1. Acute limb ischemia is a medical emergency that occurs when there is a sudden decrease in blood flow to a limb, threatening the viability of the limb. It requires urgent evaluation and management within 2 weeks of symptom onset.
2. The main treatment options are endovascular therapies like catheter-directed thrombolysis or mechanical thrombectomy, or surgical interventions like thrombectomy or bypass surgery. The goal is to rapidly restore arterial blood flow while minimizing risks to the patient.
3. Factors like the severity of ischemia, time since symptom onset, and patient characteristics help determine which treatment - thrombolysis, surgical thrombectomy, or in some cases immediate amputation - is most appropriate to salvage the limb.
2. DEFINITION
“Acute limb ischemia is Sudden decrease in limb perfusion that
threatens limb viability (within 2 weeks of the onset of symptoms) and
requires urgent evaluation and management.”
3. Introduction
■ Acute limb ischemia (ALI) is one of the most treatable and potentially devastating
presentations of Peripheral Artery Disease (PAD)
■ Critical limb ischemia (CLI) is defined as limb pain that occurs at rest or impending
limb loss caused by severe compromise of blood flow to the extremity.
■ Chronic ischemia induces the development of collateral blood vessels and results in
skin changes secondary to progressive ischemia.
4. Burden of Acute Limb Ischemia
■ Acute limb ischemia is a surgical emergency with significant morbidity and
mortality.
■ The incidence of ALI is 9–16 cases per 100,000 persons per year for the lower
extremity and around 1–3 cases per 100,000 persons per year for the upper
extremity.
■ Most published series report a 10% to 30% amputation rate
■ The short-term mortality is 15% to 20% (3-year).
■ This is a time-sensitive condition, and the diagnosis is primarily clinical.
5. Pathophysiology
■ Insufficient oxygenated blood to meet the metabolic demand of the tissues.
■ Ischemia → shift aerobic to anaerobic metabolism → lactate production.
→ depletion of ATP → leakage of extracellular calcium into muscle cells → cell death.
■ Severity Depends on
– degree of obstruction
– Site of occlusion,
– Presence of collaterals
– Affected tissues
– systemic perfusion, such as cardiac output and peripheral vascular resistance
6. Pathophysiology
■ The tissues most sensitive to ischemia are
– peripheral nerves, (irreversible damage after 6 hours)
– skin,
– subcutaneous tissues,
– skeletal muscle (up to 10 hrs)
7. Pathophysiology : Reperfusion injury
■ Ischemic tissue → free radicals → trigger peroxidation of membrane lipids →
increased capillary permeability and filtration → swelling → compartment syndrome.
■ Inflammation → leukocyte-activated platelet aggregation and complement system
activation → occlusion of the reperfused vessels (no-reflow phenomenon)
■ Byproducts of cell death are released into the systemic circulation and include
potassium, phosphate, myoglobin, creatine kinase, and thromboplastin.
– and can lead to rhabdomyolysis, cardiac dysrhythmia, multiorgan failure,
disseminated intravascular coagulation, and death.
8. Etiology
The etiology of lower extremity ALI is traditionally either
■ embolism,
■ in situ thrombosis with preexisting peripheral arterial
disease (PAD),
■ graft/stent thrombosis ,
■ trauma, or
■ peripheral aneurysm with embolism or thrombosis .
