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25/02/2012

ABDOMINAL AND THORACIC AORTIC ANEURYSMS

DR N. GOVENDER

Commentators: Dr Z. Moolla & Dr T. Mbebe Moderator: Ms A. Ramnarain

In 1948, Dr. Rudolph Nissen, performed an exploratory laparotomy for abdominal pain on Albert Einstein at the Brooklyn Jewish Hospital. A "grapefruit-sized" aortic aneurysm was discovered. During that era, ligation of the abdominal aorta had already proved to be ineffective, and replacing the aorta with a graft was still a decade away. The only available treatment was to attempt to reinforce the aortic wall and delay the inevitable rupture. Dr. Nissen wrapped the visible anterior portion of the aneurysm with cellophane (a tissue irritant), in the hopes of stimulating an intense fibrous tissue reaction that would strengthen the bulging aortic wall. Einstein recovered from the operation after a 3-week hospital stay. On April 12, 1955, Einstein developed worsening abdominal pain. Einstein refused surgery, saying: “I want to go when I want. It is tasteless to prolong life artificially. I have done my share, it is time to go. I will do it elegantly” He demised on April 18, 1955.

DEFINITIONS 1

Aneurys : focal permanent dilatation of an artery more than 1.5 times the normal diameter

The normal infrarenal aortic diameters in patients older than 50 years are[pic] 1.5

cm in women and ±1.7 cm in men.

By convention, an infrarenal aorta ≥ 3-5 cm in diameter is considered aneurismal.

Arteriomegaly: diffuse arterial enlargement with an increase in the diameter more than 50%

of normal.

Ectasia : permanent dilation of an artery of less than 50% of the normal diameter.

Pseudo aneurysm/False aneurysm: is the contained extravasated blood from an arterial wall

disruption and is contained by the adjacent structures. It does not contain all 3 layers of

the vessel wall.

ABDOMINAL AORTIC ANEURYSMS (AAA’S) AETIOLOGY2

|Degenerative |Atherosclerotic, Fibromuscular dysplasia |

|Infective/Mycotic | Bacterial, fungal, syphilis, viral |

|Pseudoaneurysm | Trauma and anastamotic disruption |

|Congenital |Idiopathic |

| |Tuberous sclerosis |

| |Turner’s syndrome |

| |Menke’s syndrome |

| |Persistant sciatic artery |

|Inflammatory |Takayasu’s disease |

| |Behçet’s disease |

| |Kawasaki’s Disease |

| |Polyarteritis Nodosa |

| |Giant cell arteritis |

| |Periarterial(pancreatitis) |

|Connective tissue disorders |Marfan’s syndrome |

| |Ehler’s Danlos syndrome |

| |Cystic medial necrosis |

| |Berry(cerebral) |

|Post dissection |Idiopathic, Cystic Medial necrosis, Trauma |

|Post Stenotic |Thoracic outlet syndrome, Coarctation |

|Miscellaneous |Pregnancy induced, Inflammatory |

PATHOPHYSIOLOGY3,4

• Loss of elastin is the initiating event in abdominal aortic aneurysm (AAA) formation, whereas loss of collagen is required for continued expansion

• The primary event in the development of an AAA involves proteolytic degradation of the extracellular matrix proteins elastin and collagen by various proteolytic enzymes, including matrix metalloproteinases

• There is a reduced amount of vasa vasorum in the abdominal aorta (compared to the thoracic aorta); consequently, the tunica media relies mostly on diffusion for nutrition which makes it increasingly susceptible to damage.

• Haemodynamics affect the development of AAA which has a predilection for the infrarenal aorta as the diameter decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a lesser proportion of elastin. The mechanical tension in abdominal aortic wall is therefore higher than in the thoracic aortic wall. The elasticity and distensibility also decline with age, the half life (t½) of elastin being 71years, which can result in gradual dilatation of the segment.

• Higher intraluminal pressure in patients with arterial hypertension contributes to the progression of the pathological process.

SYMPTOMS3

1. Local compression

• Compression of the duodenum usually present with early satiety, nausea and vomiting

• Compression of ureters occurs less frequently and presents with obstructive uropathy and recurrent urinary tract infections

• Erosion of vertebral bodies presents with back pain

2. Rupture/imminent rupture

• The classical triad of acute abdominal pain, haemodynamic instability and pulsatile abdominal mass is only present in 50%

• Retroperitoneal rupture is usually secondary to a small posterolateral tear in the aortic wall. The bleeding is initially contained within the retroperitoneum, but is followed at unpredictable interval by frank intraperitoneal rupture

• Free intraperitoneal rupture is catastrophic and is heralded by acute abdomen and cardiovascular collapse

• Expansion presents similar to rupture without haemodynamic instability. The pain associated with expansion is poorly understood but may be related to stretching of layers of the aortic wall or pressure on adjacent somatic nerves

3. Embolism

• Distal macroembolism presents with acutely threatened limb,

• Distal microembolism presents with blue toe syndrome

4. Fistulation

• Aortoduodenal fistulas are less frequent, present classically with intermittent unexplained haematemesis and maelena or massive uncontrollable haematemesis.

• Aortocaval fistula is also less common, and presents with abdominal bruit, widened pulse pressure, venous hypertension and high output cardiac failure

INVESTIGATIONS 4

CT ANGIOGRAM

• Gold standard

• Characteristic findings of AAA on CT are dilation of the calcified wall of the aorta with varying degrees of surrounding thrombus

• Accurate for defining anatomy and anomalies including:

➢ Aneurysm rupture(disruption of calcifications with obliteration of surrounding soft tissue

➢ InflammatoryAAA (thickening of the aortic wall and adherence to surrounding structures)

➢ Mycotic Aneurysm(eccentric thickening of aortic wall with intramural air)

• Enables assessment of graft function as well as complications following open repair

• Vital in selection of candidates for endograft repair (reconstructed images allows for precise length measurements within aorta and tortuous iliac arteries, crucial to proper graft sizing and success of the endovascular repair)

• Disadvantageous as it is expensive and exposes the patient to both contrast and ionising radiation

ANGIOGRAM

• Shows visceral and occlusive disease(can clearly identify mesenteric and/or renal artery stenosis, accessory renal arteries, inferior mesenteric artery occlusion)

• Can determine the exact relation of aneurysm to major aortic branches.

