Vascular Surgery Emergencies (not AAA)

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Transcript Vascular Surgery Emergencies (not AAA)

Vascular Emergencies
(Not including
ruptured aneurysms)
Adrian P. Ireland
BA(mod) MB MCh BAO FRCS(I)
RCSI final meds 12 Jan 2004
Outline
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What are the Vascular Emergencies?
Review of the circulation
Pathogenesis of blocked arteries
Manifestations of blocked arteries
Monitoring the circulation
Occlusive peripheral vascular disease
– Acute and Chronic Ischemia
Vascular Emergencies
(not aneurysms)
• Arterial
– Acute ischaemia
– Bleeding due to trauma (incl. iatrogenic)
• Venous
– Deep Venous Thrombosis (Phlegmesia Caeurlia
Dolens)
– Pulmonary Embolism
• Lymphatic
– Cellulititis
• Compartment Syndrome
Occlusive Peripheral Vascular
Disease
• Peripheral vascular disease
– Includes any disease affecting the
peripheral vascular system
• Occlusive – essentially blocked arteries
Review Of Circulation
• Cells need supply of nutrients and
removal of by products
• In a unicellular organism this may occur
via the cell membrane into say a pond
or sea
• Multicellular organisms need a
circulatory system
William Harvey (1578-1657)
On the Motion of the Heart and Blood in Animals
(1628)
Problem With Blocked Circulation
• Tissues lack adequate supply of nutrients
• Tissues suffer build of toxic by products
• May cause symptoms and signs particularly
when more blood flow is required;
– To muscles during exercise
– To tissues that are injured (more blood needed)
Pathogenesis Of Blocked Arteries
• Atherosclerosis
– Genes, hyperlipidemias
– Lifestyle
• Smoking
• High fat diet
• Lack of exercise
– Co-morbidities
• Diabetes, hypertension, hypothyroidism,
homocysteine
Manifestations Of Blocked Arteries
• Depends on circulation affected
– Heart
• Stable angina, unstable angina, myocardial infarction
– Brain
• Transient ischemic attact, stroke
– Kidney
• Hypertension, renal failure
– Legs
• Claudication, rest pain, necrosis
Principal causes of death in
Ireland (males)
other
12%
circulatory
disesases
43%
Injury and
poisining
6%
respiratory
diseases
15%
malignant
neoplasms
24%
Report on Vital Statistics Central Statistics Office Ireland, 1995
Annual Deaths Due to
Cerebrovascular Disease and
Ischemic Heart Disease
2500
IHD
Male
2000
Deaths
per
100,000
1500
IHD
Female
1000
CVA
Male
500
CVA
Female
75
+
35
-4
4
45
-5
4
55
-6
4
65
-7
4
0
Age Range
Report on Vital Statistics Central Statistics Office Ireland, 1995
Manifestations Of Blocked Arteries
• Depends on speed of development of
blockage
– Slow blockage
• Permits development of collateral blood supply
so that occlusion may be asymptomatic
– Rapid blockage
• No time for development of collaterals
– Symptoms/ signs depend on adequacy of preexisting
collaterals
Monitoring Circulation
• Mottling, colour, temperature,
movements, sensation
• Palpable pulses, doppler signals
• Non invasive pressure studies (Doppler)
• Duplex imaging
• Angiography (IAA, DSA, MRA)
Non Invasive
Pressure
Studies
(NIPS)
Duplex of carotid stenosis
Angiography
(DSA)
MRA
Occlusive Peripheral Vascular
Disease
• Classification based upon clinical
presentation
– Acute ischemia
– Chronic ischemia
• Anatomic classifcation based upon
site(s) of disease
OPVD Anatomic Classification
• Aorto-iliac
– Le-Riche
• Femero-popliteal
• Tibio-peroneal
Acute Ischemia
Effects Of Acute Ischemia
• Reduced blood flow
– Pulseless, pallor, perishing cold
• Nerve ischemia
– Pain, paralysis, Paresthesia
• Muscle ischemia
– Rhabdomyolysis
• Compartment syndrome
• Ischemia reperfusion syndrome
Compartment Syndrome
• Pathophysiology
• Diagnosis
• Management
Compartment Syndrome
Pathophysiology
• Strong fascia encases the limb to aid muscle
function and return of venous blood
• Injury results in swelling
• Swelling raises pressure
• Pressure occludes lymphatic return, then
venous return, then arterial inflow
– Result is dead or severly damaged tissues due to
pressure and ischemia
Compartment Syndrome
Diagnosis
• Strong index of suspicion
– Nature of injury and duration of ischemia
• Clinical manifestations
– Nerve and muscle dysfunction
– Decreased perfusion
– Tense compartment
• May measure compartment pressure as
adjunct to treatment > 40 mm hg
Compartment Syndrome
Management
• Fasciotomy
Acute Ischemia
• Causes
– Thrombosis
– Embolism
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The P’s
Thrombosis or embolism?
Clinical assessment of severity
Clinical algorithm
Causes of Acute Ischemia
• Trauma
• Thrombosis
• Embolism
• Small print
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Aneurysm
Thrombophilia
Paradoxial embolism
Anatomic variation
Csytic adventitial disease
Thrombosis
• Occlusive atherosclerosis
• Aneurysm
• Malignancy
• Thrombophilia
Embolism
• Macro-embolism
– arterial side
– venous side (patent foramen ovale)
• Micro-embolism
– ulcerated atherosclerotic plaques
– aneurysm
The P ’s
• No flow in artery
– Pallor
– Pulse absent
– Perishing cold
• Nerve becomes ischemic
– Pain
– Paresthesia / anesthesia
– Paralysis
Thrombosis or Embolism?
