ACUTE UPPER EXTREMITY ISCHEMIA

June 3, 2024
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TOPIC 9. ARTERIAL TROMBOSIS AND EMBOLISM

 

ACUTE UPPER EXTREMITY ISCHEMIA

 

Acute ischemia in the upper extremity constitutes 10–15% of all acute extremity ischemia. The etiology is emboli in 90% of the patients. The reason for this higher rate compared with the leg is that atherosclerosis is less common in arm arteries. Emboli have the same origins as in the lower extremity  and usually end up obstructing the brachial artery. Sometimes  plaques or an aneurysm in the subclavian or axillary arteries is the primary source of emboli. Embolization to the right arm is more common than to the left due to the vascular anatomy. For the 10% of patients with atherosclerosis and acute thrombosis as the main cause for their arm ischemia, the primary lesions are located in the brachiocephalic trunk or in the subclavian artery. Such pathologies are usually asymptomatic due to well-developed collaterals around the shoulder joint until thrombosis occurs, and they cause either micro- or macroembolization. Other less frequent causes of acute upper extremity ischemia are listed in Table 1

 

Table 1. Less common causes of acute upper extremity ischemia

 

 

 

Subclavian artery thrombosis is a condition in which the blood flow through the vessel is obstructed. The condition usually occurs secondary to some form of antecedent injury to the vessel, hypercoagulable state, or atherosclerotic changes. The condition is common in young athletic individuals who exert a significant amount of upper body activity. Sudden occlusion from emboli followed by thrombosis of the artery is common in the population with signs of significant atherosclerotic disease.

 

The patient presenting with acute subclavian artery occlusion usually has a history of repetitive use and/or stress injury to the upper extremity on the affected side. A history of upper extremity claudication is common.

 

In situations in which the occlusion is secondary to atherosclerosis, acute thromboses of the artery are generally asymptomatic. In fact, in 9% of autopsy series, the left subclavian artery was either stenotic or occluded. If symptoms are present, upper extremity claudication on the affected side is most common. The patient may also present with dizziness, vertigo, imbalance, visual disturbances, or hemisensory dysfunction indicative of a subclavian steal syndrome. However, note that subclavian steal is observed on 2% of cerebral angiograms and causes no symptoms.

EMBOLISM

Embolism is considered the most common cause of acute arm ischemia (74%). The emboli are attributed to a variety of sources. Cardiac embolism is the most frequently reported cause of acute arm ischemia (58% to 93%) and atrial fibrillation is the usual etiology. Over the years the incidence of atrial fibrillation has remained fairly constant although the cause of fibrillation has changed from valvular heart disease as a result of rheumatic fever to ischemic heart disease and myocardial infarction. Rare causes include endocarditis, atrial myxoma, ventricular aneurysm, cardiac failure, and paradoxical embolism.

Non-cardiac embolism determines 1% to 32% of the acute arm emboli. Proximal upper limb stenosis caused by atherosclerotic plaque or external compression (cervical ribs) can result in thrombo-embolism or atheroembolism, which may cause large vessel occlusion or acute digital ischemia.

Other causes include atheroma in the aortic arch, primary subclavian aneurysm or aneurysm secondary to extrinsic compression from thoracic outlet syndrome, old fracture, and chronic trauma such as that from the use of crutches. Rarer sources are the proximal end of an occluded axillofemoral graft, arteritis, malignant emboli, and fibromuscular dysplasia. Despite a classic embolic presentation and operative findings, an embolic source may not be found in at least 12% of patients.

 

THROMBOSIS

Reports suggest that 5% of cases in population studies and 9% to 35% in surgical series are due to thrombosi. Jivegard et al. estimated that in patients who had embolectomy, the chance of thrombosis being the true cause was 5.5% in the arm. Most of the proximal arterial lesions that can cause emboli can also result in thrombosis, including atherosclerotic plaques, aneurysm, acute aortic dissection, and arteritis (Takayasu’s disease).

Atherosclerosis in the upper extremity appears especially prominent in older men. The disease may be at the origin of the great vessels or distally in the axillary or brachial arteries. Aneurysms of the subclavian or axillary arteries may also result in upper extremity ischemia through two mechanisms. They may directly cause ischemic symptoms by thrombosis or by producing emboli that occlude the distal circulation (Raynaud’s phenomenon).

Less common causes include arteritis from connective tissue disorders (scleroderma), radiation arteritis, hyperthrombotic conditions and thrombosis associated with malignancy or steroid use.

 

Clinical Presentation

 

Acute arm ischemia is usually apparent on the basis of the physical examination. The symptoms are often relatively discreet, especially early after onset. The explanation for this is the well developed collateral system circumventing the brachial artery around the elbow, which is the most common site for embolic obstruction. The “six Ps” – pain, pallor, paresthesia, paralysis, pulselessness, poikilothermia – are applicable also for acute arm ischemia, but coldness and color changes are more prominent than for the legs. Accordingly, the most common findings in the physical examination are a cold arm with diminished strength and disturbed hand and finger motor functions. Tingling and numbness are also frequent. The radial pulse is usually absent but is pounding in the upper arm proximal to the obstruction. Gangrene and rest pain appear only when the obstruction is distal to the elbow and affects both of the paired arteries in a finger or in the lower arm. Ischemic signs or symptoms suggesting acute digital artery occlusion in only one or two fingers, imply microembolization.

 

Diagnostics

 

Only the few patients with uncertain diagnosis, and those with a history and physical findings that indicates thrombosis, need additional work-up. Examples include patients with a history of chronic arm ischemia (arm fatigue, muscle atrophy, and microembolization) and bruits over proximal arteries. Angiography should then be performed to reveal the site of the causing lesion. Duplex ultrasound is rarely needed to diagnose acute arm ischemia but may occasionally be helpful.

 

 

Management Before Treatment

 

Even though symptoms and examination findings may be so subtle that conservative treatment is tempting, surgical removal of the obstruction is almost always preferable. It has been suggested that in patients with a lower-arm blood pressure >60 mmHg embolectomy can be omitted, but such a strategy has not to our knowledge been evaluated systematically. In a patient series of nearly symptomless acute arm ischemia, which was left to resolve spontaneously or with anticoagulation as the only treatment, late symptoms developed in up to 45% of the cases. Surgical treatment is also fairly straightforward. It can be performed using local anesthesia and is associated with few complications. Very often an embolus is a manifestation of severe cardiac disease, so the patient’s cardiopulmonary function should be assessed and optimized as soon as possible. Preoperative preparations include an electrocardiogram (ECG) and laboratory tests to guide anticoagulation treatment. Heparin treatment is started perioperatively and continued postoperatively in most patients.

 

Operation

 

Embolectomy

 

As mentioned previously, the most common site for embolic obstruction is the brachial artery.

 

The arm is placed on an arm table. We prefer to perform embolectomy using local anesthesia. Often a transverse incision placed over the palpable brachial pulse can be used. If proximal extension of the incision is required, this should be done in parallel with and dorsal to the dorsal aspect of the biceps muscle. It has to be kept in mind that 10–20% of patients may have a different brachial artery anatomy. The most common variation is a high bifurcation of the radial and ulnar arteries, and next in frequency is a doubled brachial artery.

An alternative location for embolectomy in the arm is to expose the brachial artery in the bicipital groove. A longitudinal incision starting 10 cm above the elbow that is extended proximally is then used.

If it is hard to achieve a good inflow, a proximal lesion may cause the embolization or thrombosis. More complicated vascular procedures are then required to reestablish flow. The embolectomy attempt is then discontinued and the patient taken to the angiography suite for a complete examination. If practically feasible, an alternative is to obtain the angiogram in the operating room. Frequently, however, the preferred treatment is endovascular, and this is better done in the angiography suite. Occasionally the films will reveal a proximal obstruction that needs open repair. Examples of such are carotid-subclavian, subclavian-axillary, and axillary-brachial bypasses.

 

Embolectomy via the Brachial Artery

 

Brachial Artery in the Upper Arm

 

The incision is made along the posterior border of the biceps muscle; a length of 6–8 cm is usually enough.

 

Fig.  Transverse incision in the elbow for exposing the brachial artery and with possible elongations (dottedlines) when access to the ulnar and  radial branches as well as to more proximal parts of the brachial artery is needed

 

The muscles are retracted medially and laterally, and the artery lies in the neurovascular bundle immediately below the muscles. The sheath is incised and the artery freed from the mediaerve and the medial cutaneous nerve that surrounds it.