• Useful in evaluating distal runoff, in patients with symptoms of claudication

• Reserved for patients with abnormal anatomy, juxtarenal, supracoeliac, and complex aneurysms

• Expensive and exposes patient to contrast load

• Invasive (local complications)

✓ Haematoma, AV fistula and/or a pseudoaneurysm at arterial puncture site

✓ Intimal tear, resulting in arterial rupture, thrombosis, pseudoaneurysm formation;

✓ Distal embolization related to atheroemboli or pericatheter thrombosis.

• Incorrect assessment of aneurysm size in the presence of thrombus

MRA

• Avoids radiation and invasive angiography but is expensive with limited availability

• Motion artefact in breathing patient

• Patient Contraindications (Cardiac pacemakers etc)

SCREENING5

Screening for AAA would most benefit those who have a reasonably high probability of having an AAA that is large enough or will become large enough to benefit from surgery. U.S. Preventive Services Task Force recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men aged 65 to 75 who have smoked, as this was proven to lead to decreased AAA-specific mortality and showed a benefit for all-cause mortality

Because of the low prevalence of large AAA’s in men who have never smoked and in women, the number of AAA-related deaths that can be prevented by screening this population is small. There is good evidence that screening and early treatment result in important harms, including an increased number of surgeries with associated morbidity and mortality, and psychological harms.

MANAGEMENT: 1,5,6,7

Intervention should be considered when the risk of rupture outweighs the operative risk. As such, the diameter is considered the most important factor in predicting the risk of rupture. The law of Laplace decrees that the tensile strength of the arterial wall is a function of the pressure multiplied by the radius. Consequently larger vessels are more likely to rupture.

|Greatest Diameter(cm) |Annual Rupture Risk(%) |

|3.0 – 5.5 |0.6 |

|5.6 – 5.9 |5 – 10 |

|6.0 – 6.9 |10 – 20 |

|7.0 – 7.9 |20 – 30 |

|>8.0 |30 – 50 |

Other factors such as rate of expansion and risk factors associated with rupture are taken into account and the risk can be categorised into low, average or high.

| |Low |Average |High |

|Diameter | 6.0 cm |

|Expansion |< 0.3 cm / year |0.3 – 0.6 cm / year |> 0.6 cm / year |

|Smoking / COPD |Mild |Moderate |Severe / steroids |

|Family History |No relatives |One relative |More than one |

|Hypertension |Normal BP |Controlled |Poorly controlled |

|Shape |Fusiform |Saccular |Very eccentric |

|Wall stress |Low ( 35 N / cm2) |Med ( 40 N / cm2 ) |High ( 45 N / cm2 ) |

|Gender | |Male |Female |

|Anticipated mortality |1-3% |3-7% |5-10% add 3-5% for each co-morbid |

| | | |condition |

Guidelines for the Management of AAA’s

Joint Council of the American association for Vascular Surgery and Society for Vascular Surgery)

➢ The arbitrary setting of a single threshold diameter for elective AAA repair that is applicable to all patients is not appropriate ,and the decision for repair must be individualized in each case

➢ Randomised control trials, including the ADAMS trial, and UKSAT have shown that the risk of rupture of small (< 5 cm) AAA’s is quite low and that a policy of careful surveillance up to a diameter of 5.5 cm is safe ,UNLESS rapid expansion(>1cm/yr) or symptoms develop.(However early surgery is comparable to surveillance with later surgery , so patient preference is important, especially for AAA’s 4,5 to 5,5cm in diameter)

➢ A diameter of > 5.5cm is an appropriate threshold for repair in an average patient

• Younger , low risk patients with longer life expectancy may prefer earlier repair

• If surgeons documented operative mortality rate is low, repair may be indicated at smaller sizes (4.5 to 5.5cm) if that is the patients preference.

➢ For women or AAA’s with greater-than-average risk for rupture , 4.5 – 5.0 cm is an appropriate threshold for elective repair.

➢ For high risk patients , delay in repair until larger diameter is warranted , especially if endovascular repair is not possible.

➢ In view of its uncertain long term durability and effectiveness , as well as increased surveillance burden, EVAR is most appropriate for patients at increased risk from open aneurysm repair

➢ EVAR may be the preferred treatment method if anatomy is appropriate for older, high risk patients , those with ‘hostile abdomens’, or other clinical circumstances likely to increase the risk of conventional open repair

➢ Use of EVAR in patients with unfavourable anatomy markedly increases the risk of adverse outcomes, need for conversion to open, or AAA rupture

➢ There does not appear to be any justification that EVAR should change the accepted size thresholds for intervention in most patients.

BEST MEDICAL MANAGEMENT 6

The therapeutic goal is to prevent small aneurysms from reaching a size at which the rupture risk is higher than the operative risk or decrease the expansion rate for larger aneurysms.

Medical management should focus on reducing co morbid conditions and monitoring the aneurysm for enlargement

• Ultrasound surveillance is recommended at

➢ 3 monthly for 4.5 to 5.5cm

➢ 6 monthly for 3 to 4.5cm

• The approaches proposed to prevent progression of aneurysmal disease include haemodynamic management, inhibition of inflammation, and protease inhibition.

• Beta blockade has been postulated to decrease the rate of AAA expansion. Two randomized trials failed to show any reduction in growth rate with beta blockade. A randomized trial from Toronto showed that patients taking beta blockers had worse quality of life and did not tolerate the drug well.

• Doxycycline (150 mg daily) shown to slow the rate of AAA expansion in one small randomized trial .This antibiotic has activity against C. Pneumonia (present in many AAAs. (Level B evidence)

• A number of studies agree that tobacco use is associated with an increased rate of aneurysm expansion. Level B and C evidence is available to suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may inhibit aneurysm expansion.

• There are animal data but no human data demonstrating that angiotensin-converting enzyme inhibitors or losartan, an angiotensin receptor blocker, will decrease the rate of AAA expansion.

