Things That Bring Me In
At Night
(Vascular Emergencies)
Abdominal Pain
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69 year old male
Sudden onset abdominal
pain, passed out at work
PMH: HTN
PSH: Hartman’s
procedure for diverticulitis
Meds: None
SH: Retired, plays golf
daily
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PE: BP 65/40, HR 120
Lungs: Coarse
Heart: Tachy
Abd: Hugely distended,
midline scar
Ext: Weak pulses
Referred from outside
hospital, 45 minutes in
ambulance
AAA
 Prevalence
2-5 %
 Men
4:1
 Rupture Risk
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Size does matter
•
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•
5-5.9 cm 5% per year
6-7 cm 6.6% per year
> 7cm 20% per year
Grow at 0.5 cm/year
Etiology of Ruptures
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Aortic wall contains vascular smooth muscle as
well as elastin and collagen
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Gradual reduction of medial elastin layers and
collagen content
• Medial thinning and intimal thickening
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Elastin is principal load-bearing element that resists
aneurysm formation
Collagen acts as “safety net” to prevent rupture
Excessive collagenase activity/ elastase activity
Laminated thrombus lines aneurysm
Law of Laplace
 Relationship
between tangential stress (T)
tending to disrupt the wall and radius ( R)
and the transmural pressure (P)
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T=P*R
Diagnosis
 High
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index of suspicion is critical
< 15% know they have AAA prior to rupture
 Mean
time from Sx to ER is 37 hrs
 Lower back, flank or groin pain
 Pulsatile abd mass, hypotension, anemia
 No imaging in an unstable pt
Treatment
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60 % of ruptures die prior to arrival
48 % operative mortality
Overall ~ 90% mortality for ruptures
Take promptly to OR
“I feel no significant attempt should be made for
blood volume resuscitation until the time of
operation. The SBP should be maintained 50-70
mm Hg until the aorta is clamped.”
Prepped/draped then anesthesia
Bulging Groin
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79 year old male
 History of bulge right
groin, recent difficulty
walking, no recent trauma
 Poor historian
 PMH: COPD, HTN
 PSH: No vascular
surgeries
 Meds: Inhaler
 FH: No aneurysms
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PE:
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Thin black male
148/87
No acute distress
RRR
CTA
Pulsatile mass right groin
Cool lower extremities, no
palpable pulses
 Embolization
L hypogastric 12/20
 EVAR of L Iliac aneurysm 12/22
 R femoral aneurysm repair 12/31
 Bilateral AKAs 2/19
 Returns
7/04 with enlarging pulsatile mass
in left groin
Head
Aneurysms
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AAA identified in 6-9% of men over 65
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Family history discernible in up to 20%
Specific genetic defects only identified in 5% of familial AAA
Pathology of aneurysm wall:
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Decreased elastin (especially in Marfan’s)
Altered type III collagen (Ehlors-Danlos)
Endogenous proteases produced by inflammatory cells
Matrix metalloproteinases (esp. MMP-9 and MMP-12)
• Activity reduced by doxycycline with decreased aneurysm formation
in rat models
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Alpha-1 anti-trypsin association in familial AAA
Lipoprotein (a) increased levels in familial AAA
Aneurysms
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Isolated iliac/femoral artery aneurysms rare
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Usually associated with aortic aneurysms
Both more common in men
For iliac, incidence is 1% that of AAA (500/year US)
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Common > Internal > External
Natural history not well known, although rupture rare if <3 cm
Rupture more common than embolus or thrombosis, especially if
greater than 5 cm
Treatment must consider likelihood of AAA development in the
future
Aneurysms
 Femoral
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Type 1 CFA only, Type 2 involves origin of profunda
Rare, seen in only 3% of AAA
Of pts with CFA aneurysm
• 95% have second aneurysm
• 92% had aortoiliac aneurysm
• 59% bilateral femoral aneurysm
-Dent et al. Arch Surgery, 1972
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Natural history also not well known
Thrombosis more common than rupture, 12-40%
estimated
GSW Left shoulder
 37
year old female
 GSW to left shoulder
 Hemodynamically stable
 Previous GSW abdomen
 BP 150/70 R, 70/30 L
 Left hand cool
Etiology
 Emboli
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vs Thrombosis
Emboli primarily from the heart (AAA’s)
Thromboses occur most freq in setting of
aortoiliac occlusive dz
• Low flow states (dehydration / decreased CO)
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Intraplaque hemorrhage
Hypercoaguable states
Dissection / Trauma
Diagnosis
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Six p’s of acute extremity ischemia
Severity dependent on extent of thrombus,
distal embolization, adequate collaterals
Focus on neuro deficits often cause delay
Presence of abd pain, severe HTN, anuria
suggest renal and mesenteric involvement
Utility of imaging is uncertain
• Dossa: helpful in 2/24
• Littooy: helpful in 1/6
Treatment
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Requires prompt definitive treatment
• Severity of ischemia correlates with outcome more
than duration
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Several case reports of endovascular tx
• Reserve for high-risk, minimal sx