 

 

Brachial Artery at the Elbow

 

The incision is placed 2 cm below the elbow crease and should continue up on the medial side along the artery. If possible, veins transversing the wound should be preserved, but they can be divided if necessary for exposure. The medial insertion of the biceps tendon is divided entirely, and the artery lies immediately beneath it. By following the wound proximally, more of the artery can be exposed . If the origins of the radial and ulnar artery need to be assessed, the wound can be elongated distally on the ulnar side of the volar aspect of the arm. The mediaerve lies close to the brachial artery, and it is important to avoid injuring it.

A transverse arteriotomy  in the brachial artery is made as close as possible to the bifurcation of the ulnar and radial arteries. The embolectomy is performed in proximal and distal directions with #2 and #3 Fogarty catheters. Separate embolectomy in each branch should be done if technically simple. The Fogarty catheter otherwise slips down into the larger and straighter ulnar artery. The route of the catheter can be checked by palpation at the wrist level when the inflated balloon passes. On the other hand, restored flow in one of the arteries is usually enough for a result that is sufficient for adequate hand perfusion. The arteriotomy is closed with interrupted 6-0 sutures, and distal pulses and the perfusion in the hand are evaluated. If the result is inadequate – poor backflow after embolectomy, absence of pulse, a weak continuous-wave Doppler signal, and questionable hand perfusion – the arteriotomy should be reopened and intraoperative angiography performed.

 

 Endovascular Treatment

 

Thrombolysis is as feasible for acute upper extremity ischemia as it is in the leg. The limited ischemia that often occurs after most embolic events because of the collateral network around the elbow also allows the time needed for planning and moving the patient to the angiosuite. The technique involves cannulation in the groin with a 7-French sheath. Long guide wires and catheters are required to reach the occluded site and makes identification of proximal lesions possible. A new arterial puncture in the brachial artery may be necessary for thrombolysis of distal occlusions.It can be argued that thrombolysis in spite of acceptable results, rarely is needed for treating this disease because open embolectomy can be performed under local anesthesia with good results and little surgical morbidity. The advantages with endovascular treatment are indeed limited. For patients in whom suspicion of thrombosis is strong or when proximal lesions are likely, it should be attempted first. However, case series indicates that results of thrombolysis are inferior for forearm occlusions. In summary, thrombolysis is an alternative but has little to offer in reducing risk or improving outcome compared with embolectomy for most patients.

 

Management After Treatment

 

Patients usually regain full function of their hand immediately after the procedure, and postoperative regimens consist of anticoagulation and a search for the embolic source.  The search for cardiac sources may advocate repeated ECGs, echocardiography, and duplex ultrasound of proximal arteries.

 

Results and Outcome

 

The number of salvaged arms after surgical intervention is very high, 90–95 %, and arm function is usually fully recovered. The remaining 5–10% represents patients with extensive thrombosis involving many vascular segments and most branches of the distal arteries. The postoperative mortality is around 10–40% in most patient series, reflecting that embolization often is a consequence of severe cardiac disease. Postoperative mortality is similar for thrombolysis to treat acute arm ischemia, while early technical success is slightly lower or similar. Less favorable results with thrombolysis are achieved when the distal arteries also are obstructed.

 

 

ACUTE LEG ISCHEMIA

 

 

Acute leg ischemia is associated with a great risk for amputation and death. The age of the patients is high, and to some extent acute leg ischemia can be considered an end-of-life disease. Patients’ symptoms and the clinical signs of the afflicted leg vary. Sometimes grave ischemia immediately threatens limb viability, such as after a large embolization to a healthy vascular bed. Other times the symptoms are less dramatic, appearing as onset of rest pain in a patient with claudication. This is usually due to thrombosis of a previously stenosed artery.

 

 

Table 2.Incidence of acute leg ischemia

 

 

It is the severity of ischemia that determines management and treatment. To minimize the risk for amputation or persistent dysfunction it is important to rapidly restore perfusion if an extremity is immediately threatened. When the leg shows signs of severe ischemia but is clearly viable, it is equally important to thoroughly evaluate and optimize the patient before any intervention is initiated. These basic management principles are generally applicable. Accordingly, we recommend “management by severity” rather than “management by etiology” (thrombosis versus embolus) but recognize that the latter can also be an effective strategy.

 

Embolism

 

Embolism is by far the most common cause of acute arm ischaemia, accounting for 74–100% of cases.

In the lower extremities, controversy exists regarding the ratio between arterial embolism and thrombosis, with diferent studies giving numbers ranging from 4:1 to 1:9.

The heart is invariably the most common origin of peripheral arterial emboli, and is responsible for 58–93% of cases. However, the pattern of the underlying heart disease has changed recently as the incidence of rheumatic valvular disease has decreased significantly

 

Cardiac Sources of Emboli

 

Nowadays, the most common sources of arterial emboli of cardiac origin are:

atrial ibrillation due to atherosclerotic heart disease, accounting for 32–75% of cases, followed by

myocardial infarction with mural thrombi formation, which is responsible for 21–32% of peripheral emboli.

 

Less common cardiac sources of emboli are:

idiopathic dilated cardiomyopathy

prosthetic valves

rheumatic mitral valve disease

intracavitary cardiac tumours (mainly myxomas)

paradoxical embolization through an intracardiac defect, usually a patent foramen ovale

fungal or bacterial endocarditis.

 

Noncardiac Sources

 

Noncardiac sources  of emboli are being identiied with increasing frequency, at the expense of undetermined causes, the frequency of which has steadily decreased due to improvements in diagnostic methods. Noncardiac sources of emboli are nowadays found in 5–12% of patients, while in 9–12% the source of the emboli remains unknown.

Aneurysms are the most commooncardiac source of peripheral embolism, accounting for about 5% of distal emboli.

Ulcerated atherosclerotic plaques follow in order of frequency, carrying the risk of distal embolism from white thrombi adherent on their surface. Such emboli are usually sizeable, capable of obstructing major peripheral arteries.

A distinct variant of peripheral embolization due to an atherosclerotic plaque is atheroembolism, in which a portion of the plaque breaks of and undergoes embolization to peripheral arteries. Such emboli may evolve in three clinical forms:

1. The asymptomatic form, not diagnosed during the subject’s lifetime and only recognized in autopsy studies.

2. A benign form such as blue toe syndrome or cutaneous livedo, with a spontaneous mild prognosis.

3. A difuse multisystemic form with a very poor prognosis.

Cryptogenic Emboli

 

Despite complete diagnostic work-up, including complex investigations, the precise source of the emboli cannot be identiied in 5–12% of cases. Such emboli are called cryptogenic and represent either the limited sensitivity of current diagnostic modalities or, in some cases, confusion with local thrombosis in situ.

 

Thrombosis

 

Thrombosis of an atherosclerotic artery or a vascular grat is another major cause of acute arterial occlusion of the extremities. As Virchow suggested in 1856, thrombus formation is the result of an interaction between an injured surface, stasis and the hypercoagulability of blood:

Arterial thrombosis most oten develops at the points of severe stenosis. Since the course of atherosclerotic disease is chronic, a collateral network will have already developed and the clinical picture will be milder compared with arterial embolism. However, a thrombus can be formed in the absence of signiicant pre-existing stenosis, particularly when the surface of the plaque is ulcerated or ater an intraplaque haemorrhage resulting in sudden arterial occlusion.

Low-low conditions, such as congestive heart failure, hypovolaemia, hypotension of any cause or decreased blood low due to a more proximal stenosis.

Hypercoagulable  states, such as myeloproliferative disorders, hyperviscosity syndromes and coagulation disorders, may contribute to thrombosis of the diseased artery.

Other causes of arterial thrombosis include:

Arterial aneurysms, with the risk of thrombosis being higher the more peripherally the aneurysm is located.

Arterial by-pass  grat thrombosis, which frequently induces acute limb-threatening ischaemia, as the grat has usually allowed collateral vessels to regress. Early grat failure, within the irst postoperative month, is usually due to a technically suboptimal result, inappropriate indication or a transient episode of hypotension. Late grat failure, ater 1 month, is secondary to intimal hyperplasia at the anastomotic sites or to progression of atherosclerotic disease.

Aortic dissection.

Fibromuscular dysplasia, occasionally involving the iliac arteries.

Cystic adventitial disease, usually afecting the popliteal artery and rarely the femoral.

hromboangiitis obliterans, involving medium-sized muscular arteries.

Various arteritides, such as Takayasu’s aortitis and giant cell arteritis.

Compartment syndrome.

Еhoracic outlet syndrome.

Popliteal entrapment syndrome.

Ergotism.

 

Magnitude of the Problem

 

It is difficult to find accurate incidence figures on acute leg ischemia. Data from some reports are given in Table 2. The numbers listed do not include conservatively treated patients or those whose legs were amputated as a primary procedure. The incidence increases with age and is seen with equal frequency in men and women. Regardless, the frequency indicates that it is a very common problem.

