VSITE Review - Acute Limb Ischemia

 

 

Script and Outline by Alex Forsyth

 

**If you are interested in creating a VSITE/Vascular Boards review episode Please email  mcpsmith@uw.edu  or  Audible.bleeding.podcast@gmail.com  and let me know,  I’ll walk you through how to do it and set you us with a credible Faculty member to discuss your topic with!**

 

Alex Forsyth is a 4th  year medical student at Boston University She’s a cofounder of the Vascular surgery student interest group and is exciting to be applying to Integrated Vascular surgery programs this season

Dr.  Sarah Carlson is an assistant Professor of Vascular Surgery at Boston University where she practices at the Boston VA Medical Center.  She completed her general surgery training at Beth Israel Deaconess in Boston followed by a fellowship in Vascular Surgery at Dartmouth-Hitchcock Medical center in new Hampshire.

 

What is acute limb ischemia and what does it encompass? 

 

Acute limb ischemia is defined as any process that leads to an abrupt cessation of blood flow to a limb resulting in ischemia. There are a few causes, but the most common two are embolic and thrombotic. 

 

• Embolic

• • Cardiac

  • • Typically due to a fib

    • Arm ischemia is most commonly due to cardiac embolism 

    • Endocarditis – as seen in IV drug users or patients with bacteremia from other causes

    • Cardiac tumors – such as atrial myxoma

  • Atherosclerotic (e.g. iliac disease embolizing downstream to the lower leg)

  • Paradoxical embolism (Thromboembolic venous system with PFO) 

  • Aneurysm (e.g. thrombus from within an aortic aneurysm embolizing downstream to the leg)

• Thrombosis

• • Aneurysm

  • Bypass graft

  • Acute on chronic progression of atherosclerosis

• Dissection

• Thoracic outlet syndrome (in the upper extremity)

• Vasospasm (severe)

 

For clarification: (1) Acute on chronic progression of atherosclerosis:  – e.g. once a chronic stenosis becomes critically tight, platelet thrombus can develop leading to an acute occlusion; or unstable plaque can “rupture” leading to an acute occlusion of a chronic lesion.  And (2) Regarding aneurysms – especially small aneurysms (such as popliteal) – these are less likely to rupture, but more likely to thrombose and cause an acute limb ischemic event.

What is the patient presentation of ALI? Are there any differences for upper vs. lower extremity presentations? 

 

Classically remembered by the 5 or 6 Ps depending on who you ask

• Pain: usually located distal to the occlusion and gradually increases in severity as the duration of ischemia continues. The pain may also decrease after a time due to ischemic sensory loss

• Pallor: the limb appears pale compared to the non ischemic limb. There is delayed capillary refill as well

• Poikiolothermia: (just a way to make “cold” into a “P” – really means cold limb) means literally the inability to regulate one’s body temperature, or dependent on ambient temperature as cold blooded animals are. If there is no perfusion of warm blood to the limb, it acclimates to the ambient temperature. 

• Pulseless: self explanatory, but a good thing to think about is if the contralateral limb has normal pulses, it suggests the absence of chronic limb ischemia and that an embolus or other cause of ALI. 

• Paresthesia and Paralysis are the last two Ps. Paresthesias are an earlier sign of ischemic nerve dysfunction and paralysis is a later sign. In the lower extremity, ischemic changes often affect the anterior compartment first, and sensory loss over the dorsum of the foot is one of the earlier neurologic deficits in ALI

This is why a thorough physical exam is key; comparison of both limbs and a good pulse exam including handheld doppler exam.  It can be difficult for a junior resident to tell whether a limb is acutely threatened, especially in patients with chronic disease where the presentation of an acute change can be more subtle.  This is why the attending surgeon will always ask the consult resident “how is the motor and sensory function” in addition to the pulse exam…this helps us gauge the chronicity and therefore the urgency of intervention.

 

How is ALI classified?

 

From Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg. 1997;26:517–538.

 

 

What does the work up for an acute limb entail? How is the diagnosis made? 

 

• The diagnosis can often be made on history, physical exam, and bilateral ABIs. Imaging can be done in patients in who the diagnosis is uncertain

• As with most urgent cases, the type of imaging done depends on the availability of at your institution, but generally imaging, such as a CT angiography or arteriography should be done on viable and marginally threatened limbs. Arteriography often can distinguish between embolic vs arterial thrombosis which may help to direct therapy. 

 

The situation varies depending on how severe the presentation is and how quickly you can obtain imaging.  Also depends on renal function and whether you want accept two contrast loads (CT followed by endovascular intervention).  As a rule of thumb, if I can feel femoral pulses I would typically be more inclined to proceed with on-table angiogram without a CT scan.  If femoral pulses are absent I would be more concerned about aortoiliac disease and I would prefer to have a CT scan so I know what I’m getting into in the operating room and can have a better plan.