PREOPERATIVE OPTIMISATION 9

• Cessation of smoking and structured exercise programme may improve cardiopulmonary reserve

• Antiplatelet medication to protect against thromboembolic complications, if aspirin is not tolerated clopidogrel should be given

• Statins - improve both the short- and long-term outcomes following non- cardiac surgery due to plaque stabilisation. Statins should be given irrespective of serum cholesterol concentrations

• Β-blockers for inducible ischemia

• Hypertension should be controlled preferably with ACE inhibitor

OPERATIVE MANAGEMENT10,11,12

The relative indication for OPEN repair versus Endovascular repair (EVAR) is in a constant state of evolution, and currently the choice is left to the surgeon.

Outcome of Trials in the decision for Open versus Endovascular management of AAA’s

• The endovascular aneurysm repair (EVAR) 1 and 2 and Dutch Randomized Endovascular Aneurysm Management (DREAM) trials address management of abdominal aortic aneurysms (AAAs) larger than 5.5 cm in diameter.

• The DREAM and EVAR 1 trials randomized patients appropriate for open repair between endovascular repair (EVAR) and open repair (OR), and the EVAR 2 trial randomized patients unfit for OR between EVAR and conservative non-operative management (No Rx).

• The EVAR 1 trial showed a 3% lower initial mortality for EVAR, with a persistent reduction in aneurysm-related death at 4 years. Improvement in overall late survival was not demonstrated. Similarly, the DREAM trial observed an initial mortality advantage for EVAR, but overall 1-year survival was equivalent in both groups. Both trials found significantly higher complication and intervention rates and higher hospital costs with EVAR, and by 1 year a quality of life (QOL) benefit was not evident.

• The EVAR 2 trial did not demonstrate a survival advantage of EVAR with respect to non-operative management; noted that EVAR was associated with greater likelihood of treatment complications, subsequent interventions, and threefold higher costs.

• Both EVAR trials were limited by long delays between randomization and treatment. Moreover, 27% of patients in EVAR 2 crossed over from non -operative to endovascular repair, and these patients had a lower procedure mortality from EVAR than those originally assigned to it (2% v 9%)

• Outcomes of the EVAR 2 trial have not settled the choice between EVAR and no treatment in this scenario to everyone's satisfaction. In patients with large AAAs who are fit for OR, EVAR offers an initial mortality advantage over OR, with a persistent reduction in AAA-related death at 4 years. However, EVAR offers no overall survival benefit, is more costly, and requires more interventions and indefinite surveillance with only a brief QOL benefit. It may or may not offer a mortality benefit over nonoperative management in patients with large AAAs who are unfit for open repair, but the statistical significance of this comparison is inconclusive

PREOPERATIVE ASSESSMENT OF THE ELECTIVE AAA REPAIR9,10

Patients presenting for abdominal vascular surgery have a high incidence of co morbidities

• Coronary artery disease, often with left ventricular dysfunction which is responsible for 50-60% of all peri-operative and late deaths

The ability to exercise is an excellent indicator of cardiovascular and respiratory fitness. Patients who cannot climb a flight of stairs frequently have adverse outcomes

Other major cardiac risk factors include:

• recent myocardial function (MI) < 1 month

• unstable or severe angina

• decompensate heart failure

• significant arrhythmias

• severe valvular heart disease

• coronary artery bypass graft or percutaneous transluminal coronary angioplasty < six weeks

The risk of surgery in elective repair can be stratified on the basis of the presence of the following preoperative conditions and co-morbidities

Risk Stratification for Open AAA repair

|Risk Factor |Low Risk |Intermediate Risk |High Risk |

|Age |Before 8th Decade |8th Decade |9th Decade or later |

|Functional Status |Active regular physical exercise |Sedentary but otherwise |Minimally able to accomplish |

| | |independant |daily activites |

|Cardiac |No or minor ACC clinical |Intermediate ACC clinical |Severe ACC clinical predictors |

| |predictors |predictors | |

|Pulmonary |No Clinical Disease |Mild COPD, FEV1> 1L/sec |O2 dependant , FEV1 3.0 |

|Other |Non-inflammatory infrarenal AAA |Juxtarenal,suprarenal or |Pugh-Child’s class B or C liver |

| | |Inflammatory AAA |failure |

Low risk patients: no clinical predictors, not associated with postoperative cardiac events, no need for further cardiac testing

Intermediate risk patients: at least two major cardiac risk factors – non invasive evaluation of cardiac status with dobutamine stress echocardiogram. Patient with positive stress test should have coronary angiogram

High risk patients: multiple major risk factors should undergo coronary angiogram. If necessary coronary revascularisation should be performed prior to aneurysm repair

Local practise: CPX (Cardiopulmonary exercise testing) has been used to identify high-risk surgical patients and to predict long-term outcome in patients with heart failure This test measures four variables associated with survival: anaerobic threshold, ˙V O2 peak,˙VE/˙VO2 and ˙V E/˙VCO2. CPET is performed on a cycle ergometer with respiratory gas analysis and simultaneous ECG recording

Patients who underwent preoperative CPX testing were found to have improved 30-day and mid-term survival if the ˙V E/˙VCO2was less than 43

An anaerobic threshold of < 11ml/kg/min, particularly if associated with ECG evidence of ischaemia, is associated with high operative mortality. Low risk patients are considered for open repair, the high risk patients are subjected to endovascular repair

Patients identified as unfit by a preoperative test may benefit from the opportunity to improve their chances of survival through interventions such as drug therapy (statins), an exercise programme and dietary advice.