Sex
Embolic source
Onset
Ischemia
PHx
Other leg
Thrombosis
Male
No
Progressive
Milder
Claudication
Abnormal
Embolism
Female
Yes
Acute
Severe
None
Normal
Clinical Assessment of
Severity
• Viable
• Threatened
– Marginally
– Immediately
• Irreversible
no immediate threat
ok if treated
promptly
ok if treated
immediately
dead leg
Irreversible Ischemia
• Sensory loss
Profound,
anaesthetic
• Muscle weakness Profound,
paralysis
• Arterial doppler
Inaudible
• Venous doppler Inaudible
Amputation
Viable no immediate threat
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Sensory loss
None
Muscle weakness None
Arterial doppler
Audible
Venous doppler
Audible
Restore perfusion
Clinical Assessment of
Severity
• Viable
No immediate threat
• Threatened
–marginally
–immediately
• Irreversible
Ok if treated
promptly
Ok if treated
immediately
Dead leg
Threatened Marginally
• Sensory loss
Minimal (toes)
to none
• Muscle weakness None
• Arterial doppler
Inaudible
• Venous doppler
Audible
Restore perfusion
Threatened Immediately
• Sensory loss
More than toes,
Pain
• Muscle weakness Mild to
moderate
• Arterial doppler
Inaudible
• Venous doppler
Audible
Restore perfusion
Practical Questions
• Is this ischemia? (DDx stroke, TIA, cord)
• Is the limb viable, threatened or lost?
• If threatened how long can reperfusion be
delayed?
• Is there a need for duplex or angiography?
• Should the patient be immediately
heparinised?
acute non traumatic ischemia
Irreversible
Threatened
Viable
Clear embolus
?Thrombosis
Duplex
Adequate
Inadequate
Angiogram
Treat
Amputation
Embolectomy Thrombolyse Reconstruct
+/- PTA
Prognosis
• Embolism
– Overall 60% dead within three years
– One episode 15-20% mortality (in hospital)
– Two episodes 40% mortality (in hospital)
• Thrombosis
– Overall 40% dead within three years
Chronic Ischemia
LaFontaine Classification
Stage 1
Stage 2
Stage 3
claudication
rest pain
necrosis/ulceration
Definition Of Critical Ischemia
• Presence of tissue loss
OR
• Rest pain with ankle pressure less than
50 mm Hg
FOR
• More than 2 weeks
Acute on Chronic
Bypass
J.C. 68 year old male
• Emergency admission 24.3.2000 to
vascular service SVUH, via A/E
– Ischemic right foot
History of Presenting
Complaint
• Awoke with coldness and numbness in
the right foot 2 hours ago
• Gradually sensation returned and foot
became warm again
• Worsening claudication for two years,
100 metres
Past History
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1996 angina, failed angioplasty (aspirin)
1996 hypertension (atenalol)
1996 Hypercholesterolemia (diet)
June 1999 dizzyness ? cause
– Carotid duplex showed non critical stenosis
Social History
• Retired
• Lives with wife
• Ex smoker 20 cigarettes per day for 20
years (gave up 20 years ago)
Clinical Examination
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No distress, vitals normal
Regular pulse
Left carotid bruit
Normal examination of chest
Normal examination of abdomen
Examination - Right foot
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Absent pulses below femoral
Pallor at 30 degrees
Movements and sensation intact
Hand held doppler reveals arterial
signals over dorsalis pedis and
peroneal, posterior tibial signal absent
Investigations
• CXR - normal
• ECG BSR, Left axis deviation
– Old lateral MI
• U+E - U 7.7, Creatinine 118
• FBC - Normal
• COAG - Normal
Non Invasive
Pressure
Studies
Digital Subtraction Angiogram
Summary
• 68 year old male
• Acute on chronic
ischemia right foot
• Previous, MI, OCD
(dizzy turn)
• Critical ischemia
• Probable poor run off
on angiogram
Pre operative course
• Elected initial conservative management
• Anticoagulation with Heparin
• 28.3.2000 decision to proceed to elective
surgery (next list 6.4.2000)
• 29.3.2000 further episodes of numbness,
twice, and pallor on the flat
– proceed to urgent vascular reconstruction
Vascular Reconstruction
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Right fem pop below knee bypass
General anaesthesia
Commenced 16:05 finished 19:10
No transfusion
Vascular Reconstruction
• Conduit - thin wall 6mm PTFE
– Long saphenous vein thrombosed below
knee
– Poor quality vein in groin
• Inflow - CFA s/e 5/0 prolene
• Outflow
– Miller cuff to BK pop 6/0 prolene
– e/s PTFE to cuff 6/0 prolene
Miller Cuff - technique
Miller Cuff - technique
Post Operative Course
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Day 14
Palpable DP pulse in foot
Wounds healing
Discharge to Convalescence
Chronic
Endarterectomy
Chronic
In situ distal bypass
Fem to distal 1/3 posterior tibial
with insitu long saphenous vein
Critical Limb Ischemia Sweedish Data
• 30 d mortality 5.3%
• 1 year mortality 22.9%
• For those aged > 75
– 30 d mortality 6.4%
– 1 year mortality 26.4%
Eur J Vasc Endovasc Surg 16:137-141, 1998
Critical Limb Ischemia Finnish Data
Mortality
Bypass
Amputate
30 day
8%
24%
1 year
20%
43%
5 year
57%
84%
Ann Chir Gyn 86:213, 1997
Effect of Vein Cuff on patency
of PTFE fempop Bypass
100
90
80
70
60
50
40
30
20
10
0
AK PTFE cuff
AK PTFE no
cuff
BK PTFE cuff
BK PTFE no
cuff
1 year
2 year
n = 261 Randomised, BK 84:62% 2 y salvage cuff:nocuff
Stonebridge, Prescott and Ruckley. J Vasc Surg 26(4):543-50, Oct 1997