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Abdominal Ao and LE Aneurysms yrs later (4.5% vs. almost 10%). It‘s very cost  At 6 yrs, both groups had comparable survival

efficient. Thus, we should screen for AAA in men. rates (64%) (if died, from any cause, not just

Definitions: rupture)

 Aneurysms: permanent localized dilation, diam Expansion rate  Thus, if aneurysm 50% of expected nl  About 10% diameter ↑ in diameter / yr have to treat it

 Ectasia: dilation 50% of nl o Rapid growth  increased rupture risk o If 4-5.5 cm diam, annual risk for

 Median expansion rate = 3^(0.106t) rupture is 2.2% / yr

Epi: o But this rate is higher with the

 M:F ratio 5-7:1 (so M>F) Rupture following RFs

 Prevalence  Diameter is the primary determinant RF for  F

o AAA > 3 cm : 3-10% for pts > 50 yo rupture  Larger initial diam

o AAA > 3 cm : 4-6% for VA pts bw 50-  LaPlace: T=Pr/h  Current smoking

79 yo o 4 cm: 1.4% o 4-5 cm 0.5-5%  Higher BP

 3.5 Caucasian: 1 AA o 5-6 3-5%

 Seasonal: Fall, winter o 6-7 10-20% Risk fo rupture of Larger (>5.5 cm) aneurysms

 Present in 6% of CAD pts, 9% PAD pts, 50% o 7-8 20-40  Lancet (2002): 198 vets w/ AAA >5.5 cm who

of pts w/ femoral or popliteal aneurysms o >8 30-50 refused /unfit for surg

 Location: 95% of arterial aneurysms in Al  RFs  Mean f/u 1.52 yrs showed 112 deaths, 45 from

o 95% of Ao aneurysms are infrarenal o HTN ―probable‖ AAA ruptures

o Thrombosis, embolism can occur but o COPD  Found that diam was correlated w/ risk for

rupture is more common o Smoking – strong RF rupture per yr

 Ruptured AAA: 13 leading cause of death

th o FHx o 5.5-5.9 cm 9.4%

(USA) o Shape/wall tension: (saccular/bowing o 6-6.9 10.2

out = high risk; fusisform lwr risk) o >7 32.5

Diagnosis o Thrombus  Anything >7 is considered very large

 directed PE is accurate if abd growth 15 mm

o plain abn x-rays  Good results: > that of open surg

the prosthesis but within the aneurysm sac U/S

 not an aneurysm Counseling your pts:  Rate of rupture w/ observation of sm

 Classification Types:  Open AAA surg is appropriate for fairly healthy aneurysms: ~2%/yr

o I: attachment site leak pts w/ AAA‘s >5.5 cm  Endovasc aneurysm repair is an option for

 IA: prx end  Not indicated in pts w/ chronic fatal dz: severe ~60% of pts

 IB: distal end COPD, CHF, cancer  Mortality lwr for endovasc repair than open

o II: branch leak- retrograde blood  Problematic in ―healthy‖ elderly (>80 yo) surg

 Most AAA are silent

comes from mesenteric a or collaterals  Long term outcomes for endovasc repair similar

 IIA: simple (1 branch)  Primary role of AAA repair: prevent rupture to open surg

 IIB: complx (2+ branches)  Poorer risk pts more likely to develop  but endo vasc repair is more $$$ and requires

o III: Device defect functional impairment after open surg indefinite monitoring due to higher re-

 IIIA: junction leak intervention rate (10-20%)

 IIIB: fabric disruption Popliteal aueurysms

o IV: Fabric porosity  Much less common Predisposing conditions

o 1% of 65-85 yo M pts  Marfans: fibrillin plays greater role in

What connects IMA to SMA? o present in 2-3% of AAA pts upper/thoracic Ao; collagen plays bigger role in

1. Marginal artery of Drummond o but 40-50% of pts w/ popliteal lower/abdominal Ao

(collection of arcades) and aueurysms also have Ao ones o so Marfan‘s pts have defects in

2. Arc of Riolan (meandering mesenteric a)  Clinical pres ascending Ao

(more variable). o Most silent  Ehlers Danlos

Coils can be placed in these to prevent type II o Thromboembolism – the knee bends a o Spont arterial rupture w/o necessarily

endoleaks lot which can break off emboli having aneurysms

o Large (4 cm) ones may cause  Lowes Deeps (?) syndrome

Trial comparing conventional and endovascular compression o Defect assoc‘d w/ premature aneurysm

repair of AAAs o Rarely rupture formation

 Lancet (2004) (EVAR Trial): For pts with >5.5

diam AAA, underwent open surgery or Repair of Popliteal aneurysm Gallbladder and Pancreas

endovascular repair  Indications Gallbladder anatomy…tricky ones: Spiral valves of