 

Pathogenesis

 

Acute leg ischemia is caused by a sudden deterioration of perfusion to the distal parts of the leg. While the abrupt inhibition of blood flow causes the ischemia, its consequences are variable because acute leg ischemia is multifactorial in origin. Hypercoagulable states, cardiac failure, and dehydration predispose the blood for thrombosis and make the tissue more vulnerable to decreased perfusion. Besides the fact that a healthy leg is more vulnerable than one accustomed to low perfusion, it is unknown what determines the viability of the tissue. The most important factor is probably the duration of ischemia. The type of tissue affected also influences viability. In the leg, the skin is more ischemia-tolerant than skeletal muscle.

 

 Embolus and Thrombosis

 

The etiology of the occlusion is not what determines the management process. It is, however, of importance when choosing therapy. Embolus is usually best treated by embolectomy, whereas arterial thrombosis is preferably resolved by thrombolysis, percutaneous transluminal angioplasty (PTA), or a vascular reconstruction. The reason for this difference is that emboli often obstruct a relatively healthy vascular bed, whereas thrombosis occurs in an already diseased atherosclerotic artery. Consequently, emboli more often cause immediate threatening ischemia and require urgent restoration of blood flow. Thrombosis, on the other hand, occurs in a leg with previous arterial insufficiency with well-developed collaterals. In the latter case it is important not only to solve the acute thrombosis but also to get rid of the cause. It must be kept in mind that emboli can be lodged in atherosclerotic arteries as well, which then makes embolectomy more difficult.

 

Table 3 summarizes typical findings in the medical history and physical examination that suggest thrombosis or embolism. Many risk factors, such as cardiac disease, are common for both embolization and thrombosis. Atrial fibrillation and a recent (less than 4 weeks) myocardial infarction with intramural thrombus are the two dominating sources for emboli (80–90%). Other possible origins are aneurysms and atherosclerotic plaques located proximal to the occluded vessel. The latter are often associated with microembolization (discussed later) but may also cause larger emboli.

 

 

Table 3. History and clinical indings diferentiating the etiology of acute ischemia

 

 

 

Plaque rupture, immobilization, and hypercoagulability are the main causes of acute thrombosis. Severe cardiac failure, dehydration, and bleeding are less common causes. Hypoperfusion due to such conditions can easily turn an extremity with longstanding slightly compromised perfusion into acute ischemia.

Location of embolic obstruction

 

Clinical Presentation

 

Medical History

 

The typical patient with acute leg ischemia is old and has had a recent myocardial infarction. He or she describes a sudden onset of symptoms – a few hours of pain, coldness, loss of sensation, and poor mobility in the foot and calf. Accordingly, all signs of threatened leg viability are displayed. The event is most likely an embolization, and the patient needs urgent surgery. Unfortunately, such patients are unusual among those who are admitted for acute leg ischemia. The history is often variable, and sometimes it is difficult to decide even the time of onset of symptoms. It is important to obtain a detailed medical history to reveal any underlying conditions or lesions that may have caused the ischemia. Moreover, identifying and treating comorbidities may improve the outcome after surgery or thrombolysis.

 

 

Clinical Signs and Symptoms

 

The symptoms and signs of acute ischemia are often summarized as the “five Ps”: pain, pallor, pulselessness, paresthesia, and paralysis. Besides being helpful for establishing diagnosis, careful evaluation of the five Ps is useful for assessing the severity of ischemia. Sometimes a sixth P’s is used – poikolothermia, meaning a low skin temperature that does not vary with the environment.

Pain:  For the typical patient, as the one described above, the pain is severe, continuous, and localized in the foot and toes. Its intensity is unrelated to the severity of ischemia. For instance, it is less pronounced when the ischemia is so severe that the nerve fibers transmitting the sensation of pain are damaged. Patients with diabetes often have neuropathy and a decreased sensation of pain.

Pallor: The ischemic leg is pale or white initially, but when ischemia aggravates the color turns to cyanotic blue. This cyanosis is caused by vessel dilatation and desaturation of hemoglobin in the skin and is induced by acidic metabolites in combination with stagnant blood flow. Consequently, cyanosis is a graver sign of ischemia than pallor.

Pulselessness: A palpable pulse in a peripheral artery means that the flow in the vessel is sufficient to give a pulse that is synchronous with vessel dilatation, which can be palpated with the fingers. In general, palpable pulses in the foot therefore exclude severe leg ischemia. When there is a fresh thrombus, pulses can be felt in spite of an occlusion, so this general principle must be applied with caution. Palpation of pulses can be used to identify the level of obstruction and is facilitated by comparing the presence of pulses at the same level in the contralateral leg.

When the examiner is not convinced that palpable pulses are present, distal blood pressuresmust be measured. It is prudent to always measure the ankle blood pressure. This is a simple way to verify ischemia and the measurement can be used to grade the severity and serve as a baseline for comparison with repeated examinations during the course of treatment. (This will be discussed further later.) The continuous-wave (CW) Doppler instrument does not give information about the magnitude of flow because it registers only flow velocities in the vessel. Therefore, an audible signal with a CW Doppler is not equivalent to a palpable pulse, and a severely ischemic leg can have audible Doppler signals.

 

Paresthesia:  The thierve fibers conducting impulses from light touch are very sensitive to ischemia and are damaged soon after perfusion is interrupted. Pain fibers are less ischemia-sensitive. Accordingly, the most precise test of sensibility is to lightly touch the skin with the fingertips, alternating between the affected and the healthy leg. It is a common mistake to believe that the skin has been touched too gently when the patient actually has impaired sensitivity. The examiner then may proceed to pinching and poking the skin with a needle. Such tests of pain fibers evaluate a much later stage of ischemic damage. The anatomiclocalization of impaired sensation is sometimes related to which nerves are involved. Frequently, however, it does not follow nerve distribution areas and is circumferential and most severe distally. Numbness and tingling are other symptoms of ischemic disturbance of nerve function.

 

Paralysis: Loss of motor function in the leg is initially caused by ischemic destruction of motor nerve fibers and at later stages the ischemia directly affects muscle tissue. When palpated, ischemic muscles are tender and have a spongy feeling. Accordingly, the entire leg can become paretic after proximal severe ischemia and misinterpreted as a consequence of stroke. Usually paralysis is more obscure, however, presenting as a decreased strength and mobility in the most distal parts of the leg where the ischemia is most severe. The most sensitive test of motor function is to ask the patient to try to move and spread the toes. This gives information about muscular function in the foot and calf. Bending the knee joint or lifting the whole leg is accomplished by large muscle groups in the thigh that remain intact for a long time after ischemic damage in the calf muscle and foot has become irreversible.

 

Evaluation of Severity of Ischemia

 

Classiication

 

When a patient has been diagnosed to have acute leg ischemia, it is extremely important to evaluate its grade. Ischemic severity is the most important factor for selecting a management strategy, and it also affects treatment outcome. Classification according to severity must be done before the patient is moved to the floor or sent to the radiology department. We have found that the simple classification suggested by the Society for Vascular Surgery ad hoc committee (1997) is helpful for grading. It is displayed in Table 4.

 

Table 4. Categories of acute ischemia

 

 

Viable Leg

 

As indicated in Figure 2, a viable ischemic leg is not cyanotic, the toes can be moved voluntarily, and the ankle pressure is measurable. The rationale for choosing these parameters is that cyanosis and impaired motor function are of high prognostic value for outcome. The limit of 30mmHg for the ankle pressure  is not important per se but is a practical limit useful to make sure that it is the arterial, and not a venous, pressure that has been measured. The dorsalis pedis, posterior tibial arteries, or branches from the peroneal artery can be insonated. The latter can be found just ventral to the lateral malleolus. If no audible signal is identified in any of these arteries or if there only is a weak signal that disappears immediately when the tourniquet is inflated, the ankle blood pressure should be recorded as zero. It is important to rely on the obtained results and not assume that there is a signal somewhere that is missed due to inexperience. Qualitative analysis of the Doppler signal is seldom useful when evaluating acute leg ischemia.

 

 

Fig. 2. Simpliied algorithm to support the management of acute

leg ischemia

 

Threatened Leg

 

As shown in Table 4, the threatened leg differs from the viable one in that the sensibility is impaired and there is no measurable ankle blood pressure. The threatened limb is further separated into marginally threatened and immediately threatened by the presence or absence of normal motor function. The threatened leg differs from the irreversibly damaged leg by the quality of the venous Doppler signal. In the irreversibly damaged leg, venous blood flow is stagnant and inaudible.

