired aneurysm to monitor pressure within the sac has been developed

38. Complications Endoleak – 5 types Access related complications – hematoma, pseudo aneurysm, arterial occlusion or dissection, iliac artery rupture or transaction, peripheral embolization Renal insufficiency Local wound complications Renal or hypo gastric artery occlusion Colon or spinal cord ischemia Graft limb occlusion Device migration Device failure

39. Endoleak Most common cause of re intervention after EVAR Type 1 endoleak – Failure to achieve satisfactory proximal or distal seal which means failure to exclude aneurysm sac. Must be addressed at the time of detection on follow up scans with the aim to increase radial force and improve wall apposition Managed by more aggressive balloon inflation inside the seal zone, placement of additional graft components to extend the seal zone, or placement of balloon expandable stents within the seal zone Type 2 endoleak – most common form

40. Type 2 endoleak – most common form Continued filling of aneurysm sac by lumbar branches or IMA Intervention is indicated if there is persistent type 2 endoleak with increase in sac size Managed by – selective embolization of feeding branches, direct sac puncture, open or laparoscopic ligation of feeding branches Pre operatively – max aneurysm sac diameter at the level of IMA and parent lumbar arteries have been associated with persistent type 2 endoleak Type 3 endoleak – failure of individual graft components or seal between components of a modular graft All must be treated at the time of detection Managed with – reliningofffending area with new graft components

41. Type 4 endoleak – seepage through porous graft material Usually self limiting and resolved once operative anti coagulation is reversed Type 5 endoleak – or endotension Persistent growth of aneurysm sac in the absence if a detectable leak or feeding branch Said to be due to seepage of serous fluid through the graft fabric or presence of an other type of endoleak that has not been detected

42. Ruptured AAA It is a medical emergency Presents as a triad of – severe abdominal or back pain, hypotension, pulsatile abdominal mass Nearly half of all patients die before reaching the hospital and the operative mortality for the rest is 45 to 50% Overall mortality is 71 to 77% Can rupture anteriorly into the peritoneal cavity (20%) causing free bleeding into peritoneal cavity or into retro peritoneal space (80%) causing retro peritoneal hematoma

43. If patient is hemodynamically stable, a CT scan is done which shows periaortic stranding, retroperitoneal hematoma and extravasation of IV contrast Management Early clinical diagnosis (history, abdominal or back pain, Pulsatile mass, shock) Immediate resuscitation Permissible hypotension at systolic BP Just above 100 mm Hg Arrange for blood transfusion and rapid transfer to operating theatre Draping and preparation is done prior to induction of anaesthesia as process if induction can cause further hemodynamic instability and waste precious time in resuscitation

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