 30 day mortality (all-cause) o Symptomatic Heister and Triangle of Calot

o Open surg: 4.7% o 2 cm diam generally

o Endovasc: 1.7% o Intraluminal thrombus Bile formation:





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 liver excretes bile continuously, 500-1000 mL /  LFTs for Tbili, AST, ALT, AP  Hepatobiliary Radionuclide Scanning (HIDA

day  ↑ WBC may indicate cholecystitis scan)

 w/ intact Sphincter of Oddi, bile flow is  ↑ TBili and AP suspicious for o Nuclear med study

directed into gallbladder choledocholithiasis o T-99 labeled protein injected IV, taken up

 bile composition: water, e-lytes, bile salts,  ↑ bili, AP, and transaminases in cholangitis by Kupffer cells of liver, excreted by bile

protein, lipid, pigments o Scarred/ inflamed GB (cholecystitis) will

 Enterohepatic circ: Ways to evaluate the GB show the Technetium never taken up by the

o 80% bile salts reabsorbed in terminal  U/S GB, never ends up in duodenum

ileum o Gen info  Magnetic Resonance

o 15% reabsorbed by colon  Non-invasive, painless, no Cholangiopancreatography (MRCP)

o 5% excreted by stool radiation o Typically used for pts w/ GB/BD/head of

 Operator/technician dependent pancreas cancers to assess invasion of

Gallbladder (GB) fxn  Demonstrates gallstones w/ 90% vasculature

 GB stores 80% of bile secreted by the liver sens and spec o 95% sens, 89% spc for choledocholithiasis

 GB mucosa reabsorbs Na, Cl, water  o Cholelithiasis: stones in GB o Single, non-invasive test for the dx of

concentrating bile 10x o Choledocholithiasis: stones in CBD. biliary and pancreatic dz

 Releases bile in response to hormones: Secondary sign = Biliary ductal dilatation

o (+) CCK, vagal stim‘n, distension of (proximal dilatation, distal stricture) Gallstone Dz

gastric antrum o Acute cholecystitis: GB wall thickening, Gallstone Formation

o (-) VIP, splanchnic symp stim‘n, pericholecystic fluid (edema around GB),  Formed from solids settling out of bile soln in

somatostatin sonographic Murphy‘s sign (+ Murphy as a the GB: bili, bile salts, phospholipids,

result of pressure from U/S probe) cholesterol

Sphincter of Oddi o Chronic cholecystitis: contracted, thin-  Cholesterol stones 80%, pigmented stones 15-

1. Regs flow of bile and pancreatic enzymes into walled GB 20% (Western world)

duod  Intraoperative Cholangiogram –

2. prevents regurg of duod‘l contents into biliary o Gen info: to confirm there are no stones, Epi and Nat Hx

tree you need  Autopsy studies show prev of cholelithiasis 11-

3. diverts bile into the GB, resting pressure 13 torr  go through cystic duct 36% so gallstones are common

4. CCK causes sphincter relax‘n and GB  Filling of R and L hepatic ducts  RFs: Female, age, obesity, pregnancy, gastric

contraction in response to acid, fat, amino acids  Absence of filling defects in CBD bypass surg, term ilium resection, diet,

in the duod tells you there are no stones hereditary spherocytosis, sickle cell dz

5. morphine sulfate can cause Sphincter of Oddi  Free flow of contrast into duod  Comps

spasm (causes RUQ tenderness so don‘t give  Endoscopic Retrograde o Acute cholecystitis

someone with biliary colic morphine) Cholangiopancreatography (ERCP) o Choledocholithiasis (stone in CBD) +/-

6. Glucagon relaxes Oddi – can help when have o Performed by gastroenterologist, use cholangitis (infxn of extrahepatic biliary

trouble getting contrast through endoscope to cannulate the CBD ducts)

o Can perform retrograde sphincterotomy o Gallstone pancreatitis

Labs (cut Oddi, let stones come out) o Cholecystoduodenal fistula +/- gallstone

 get CBC for wbc, hct, hbg, platelets o 5% complication rate-- Complications ileus (gallstone so big, size of golf ball,

include perforation and pancreatitis causes scaring and fistula through which it

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goes through to duodenum, small intestine,  PE  Rare, aggressive tumor w/ poor prognosis (5 yr

gets trapped in ileocecal valve ) o Scleral icterus survival = 5%)