 

Management Strategy

 

A viable leg does not require immediate action and can be observed in the ward. A threatened leg needs urgent operation or thrombolysis. The latter is more time-consuming and recommended for the marginally threatened leg. The immediately threatened leg must be treated as soon as possible, usually with embolectomy or a vascular reconstruction. Irreversible ischemia is quite unusual but implies that the patient’s leg cannot be saved. Figure 2 is intended to show a simplified algorithm to further support the management of acute leg ischemia.

 

Diagnostics

 

A well-conducted physical examination is enough to confirm the diagnosis of acute leg ischemia, determine the level of obstruction, and evaluate the severity of ischemia. When the leg is immediately threatened, further radiologic examinations or vascular laboratory tests should not under any circumstances delay surgical treatment. When the extremity is viable or marginally threatened, angiography should be performed. Duplex ultrasound is of limited value for evaluating acute leg ischemia and angiography is recommended for almost all patients in these two groups. If angiography is not available or if examination of the patient has verified that emboli is the cause and probably is best treated by embolectomy, angiography can be omitted. This situation is rare, however.

The arteriogram provides an anatomical map of the vascular bed and is very helpful in discriminating embolus and thrombosis. The former is essential for planning the surgical procedure, and the latter may be of importance for selecting the treatment strategy.

 

An arteriogram representing an embolus is shown in Fig. 3.

 

 

 

Fig. 3. Embolus lodged at the origins of the calf vessels (arrow).

Angiograms display ilms before and after thrombolysis

 

Angiographic signs of embolism are an abrupt, convex start of the occlusion and lack of collaterals. Thrombosis is likely when the arteriogram shows well-developed collaterals and atherosclerotic changes in other vascular segments.

For most patients with viable and marginally threatened legs the diagnostic angiography is followed by therapeutic thrombolysis right away.

 

Angiography can be performed during daytime when qualified radiology staff is available. The patient should be optimized according to the recommendations given in the next section. Before angiography it is important to keep the patient well hydrated and to stop administration of metformin to reduce the risk of renal failure. Disturbances in coagulation parameters may interfere with arterial puncture and must also be checked before the investigation. The information is also important as baseline values in case of later thrombolysis.

The groin of the contralateral leg is the preferred puncture site for diagnostic angiography. A second antegrade puncture can be done in the ischemic extremity if thrombolysis is feasible.

 

Management and Treatment

 

Management Before Treatment

 

Viable Leg

 

If the leg is viable the patient is admitted for observation. A checklist of what needs to be done in the emergency department follows below:

 

1.Place an intravenous (IV) line.

 

2. Start infusion of fluids. Because dehydration is often a part of the pathogenic process, Ringer’s acetate is usually preferred. Dextran is another option that also is beneficial for blood rheology.

 

3. Draw blood for hemoglobin and hematocrit, prothrombin time, partial thromboplastin time, complete blood count, creatinine, blood urea nitrogen, fibrinogen, and antithrombin. Consider the need to type and cross-match blood.

 

4.Order an electrocardiogram (ECG).

 

5.Administer analgesics according to pain intensity. Opiates are usually required (morphine 2.5–10mg IV).

 

6.Consider heparinization, especially if only Ringer’s acetate is given. Heparin treatment should be postponed until after surgery if epidural anesthesia is likely.

 

Repeated assessments of the patient’s clinical status are mandatory in the intensive care unit and when the patient has been moved to the ward. The time interval depends on the severity of ischemia and the medical history. This examination includes evaluating skin color, sensibility, and motor function as well as asking the patient about pain intensity.

Dextran is administered throughout the observation period. The risk for deterioration of heart failure due to dextran treatment is substantial and for patients at risk the volume load must be related to the treatment’s expected possible benefits. For such patients it is wise to reduce the normal dose of 500ml in 12h to 250ml. Another option is to prolong the infusion time to 24h.

 

Heparin only or in combination with dextran is recommended when patients do have an embolic source or a coagulation disorder. There are two ways to administer heparin. The first is the standard method, consisting of a bolus dose of 5,000 units IV followed by infusion of heparin solution (100units/ml) with a drop counter. The dose at the start of infusion should be 500 units of heparin per kilogram of body weight per 24h. The dose is then adjusted according to activated partial thromboplastin time (APTT) values obtained every 4h. The APTT value should be 2–2.5 times the baseline value.

Low molecular weight heparin administered subcutaneously twice daily is the other option. A common dose is 10,000 units/day but it should be adjusted according to the patient’s weight.

It is important to optimize cardiac and pulmonary function while monitoring the patient. Hypoxemia, anemia, arrhythmia, and hypotension worsen ischemia and should be abolished if possible. A cardiology consult is often needed.

The above-mentioned treatment regime of rehydration, anticoagulation, and optimization of cardiopulmonary function often improves the ischemic leg substantially. Frequently this is enough to sufficiently restore perfusion in the viable ischemic leg, and no other treatments are needed. If no improvement occurs, angiography can be performed during the daytime, followed by thrombolysis, PTA, or vascular reconstruction.

 

Threatened Leg

 

If the leg is immediately threatened, the patient is prepared for operation right away. This includes the steps listed above for the viable leg, including contact with an anesthesiologist. When there is no cyanosis and motor function is normal – that is, the extremity is only marginally threatened – there is time for immediate angiography followed by thrombolysis or operation. An option is cautious monitoring and angiography as soon as possible.

Before starting the operation, the surgeoeeds to consider the risk for having to perform a complete vascular reconstruction. It is probable that a bypass to the popliteal artery or a calf artery will be needed to restore circulation. If thrombosis is the likely cause and the obstruction is distal (a palpable pulse is felt in the groin but not distally), a bypass may also be required even when embolization is suspected.

 

Operation

 

Exposure of Different Vessel Segments in the Leg

 

Femoral Artery in the Groin, Fig. 4 A, B, C.

 

a A longitudinal skin incision starting 1–2 cm cranial to the inguinal skin fold and continued  lateral to the artery is used to avoid the inguinal lymph nodes. A common mistake is to place the incision too far caudally, which usually means the dissection is taking place distal to the deep femoral.

 

b The dissection  is continued sharply with the knife straight down to the fascia lateral to the lymph nodes and is then angulated 90° medially to reach the area over the artery. It should then be palpable. Lymph nodes should be avoided to minimize the risk for infection and development of seroma. The fascia is incised, and the anterior and lateral surfaces of the artery are approached.

 

c At this stage the anatomy is often unclear regarding the relation of branches to the common femoralartery. Encircle the exposed artery with a vessel-loop, and gently lift the artery. Continue dissection until the bifurcation into superficial and deep femoral artery is identified. Its location varies from high up under the inguinal ligament up to 10 cm further down. At this stage, the surgeon must decide whether exposure and clamping of the common femoral are enough. This is usually the case for proximal control in trauma distally in the leg. In acute ischemia it is more common  that the entire bifurcatioeeds to be exposed.

 

During the continued dissection, attention must be given to important branches that should be controlled and protected from iatrogenic injuries. These are, in particular, the circumflex iliac artery on the dorsal aspect of the common femoral artery and the deep femoral vein crossing over the anterior aspect of the deep femoral artery just after its bifurcation. To provide a safe and good exposure of the deep femoral to a level below its first bifurcation, this vein must be divided and suture-ligated. Partial division of the inguinal ligament is occasionally needed for satisfactory exposure.

 

Fig. 4 A. Exposure of femoral artery in the groin

 

 

 

Fig. 4 B. Exposure of femoral artery in the groin

 

Fig. 4 C. Exposure of femoral artery in the groin

 

 Superficial Femoral Artery, Fig. 5

 

A skin incision is made along the dorsal aspect of the sartorius muscle at a midthigh level. It is important to avoid injuries to the greater saphenous vein, which usually is located in the posterior flap of the incision. The incision can be elongated as needed. After the deep fascia is opened and the sartorius muscle is retracted anteriorly, the femoral artery is found and can be mobilized.  Division of the adductor tendon is sometimes required for exposure.

 

 

Fig. 5. Incision for exposure of the supericial femoral artery

 

Popliteal Artery Above the Knee,  Fig. 6 A, B.

 

a The knee is supported on a sterile, draped pillow. The skin incision is started at the medial aspect of the femoral condyle and follows the anterior border of the sartorius muscle 10–15 cm in a proximal direction. Protect the greater saphenous vein and the saphenous nerve during dissection down to the fascia. After dividing the fascia longitudinally, continue the dissection in the groove between the sartorius and gracilis muscles, which leads to the fat in the popliteal fossa.

b The popliteal artery and adjacent veins and nerve are then, without further division of muscles, easily found and separated in the anterior aspect of the fossa.