Alternatively a transthoracic echocardiogram is performed to assess left ventriclar ejection fraction, and lung functions to evaluate pulmonary reserves

All patients undergo objective test to assess the quality of renal function (Creatinine Clearance)

OPEN REPAIR: 11,12

Exposing the aorta for repair can be achieved via a transperitoneal /transabdominal (TPA) or Retroperitoneal (RPA) approach

COMPLICATIONS

Risk factors for postoperative complications are age, emergency operation, duration of clamp time and operation, the amount of transfusion during clamp and operation, the amount of crystalloid during clamp, and blood loss.

|Cardiac |Usually occur in first 48hrs post-op |

| |Cross clamping of the infrarenal aorta causes increased vascular resistance → arterial |

| |hypertension |

| |A diseased coronary system may be unable to respond to increases in cardiac load, resulting in |

| |cardiac failure and myocardial ischaemia. |

|Haemorrhage |Problematic haemorrhage intra-operatively is due to bleeding from the proximal suture line, or |

| |inadvertent iatrogenic vein injury |

|Iatrogenic |Urethral |

| |Splenic |

| |Pancreatitis(secondary to handling of mesenteric base) |

|Renal Failure |Related to Ischaemic clamp time |

| |Premorbid renal impairment important risk factor |

|GI Complications |Paralytic Ileus(Retroperitoneal dissection) |

| |Colonic Ischaemia may occur due to inappropriate inferior mesenteric artery ligation, inadvertent |

| |collateral vessel damage or internal iliac artery thromboembolic event |

|Limb Ischaemia |Due to either distal embolization of debris from aneurysm sac or more rarely graft thrombosis. |

|Impaired sexual function |May result from damage to autonomic pathways found on the left side of the infrarenal aorta |

Late Complications

• Less than 10% of patients experience late complications of AAA repair during their lifetime. Most of these are severe, however, and often fatal.

• Anastomotic disruption resulting in a pseudoaneurysm

• Aortoenteric fistula

• Thrombosis of an aortoiliac graft after

• In long-term follow-up after AAA repair, approximately 5% of patients develop complications secondary to other aneurysms. If these secondary aneurysms rupture, less than 5% of patients survive. It is important to detect these aneurysms before rupture occurs. Hypertension significantly increases the risk of secondary aneurysm development.

ELECTIVE ENDOVASCULAR AAA REPAIR (EVAR)11,15

The basic principle of EVAR is the exclusion of the AAA from the systemic circulation by means of a preoperatively sized deployment stent graft, thus preventing further aneurysm expansion and elimination of the rupture risk.

Patient selection

• Patient factors

➢ High risk for the open procedure(as mentioned previously)

• Aneurysm factors

o Aneurysm neck morphology

➢ Straight neck minimal length of 10mm

➢ 60° angulation

➢ Maximum diameter of 3cm

➢ Funnel shaped ,thrombus extending to the neck and excessive calcifications are absolute contraindications to EVAR

o Iliac vessels

➢ Iliac arteries of sufficient calibre > 7mm to tolerate passage of the graft

➢ Calcified , tortuous vessels are unfavourable

o Aortic bifurcation diameter must be wide enough to accept both graft limbs without their compressing each other

Device selection

• Successful endovascular repair requires achievement of three objectives

1. Transluminal access to target site

2. Proximal and distal endograft fixation

3. Haemostatic seal between graft and native vessel

• An endograft is composed of two components: the fabric graft and the metallic skeleton. Both PTFE and Dacron have been used for the fabric component, the fabric can be attached outside the metal stents or embedded in it.

• A variety of exoskeleton grafts have been developed, the biocompatible metals used are stainless steel(Zenith), or Nitinol

Graft design

• Uni-iliac grafts allows for smaller sheath sizes, requires embolization of the contralateral common iliac artery and revascularisation with the bypass graft

• Bifurcated grafts may be unibody or modular, avoids embolisation of the contralateral iliac artery but requires cannulation of the contralateral iliofemoral arteries.

Complications

Iatrogenic vessel injury

The introduction of guide wires, large bore catheters, and a stent graft poses the risk of arterial and proximal vessel injury such as rupture or dissection, delayed Pseudoaneurysm at the cannulation site.

Endoleak

• Endoleak refers to the presence of arterial flow of blood into the excluded aneurysm sac but outside the lumen of the deployed stent graft

• The endoleaks regardless of size or type can transmit some proportion of systemic pressure to the aneurysm sac; the aneurysm may continue to expand, thus carrying risk of rupture.

• Incidence 12-44%

|Classification |Forms |

|Type IA |Proximal neck |

|IB |Distal Iliac End |

|Type IIA |Inferior Mesenteric Artery |

|IIB |Lumbar Artery |

|Type IIIA |Leakage from overlap site |

|IIIB |Defect in Endograft Material |

|Type IV |Graft porosity |

|Type V |Endotension ( aneurysm enlargement without identifiable |

| |endoleak |

• 70% of all endoleaks are type II, these tend to close spontaneously

• Type I and III tend to persist and are dangerous

• The most dreaded late complication of aortic endograft procedures is the development of a late type I or III endoleak, both of which are associated with a sudden recurrence of systemic pressurization of the aneurysm sac, a smaller contracted aneurysm sac with atrophy of the aortic wall is prone to immediate rupture on re-pressurization.

• Endoleaks are initially managed with simple observation, if after a prescribed time period, the endoleak persists or rapid aneurysm expansion is observed further intervention such as endoluminal graft extension, band ligation of the aortic aneurismal neck, or even open repair may be required

Embolization

Graft migration, dislocation and displacement

Postimplant syndrome

Postimplant syndrome refers to the presence of early back pain and fever without leucocytosis following EVAR. It last for up to 1 week after insertion, the condition is self-limiting and is managed conservatively. The cause is unknown.

Contrast nephropathy

Haemorrhage

Graft sepsis

Graft limb thrombosis

RUPTURED AAA (RAAA)15,16

Rupture is the most lethal complication of an AAA. Rupture AAA carries overall mortality in the region of 80 to 90%, it has an operative mortality rate of 50%

Pathophysiology

• The exact process that triggers rupture of AAA remains unknown. Several factors are known to suggest an increased likelihood of rupture and the most important of these is aneurysm size.

• The haemorrhagic shock and lower torso ischaemia-reperfusion injury which accompanies RAAA activates multiple inflammatory pathways in the body inducing harmful proliferative SIRS characterised by wide spread vital organ injury. The sequential failure of these organs despite intensive care support, once established leads to death in 90% of cases.

