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250
Fig. 21.8 Example of aortic measurement of TL and FL in the dissected aortic segment
I. A. Laskowski et al.
All TBAD patients are admitted to the inten­sive care unit for initial management and neces­sary evaluation. If additional better-quality imaging is required prompt thin cut contrast enhanced computed tomography of the thorax, abdomen and pelvis (CTA) is performed. If abso­lute contraindications to iodinated contrast exist, Magnetic Resonance Angiography (MRA)may be utilized for further anatomic evaluation.
When isolated TBAD with organ malperfu­sion is present, an emergent repair using endo­vascular options is considered as the rst line of therapy. In cases of frank aortic rupture, patients either undergo emergent open repair or multi­disciplinary approach by vascular and cardio­thoracic senior team members used to evaluate endovascular options and formulate treatment plan.
For patients with non-complicated, high risk features dissection with presence of two lumens, immediate medical management with blood pres­sure and impulse control is implemented. High risks feature TBAD is dened in cases when total aortic lumen is >40 mm, false lumen >22 mm, proximal aortic tear >10mm, there is presence of ongoing chest pain regardless of blood pressure
control, history of poor compliance with medical management of hypertension, and evidence of organ malperfusion on imaging [31]. Following qualication for surgical intervention timing of repair is dened as hyperacute when treated within rst 24h of presentation, acute-days 1–14 and subacute for those treated between day 15 and 90th day of presentation. Majority of our patients undergo repair during acute phase for isolated TBAD, and subacute for the residual dis­section following TAD repair.

Imaging: CTA, MRI, TEE

All patients undergo baseline imaging evaluation that consisted of computed tomography angiog­raphy (CTA) with multiplanar reconstruction or gadolinium-enhanced magnetic resonance angi­ography when needed. Interprocedurally, all patients undergo transesophageal echocardiogra­phy for baseline assessment of aortic arch and ascending and proximal descending aorta for evaluation of a possibility of retrograde Type A dissection, new pericardial effusion, or any other acute changes.
21 Surgical Decision-Making in Vascular Surgery: Practical Approaches to New Innovative Techniques…
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Morphologic Aortic Assessment

Preoperative imaging was used for morphologic assessment of the entire aorta with assessment of aortic false lumen patency status, aortic arch involvement, and proximity to left subclavian artery, patency of aortic branch vessels with determination of the take-off from true or false lumen, and degree and symmetry of end-organ perfusion. Femoral access is evaluated in detail with particular attention to the extent of dissec­tion and patency and diameter of iliac arteries, quality and diameter of femoral arteries with potential involvement in dissection, presence of atherosclerotic disease, and the level of femoral bifurcations bilaterally. This is especially impor­tant since we routinely use preclose technique with Perclose, Proglide devices (Abbott Cardiovascular Systems, IL, USA).
Preoperative Planning andAortic Dissection
As a rst step of preoperative planning of aortic dis­section, we assess proximal extent of the dissection based on Ishimaru Zones. We always want to select aortic segment free of pathology as close to 2cm in length for the proximal landing zone of the aortic stent graft. For elective cases, we attempt to pre­serve ow into left subclavian artery that is achieved by either revascularization with carotid to subcla­vian bypass grafting or with the use of Thoracic Branch Endograft (Gore and Ass, Flagstaff, AZ, USA). In all cases of FL visceral branch origin, we protect the branch vessels with a Glide Wire or end lumen catheter during distal aortic stenting with subsequent branch vessel patency and adjunct branch vessel stenting as needed (Fig.21.8).