11. THROMBOSIS: mechanisms
■ Atherosclerosis
■ Low-flow states
– Congestive heart failure
– Hypovolemia
– Hypotension
■ Hypercoagulable states
■ Vascular grafts
– Progression of disease
– Intimal hyperplasia
– Mechanical
■ Arterial plaque rupture
■ Trauma
■ Aortic/arterial dissection
■ HIV arteriopathy
■ Arteritis with thrombosis
■ Popliteal adventitial cyst
with thrombosis
■ Popliteal entrapment with
thrombosis
■ Vasospasm with thrombosis
(e.g., ergotism, cocaine)
■ External compression
■ Iatrogenic – catheter induced
12. Embolism versus Thrombosis
Embolism Thrombosis
Sources Frequently detected Not specified
Onset Sudden Acute
Site Normal vessels On stenosis, calcified
Previous history a known embolic source,
such as cardiac arrhythmias
Symptoms of chronic
ischemia
Findings Normal pulses in uneffected
limb
Evidence of peripheral
arterial disease
Multiplicity Multiple sites Single site
Angiography multiple occlusions, no
collaterals
Diffuse atherosclerosis
Collaterals present
The timing of presentation depends on the severity of ischemia, which is
linked to the etiology. Patients with embolism, trauma, and popliteal
aneurysms present early (hours), compared to those with in situ thrombosis
presenting later (days)
13. Nonatherosclerotic causes
■ arterial trauma,
■ vasospasm, drugs(cocaine, vasopressors)
■ low flow states: eg cardiogenic shock/sepsis
■ vasculitis,
■ hypercoagulable states,
■ aortic dissection, - should be strongly considered in patients with unilateral or
bilateral iliac occlusion.
■ external arterial compression, such as with popliteal cyst, popliteal artery
entrapment syndrome. – should be considered in younger patients with absent
atherosclerotic risk factors.
■ Iatrogenic; arterial catheterization
14. Clinical features of acute ischemia
Pain : symptom
PALLOR
POIKILOTHERMIA
PULSELESS
PARASTHESIA
PARALYSIS
Either constant or elicited by
passive movement of the
involved extremity.
Embolic occlusions are
usually very sudden and of
great intensity, such that
patients often present within
a few hours of onset.
15. Clinical features of acute ischemia
Pain : symptom
PALLOR
POIKILOTHERMIA
PULSELESS
PARASTHESIA
PARALYSIS
COLOR
Early: Pale
Later: Cyanosed → Mottling → fixed mottling &
cyanosis
Pallor
An area of fixed
cyanosis surrounded
by reversible mottling
Empty veins:
compare with normal
limb
16. The limb is cold
sudden loss of previously
palpable pulse implies
embolic cause.
compare with the other
side
Slow capillary refilling of
the skin after finger
pressure
Bounding water hammer
pulses proximal to
occlusion
Clinical features of acute ischemia
Pain : symptom
PALLOR
POIKILOTHERMIA
PULSELESS
PARASTHESIA
PARALYSIS
17. Loss of sensory function
Numbness will progress
to anesthesia
Progress of Sensory loss
Light touch
Vibration sense
Proprioreception
Deep pain
Pressure sense
Clinical features of acute ischemia
Pain : symptom
PALLOR
POIKILOTHERMIA
PULSELESS
PARASTHESIA
PARALYSIS
18. Loss of motor function:
Indicates advanced limb threatening
ischemia
fine movement affected first
Late irreversible ischemia: Muscle
turgidity
Intrinsic foot muscles are affected first,
followed by the leg muscles
Detecting early muscle weakness is
difficult because toes movements are
produced mainly by leg muscles
Clinical features of acute ischemia
Pain : symptom
PALLOR
POIKILOTHERMIA
PULSELESS
PARASTHESIA
PARALYSIS
19. other clinical features
■ Signs-
■ Limb blood pressure (<50mm hg)
■ Edema does not occur, however, with acute arterial occlusion unless diagnosis is
delayed and swelling begins to develop
20. Differential diagnosis
■ low cardiac output (especially when superimposed on chronic lower extremity PAD)
■ acute deep vein thrombosis (DVT), (especially when associated with features of
phlegmasia cerulea dolens)
■ Chronic peripheral neuropathy (diabetic neuropathy), or
■ acute compressive peripheral neuropathy (compartment syndrome)
■ Potential causes of nonischemic limb pain include acute gout, spontaneous venous
hemorrhage, or traumatic soft tissue injury.
23. Diagnosis and Management
■ Diagnosis of ALI is primarily clinical.