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Nonoperative Tx carries > 80% mortality
Heparin at time of Dx (except with HAT)
Measure bilateral upper extremity BP’s
Treatment
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Thromboembolectomy
• All pts should undergo initially unless severe
aortoiliac dz is known
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Axillobifem
• “Simple” with potential lower mortality
• Inferior long term patency (5 yr 37-81%) vs (8090%)
• Potential for clot propagation
Summary
 Outcome
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Mortality 23-53%
High Complication rate (70%)
Limb salvage approaches 95% in surviviors
Pts with embolic occlusions noted to have
27%-37% recurrent emboli – underscores
need for long term anticoagulation
52 yo AA male c/o left foot rest pain
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PMHX: pancreatitis,
arterial occlusive
disease
PSHx: Bilat iliac stents,
Left CFA
endarterectomy, L SFA
stent
Meds: tylenol,
coumadin
Social: Heavy tobacco
history
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Exam:
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Alert, responsive
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No JVD, no bruits
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RRR, no murmurs
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Abd soft, no masses
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Palpable femoral pulses
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Palpable distal pulses on
right
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Non palpable distal
pulses on the left
Acute Arterial Occlusion
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Sx depend on level/severity of obstruction and
existence of collaterals
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Pts without hx of claudication or previous
reconstructions – most likely embolic
6 “P”s
Ischemic manifestations usually most severe
one joint space distal to occlusion
 Pain – sensory deficits – numbness – paralysis
 Pallor – blanching mottling – nonblanching
mottling
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Management
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Embolism: Thromboembolectomy
Pts with preexisting vascular disease are much
more complicated
 Heparinization
 Arteriography when cause is uncertain
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Emboli: Meniscus sign, lodge in bifurcations, multiple
filling defects
Doppler exam: help determine patent distal
outflow tract
 Bypass
Fasciotomy
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Capillary leak after prolonged ischemia and reperfusion
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As compartment pressure rises, tissue perfusion
decreases
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Inflammatory mediators and free radicals
Neutrophil adherence to endothelium leads to oxidant release
20 mmHg: impaired
< 30 mmHg from DBP, flow is sig decreased
Need for fasciotomy increases with
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> 6 hours
Arterial and Venous injury
Soft tissue crush injury or Fx
Fibinolytic agents
 Streptokinase
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Combines with plasminogen to form activator
complex which acts within the clot and in
circulating plasma
 Urokinase
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Directly converts pasminogen to plasmin
Higher affinity for clot bound plasminogen
 tPA –
even greater clot specificity
Case Presentation
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65 yo male with acute slurred speech and loss of vision
in the inferior field of the R eye
PMH: B carotid stenoses on recent US, HTN, CHF,
hypercholesterolemia
PSH: appendectomy
Social: quit smoking 1973
Meds: plavix, norvasc, lisinopril, simvastatin
Case Presentation
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Exam: B carotid bruits (L>R), heart regular, visual deficit
inferior hemifield of R eye, normal speech, no focal
weakness
EKG: sinus rhythm
Echo: no thrombus or vegetation
Head CT (admission): negative
MRI (day 2): multiple infarcts involving R frontal lobe, L
caudate nucleus, and L occipital lobe
Amaurosis Fugax
R superior retinal infarct
Ophthalmic artery
(1st
branch of ICA)
Retinal arteries
Visual Deficit
R inferior hemifield
deficit
R superior retinal infarct
Carotid Duplex
Class
1
2
3
4
5
Category
0-39%
40-59%
60%
60-99%
occluded
Vp (cm/s)
<160
>160
>160
>160
0
Vd
<80
<80
80-109
>110
0
R Carotid
Duplex
Class 3
L Carotid
Duplex
Class 4
Arch vessels
R carotid arteries
R carotid arteries
L carotid arteries
Controversies in Carotid Surgery
General anesthesia vs. local anesthesia
Intraoperative monitoring of cerebral ischemia
Selective shunting vs. routine shunting
Primary closure vs. patch angioplasty
Carotid Endarterectomy with Intraluminal Shunt
Complications of Internal Shunts
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1-3% complication rate
Damage to the arterial
wall
Embolization
Arterial Closure Following Shunt Placement
Measurement of ICA Stump Pressure
PICA ~ PMCA
Local Anesthesia with Mental Status Monitoring
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“The time-honored technique is trial occlusion with local
anesthesia.” (Rutherford Vascular Surgery)
Considered the gold standard
Carotid occlusion for 3 minutes with evaluation of speech
and contralateral movement
85-90% pass this test, but 10-15% require a shunt
This technique yields the lowest stroke rate and lowest
rate of shunt use
Common Indications for Shunt Placement
1.
2.
3.
4.
5.
Deterioration of mental status exam or contralateral
extremity function
EEG changes
ICA stump pressure <40 (range 25-50)
Recent stroke
Complete occlusion of contralateral ICA