Clinical presentation

• Any patient with a known AAA who presents with sudden severe abdominal or back pain has a ruptured AAA until proven otherwise

• The classical triad of acute abdominal pain, hypotension and pulsatile abdominal mass is seen in only 50% of the cases

Operative management

Immediate management of these patients is principally resuscitation with a view to expedient transfer to theatre for definitive treatment to take place. Large bore intravenous access should be established and fluid resuscitation commenced. The concept of permissive hypotension has been accepted as the standard practice. Limited resuscitation can buy adequate time to effect endovascular repair

Patient selection

Hardman et al identified five important factors that influence post operative mortality

➢ Age > 76

➢ Creatinine > 190mmol/l

➢ Hb < 9g/dl

➢ ECG evidence of ischaemia

➢ Loss of conscious

The presence of ≥ 3 factors predict mortality of 100%

OPEN REPAIR OF RUPTURED AAA15,16

• Surgeons should be ready before the anaesthesia is given

• Prophylactic antibiotics should be given

• Transperitoneal approach is preferred locally

• Proximal control at aortic diaphragm hiatus is a priority

• The operation proceeds as for elective repair

Aortic Cross-clamping

Aortic clamping is used both as an adjunct to resuscitation and a means of partially controlling torrential arterial haemorrhage. Aortic clamping can be performed at several sites:

➢ The supracoeliac aorta can be approached through the lesser omentum and clamped at the diaphragmatic hiatus. The peritoneum anterior to the oesophagus is opened, and the oesophagus is rapidly mobilized to the patient's left. An opening is made bluntly in the left diaphragmatic crus, and the aorta is clamped through it, thus avoiding the thick peri-aortic tissue below the diaphragm. Using this technique, the clamped aortic segment is in fact the lowermost portion of the thoracic aorta.

➢ The suprarenal aorta can be clamped or compressed directly through an opening in the lesser sac, or approached in the retropancreatic area by performing an extended Kocher maneuver

➢ The infrarenal aorta is clamped beneath the left renal vein after a rightward reflection of the small bowel, division of the ligament of Treitz, and incision of the posterior peritoneum overlying the aorta.

➢ The aorta can also be occluded by retrograde insertion of an occluding balloon from the groin, via the femoral and iliac arteries.

➢ The descending thoracic aorta can be clamped above the diaphragm through a left anterolateral thoracotomy. Used mainly as one of the steps in resuscitative thoracotomy, it also enables the surgeon to gain aortic control before laparotomy. However, it entails opening another visceral compartment, with inevitable loss of time and body heat, and is therefore not commonly used.

Aortic clamping through the lesser sac is not always quick and easy, especially when performed in a pool of blood. Meticulous dissection is often impossible, proper positioning of the clamp is made difficult by the dense periaortic tissue, and iatrogenic injury (to the coeliac axis, oesophagus, left gastric artery, and the aorta) may also occur. Therefore it is often advisable to use firm digital pressure to compress the aorta through the lesser sac against the vertebral body instead of formal clamp placement.

Another problem with aortic clamping is its physiologic effect, sudden afterload augmentation and peripheral ischaemia are detrimental to the patient's already borderline physiologic reserves.

Although at times a lifesaving manoeuvre vital for the rapid control of aortic injuries in a "crashing" patient, its use as a resuscitative adjunct should be judicious and not reflexive.

ABDOMINAL EXPOSURE MANOEUVRES

The abdominal aorta is retroperitoneal and relatively inaccessible. The key to correct exposure is rapid mobilization of the overlying peritoneal viscera. This can be achieved using two visceral rotation manoeuvres

Medial rotation of the left-sided abdominal viscera (Mattox manoeuvre)

• affords rapid access to the entire intra-abdominal aorta and its branches, except the right renal artery

• It is the key to exposing the supra-mesocolic aorta and its branches, an area that is otherwise almost inaccessible

Right-sided medial visceral rotation (extended Kocher or Cattel-Braasch manoeuvre)

Consists of medial reflection of the right colon and duodenum by incising their lateral peritoneal attachments

Provides wide exposure of the infrarenal cava, aorta, and their bifurcations

This technique also exposes the superior mesenteric vessels and the entire length of the right iliac vessels as well as the proximal part of the left iliac vessels

ENDOVASCULAR RUPTURED AAA REPAIR15,16

Pre operative CTA

• CTA is used to assess the morphology aneurysm and to select the device. Initially surgeons believed that the time spent in obtaining a CT scan may be detrimental to the patient but recent studies suggest CTA assessment can be safely carried out in ruptured patients

• Some centres advocate intra-operative calibrated angiography as an effective alternative in order to reduce pre-operative delays. However, angiography does not clearly show luminal thrombus, which could adversely affect the ability to obtain a secure seal at the proximal fixation site risking endoleak or late device migration.

Device selection

Generous device oversizing is advocated and can improve the chances of a primary seal

Uni-iliac system

The advantage of the uni-iliac system is more rapid exclusion of the aneurysm from the systemic circulation, but this technique also requires revascularisation of the contralateral limb with femoro-femoral crossover graft .The major disadvantage of this system is the potential for infection of the crossover graft because of suboptimal groin sterility in emergency setting

Bifurcated system

Advantage is that it is more anatomical. The problem lies with necessity for rapid cannulation of the stump of the main body for deployment of the contralateral limb, this may be problem particularly with large aneurysm sac.

Radiologic considerations

• The procedure should be performed in a designated endovascular suite, in case urgent conversion is required.

• Contrast exposure in a haemodynamically unstable patient is serious challenge

THORACIC AND THORACOABDOMINAL ANEURYSM20,21

Aetiology

• Atherosclerosis is the most commonly implicated factor in the development of TAAA disease. The classical fusiform aneurysm that results is typically seen in men over the age of 50 years, usually with evidence of arterial atherosclerotic disease elsewhere.