■ In patients with suspected ALI, initial clinical evaluation should rapidly assess limb
viability and potential for salvage and does not require imaging
■ The severity of the ischemia, according to the classification presented above, will
dictate the extent of diagnostic tests performed for systemic risk factor assessment.
24.
25. Management: initial work-up
■ Routine blood studies should be performed before heparin is administered.
– CBC: elevated platelet in thrombotic disease
– Creatinine kinase: predictive of major amputation.
– Hypercoagulable state and Homocysteine: prothrombin time, partial
thromboplastin time, thrombin time, lupus anticoagulant, anti-cardiolipin
antibody, activated protein C resistance, factor V Leiden
– Renal function test: elevated in DM,HTN. No contrast study if deranged
– Lipid profile: hyperlipidemia
– FBS and HbA1c
– ESR: elevated in collagen vascular disease
– CRP: marker of worsening PVD
■ A plain chest x-ray and electrocardiogram should be obtained from every patient.
■ Echocardiogram: In suspected embolism, as soon as time allows.
26. Management: Early heparinisation
■ early heparinization is remains one of the mainstays in the treatment of ALI.
– immediate full-dose heparinization can result in symptomatic improvement in
some patients, either from the anticoagulation effects of heparin or volume
expansion
– prevents proximal and/or distal thrombus propagation and preserves the
microcirculation
– IV unfractionated heparin 80-150 U/kg bolus, followed by infusion of 18 U/kg/hour
– aPTT ratio 2-2.5
– If the patient has a known history of HIT or an anti-thrombin III deficiency,
alternative agents, such as direct thrombin inhibitors (lepirudin or argatroban),
can be used.
27. Management
■ Adequate analgesia
■ IV fluid resuscitication
■ Oxygen delivered by face mask
■ Correction of underlying electrolyte imbalances and systemic anticoagulation
should proceed concomitantly.
■ Aspirin initiated.
■ Limb placed in dependent position and kept warm
29. Duplex Ultrasonography
■ First-Level Noninvasive Diagnostic test
■ Low cost
■ In experienced hands may offer quality data as high as coming from the angiography
■ Thromboemboli: anechoic in the acute phase and gradually increasing in
echogenicity in a later phase. (possible to hypothesize the onset of the disease)
■ Also assess vessel wall status
30. Duplex
Ultrasonography
Duplex ultrasound findings at different limb
levels:
( a ) Doppler spectral analysis above the acute
occlusion (“stump” signal).
( b ) The vessel profile is irregular, some
calcifications appear as hyperechoic
thickening of the vessel wall, and hypoechoic
material is present intraluminally at the level
of thrombotic occlusion.
( c ) Downstream to the occlusion a
monophasic flowmetry (reduced PSV and
significant systolic phase prolongation) with
low resistance patterns may be appreciated.
31. CT Angiography
■ accurate analysis of the location, extent, and
grading of steno-obstructive disease
■ Still uses ionizing radiation and iodinated
contrast agent.
■ Limitation: “blooming artifact,” which affects
the evaluation of the lumen of diffusely
calcified vessels and pronounced in small
caliber vessels particular below-the-knee
vessels.
absence of flow in the right common iliac artery
(white arrow)
32. MR Angiography
■ Better for distal small and pedal vessels as compared to CT angiography
■ Higher cost, large number of artifacts.
■ More time consuming than CT.
■ Gadolinium worsens CKD patients and precipitates nephrogenic systemic fibrosis
33. Angiography
■ Invasive
■ Used to be gold standard test for road mapping before surgery
■ Replaced by CTA and MRA
■ On table arteriography has an established place intraoperatively as a guide for
extension of the procedure to ensure complete clearance of the arterial tree and
distal patency and for the evaluation of immediate results after surgical treatment.