 

 

 

Fig. 6 A. Exposure of popliteal artery above the knee

 

 

 

Fig. 6 B. Exposure of popliteal artery above the knee

 

Popliteal Artery Below the Knee, Fig. 7 A,B.

 

a A sterile pillow or pad is placed under the distal femur. The incision is placed 1 or 2 cm posterior to the medial border of the tibia, starting at the tibial tuberosity and extending 10–12 cm distally. Subcutaneous fat and fascia are sharply divided, with caution to the greater saphenous vein.

b The popliteal fossa is reached by retracting the gastrocnemius muscle dorsally. The deep fascia is divided and the artery usually easier to identifiy. Occasionally, pes anserinus must be divided for adequate exposure. The popliteal artery is often located just anterior to the nerve and in close contact with the popliteal vein and crossing branches from concomitant veins. If it is necessary to expose the more distal parts of the popliteal artery, the soleus muscle has to be divided and partly separated from the posterior border of the tibia.

 

 

 

Fig. 7 A. Exposure of popliteal artery below the knee

 

 

 

Fig. 7 B. Exposure of popliteal artery below the knee

 

 

 

Embolectomy

 

It is beyond the scope of this book to cover the technique for vascular reconstructions. But because embolectomy from the groin with balloon catheters (known as Fogarty catheters) is one of the most common emergency vascular operations in a general surgical clinic and may be performed by surgeons not so familiar with vascular surgery.

 

TECHNICAL TIPS

 

Embolectomy

 

Use an operating table that allows x-ray penetration. Local anesthesia is used if embolus is likely and the obstruction seems to be in the upper thigh or in pelvic vessels (no pulse in the groin). Make a longitudinal incision in the skin, and identify and expose the common, superficial, and deep femoral arteries . If the common femoral artery is soft-walled and free from arteriosclerosis – especially if a pounding pulse is felt proximal to the origin of the deep femoral artery – an embolus located in its bifurcation is likely. Make a short transverse arteriotomy including almost half the circumference. Place the arteriotomy only a few mm proximal to the origin of the profunda artery so it can be inspected and cannulated with ease. In most other cases, a longitudinal arteriotomy is preferable because it allows elongation and can be used as the site for the inflow anastomosis of a bypass. For proximal embolectomy, a #5 catheter is used.

Before the catheter is used the balloon should be checked by insufflation of a suitable volume of saline. Check the position of the lever of the syringe when the balloon is starting to fill, which gives a good idea of what is happening inside the artery. Wet the connection piece for the syringe to get a tight connection. It is smart to get external markers of the relationship between the catheter length and important anatomical structures; for example, the aortic bifurcation (located at the umbilicus level), the trifurcation level (located approximately 10 cm below the knee joint), as well as the ankle level. The catheters have centimeter grading, which simplifies the orientation.

It is common for the embolus to already be protruding when the arteriotomy is done and a single pull with the catheter starting with the tip in the iliac artery is enough to ensure adequate inflow. This means that a strong pulse can be found above the arteriotomy, and a pulsatile heavy blood flow comes through the nole. For distal clot extraction, a #3 or #4 catheter is recommended. A slight bending of the catheter tip between the thumb and index finger might, in combination with rotation of the catheter, make it easier to pass down the different arterial branches (Fig. 8).

 

 

Fig. 8. Use of Fogarty catheter for embolectomy. Note that withdrawal is parallel to the artery

 

When the catheter is inserted into the artery and while the surgeon is working with it, hemostasis of the arteriotomy is achieved by a vessel-loop or by a thumb–index finger grip over the artery and the catheter. In a typical case, an embolus, including a possible secondary thrombus, can be passed relatively easily or with only slight resistance. If a major part of the catheter can be inserted the tip will be located in one of the calf arteries, most probably the posterior tibial artery or the peroneal artery. The balloon is insufflated simultaneously as the catheter is slowly withdrawn, which makes it easier to get a feeling for the dynamics and to not apply too much pressure against the vascular wall.

A feeling of “touch” is preferable, but a feeling of “pull” against the vascular wall should be avoided.

To get the right feeling the same persoeeds to hold the catheter, pull it, and insufflate the balloon at the same time. To avoid damage in the arteriotomy, the direction of withdrawal should be parallel with the artery .

 

 

When the catheter is withdrawn it moves into larger segments of the artery and has to be successively insufflated until it reaches the arteriotomy. The reverse is, of course, valid when the embolectomy is done in a proximal direction. The thromboembolic masses can be suctioned or pulled out with forceps, and the arteriotomy should be inspected to be clean from remaining materials before the catheter is reinserted. The maneuver should be repeated until the catheter has been passed at least once without any exchange of thromboembolic materials and until there is an acceptable backflow from the distal vascular bed.

Depending on the degree of ischemia and collaterals, the backflow is, however, not always brisk.

If a catheter runs into early and hard resistance, this might be due to previously occluded segment that forced the catheter into a branch. It should then be withdrawn and reinserted, using great caution to avoid perforation. If the resistance cannot be passed and if acute ischemia is present, angiography should always be considered to examine the possibility of a vascular reconstruction.

Besides performing embolectomy in the superficial femoral, popliteal, and calf arteries, the deep femoral artery must be checked for an obstructing embolus or clot that needs to be extracted. Separate declamping of the superficial femoral and deep femoral arteries to check the backflow is the best way to do this. Remember the possibility that backflow from the distal vascular bed after embolectomy might emanate from collaterals located proximal to distally located clots. Back flow does not always assure that the peripheral vascular bed is free from further embolic masses. A basic rule is that every operation should be completed with intraoperative angiography  to ensure good outflow and to rule out remaining emboli and secondary thrombus. To dissolve small amounts of remaining thrombus local infusion of 2–4 cc recombinant tissue plasminogen activator (rtPA) can be administered before the angiography catheter is pulled out.

Finally, the arteriotomy is closed. If necessary a patch of vein or synthetic material is used to avoid narrowing of the lumen. As mentioned before, the embolectomy procedure includes intraoperative angiography. If this examination indicates significant amounts of emboli remaining in the embolectomized arteries or if the foot still appears as being inadequately perfused after the arteriotomy is closed, other measures need to be taken. If there are remaining emboli in the superficial femoral or popliteal arteries, another embolectomy attempt from the arteriotomy in the groin can be made. Clots, if seen in all the calf arteries, need to be removed through a second arteriotomy in the popliteal artery. This is done by a medial incision below the knee; note that localanesthesia is not sufficient for this. It is usually necessary to restore flow in two, or occasionally in only one, of the calf arteries.

Embolectomy at the popliteal level is the first treatment step when ischemia is limited to the distal calf and foot and when there is a palpable pulse in the groin or in the popliteal fossa.

 

Thrombosis

 

The preliminary diagnosis of embolus must be reconsidered if the exposed femoral artery in the groin is hard and calcified. In most situations, clot removal with Fogarty catheters will then fail. It is usually difficult or even impossible to pass the catheter distally, indicating the presence of stenoses or occlusions. Even if the embolectomy appears successful, early reocclusion is common. Such secondary thrombosis is usually more extensive and will aggravate the ischemia. Accordingly, angiography should be considered as the first step if the femoral artery is grossly arteriosclerotic and if it is hard to pass the catheter down to the calf level. It will confirm the etiology and reveal whether a bypass is required and feasible. Vascular reconstruction in acute leg ischemia is often rather difficult andexperience in vascular surgery is required.

 

 Intraoperative angiography

 

With the proximal clamp in position a 5 or 8French baby-feeding catheter is inserted into the arteriotomy. The tip of the catheter is placed 5cm into the superficial femoral artery and distal control around it is achieved with a vessel-loop. Contrast for intravasal use containing 140–300 mg iodine/ml is infused with a 20ccsyringe connected to a three-way valve. Heparinized Ringer’s or saline (10units/ml heparin) is flushed through the catheter before and after contrast injection to prevent thrombosis in the occluded vascular bed. If the patient is suspected to have renal failure, the amount of contrast used is kept at a minimum. Angled projections can  be obtained without moving the C-arm by rotating the patient’s foot.

 

The use of contrast in the Fogarty catheter balloon during fluoroscopy allows the calf vessel into which the catheter slides to be identified. The technique for intraoperative angiography is also a prerequisite for interoperative use of endovascular treatment options such asangioplasty (Fig. 9).

 

 

Fig. 9. Intraoperative angiography

 

Thrombolysis

 

Thrombolysis is performed in the angiosuite. A consultation with a specialist in coagulation disorders or a specialist in vascular medicine is sometimes needed to discuss possible problems related to coagulation before the procedure.