Technique

We perform all aortic dissection cases under gen­eral anesthesia in the hybrid operating room with the use of digital subtraction angiography. All patients undergo neuromonitoring with somato­sensory evoked potential (SSEP) and motor evoked potential (MEP) throughout the case. We
do not use cerebrospinal uid drainage on routine basis. Bilateral ultrasound-guided percutaneous access with use of preclose Perclose ProGlide sys­tem technique is applied for the main device deliv­ery. If ilio-femoral dissection is present, preferentially the non-dissected side is used for the device deployment. For initial vascular access, a Bentson wire (Boston Scientic, Marlborough, MA, USA) with 100 cm Pig tail catheter (Cook Medical) support is advance to ascending aorta with subsequent exchange for a 300 cm double curve Lunderquist® extra-stiff wire (Cook Medical). Contralateral diagnostic Pigtail catheter is advanced in a similar fashion and positioned in the ascending aorta. Femoral venous access is rou­tinely established for temporary percutaneous pac­ing wires that are placed in the right ventricle. They are used for rapid cardiac pacing during stent deployment and during aortic angioplasty with rate set to 180 to 200bpm. In the next step, aortic arch angiogram is performed and using informa­tion from the preoperative CTA, intraoperative conrmation of the position of arch vessels is made and nal level of the proximal deployment of the rst stent is selected. In cases where L SCA is involved and when GORE Thoracic Branch Endograft (TBE) is used, we obtain additional through and through wire access from the left wrist and out of the large sheath of the main device delivery as per Gore device IFU.In all other cases, our to go to device is Zenith TX2 when deployed into the native aorta or Zenith Alpha (Cook Medical) covered stents when deployment is into preexisting Dacron graft of either ascending aortic repair or an elephant trunk repair. For all cases requiring left SCA coverage that do not meet ana­tomic criteria for TBE, we perform carotid -to­subclavian bypass usually a day or two prior to the aortic stenting procedure.
Once proximal stent graft is in place, we continue to deploy covered stents to the level just proximal to celiac trunk. We do that to assure that all secondary tears of the aortic dissection ap are excluded as dis­tally as possible. In our experience, this prevents ongoing false lumen ow that may lead to early repair failure. Once all covered stents are in place, we proceed with Zenith Dissection uncovered stents
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deployment in the remaining abdominal aorta all the way to the level of iliac bifurcation. At this point for those patients that Petticoat approach is intended, this completes the procedure.
Since in our experience, STABILISE tech­nique has excellent outcomes we attempt it in all patients with TBAD that meet anatomic criteria of aortic diameters. We use modied criteria rst established by Melissano and his group [32].
That part of the procedure is performed with a 46 mm Coda molding balloon (Cook), and the entire stented segment of the aorta to the infrare­nal segment is angioplastied while rapid cardiac pacing is employed (Fig. 21.7). The goal is to dilate true aortic lumen to the total aortic diame­ter as per measurements from the preoperative imaging. In the next step, we perform conrma­tory intravascular ultrasound of the entire aorta to determine presence of residual false lumen and we repeat aortic angioplasty at these levels until false lumen obliteration was achieved.
We routinely employ wire protection of all aortic branch vessels that come off the false lumen during aortic angioplasty (Fig.21.9).
After intervention patients are observed in the intensive care unit with routine neurovascular checks and to maintain mean arterial pressures in the 90–100mmHg range for rst 72h. Patients
are on standard DVT prophylaxis, and antiplate­let regimen with aspiring 81mg daily is imple­mented in those cases where TBED or adjunct branch vessel stenting was performed.
Patient undergo repeat CTA chest abdomen and pelvis evaluation before discharge to assess aortic remodeling results with particular atten­tion to false, true and total lumen diameters, false lumen ow, and presence of endoleaks, type A retrograde dissection, and all organ perfusion.
To date, over 30 patients were treated using this approach with no intraoperative mortality and no aortic rupture in the course of aortic mold­ing balloon. When compared to Petticoat, STABILISE technique achieved signicantly smaller false lumen diameter and resultant abro­gation of false lumen ow on follow-up imaging (Fig.21.10). In addition, we did not observe ret­rograde type A dissection, open conversion, and new aortic branch vessel compromise or occlu­sion. We also did not observe neurologic compli­cations both during the intervention and in the postoperative period. Realizing that more studies are needed to fully evaluate this approach, we feel that our treatment algorithm allows thera­peutic options for patients with this challenging condition.
Fig. 21.9 Branch vessel wire protection and stenting after completion of aortic remodeling
21 Surgical Decision-Making in Vascular Surgery: Practical Approaches to New Innovative Techniques…
Fig. 21.10 Aortic remodeling after STABILISE technique on pre- and postoperative CTA imaging
253
Carotid Endarterectomy—Can WeMake aGood Operation Better? Technical Considerations