• Previously the most common cause of this type of aneurysm was syphilitic aortitis leading to the classical Crawford type I Saccular TAAA

• Other causes include cystic medial necrosis, Takayasu’s disease and trauma leading to false aneurysm

Crawford Classification

|Type I |Involves the descending thoracic aorta as far as visceral branches |

|Type II |Extends from the aortic arch ,just distal to the left subclavian artery as far as the aortic bifurcation |

|Type III |Commences in the midthoracic aorta and extends to aortic bifurcation |

|Type IV |Involves the entire abdominal aorta from the diaphragmatic hiatus to aortic bifurcation |

[pic]

Clinical presentation

40% are asymptomatic

Symptomatic TAAA usually result from local pressure effects

• Chest pain radiating to the back

• Irritation of the recurrent laryngeal nerve and bronchial structures result in stridor, voice changes and dyspnoea

• Dysphagia due to compression the oesophagus

• Distal embolization

• Haemoptysis or haematemesis with haemodynamic instability indicate ruptured TAAA in the bronchial structures or oesophagus

Diagnosis

• CTA is the investigation modality of choice, it gives all the required preoperative information regarding aneurismal size, visceral artery relation, and its proximal extent

• Conversional angiography is indicated to give sufficient information regarding relationship to visceral (especially renal) arteries and evaluation of possible visceral artery stenosis

• Trans-oesophageal echocardiogram assess cardiac status, the extent of intraluminal thrombus, fistula presence, aortic valve incompetence and pericardial collections

MANAGEMENT20

• Indications for surgery

• Aortic size

o Ascending aortic diameter ≥5.5 cm or twice the diameter of the normal contiguous aorta

o Descending aortic diameter ≥6.5 cm

o Subtract 0.5 cm in the presence of Marfan syndrome, family history of aneurysm or connective tissue disorder, bicuspid aortic valve, aortic stenosis, dissection

o Growth rate ≥1 cm/yr

• Symptomatic aneurysm

• Pseudoaneurysm

• Large saccular aneurysm - increased propensity to rupture

OPEN REPAIR OF TAAA

• Crawford Inclusion Technique

• Multiple Side Arm Technique ( Local Technique )

Endovascular repair of TAAA

• Requirements for aortic neck

Proximal neck should be 2cm or more distal to the left subclavian orifice, if aneurysm begins more proximal the left subclavian orifice can be covered with stent graft, revascularisation of the subclavian artery is not necessary in most of the cases.

• Distal fixation

There must be an adequate length of normal, non-aneurismal aorta above all visceral vessels. A 2cm neck length above the celiac take off is recommended. Celiac axis may be covered without sequelae.

The diameter of the aorta at proximal and distal attachment sites should be a maximum of 10% smaller than the diameter of the expanded stent graft.

• Requirements for iliac vessels

The large diameter of the thoracic aorta requires the use of larger diameter stent graft and their associated delivery systems. The larger size of these delivery systems can be problematic when the iliac vessels are small in diameter, tortuous, or calcified

• Maintenance of spinal perfusion

Lumbar vessels can be covered without sequelae , occlusion of intercostals vessels has been associated with paraplegia

Hybrid approaches

Hybrid approaches offer the advantages of versatility, avoidance of bicavitary surgical incisions and exposures, and a combination of open and endovascular techniques and potentially offer a broader range of therapies to patient population that would not otherwise be considered for aortic surgical repair. The durability of these procedures currently remains in question

COMPLICATIONS2,20

Paraplegia

Remains a major cause of mortality and morbidity following extensive TAAA repair.

Incidence varies between 4% to 16% depending on extent of aneurysm, co-morbidities of the patient and the protective strategies used.

Highest incidence in Type I and Type II aneurysms.

Mechanism of spinal cord injury

• Distal hypoperfsion

• Increased CSF pressure

• Reperfusion injury

Spinal protection

Continuous CSF drainage

• The use of continuous CSF drainage via a lumbar thecal drain has become the accepted standard of care

• Spinal fluid drainage has been shown to decrease neurologic complications (paraplegia and paraparesis), especially in patients with Type II TAAA and longer clamp times.

Epidural cooling

• Performed through a separate epidural catheter has been proposed to give added protection from neurologic injury.

• Cold saline infused in catheter to achieve spinal cord temperatures of 25-28 degrees.

Reimplantation of patent intercostal arteries

• Although preoperative angiographic location of the artery of Adamciewicz, the major arterial supply to the spinal cord, has been proposed to assist in selective reimplantation, it is technically difficult and sometimes not possible.

• Current data suggest that emphasis should be placed on the implantation of patent intercostal arteries at the level of T11, T12, and L1, and when technically feasible any patent artery from T7 to L4.

Pharmacotherapy

• Options include corticosteroids, papaverine, nalaxone, mannitol, calcium channel blockers, magnesium and barbiturates.

• Currently no convincing data regarding their efficacy.

Delayed post operative paraplegia

• Develop neurology in the post operative period.

• Reasons postulated are that the spinal cord blood supply post aneurysm repair is dependent on a tenuous collateral circulation.

• Compromising these collateral results in ischaemia with resultant neurological deficit.

• Most common causes are hypotension or elevation in spinal pressure

• Treatment directed at maintaining blood pressure and reducing spinal pressure via spinal tapping.

Renal failure

• Significant and potentially lethal complication.

• May be minimized when renal protection implemented.

• These include:

➢ Renal preservation solution – hypothermic renal artery perfusion

➢ Atrial – femoral bypass with use of ‘octopus’ catheter

➢ Minimize renal ischaemic time

Multiple side arm technique which minimizes ischaemic time

Other strategies

Systemic hypothermia

• Left heart Bypass

➢ Shown to be beneficial in type I and II aneurysm.

➢ For the less extensive type II and IV distal perfusion techniques are really required

Inflammatory AAA

• The definition of inflammatory AAA depends on the presence of a triad of factors

1. Thickened aneurysm wall

2. Marked perianeurysmal/ retroperitoneal fibrosis

3. Dense adhesions involving adjacent abdominal viscera to the aneurysm

• These aneurysms comprise 5 to 10% of all AAA, the typical patient is male in his sixth decade, and females are rarely affected, with average age at diagnosis 10 years younger than patients presenting with non-inflammatory aortic aneurysm

• Risk factors include smoking and genetic predisposition

• The inflammatory aneurysms are usually larger than their atherosclerotic counterpart and it is generally accepted that the risk of rupture is lower (due to the paradoxical strengthening of the peri-aortic tissues by fibrotic changes)

• The presence of abdominal or back pain, weight loss and elevated ESR in patients with known AAA confers a diagnosis of inflammatory aneurysm until proven otherwise.