■ Safer in recent years due to fine 3-4 F catheters
35. Management of ALI
■ Main target: Rapid restoration of arterial flow with least risk to patient
■ For viable limbs (Category I ALI), revascularization should be performed an on
urgent basis (within 6–24 hours).
■ For marginally or immediately threatened limbs (Category IIa and IIb ALI),
revascularization should be performed emergently (within 6 hours).
■ For nonsalvageable limb (Category III), Amputation should be performed as the first
procedure.
36. Management of ALI
■ The revascularization strategy can range from catheter-directed thrombolysis to
surgical thromboembolectomy.
■ The technique that will provide the most rapid restoration of arterial flow with the
least risk to the patient should be selected.
■ Prolonged duration of ischemia (> 6-8 hrs.) is the most common factor in patients
requiring amputation for treatment of ALI.
38. Intra-arterial thrombolysis
■ Catheter passed into occluded vessel, left embedded in clot and thrombolytic agent
infused over 24 to 48 hrs.
■ The method abandoned if no progression of dissolution of clot with time (>24 hours)
■ Thrombolytic agents: tPA, alteplase, reteplase & tenecteplase.
■ Patients with profound ischemia who may not tolerate such a prolonged procedure
are not candidates for catheter-directed thrombolysis.
■ Percutaneous endovascular thrombolysis options are more effective in patients with
– viable or marginally threatened limb and recent occlusion (<2 weeks),
– Arterial thrombosis,
– thrombosis of synthetic grafts, and stent thrombosis
39. Catheter directed thrombolysis
Pros:
■ Direct delivery of drug into existing thrombus
■ Reduces thrombolytic drug dosages
■ Lyses clot in both large and small vessels
■ Lower reperfusion syndrome than embolectomy
■ Done via percutaneous approach with local anaesthesia
Cons: takes >24 hours to be effective, Risk of major bleeding (6-9%),
40. Contraindications to thrombolytic
therapy
Absolute contraindications
■ Established cerebrovascular events (including transient ischemic attack) within last
2 months
■ Active bleeding diathesis
■ Recent (<10 days) gastrointestinal bleeding
■ Neurosurgery (intracranial or spinal) within last 3 months
■ Intracranial trauma within last 3 months
■ Intracranial malignancy or metastasis
41. Contraindications to thrombolytic
therapy
Relative major contraindications
■ Cardiopulmonary resuscitation within last
10 days
■ Major nonvascular surgery or trauma within
last 10 days
■ Uncontrolled hypertension (>180 mmHg
systolic or >110 mmHg diastolic)
■ Puncture of noncompressible vessel
■ Recent eye surgery
Minor contraindications
• Hepatic failure,
particularly with
coagulopathy
• Bacterial endocarditis
• Pregnancy
• Diabetic hemorrhagic
retinopathy
42. Mechanical thrombectomy
Percutaneous mechanical thrombectomy (PMT) with mechanical pulse spray/
suctioning with catheter as adjunctive therapy to thrombolysis (Angiojet catheter)
■ Pros:
– Disrupts the thrombus- allows better penetration of the clot by a thrombolytic
agent
– Reduces thrombolytic dosing
– Reduces therapy time- increasingly being used in class IIb
– Done via percutaneous approach with local anaesthesia
– Less vessel injury
■ Cons:
– Can be used only large vessel
– Expensive device
44. SURGICAL THROMBOEMBOLECTOMY
■ Local or general anesthesia
■ The artery (usually the larger proximal), exposed and held in
slings and longitudinal or transverse incision given
■ Fogarty balloon catheter introduced past the occlusion,
inflated and withdrawn with the clot.
■ Good back-bleeding and antegrade bleeding suggest that the
entire clot has been removed.
■ Completion angiography to ascertain adequacy.