 Symptomatic gallstone dz develops in 3% of o Mild tenderness epigastrum, RUQ  Calcified ―porcelain‖ GB (stiff, hard) = 20%

asymptomatic pts / yr  Dx malignancy. 80-90% of adenocarcinomas

 Complicated gallstone dz develops in 3-5% of o RUQ u/s  choledocholithiasis, dilated  Corvoisier’s sign: enlarged, palpable GB

symptomatic pts / yr CBD (proximal to obstruction, >8 mm)  Found incidentally in 1% of pts undergoing

o MRCP / ERCP cholecystectomy for gallstones

Chronic Cholecystitis o Hi bili, AP (bile ducts are irritated; bile

Repeated inflammation of GB (biliary colic) Cholangiocarcinoma – cancer of extrahepatic

ductal tissue produces AP), transaminases

 Tx – both these methods are done: billiary ducts

Acute Cholecystitis o ERCP  sphincterotomy, stone extraction  rare, most often at hepatic duct bifurcation

Obstruction (usu stone) causes cystic duct o Laparoscopic cholecystectomy (Klatskin tumor)

inflamm‘n  GB distention, inflamm‘n, secondary  Survival unresectable dz: 5-8 mo, 5-yr survival

bac infxn (due to stasis) Cholangitis – typical comp of stones stuck in CBD, resected dz 10-30% (poor prognosis)

 Presentation stasis  ascending bacterial infxn, usu gm (-) and  RFs: primary sclerosiing cholangitis,

o RUQ/epigastric pain, lasting 1-2 days anaerobes choledochal cysts, UC, Clonarchis

o Not hungry

o N/V  Presentation Three Rules of Surgery!

o +/- Fever o Charcot‘s triad: F, RUQ pain, jaundice 1. Eat when you can!

 PE o Raynaud‘s pentad: above + septic shock + 2. Sleep when you can!

o Focal tenderness in RUQ MS change 3. Don‘t mess w/ the pancreas

o Palpable mass sometimes  PE

o + Murphy‘s o Febrile, focal tenderness and guarding RUQ ANESTHESIA – Dr. Ken Abbey

 Dx  Dx

o RUQ U/S  stones in GB, GB wall o RUQ u/s  choledocholithiasis, dilated Case: hernia repair for Al

thickening, edema, sonographic Murphy‘s biliary ducts  Al = 46 yo shoe salesman married to Peg

sign o ERCP  gold standard visualization. Do  HPI: was swuatting to fit a shoe, felt pop in

o HIDA scan  non-visualization of GB this right away – stones must be removed groin

 Mild leukocytosis (12-15,000) +/- mildly ↑ quickly  PMH: low IQ, low self esteem

LFTs o Elevated bili, AP, LFTs; leukocytosis  PSH: removal of ‗will to live‘ by Peg

 Tx  Tx

o IV fluids, pain control, IV Abx (3rd gen o IV abx, fluids, ICU admission, vasopressor You speak to surgeon, Brett, who asks:

cephs), remove GB w/in 24 hrs typically support  what are the 4 goals of anesthesia?

o Emergent biliary decompression by ERCP, o Amnestic - you don‘t remember

Choledocholithiasis – stuck in CBD, so no bile eventual GB removal o Hypnotic – you‘re not aware

passes from liver to small bowel o Analgesic - not in pain

Laparoscopic Cholecystectomy (Lap Chole) video o Paralyzed - not moving

 Pres  What does MAC mean?

o RUQ / epigastric pain Billiary neoplasms - rare o Minimum alveolar concentration

o N/V GB carcinoma

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o Amt of anesthetic necessary to prevent  If adult, then give muscle relaxant (ie

movement in 50% of pts on incision pancuronium) before intubation (cords won‘t Opiates:

o We aim for 1.3 MACs (95% of rats don‘t slam together, helps give good view w/  Morphine

move) Laryngoscope)  Hydrocodone

 Caution w/ morbidly obese pts: if give m  Methadone

So, why do we do anesthesia? relaxant, may then be in a position where you  Fentanyl