Treatment is usually directed toward resolving a fresh, thrombotic occlusion, but emboli and thrombi several weeks old can also be successfully lysed. The procedure starts with a diagnostic angiography via contralateral or antegrade ipsilateral arterial punctures. If thrombolytic treatment is decided the procedure continues right away, and the tip of a pulse-spray catheter is placed in the thrombus. The lytic agent is then forcefully injected directly into it to cause fragmentation. The primary choices for lytic agent are recombinant tissue plasminogen activator (rtPA) or urokinase. Because of the risk of allergic reactions, streptokinase should be avoided. Intermittent injections of 1 ml every 5–10 min to a total dose of 10–20 ml rtPA over 1–3 h is followed by angiographic control of the result. If the thrombus is completely lysed any underlying lesion is treated. If thrombus still remains, the rtPA infusion is continued slowly over 6–12h with 1mg/h. If the initial thrombolysis fails, a variety of mechanical catheters can be used to try to further dissolve and aspirate the thrombus. Examples include the AngioJet and the Amplatz.

Because of the risk of bleeding and systemic complications, and also because the ischemic leg may deteriorate, careful monitoring during con-tinued thrombolysis is necessary. This is best done in an intensive care or step-down unit. The patient should be kept supine in bed throughout the procedure. During this time the other measures suggested for optimizing coagulation and central circulation are continued. It is also necessary to check fibrinogen concentration to make sure the value does not decline to <1.0 mg/ml. Below this level surgical hemostasis is insufficient and the infusion should be stopped. Angiographic control of the result is performed afterwards, usually the following morning, and occasionally during the slow infusion to check the effect and allow repositioning of the catheter. The part of the thrombus surrounding the catheter is lysed first, which is why it often is beneficial to advance the catheter further into the thrombus after a few hours.

Finally, the lesion that caused the thrombosis is treated with angioplasty. To avoid unnecessary bleeding from the puncture site, the fibrinogen concentration is checked again before the sheath is withdrawn to ensure that the level exceeds 1.0 mg/ml.

 

Management After Treatment

 

Anticoagulation

 

Patients with embolic disease caused by cardiac arrhythmia or from other cardiac sources proven by ECG, medical history, or clinical signs should be anticoagulated postoperatively. Treatment regimens described previously are employed, followed by treatment with coumadin. Anticoagulation has no proven positive effect for the prognosis of the ischemic leg but is administered to reduce the risk of new emboli. The patient’s abilities to comply with treatment and the risk for bleeding complications have to be weighed against the benefits. If the source of the emboli is not clear, it should be investigated. Findings of atrial fibrillation and heart thrombus can then be treated. If the ECG is normal, echocardiography is ordered to search for thrombus and valve deficiencies. If the left atrium is a likely embolic source, transesophageal echocardiography may be indicated.

When the etiology of leg ischemia is uncertain it is difficult to give general advice. There is no scientific evidence that long-term postoperative anticoagulation reduces the risk of reocclusion or influences patient survival. Continued treatment with dextran or low molecular weight heparin is recommended at least during hospitalization.

If hypercoagulable states are suspected the patient needs to be worked up during the postoperative period to reduce the risk of reocclusion. Examples are patients with hyperhomocysteinemia, who may be treated with folates, and patients with antiphospholipid antibodies, who need coumadin and salicylic acid.

 

Reperfusion Syndrome

 

Patients treated for severe acute leg ischemia are at risk of developing reperfusion syndrome. This occurs when ischemic muscles are reperfused and metabolites from damaged and disintegrated muscle cells are spread systemically. A part of this process consists of leakage of myoglobin; it may be nephrotoxic and colors the urine red. The metabolites also affect central circulation and may cause arrhythmia and heart failure. The risk for reperfusion syndrome is higher when occlusions are proximal and the affected muscle mass is large. One example is saddle emboli located in the iliac bifurcation. The risk is also higher when the ischemia time is longer than 4–6 h.

The elevated mortality associated with severe acute leg ischemia may be due to reperfusion syndrome. Survival may therefore be improved by avoiding reperfusion and a lower mortality has been reported from hospitals where primary amputation is favored. It has also been suggested that thrombolysis saves lives by restoring perfusion gradually. For a threatened leg this is seldom an option because rapid restoration of perfusion is necessary to save it.

The best treatment for reperfusion syndrome is prevention by expeditious restoration of flow.

There are no clinically proven effective drugs but many have been successful in animal models, including heparin, mannitol, and prostaglandins.

Because heparin and mannitol also have other potential benefits and few side effects they are recommended during the postoperative period. Obviously, acidosis and hyperkalemia must be corrected, and the patient needs to be well hydrated and have good urine output. For patients with suspected reperfusion syn-

drome – urine acidosis and high serum myoglobin levels – alkalinization of the urine is often recommended in order to avoid renal failure despite weak support in the literature. If the urine is red, the urine pH <7.0, and serum myoglobin >10,000 mg/ml, 100 ml sodium bicarbonate is given IV. The dose is repeated until the pH is normalized.

 

Compartment Syndrome

 

 

The acute inflammation in the muscle after reestablishing perfusion leads to swelling and a risk for compartment syndrome. The available space for the muscles is limited in the leg and when the increased pressure in the compartments reduces capillary perfusion below the level necessary for tissue viability, nerve injury and muscle necrosis occur.

The essential clinical feature of compartment syndrome is pain – often very strong and “out of proportion,” which is accentuated by passive extension. The muscle is hard and tender when palpated. Unfortunately, nerves within the compartments are also affected, causing disturbance of sensibility and motor function. This makes diagnosis more difficult. Moreover, the patient is often not fully awake or disoriented, but early diagnosis is still important to save the muscle tissue. For that reason measurement of intracompartmental pressure is performed for diagnosis in some hospitals.

There are no precise limits that advocate fasciotomy, but 30mmHg has been proposed. The specificity for a correct diagnosis using this limit is high, but the sensitivity is much lower.

To notice signs of compartment syndrome after operation or thrombolysis for acute ischemia, frequent physical examinations are vital. Fasciotomy should be performed immediately following the procedure if any suspicion of compartment syndrome exists. Common advice is to always perform fasciotomy right after the vascular procedure when the ischemia is severe and has lasted over 4–6 h. To open all four compartments, we recommend using two long incisions, one placed laterally and one medially in the calf.

 

Results and Outcome

 

The outlook for patients with acute leg ischemia has generally been poor. The 30-day mortality when an embolus is the etiology varies between 10% and 40%. Survival is better when arterial thrombosis is the cause, around 90%. When considering the amputation rate after surgical treatment the figures are reversed – lower for embolic disease, at 10–30%, than for thrombosis, which of ten has an early amputation rate of around 40%.

A substantial number of the patients die or require amputation after 30 days. This is due to a combined effect of the patients’ advanced age and comorbidities. In studies not differentiating between etiologies, only 30–40% of the patients were alive 5 years after surgery, and among those, 40–50% had had amputations.

Because the gradual release of ischemia is thought to reduce the risk for reperfusion syndrome and thereby the negative effects on the heart and kidneys mortality after thrombolysis is thought to be lower. It is difficult, however, to find data on thrombolytic therapy comparable to surgical results. A majority of patients will undergo surgery when thrombolysis is not technically possible, leaving a selected group to follow up. In the few randomized controlled trials that compare surgery and thrombolysis the short-term and long-term amputation rates are alike. Survival is also similar, but in one study it was lower after thrombolytic therapy at 1 year, 80%, compared with surgically treated patients, of whom only 60% were alive at that time.

 

 

Conditions Associated with Acute Leg Ischemia

 

Chronic Ischemia of the Lower Extremity

 

It is sometimes difficult to differentiate between acute leg ischemia, deterioration of chronic leg ischemia, and just severe end-stage chronic disease in general. Periods of pain escalation bring patients with chronic ischemia to the emergency department. Accentuated pain in these patients has a wide range of origins. Decreased foot perfusion can be due to dehydration or lowered systemic pressure as a consequence of heart failure or a change in medication. Ulcers are frequently painful, especially when complicated by infection or when dressings are changed. History and examination of vital functions and the leg usually disclose such conditions and can also sufficiently rule out acute leg ischemia that needs urgent treatment.

Patients with chronic ischemia benefit from careful planning of their treatment and should not – with few exceptions – be expeditiously treated. Elective therapy includes weighing risk factors against the outcome of the proposed treatment and all the work-up that is needed to get this information. (It is beyond this book’s purpose to describe the management of chronic ischemia.) In the emergency department it is sensible to identify and directly treat the patients with true acute leg ischemia and schedule treatment of patients with chronic disease for later. Examples of findings in medical history and physical examination are listed in Table 5 .