• Ultrasound is unreliable in distinguishing inflammatory from non-inflammatory variant

• CT scan can sensitively detect aneurysm wall thickening and perianeurismal fibrosis

• Oral corticosteroids to attenuate the inflammation is not recommended.

• Surgery remains the treatment of choice

HIV ASSOSCIATED ANEURYSMS18,19

HIV related aneurysms are unusual in that they affect young patients, occur in atypical sites and tend toward multiplicity. These aneurysms have a predilection for superficial and carotid arteries

Pathogenesis

The exact mechanism is unknown but there are 3 major possibilities: (1) immunodeficiency allows bacteria that are known to cause mycotic aneurysms to proliferate without immune restraint; (2) one or more of the HIV envelope proteins sufficiently resemble one or more artery-specific-antigenic proteins (ASAPs) that may trigger an autoimmune response (molecular mimicry); and (3) the HIV virus itself infects arterial-resident cells that maintain the integrity of the load-bearing matrix.. Accordingly, direct infection of aortic fibroblasts by the HIV virus is more likely to be the pathogenetic mechanism than the process of molecular mimicry.

Ultrasound Features

The ultrasound features of large symptomatic HIV-related femoral and carotid aneurysms were typical of pseudoaneurysms with a defect or “blow-out” in the vessel wall and turbulent pulsatile flow. The presence of marked thickening of the vessel adjacent to the aneurysm and hyperechoic “spotting” of the arterial wall are features on U/S that may be unique to HIV vasculopathy.

Management

• Patients with full blown AIDS, the perioperative morbidity and mortality is high with a poor long term survival as such reconstructive surgery should not be offered

• Patients with symptomatic aneurysm ,when risk of surgery is favourable with respect to comorbidities, should be offered surgery

• Asymptomatic patients with no signs of advanced disease are managed as seronegative patients

• The conduit of choice for reconstruction is the autogenous vein grafts for peripheral aneurysms. Prosthetic graft can be utilised when autogenous vein graft is unsuitable

• Ligation is viable if ischaemia of the distal tissues is not a problem

The role of endovascular intervention in patients predisposed to infections is not yet clarified

REFERENCES

1.S Aggarwal, A Qamar, V Sharma, et al. Abdominal aortic aneurysm: A comprehensive review, Exp Clin Cardiol. 2011; 16(1): 11–15.

2.J Croenenwatt,W Johnston. Aortic Aneurysms, Rutherfords Vascular Surgery 7thEd, 2009 ; 25(1156)

3.Wilmink AB, Quick BT. Epidemiology and prevention of abdominal aortic aneurysm, Br J Surg (1998) 85: 155-62

4.D Drury,J A Michaels, L Jones et al. Systematic Review of recent evidence for the safety and efficacy of elective Endovascular repair in the management of infrarenal abdominal aortic aneurysms, Br J Surg 2005; 92:937-946

5.Jason CPT, Pery T, Statler JD. Advances in Vascular imaging, Surgical Clinics of North America (2007) 87:975-994

6. Von Allmen RS, Powell JT. The management of ruptured abdominal aortic aneurysms: screening for abdominal aortic aneurysm and incidence of rupture. Journal Cardiovasc Surg 2012 Feb;53(1):69-76.

7. Golledge J, Powell JT, Medical management of abdominal aortic aneurysm, Eur J Vasc Endovasc Surg(2007) 34: 267-273

8.Eliason JL, Clouse WD. Current Management of Infrarenal Abdominal Aneurysm. Surgical Clinics of North America(2007) 87

9.Park KW, Preoperative cardiac evaluation, Anaesthesiology clinics of N Am(2004) 22: 199-208: 1017-1035

10.Cowlishaw PJ, Telford RJ. Anaesthesia for abdominal vascular surgery, Anaesthesia and Intensive care Medicine(2007): 248-252

11.UK EVAR Trial Investigators. Endovascular versus open repair of Abdominal Aortic Aneurysms. NEJM,2010:362:1863-1871

12. The United Kingdom Small Aneurysm Trial Participants. Final 12-year follow-up of surgery versus surveillance in the UK Small aneurysm Trial. Br J Surg , (2007);94: 702-8

13.Carroccio A, Hollier LH. Abdominal Aortic Aneurysm in Haimovici’s Vascular Surgery, 5th Edition. Blackwell, Massachusetts, 2004;703-735

14. Sicard GA, Reilly JM, Rubin BG et al. Transabdominal versus retroperitoneal incision for abdominal aortic aneurysm surgery: report randomised trial. J Vasc Surg 1995;21:174-83

15.Towne JB .Review Endovascular Treatment of Abdominal Aortic Aneurysm, Am J of Surgery (2005) 189: 140-149

16.Harkin DW, Dillion M, Blair PH, et al. Endovascular ruptured AAA repair: A Systematic review, Eur J Vasc Surg (2007) 34: 673-681

17. Karmy-Jones, Simeone A, Sohn VY, Starnes BW Descending thoracic aneurysm, Surgical Clinics of North America , (2007) 87: 1047-1086

18. Nair R, Robbs JV, Chetty R, Naidoo NG, Abdool-Carrim ATO , Arterial aneurysm in patients infected with Human immunodeficiency virus; A distinct clinicopathology entity, Seventh biennial congress of vascular surgeons of Southern Africa 1997

19. Botes K, Van Marle, Surgical intervention for HIV vascular disease, Eur J of Endovascular Surgery(2007) 4: 390-396

20. Karmy-Jones, Simeone A, Sohn VY, Starnes BW Descending thoracic aneurysm, Surgical Clinics of North America , (2007) 87: 1047-1086

21.A. T. Hirsch, Z. J. Haskal, N. R. Hertzer,Mark A. Creager, Jonathan L. Halperin, Loren F. Hiratzka, William R.C. Murphy, Jeffrey W. Olin, Jules B. Puschett, Kenneth A. Rosenfield, David Sacks, James C. Stanley, Lloyd M. Taylor, Christopher J. White, John White, Rodney A. White, Elliott M. Antman, Sidney C. Smith, Cynthia D. Adams, Jeffrey L. Anderson, David P. Faxon, Valentin Fuster, Raymond J. Gibbons, Jonathan L. Halperin, Loren F. Hiratzka, Sharon A. Hunt, Alice K. Jacobs, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel et al. Thoracoabdominal Aneurysms, Journal of the American College of Cardiology ,2006( 47), 6:1239-1312

COMMENT BY DR Z MOOLLA

CURRENT MANAGEMENT OF VISCERAL ARTERY ANEURYSMS

Visceral artery aneurysms (VAA) are uncommon (overall incidence of 0.1-2%) but important as they may present with life-threatening, often fatal emergencies. The incidence is unknown as majority are asymptomatic and identified incidentally with advanced diagnostic imaging. VAA’s include both true and pseudoaneurysms.