 From 1821-46, MGH only did ~1 surgery per can‘t intubate and cannot ventilate either   Dilaudid

month (no anesthesia) disaster  Alfentanyl (short acting, quick onset)

 So a good surgeon back in those days was one  Pre-oxygenation buys you 6-7 mins in healthy  Remfentanyl – spontaneously metabolizes,

who was fast (30 seconds chop off leg!) young pt good when need quick pain relief that quickly

o Decreases oxygen demand goes away, ie head/neck cases

Gas is an anesthetic, meets all 4 goals. o When anesthetized, O2 demand goes down

Used sometimes in kids to 200 cc/min Work on mu receptors

o If you are not hooked up to O2 and you are Reversible w/ Narcan

Midazolam (Versed) = benzo, anxiolytic, amnestic apneic, the O2 gets taken from the lung

 so don‘t talk to pt until 1 hr after surgery; reservoir (FRC, what passively stays in Propofol

otherwise they won‘t remember lung after passive expiration)  O/D killed Michael Jackson – they couldn‘t

o Pre-oxygenation causes FI02 increase from manage his airway

Fentanyl = opioid, 100x more potent than 0.21 to 1  MOA: GABA-A and Na channel

morphine, given in micrograms, initially acts like o Thus when you are doing intubation, slow

 Effects

short acting drug (lipophilic; sudden onset), then down. o Euphoria

redistributes to fat. Initial effects go away fast. If o However, caution w/ obese pts, they o Hypnosis

give a lot, Vd fills up and acts like long-acting. decompensate faster. With obese pts, after o Amnesia

Cheap as dirt. Very little S/Es. Risky to use b/c of giving benzo, fentanyl, and propofol, o CV

sudden onset of action. ventilate before intubation to determine if o Resp

ventilation is even possible. Then give o V little analgesia

Propofol – common induction agent muscle relaxant o Not reversible

 other induction agents = gas induction (ceba-  Which pts do you give m relaxant right away?

fluorine, least stinky), ketamine, penthol o ―Rapid sequence induction‖ in ppl who Suggestion: use Versed instead of Propofol. And

(penafol, potent barbiturate, tastes like garlic d/t are aspiration risk (full stomach, bad have Narcan in your pocket.

sulfa groups), midaz, other barbituates reflux)

(methahexatol), ECT o If try to ventilate while pushing air in Vecuronium = non-depolarizing m relaxant.

 Propofol used a lot bc rapidly distributes and stomach, they may aspirate. Therefore they Competitive inhibitor of NMJ. Won‘t cause

causes least nausea get propofol then m relaxant right away fasiculations.

 Downside = burns upon injection

 Cheapish: $6 a vial Are benzos reversible? Yes Succinocholine = depolarizing (2 Ach‘s stuck

 Flumazenil = benzo antagonist. together), causes NMJ to be depolarized. All

Sequence: Benzo  Fentanyl  Propofol o If pt is a drinker, may cause pt to… wake muscles fire, always wake up sore. After firing,

 Propofol will cause apnea up? (not sure what he said)

o Works on NMDA receptors

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muscles have refractory period of 6-10 mins.  Bacterial, fungal o Lower specificity (detects only 60% of

Advantages = quick onset, short duration. o Inflammatory abdominal aortic AAAs)



Why doesn‘t heart stop? Pathophys Abd U/S

 it‘s smooth muscle  Chronic transmural infamm‘n  good screening tool (#1)

 gut, heart, vasculature—all smooth m, still  Destructive remodeling of extracell‘r matrix  v sens and spec

work  Depletion of vascular SM cells  accuracy 80-90%

 ppl stop breathing bc diaphragm is skeletal m  Redistribution of hemodynamic stresses of  cost effective

vessel wall  can detect AAA in their earliest stages

How about BP and CO?  Reduction of collagen and elastin content from  reproducible to within 0.3 cm

 Propofol = potent vasodilator, so is gas proximal to distal aorta  Difficulties

 That‘s why BP goes down o Loss of elastin  dilatation and aneurysm o Bowel gas interference

o Must give fluids bc capacitance has o Loss of collagen  rupture o Obese pts

increased (due to vasodilation)  58% decrease in elastin from suprarenal to o Suprarenal and iliacs not well visualized

o This increases preload infrarenal aorta o Operator dependent

o Starling: fixing preload increases BP  Elastin T ½ 40-70 yrs, not synthesized

 Scopolamine can be used to reduce awareness  Genetics: 15% with +FHx CT Scan

in trauma pts w/ less lowering of BP  Most accurate

RFs  Gold standard as preop scanning tool

ANEURYSMAL DISEASE – Mitchell  Number one: age (>65)  Excludes rupture in symptomatic pts