 

Table 5. Medical history and physical examination

findings suggesting chronic leg ischemia

 

 

Acute Ischemia After Previous Vascular Reconstruction

 

A substantial number of patients have chronic leg ischemia and have undergone vascular reconstructions, so there is a high likelihood that emergency department physicians will have to take care of problems with postoperative acute leg ischemia in the operated leg. The clinical presentation of graft failure or occlusion is variable. An abrupt change in leg function and skin temperature accompanied by the onset of pain can occur any time after surgery, but especially within the first 6 months. Several years after the reconstruction it is slightly more common for progressive deterioration to occur and an eventual graft occlusion to pass unnoticed.

As discussed previously in this chapter the management principles are roughly the same as for primary acute leg ischemia. It is the status of the leg and the severity of ischemia that lead workup and management. Most patients will undergo angiography to establish diagnosis and to provide information about possibilities to restore blood flow. Thrombolysis is often the best treatment option because it exposes the underlying lesions that may have caused the occlusion. As for patients with acute ischemia, those with an immediately threatened leg after a reconstruction should be taken to the operating room and treated as fast as possible.

 

Blue Toe Syndrome

 

A toe that suddenly becomes cool, painful, and cyanotic, while pulses can be palpated in the foot, characterizes the classic presentation of blue toe syndrome. This has occasionally led to the assumption that the discoloration of the toe is not of vascular origin, and patients have been sent home without proper vascular assessment. Although coagulation disorders or vasculitis may contribute, such an assumption is dangerous. Atheroembolism is the main cause for blue toe syndrome and atheromatous plaques in the iliac or femoral arteries or thrombi in abdominal or popliteal aneurysms are the main sources. Blue toe syndrome can also present without palpable foot pulses. The presentation may then be less dramatic.

It is common that the patient does not notice the initial insult and wait to seek medical care until after several weeks. Ischemic ulceration at the tip of the toe may then be found in the examination. During the foot examination more signs of microembolization are usually found, including blue spots or patchy discoloration of the sole and heel. When both feet are affected it suggests an embolic source above the aortic bifurcation. The clinical examination should include assessing the aorta and all peripheral arteries, including pulses and auscultation for bruits. When pulses in the foot are not palpable, ankle blood pressure needs to be measured. In the search for aneurysms and stenoses patients need to be investigated with duplex ultrasound to verify examination findings. To prevent future embolization episodes lesions or aneurysms found should be treated as soon as possible.

Occasionally the pain is transient and the blue color will disappear within a few weeks. More common, however, is an extremely intense pain in the toe that is continuous and difficult to treat. Unfortunately, the pain often lasts several months until the toe is either amputated or healed.

The pain is best treated with oral opiates, and quite high doses are often required to ease the pain. A tricyclic antidepressant drug may be added to the regimen if analgesics are not enough.

While waiting for diagnostic studies and final treatment of the lesions, the patient is put on aspirin therapy. There is no scientific evidence for using other medications such as coumadin, steroids, or dipyramidole. Still, if suspicion for a popliteal aneurysm is high we recommend anticoagulation with low molecular weight heparin until the aneurysm is corrected.

 

Popliteal Aneurysms

 

A common reason for acute leg ischemia is thrombosis of a popliteal aneurysm. Such aneurysms are also one of the main sources for embolization to the digits in the foot and blue toe syndrome. Besides the clinical signs of acute ischemia discussed previously, a prominent wide popliteal pulse or a mass in the popliteal fossa is often palpated when popliteal aneurysm is the reason for the obstrution.

Popliteal aneurysms are frequent in men but rare in women. They are often bilateral – more than 50% – and associated with the presence of other aneurysms. For instance, 40% of patients with popliteal aneurysms also have an aneurysm in the abdominal aorta. Most popliteal aneurysms are identified during angiography performed as part of the management process for acute leg ischemia. When an aneurysm is suspected during angiography or examination, duplex ultrasound is performed to verify the finding and estimate the aneurysm’s diameter.

If the severity of ischemia corresponds to the “immediately threatened” stage described earlier, the patient needs urgent surgery. The revascularization procedure is then often quite difficult. Exposure of the popliteal artery below the knee, including the origins of the calf arteries, should be followed by intraoperative angiography and an attempt to remove the thrombus. It is hoped that angiography can identify a spared calf artery distally. The calf arteries are sometimes slightly dilated in this patient group and can serve as a good distal landing site for a bypass excluding the aneurysm. Often, however, it is impossible to open up the distal vascular bed due to old embolic occlusions and the prognosis for the leg is poor. In such situations every possible alternative solution should be considered, including local thrombolysis, systemic prostaglandin infusion, and profundaplasty.

If the ischemia is less severe, thrombolysis may be considered following the angiography before surgical exclusion of the aneurysm. While thrombolysis previously has been considered questionable because of the risk for further fragmentation of thrombus within the popliteal aneurysm, this strategy may prove very favorable. Over the last few years several studies reporting restored calf vessels by thrombolysis have been published. This may lead to more successful bypasses and improved limb salvage. Once the bypass is accomplished good long-term results are probable. Interestingly, vein grafts used for bypasses in patients with popliteal aneurysms appear to be wider and stay patent longer than for other patient groups.

 

 


 

 

ACUTE INTESTINAL ISCHEMIA

 

Mesenteric artery thrombosis has the highest mortality rate of all causes of mesenteric ischemia. First described in the late 15th century, little progress was made in its treatment before the 20th century.

In 1901, a patient with a long history of postprandial pain was found to have an atherosclerotic plaque with overlying thrombus of the superior mesenteric artery (SMA). The physician concluded that if a patient could develop pain of the lower extremities secondary to atherosclerosis, it would stand to reason that a patient could present with postprandial pain due to narrowing of the mesenteric vessels. An example of complete occlusion is illustrated in the image below. The pathophysiologic mechanism by which ischemia produces pain remains poorly understood.

The arterial circulation to the gut has extensive collaterals and arcades providing multiple sources of blood inflow. This explains why vascular occlusion is well tolerated as evidenced by the relative lack of clinical intestinal ischemia despite the high prevalence of atherosclerotic disease of the aorta and visceral arteries. Certain collateral patterns are recognized, depending on which artery is blocked. When either the celiac or superior mesenteric artery (SMA) is compromised, the main collateral circulation is by the gastroduodenal and pancreaticoduodenal arteries. The main collateral channels between the SMA and inferior mesenteric artery (IMA) occur in the region of the splenic flexure between the middle and left colic arteries. In the presence of either SMA or IMA occlusion, the marginal artery of Drummond and the arch of Riolan (an ascending branch of the left colic artery anastomosing with branches of the SMA) enlarge significantly. In the presence of an IMA occlusion, another important collateral circulation is between the internal iliac artery and the left colic artery via the superior hemorrhoidal arteries.

The SMA is the critically important vessel in maintaining visceral perfusion, as demonstrated by increased blood flow after eating. This is not seen in the celiac artery. In chronic ischemia, all patients have SMA stenosis or occlusion, in addition to celiac artery and/or IMA involvement.

 

Etiology

 

OCCLUSIVE DISEASE

 

Emboli. The SMA is the most common site of embolic occlusion although the celiac artery can be affected. There is classically an underlying cardiac problem giving rise to the organized thrombus that embolizes. This is usually atrial fibrillation or less commonly a mural thrombus from an acute myocardial infarction. A history of previous embolic events is not uncommon. Other causes of emboli include iatrogenic intra-aortic manipulations, paradoxical emboli through a septal defect, atrial myxoma or primary aortic tumors.

The history is of constant severe epigastric or periumbilical pain of sudden onset. It is frequently followed by copious vomiting and explosive diarrhea.

Typically the patient has been previously well and asymptomatic. The abdominal signs are often lacking or nonspecific, with distension in association with absent or normal bowel sounds without any signs of peritonism. This combination of severe abdominal pain out of proportion to the clinical findings is typical. Peritonism or blood in the stool or vomitus indicates severe advanced intestinal ischemia with likely infarction and is generally a late clinical feature.

The presence of proximal SMA pulsation and the distribution of intestinal ischemia are intra-operative clues for an embolus. The occlusion in embolism is usually distal to the origin of the pancreaticoduodenal and middle colic branches, which allows some blood flow to the small intestine to be maintained. The stomach, duodenum, and proximal jejunum are normal with ischemia extending to the mid transverse colon.

 

Thrombosis.

 

Thrombosis of the superior mesenteric or celiac arteries is most often associated with a preexisting atherosclerotic lesion that already compromises flow. The most common preexisting pathology found in patients with acute mesenteric thrombosis is atherosclerosis.