46. SURGICAL THROMBOEMBOLECTOMY
■ Pros:
– Rapid revascularization
– Transfemoral approach can be done via local anaesthesia
– Adjunct by intraoperative thrombolysis
■ Cons:
– Risk of Vessel injury
– Reperfusion injury chances more and thus, compartment syndrome
47. Intra-operative Thrombolysis
Operative
Thromboembolectomy
Complete/ Near
complete thrombus
extraction
Incomplete thrombus
extraction with small
volume residual thrombus
Extensive residual
thrombus, Multivessel
distal occlusion
Bolus thrombolytic
agent into arterial
segment during
arterial occlusion
Bolus during arterial
occlusion(+repeat dose)
Or
20-30 min infusion
High dose isolated limb
perfusion
(Manual infusion or partial
bypass with pump
oxygenator)
48. Intra-operative Thrombolysis
■ Pros:
– Adjunct to surgical
thromboembolectomy- clear residual
thrombus in small arteries and arteriole
– Minimal risk of bleeding
■ Cons:
– Maybe inadequate in some patients
with extensive distal and small vessel
thrombosis
49. Arterial bypass surgery
■ Use in patient that
– failed other procedures- last resort!
– Severe tissue injury
– Associated Peripheral vascular disease
■ Main treatment for thrombosed popliteal
artery aneurysm
■ High surgical risk
■ Rarely used for ALI
50. Amputation
Performed as the first (index) procedure in
■ A non-salvageable (Class III limb)
■ Low potential of limb salvage
■ Risk of reperfusion syndrome
52. Reperfusion syndrome
■ Directly relates to severity and extent of ischemia
■ The myoglobin from damaged muscle precipitates in kidney tubules and causes
acute tubular necrosis.
■ Alkalinization of urine increases the solubility of myoglobin, thus preventing it from
crystallizing in the tubules.
■ In addition to alkalinization, therapy consists of forced saline diuresis and removal
of the source of dead muscle that is releasing the myoglobin.
53. Compartment syndrome
■ every reperfused patient is monitored for this complication.
■ occurs after prolonged ischemia is followed by reperfusion.
■ Capillary leak → fluid in interstitial space in fascial compartment →
■ Clinical signs:
– excessive pain in the compartment
– pain on passive stretching of the compartment, and
– sensory loss due to nerve compression
54. compartment syndrome
■ The most commonly affected compartment is the anterior compartment in the leg →
Numbness in the 1st web space between is diagnostic due to compression of the
deep peroneal nerve.
■ Compartment pressure is measured by inserting an arterial line into the
compartment.
■ pressures greater than 20 mmHg are an indication for fasciotomy
55. Fascial compartments of the lower leg
Anterior
Compartment
Lateral
Compartment
Superficial
Posterior
Compartment
Deep Posterior
Compartment
Muscles Tibialis anterior
Extensor digitorum
longus
Peroneus tertius
Extensor hallucis
longus
Extensor digitorum
brevis
Extensor hallucis
brevis
Peroneus
longus
Peroneus brevis
Gastrocnemius
Plantaris
Soleus
Tibialis posterior
Flexor digitorum
longus
Flexor hallucis
longus
Artery Anterior tibial artery Anterior and
posterior tibial
branches of the
popliteal artery
Posterior tibial
artery
Peroneal artery
Nerve Deep peroneal nerve Superficial
peroneal nerve
Tibial nerve
56. Fasciotomy
■ the medial incision, long openings are then
made in the fascia of the superficial and
deep posterior compartments.
■ Through the lateral incision, the anterior and
peroneal compartments are opened.
■ Both skin and fascial incisions should be of
adequate length to ensure full compartment
decompression.
57. References
■ Schwartz’s Principles of Surgery, 10th edition
■ Critical Limb Ischemia: Acute and Chronic, (Robert S. Dieter • Raymond A. Dieter, Jr
Raymond A. Dieter, III • Aravinda Nanjundappa), Springer, 2017
■ Acute Limb Ischemia: An Emergency Medicine Approach (Jamie R. Santistevan, MD),
Emerg Med Clin N Am - (2017), Elsevier Inc.
■ 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity
Peripheral Artery Disease: Executive Summary