 Male  Defines anatomy and anomalies

 Def: ―a widening” 1.5x normal size  Cig smoking  Reproducible to within 0.2 cm. Use 2 mm cuts

o Ectasia= dilation 5-5.5 cm if repair

common)  Reproducible to within 0.2 cm

abdominal girth 0.5 cm in 6 mo then it should be

o visceral / extremity ischemia thickness repaired

o juxtarenal and suprarenal AAA  COPD: mechanism ↑ imbalance in protease  No evidence to support regular medical mgt to

o Horseshow kidney activity prevent expansion

o Renal insuf w/ uncomtrolled HTN  Eccentric saccular aneurysm—increases risk

o generally, not used often  Rapid expansion Types of Repair

 Inflammatory: no increase in risk  Endovasc aneurysm repair (EVAR)

AAA Nat Hx  Open anerysmorrhaphy

 Grows avg 0.4 cm / yr Screening o Midline transabdominal incision

 Risk of rupture exponentially related to  Everyone agrees: o Retroperitoneal appraoach

aneurysm of diam M >65 yo with hx of smoking

 5 cm diam  avg yrly rupture rate 3-5%  More controversial: EVAR Advantages

 7 cm diam carries rupture rate of 19%/yr o Men >65 yo, FHx of AAA, females w/ mult  Reduces operating time

RFs  Shorter LOS and ICU stay

Complication of AAA  ↓ recovery time, post-op pain

 Rupture Mgmt depends on:  Blood transfusion

o only 40-50% reach hosp alive (15:13)  Size  Less chance graft infxn

o 505 operative mortality o Good risk pts w/ AAA > 5.5 cm should  Return to work faste

o Overall >75% mortality rate for repair undergo elective repair

o Clinical pres o No survival advantage for 5.5 cm) or US surveillance every 6  Probs of endoleaks, graft failures

 Distal embolization mo  Require life long graft surveillance

o Most minor affecting distal extremities/toes o 4.9 yr f/u found surgery mortality 25%,

 Long-term reports not available

o More common during repair surveillance mortality 21.5

 No difference in mortality

 Aortocaval fistula o Most deaths d/t cardiovascular dz

o Rare o Median AAA growth rate 0.33 cm/yr

Based on avail evidence, EVAR is appropriate tx

o Pres o Bottom line: no level 1 evidence to repair

for selected pts, esp those w/ hi risk for open surg

 LE edema, hematuria, rectal bleed AAA 75 yo

thrombotic dz

rupture o Disabling COPD, home O2, FEV1 2 yrs

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 Young pts – good operative risk?? o 15 mm length glues); or open conversion if all

EVAR: Preop imaging o 25 mm seal zone persist >6 mo

o +/- contrast  Extent of aortic and iliac a involvement - only worry about surg

o Need lrg volume of iodinated contrast (100- o Stent graft usu ends in common iliac a intervention if aneurism sac

150 cc) o If diam of common iliac too large, the stent continues to grow – treat w/

o Narrow collimation, 3 mm cuts can be extended to the external iliac a embolization, lap clipping

o Reformatting fo axial slices 3D o You may exclude flow from mesenteric o Late comps

reconstruction arteries which will cause sigmoid ischemia  Graft limb thrombosis – kinking in

 Pitfalls o The hypogastric a should be coil-embolized limb

o As AAA expands and lengthens, the neck as retrograde flow from the internal iliac a  Stent-graft infxn: no published

deviates anteriorly and laterally  can will cause an endoleak reports, only anecdotal reports

overestimate neck diam and  Comps  Device failure

underestimate neck lengh o Perioperative  Dilatation ofproximal neck

 Injury to access vessels  Late rupture

Angiography  Embolization

 not necessary for graft sizing - Microembolization and death EVAR results – a bunch of stuff she skipped

 can provide add‘l info from renal failure

o grade of stenosis of branches of Ao - Distal ischemia EVAR: Post-op surveillance

o renal, accessory renal  Post-implant syndrome o What to look for in the post op period

o patency of IMA - Febris eci (40 deg C)  Change in aneurysm size (ie

o lumbars - Depression continued growth = bad)