 

In patients with severe renal insufficiency, MRA or MR time-of-flight can be helpful, but these studies usually take a little longer to obtain and may not be quickly available in an acute threatened limb situation.

 

Bedside ultrasound can also be very helpful even if you’re not a certified ultrasonographer yourself, if you have access to color flow doppler US it can be very helpful.

What is normally done in the initial management of ALI? 

 

• Anticoagulation - IV unfractionated heparin is immediately administered to prevent proximal and distal progression of secondary thrombus as long as heparin is not contraindicated. The dose should be titrated to maintain activated partial thromboplastin time between 50 and 80 seconds (2-3 times normal values)

• Supportive care (IV fluids)

• A full set of labs including serum chemistry panel with BUN and Cr, CBC, baseline coagulation studies should be obtained. Baseline plasma CPK can be helpful to follow for evidence of rhabdomyolysis after reperfusion 

 

A good rule of thumb for IV heparin is to start with a bolus of 80-100 units/kg, and then drop at 18units/kg/hr – titrating to PTT at 2-3x normal

What are some of the options for treatment of ALI? 

 

• Medical primarily with anticoagulation using heparin or a direct Xa inhibitor

• Open

• • Thrombectomy – balloon catheter based (Fogarty embolectomy balloon – Dr. Fogarty invented this while he was a medical student)

  • Bypass

  • Endarterectomy – not usually the go to but might be used for the common femoral 

• Endovascular 

Who gets which kinds of treatment? Who needs emergent treatment? 

• Class I might just need medical therapy like anticoagulation and revascularization can be elective. 

• Patients presenting with class IIa do not need immediate revascularization

• • If symptoms have been present for less than 2 weeks endovascular therapy is preferred

  • If more than 2 weeks or lytic therapy has failed then surgical intervention is preferred 

• Class IIb need immediate revascularization. Historically surgical revascularization has been preferred because of its immediacy, but catheter directed thrombolysis and percutaneous mechanical thrombectomy have shortened time to revascularization. 

• Studies:

• STILE trial (1994, Annals) – one of the first large RCTs comparing catheter thrombolysis with open surgery; overall the study showed some short term benefit to open surgery however this can probably be attributed to a couple things: (1) in 28% of patients randomized to CDT they weren’t able to get a catheter in place so these patients were considered treatment failures and crossed over to the surgery arm, and (2) patients with very long durations of ischemia – up to 6 months) were randomized, and when they looked at patients who had been symptomatic for less than 2 weeks, the thrombolysis patients actually did better.

• TOPAS trial (1998, NEJM) – larger RCT which enrolled patients who had an acute arterial occlusion of less than 14 days; this showed no difference in mortality or amputation-free survival but higher major bleeding in the CDT group.

• Meta analysis released originally published in 2002 but updated in 2013 and 2018 demonstrated no difference in mortality or limb salvage between surgical and thrombolytic therapy, but endovascular demonstrated higher rates of complications including ongoing limb ischemia and bleeding within 30 days of treatment. Previously they had reported higher rates of stroke in the thrombolysis category but the most recent update is unable to support this finding (Darwood et al., 2018) 

• All this to say, it is very reasonable to think about a cathter-directed therapy especially if the presentation is acute, less than 2 weeks or so.  That said, there are certain anatomical locations that most surgeons would favor a simple open procedure – e.g. embolism to the common femoral or brachial arteries – these are typically pretty simple to treat with a cut down and balloon thrombectomy.  

• One thing it is important to consider when doing a therapeutic infusion is that you might place a tPA infusion catheter at time zero and then bring the patient back 24 hours later; patient needs to be advised that they’ll need to lie flat for a day or even two days.  Setting expectations with patients is important.

• Class III is usually treated with primary amputation because revascularization is unlikely to restore function to the limb and restoring bloodflow can cause the patient serious harm. 

What are the risks of revascularization for a class III or prolonged ischemia? 

 

• Myonephropathic metabolic syndrome: muscle cells undergo liquefactive necrosis due to ischemia. Potassium, myoglobin, lactic acid, and superoxide accumulate and can perfuse through the body or can have a sudden increase in the event of revascularization which leads to hyperkalemia, arrhythmias, pulmonary edema, metabolic acidosis, myoglobinuria, and can even cause sudden death from heart and/or renal failure (Obara et al., 2018). Treatment of this is largely supportive with fluids

What is the pathophysiology and manifestations of compartment syndrome? 