Many patients present with histories consistent with chronic mesenteric ischemia. Wasting, postprandial pain, and phagophobia (fear of eating) are all common.

Typically, the atherosclerotic lesion gradually compromises flow to the gut, causing a progressive worsening of symptoms. During a period of low flow, the artery thromboses, and flow to the gut is compromised.

Unlike embolic events that occur in arterial branches and result in limited bowel ischemia, thrombosis occurs at the vessel origin, resulting in extensive bowel involvement.

 

Superior mesenteric arterial thrombosis may occur as the result of progression of SMA stenosis that had not previously been diagnosed or treated. There is often a history of intestinal or food fear with severe weight loss, the hallmark of chronic intestinal ischemia in about 65% of patients. The typical patient is female and a heavy smoker, often with evidence of widespread arterial disease including previous myocardial infarction or daudication. As with embolic occlusion, the combination of severe abdominal pain out of proportion to the clinical findings is typical. The thrombosis of the SMA occurs at the origin of the artery.

In contrast to embolic disease, the proximal SMA pulse is absent and the distribution of intestinal ischemia is more extensive. Only the stomach, duodenum and distal colon are spared.

In the young patients, fibromuscular dysplasia can cause mesenteric arterial thrombosis with equally devastating results. Intravenous cocaine abuse is another increasing problem accounting for intestinal ischemia in the young patients. The extent of intestinal ischemia and infarction tends to be foca and less than that seen with atherosclerotic thrombosis. The mechanism of ischemia appears to be occlusive rather than due to vasospasm. Mesenteric ischemia should be considered in the differential diagnosis when evaluating a young patient with a history of cocaine abuse presenting with an acute abdomen.

Some prothrombotic states such as hyperhomocysteinemia or the 20210 A prothrombin gene mutation have resulted in primary arterial thrombosis.

 

Mesenteric venous thrombosis (MVT) is rare and accounts for 5% to 15% of all acute mesenteric ischemia. It is classified as primary (where no cause is recognized) or secondary. Secondary MVT may follow hypercoagulable states, portal venous stasis and hypertension, intra-abdominal infection and inflammation or malignancy, use of oral contraceptives and splenectomy. Long-term anticoagulation is required for MVT, because of the high recurrence rates. The clinical presentation is usually less acute than that of arterial occlusion.

Severe but vague abdominal pain that tends to be colicky and slowly progressive is usually present. Few abdominal signs are present except tenderness, distension and decreased bowel sounds. The pain is out of proportion to the physical findings. Fecal occult blood is present in the majority of patients.

There is a pyrexia of greater than 38 °C in 25% to 50% of patients, and 20% have a tachycardia. Leucocytosis ranges from 12000 to 29000.

Frank peritonitis is seen only when transmural infarction or perforation has occurred.

Surgical findings include blood-stained free peritoneal fluid at laparotomy. The affected bowel is cyanotic and edematous with a rubbery texture.

 

Mesenteric arterial pulsations are present but the veins contain fresh thrombus that extrude when the veins are cut. Infarction is most common in the mid small bowel.

 

 

 

 

 

FIG.  A – Schematic representation of the collateral circulation of the

intestine. B – Angiosraphic appearance of arch of Riolan from superior

mesenteric artery (stented at its origin). C – Angiographic appearance of

marginal artery of Drummond. D – Initial angiogram demonstrates occlu-

ded IMA. The delayed film shows the colonic supply.

 

Diagnosis

 

Acute intestinal ischemia is a life-threatening surgical emergency, yet can be a difficult diagnosis to make, with delay contributing directly to infarction.

 

The majority of cases are diagnosed more than 12 hours after the onset of symptoms. Delayed diagnosis accounts for the majority of malpractice claims involving acute mesenteric ischemia in the United States. Diagnosis depends on a high  index of suspicion. The main presenting feature is the combination of severe abdominal pain out of proportion to the clinical findings, as discussed above.

 

Serum levels of lactate and leucocytes are elevated in the majority (65% to 90%) of patients to greater than 50 U/L and 15000/mL, respectively.

Hyperamylasemia is seen in just under half the patients with acute mesenteric ischemia. Elevation of serum inorganic phosphate levels have been proposed as a marker of mesenteric ischemia, as it is extensively found in gut, but this only occurs in 15% to 33% of such patients.

 

However, in those patients who did have elevated phosphate levels, it predicted extensive injury and poor prognosis. The fibrinolytic marker D-dimer is elevated in thrombo-embolic occlusion of the SMA, although levels are also raised in other conditions of acute bowel ischemia such as strangulation or ruptured aortic aneurysm.

 

Animal studies have suggested intestinal fatty acid binding protein (I-FABP) as a serum marker reflecting bowel ischemia. Early human studies show promise, as patients with ischemic bowel disease demonstrate significantly higher I-FABP levels than either healthy subjects or patients with acute abdominal pain. Patients with mesenteric infarction had the highest serum I-FABP levels.

Plain radiographs of the abdomen may reveal nonspecific bowel dilatation or, in MVT, wall edema (thumbprinting); or gas in the bowel wall or portal vein. Unfortunately they are not helpful in most cases.

 

Mesenteric angiography will confirm the diagnosis of arterial occlusion but at the cost of delay in treatment. If there are clear abdominal signs of peritonitism, urgent laparotomy without angiography is the best course of action. In the remainder of patients suspected of acute intestinal ischemia with-out abdominal signs, angiography is indicated with lateral views of the visceral aorta and its branches.

In acute SMA thrombosis, there is usually no visualization of the entire artery because of the ostial nature of the disease, although delayed views may show slow filling of the distal SMA. SMA embolization usually allows visualization of the proximal artery to just beyond the level of the middle colic artery.

 

Treatment

 

Nonsurgical

 

In all cases, the patient should be initially resuscitated, given broadpectrum intravenous antibiotics and fully heparinized. As yet, the twin goals of mesenteric revascularization and resection of nonviable bowel can only be achieved by surgical means.

 

Surgery is indicated in all patients with peritonitis. Angiography in patients without peritonitis may demonstrate NOMI or MVT. In NOMI, treatment is nonoperative and depends on optimizing cardiac output and treating underlying conditions such as sepsis. Intramesenteric arterial infusion of papaverine at a dose of 30 to 60 mglr  may be beneficial.

Up to 65% of patients who have undergone cardiac surgery have had symptomatic improvement within hours when diagnosed early.

If MVT is diagnosed at angiography, intra-arterial thrombolytic therapy has been given successfully. Nonoperative management by full anticoagulation for acute MVT is feasible when the initial diagnosis is certain and when the bowel infarction has not led to transmural necrosis and bowel perforation. The morbidity, mortality, and survival rates are similar in cases of surgical and nonoperative management.

Other reported endovascular procedures for acute intestinal ischemia include fenestration and stent placement in aortic dissection, angioplasty and stenting in an acute occlusion in a patient with chronic mesenteric insufficiency, and angioplasty alone . This contrasts with an increasing use of angioplasty for chronic mesenteric ischemia.

 

SURGICAL

 

Laparotomy is indicated in patients with peritonitis after rapid resuscitation. The first step is to assess the degree and extent of bowel viability. Free, foul smelling peritoneal fluid is a sign of advanced necrosis even if perforation has not occurred. Ischemic bowel has a characteristic appearance with loss of its normal sheen. It is dull, gray in color and flabby in tone without any peristalsis. Infarcted bowel is purplish black in color, often friable and perforated. In many cases the bowel ischemia will be so extensive and advanced that no further surgical treatment is undertaken and palliative care given. Where there is hope of sufficient bowel viability, revascularization should be performed before any bowel resection is considered. After successful revascularization, previously precarious segments of intestine may recover and resection of clearly ischemic bowel can then take place.

 

SMA embolectomy. The proximal portion of the SMA is dissected free from the surrounding fat and lymphatic tissue just as it emerges from the pancreatic neck into the base of the mesentery. Approximately 3 to 4 centimeters of artery is cleared, with care takeot to damage the branches. Heparin (5000 units) is given intravenously. A transverse arteriotomy is made and a 3F or 4F embolectomy catheter is passed proximally and distally to clear the embolus and reestablish vigorous pulsatile flow. If proximal flow cannot be established, SMA thrombosis is likely and reconstructive surgery will be required.

 

 

 

 

FIG. A – Schematic representation of revascularization of the SMA with: bypass taking care to avoid kinking and obs-

truction B – Or re-implantation of SMA into the aorta. C – Angiographic appearance of aorto-SMA bypass with vein graft.

There is co-existing left common iliac occlusion. D – Angiographic appearance of re-implanted SMA into aorta, which has

a smal l saccular aneurysm at the site of occluded vein graft (aortoceliac bypass).

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