Indications for intervention include rupture, symptomatic VAA’s, pseudoaneurysms and mycotic aneurysms. The management of asymptomatic VAA’s lacks consensus in the literature. Aneurysms > 20mm or twice the normal vessel diameter is generally been accepted for intervention. Furthermore saccular aneurysms, aneurysms associated with portal hypertension and VAA’s in pregnancy and females of childbearing age are other recommended indications in asymptomatic patients.

The splenic artery is commonest abdominal visceral vessel affected by aneurysmal disease. Splenic artery aneurysms of the proximal vessel may be treated with aneurysmectomy and end-to-end anastomosis or simple ligation/exclusion without arterial reconstruction. Splenectomy must be performed when aneurysms are localized at the splenic hilum. Endovascular coil embolization of splenic artery is an alternate to surgery.

Hepatic artery aneurysms are the second most common VAA and amount to about 20%. The incidence has been increasing as a result of invasive biliary tract procedures. Common HAA is often treated with aneurysmectomy or aneurysmal exclusion without arterial reconstruction. Restoration of arterial blood flow is important in aneurysms involving the proper hepatic artery and its extrahepatic branches.

Renal artery is the 3rd most common site for VAA’s. Majority occur at the main renal artery bifurcation. Management of main renal artery aneurysms include ligation and bypass, stenting or nephrectomy.

Aneurysms of the SMA account for 5.5% of VAA’s and are frequently mycotic in aetiology. Surgical management with aneurysmorrhaphy and simple ligation are the most frequently used techniques. Arterial reconstruction with graft interposition, excision or aortomesenteric bypass with aneurysm exclusion are rarely performed.

Endovascular techniques such as percutaneous transcatheter coil embolization (PTCE) and stenting have been used with increasing frequency in the treatment of VAA. Although technical success has been acceptable in most series, serious procedure related complications limits its use. Endovascular techniques should be limited to centres with expertise and patients with aneurysms with favourable morphology or difficult surgical access.

REFERENCE:

Chiesa R, Astore D, Castellano R et al. Management of visceral artery aneurysms. J Vasc Br 2005; 4(1):27-34

COMMENT BY DR T MBEBE

POPLITEAL ARTERY ANEURYSMS

• Popliteal artery is the most common site of aneurysm formation, accounting for > 70% of the peripheral aneurysms

• Popliteal aneurysm occurs bilaterally in 50% of the patients

• 40% of the patients with bilateral popliteal aneurysm have AAA

• 6-12% of patients with AAA have popliteal aneurysm

• Popliteal artery aneurysms are generally perceived to be a problem of older adults because their prevalence increases with age and peaks in the sixth and seventh decades of life

• 38% are asymptomatic at the initial diagnosis, asymptomatic patients develop symptoms at rate of 14%/year

• Intermittent claudication occurs in approximately 25% of patients, local pressure occurs in approximately 5-10% of the patients, rupture is very rare

• Acute ischaemia due to artery thrombosis or distal embolization in approximately one third of the patients

Indications for surgery

• all symptomatic patient should undergo surgery

• management asymptomatic popliteal artery aneurysm is controversial

• size

aneurysms < 3cm should be followed up with ultrasound every six months

aneurysms > 3cm should be considered for surgery

Surgical options

1. By-pass procedures

Proximal and distal ligation combined with either popliteal-popliteal bypass or popliteal –femoral bypass using vein or synthetic graft. Vein grafts generally provide better results, with overall 5-year patency rate > 80%. The fate of the excluded popliteal aneurysm is unpredictable, approximately one third of the excluded aneurysm continue to enlarge as result of continued flow from collateral vessels.

Consideration should be given to fasciotomy in patients with severe ischaemia. Post operative duplex surveillance should be considered.

2. Inlay procedures

Inlay procedures is useful for a large popliteal aneurysm causing pressure symptoms .It is carried out through a posterior approach and has an advantage that all vessels arising from the aneurysm can be ligated and if necessary , the sac can be removed

3. Endovascular treatment

Gaining increasing popularity

Advantages include minimal invasiveness, reduction of wound complications and conservation of saphenous vein

However no long term reports have been reported and traditionally durability of prosthetic grafts placed across the knee joint is inferior to autogenous grafts

Management of thrombosed popliteal aneurysm

Compared with the relatively good results after elective repair, outcome after thrombosis can be poor. The main problem after thrombotic aneurysm occlusion is in general, the lack of distal run off due to previous microembolisation, hence standard aneurysm repair often results in recurrent occlusion. Mortality is approximately 5% with limb loss of > 20%

If the limb is not viable, the prompt amputation should be done

The role of arterial thrombolysis

There is no doubt that intra-arterial thrombolysis can clear acutely thrombosed distal vessels.

Pre operative thrombolysis and surgery is associated with significant complications compared with intraoperative thrombolysis and surgery. Acute deterioration of the limb caused by destabilisation and embolization of large volume thrombus within the aneurysm seems to be a particular problem of preoperative thrombolysis.

Intra-operative thrombolysis is a better option, allows clearance of the distal run off vessels without destabilisation of aneurismal thrombus

REFERENCES:

1.Galland RB, Popliteal aneurysms: controversies in their management, The Am J of Surgery (2005) 190: 314-318

2.Dawson I, Sie RB, van Bockel, Atherosclerotic popliteal Aneurysm, B J Surgery (1997)84:294-299

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