 

• Increased intramuscular compartment pressure results from increases in capillary permeability due to ischemic reperfusion. The increase in pressure leads to neuromuscular dysfunction and interferes with circulation. Irreversible damage occurs when pressures exceed 30mmHg in each compartment  

• Clinically they can have neurological dysfunction with sensory motor deficits, but the most common presentation is a tense extremity with pain on passive movement of the muscles in the compartment, which is often dorsiflexion/plantar flection of the ankle. A sensitive indicator is loss of two point discrimination

 

How do you diagnose a compartment syndrome? 

 

• Physical exam (tenderness, especially over anterior compartment), paresthesias, especially between first and second toes (anterior compartment:  deep peroneal nerve – this is a VSITE favorite)

• Compartment pressures:  how do you do this?

• • Need a needle to access the compartment and a pressure monitoring system (can be handheld Stryker kit, or just a hollow bore needle connected to an arterial pressure bag).

  • Normal compartment pressure is <10-20mmHg; greater than 30 is highly concerning.  Probably even more accurate than an absolute number is comparing the compartment pressure to the mean arterial pressure or diastolic pressure.  If the compartment pressure is within 40mmHg of the MAP (for example, MAP is 60 and compartment pressure is 25 – this is concerning) – OR – if the difference between compartment pressure and diastolic pressure is less than 10 (for example, diastolic pressure is low at 30, and compartment pressure is 22).

 

If clinical suspicion of compartment syndrome is high, I tend not to be reassured by “normal” compartment pressures.  It’s relatively low risk to do fasciotomies, but the risk of limb loss is so high for a missed compartment syndrome…I would much rather err on the side of caution if there’s any question.

Treatment is a fasciotomy – can you tell us a little about the types of fasciotomies?

 

• Forearm and upper arm fasciotomies are often performed by orthopedic or hand surgeons. The forearm fasciotomy includes dorsal and volar incisions to release the dorsal and volar compartment, and mobile wad while avoiding numerous superficial cutaneous nerves. The arm fasciotomy releases the medial, lateral, and deltoid compartments through medial lateral incisions 

• Fasciotomies can be done in the thigh as well with a medial and lateral incision to release the lateral, medial and posterior compartment

• The most common type is a lower leg 4 compartment fasciotomy 

How is a lower leg 4 compartment fasciotomy for the lower extremity performed? 

 

• A longitudinal incision is created between the fibular shaft and the crest of the tibia over the intermuscular septum and the anterior and lateral compartments are opened. If tissues are swollen occluding the view of the intermuscular septum, the perforating vessels can be followed down to it. Nerves including the peroneal nerve are most at risk near the fibular head

• A second incision is created on the medial surface of the lower leg approx. 1cm posterior to the edge of the tibia to avoid the greater saphenous vein. The superficial posterior compartment is incised. The gastrocnemius-soleus complex is taken down from its attachments to the tibia in order to access the deep posterior compartment. 

• The incisions are made generously – sometimes the skin incision can be a little short of the fascial incision, but they should be nice and long in order to fully release the compartments

• After hemostasis be sure to apply loose dressings, and the leg should be elevated to reduce edema that can complicate closure. Closure can be done in 48-72 hours but may be delayed and dressed with wound vacs to attempt primary closure. If primary closure is not possible, a split thickness skin graft can be used for closure 

Who should a prophylactic fasciotomy be performed on?

 

• Patients with high occlusion and extensive ischemia, 

• Acute ischemia of greater than 6 hours with few collaterals

• Patients with combined arterial and venous injury

• Patients who are obtunded making serial examination difficult

What is the prognosis for a patient with ALI? What are some patient factors that lead to a poor prognosis? 

 

• Amputation rates after acute limb ischemia are typically described in the 10-20% range, and mortality is also in the 10-25% range whether you’re talking about surgery or catheter-directed procedures (that’s excluding the patients who present with Rutherford class III and by definition have an unsalvageable limb).  Many factors determine likelihood of amputation; typically, patients with more medical comorbid conditions tend to do worse as you might expect:  baseline CAD, kidney disease and smoking are predictive of worse outcomes.  There is a trend toward improved limb salvage rates (decreased amputation rate) over time, and I think this speaks to wider availability of different limb salvage techniques among vascular surgeons across the globe.

 

 

References

Darwood, R., Berridge, D.C., Kessel, D.O., Robertson, I., and Forster, R. (2018). Surgery versus thrombolysis for initial management of acute limb ischaemia. Cochrane Database Syst. Rev.

Ouriel, K., Shortell, C., DeWeese, J., Green, R.M., Francis, C.W., Azodo, M.V.U., Gutierrez, O.H., Manzione, J.V., Cox, C., and Marder, V.J. (1994). A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J. Vasc. Surg.

Obara, H., Matsubara, K., and Kitagawa, Y. (2018). Acute Limb Ischemia. Ann. Vasc. Dis.  11, 443–448.