- Back pain from thrombosis  Stent migration

EVAR Anatomical Requirements - Incidence 150%  Endoleak

 Groin and wound comps  Limb stenosis

 Visceral supply

o Endoleak – failure to exclude aneurysm  Device integrity

o Access patency celiac and SMA before pt

sack from arterial blood flow o CTA

IMA overstented

 Type 1: attachment to site leaks  98% accurate in detecting

 Diameter, length, angulation, and conical nature

 Type 2: branch leaks endoleaks

of prox neck

 Type 3: structural failure  Accurate and reproducible diameter

 Calcification and mural thrombus in prox neck measurements

 Type 4: Graft wall porosity

 Diam of iliac a  Dense contrast bolus and delayed

 Type 5: endotension

 Length of distal sealing zone o Management of endoleaks images

 Tortuosity of iliac aa  Type 1 and 3  Time course: 1, 6, 12 months, and

 Extent of aortic and iliac a involvement - Require immediate repair: yearly thereafter

 Neck: use cuff or extension grafts;  2 kinds of open repair

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Midline Retroperitoneal  to maintain perfusion to pelvis and sigmoid one o #1 cause of periop mortality

- explore abdominal - hostile abdomen must maintain blood supply – may need to hook o Renal failure

viscera - stromas up the IMA  Distal embolism

- expose distal common - morbid obesity  Indications for renal a reconstruction  Severe acidosis – can be from prolonged aortic

iliac a: lrg right iliac a - aneurysm requiring o Renal a aneurysm >2 cm diam clamping, can get severe hypoTN w/ release of

aneurysm suprarenal clamping: o Involvement of renal a ostia clamp

- right renal a dz not complex aneurysm w/ o Renal failure w/ bilat pre-occlusive renal a  Graft infxn – rare, increased incidence after

amenable to celiac and sma vessel dz o Asymptomatic >80% renal a stenosis assoc‘d ischemic colitis

endarterectomy or juxta/suprarenal AAA o Renovascular HTN  Ischemic colitis – most dreaded complication

- L sided vena cava - horseshoe kidney o Best approached via retroperitoneal o Occurs ~10%, more common in setting of

-inflammatory AAA approach rupture

o Only 2-3% clinically significant

 Retroperitoneal approach Ruptured AAA o Usu 2-3 days post op

o We are on the L side of the abd, sneak  If aneurysm freely ruptures anteriorly into o Clinical manifestations

behind peritoneum down to the Ao which peritoneal cavity, rapid exsanguination  Unexplained fluid sequestration

lies over the lumbar spine occurs—pt usu doesn’t make it to hospital (BP unresponsive to resuscitation

o Advantages:  If it ruptures posteriorly, the hemorrhage goes b/c their colon is dead)

 you can get higher up on the Aorta into retroperitoneal space, may be contained, pt  Fever, leukocytosis, sepsis (L colon

than midline approach (in midline makes it to the ER bc it’s a controlled bleed – dies bc insuff blood supply bc

approach, pancreas gets in the way) there‘s no where for the blood to go you‘ve taken out the IMA)

 easier w/ morbidly obese pts  Achieve rapid proximal control by compression o Prevention: reimplant IMA if

 Midline: the peritoneum is opened, make long or clamping of supraceliac Ao through the  Lrg IMA

incision down to pelvis diaphragmatic crura  Good back bleeding

 After establishing control, move clamp to  Stump pressure <40 torr

Techniques of open repair: (she went through a infrarenal position  h/o L hemicolectomy

bunch of diagrams w/ relatively little explanation,

this is what I could catch) Goals of AAA repair Late comps

 move renal veins out of the way; give pt  Prevention of death from rupture  Aortic graft infxns

heparin; apply clips above and below the  Limb preservation by maintainance of adequate o 1% aortoiliac

aneurysm arterial perfusion o 2% aortofemoral

 ―oversew‖ lumbar arteries  Maintaining quality of life – minimize comps, o 70-80% late

 Cut a ―button‖ of tissue and sew it onto the maximize durability of reconstruction, o usu staph aureus, pseudoaneurysms in

graft preservation of sexual fxn (parasympathetic anastomotic suture line ie almost always

 sew aneurysm sack closed to prevent intestines plexus responsible for ejaculation) from graft infxn

from sticking

 tube graft = a straight shaft of graft Early comps of AAA Repair (End of lecture)

 bifurcated graft = aneurysm extends into iliac  bleeding – massive transfusion increases post

aa op M&M

 MI



9



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