Introduction

In the year 1913, James Ramsey Hunt, a young neurology attending from Columbia University presented a paper at the New York Academy of Medicine highlighting the role of carotid arteries in the causation of stroke [33]. Till that time, it was believed that stroke was essentially an intra­cranial pathology—hemorrhage, thrombosis, or tumor. Based on autopsy studies of brain and neck, Ramsey Hunt linked extracranial carotid artery disease to intracranial pathology. Miller Fisher, a Canadian neuropathologist who later headed the department in Harvard coined the term TIA (Transient Ischemic Attack) and fur­thered our understanding of stroke disorders. He postulated that one day, surgeons may be able to remove the “offending plaque.” He also explained the mechanism of stroke in atrial brillation (car­dioembolic). Egas Moniz from Portugal devel­oped cerebral angiography making it possible to visualize the extracranial arteries and the intra­cranial vascular system. By late 1940s and early
1950s, the medical community became aware of the signicance of carotid disease, there was angiography to conrm and visualize the disease, but there was uncertainty about how to treat this. Historically, Eastcott, Pickering, and Rob are credited to have done the rst published carotid surgery in Saint Mary’s Hospital in London in 1954 on a woman with carotid stenosis and TIA [34]. It is now conrmed that a surgeon in Argentina Raul Carrea performed in 1951 [35]. (Technically, the procedure was carotid artery reconstruction. Michael DeBakey performed carotid endarterectomy (CEA) in 1953, but did not publish it till much later) (Fig.21.11) [37].
By 1980s, CEA became one of the most com­mon procedures done in United States reaching 180,000 operations per year. Like so many other procedures in history of medicine, the results varied greatly from less than 3% stroke rate in some institutions to greater than 20% in some. This got the attention of media, causing public uproar. That was the force behind two large NIH sponsored studies here in US (NASCET—North American Symptomatic Carotid Endarterectomy Trial and ACAS—Atherosclerosis Carotid Artery Study) and almost similar study in Europe [38]. The conclusion of all three trials indicated
254
Fig. 21.11 Carotid endarterectomy techniques—historical perspective
I. A. Laskowski et al.
that CEA is indicated in symptomatic patients a with hemodynamically signicant carotid steno­sis, provided the operation is performed with combined stroke and mortality rates of 3–5%. The neurologic community and surgeons were now held to a high standard of care, very much similar to cardiac surgeons doing CABG and transplant surgeons doing kidney transplanta­tion. This was the beginning of accountability and a sort of code of conduct for the surgeons which also standardized the management of carotid disease—screening, diagnosis, indica­tions, and expected outcomes.

The Operation

Carotid endarterectomy is a procedure which requires high technical skill as well as an under­standing of brain physiology. This is an operation that has to be done technically perfect and physi­ologically right. The surgical team concept where every individual has the assigned role including the anesthesiologist, neuromonitoring personnel, circulating and the scrub nurse, the surgeon and his assistant—all doing work in synchrony. The postoperative care is as important as the surgery
itself. Creation of clinical pathway (Carotid path­way) further streamlines the postoperative care by the PACU nurses who are knowledgeable about certain unique features of carotid surgery. For instance, hypotension calls for starting a pressor and not uid bolus (as required in almost all other surgery cases). Similarly, the nursing staff should be aware of the signicance of neck hematoma or hoarseness, laryngeal stridor, or new neurologic decit, all of which require esca­lation of care and urgent intervention.
Regarding the conduct of surgery itself, some pointers are worth noting. Regarding type of anes­thesia, whether regional or general has been looked at, extensively. There is no difference in outcome between those who use general anesthesia and those who use regional cervical block. It comes down to individual surgeon’s preference, and the capability of anesthesia team to give a good regional block. Irrespective of the type of anesthe­sia, the conduct of operation requires, that in addi­tion to doing a complete endarterectomy, a) there is adequate brain perfusion at all times and b) attention to technical steps to prevent embolization of atheromatous debris during surgery.
Assessment of Cerebral Tolerance to Internal Carotid Artery Clamping.
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Brain is a remarkable organ, weighing 2% of the body weight, receives 15% of the cardiac out­put. Blood ow is 750-1000mls/minute. The nor­mal resting ow is 50mls/100g of tissue/minute. When brain blood ow drops to 30mls/100 g/ min., there is ischemia and reduction of ow to 20mls/100g/min or lower, thus results in cerebral infarction. It is important to maintain adequate ow when the internal carotid is clamped. There are ways of assessing the safety of internal carotid artery clamping:
1. Preoperative imaging studies—Helps to
assess contralateral carotid, vertebral arteries, and circle of Willis. If contralateral carotid is occluded or if there is incomplete circle of Willis, shunting will be needed.
2. Operating on a wake patient (regional anes-
thesia)—Assessment of motor and cognitive function with clamping (not possible if gen­eral anesthesia is used).
3. Continuous EEG monitoring, evoke poten-
tials monitoring (wave amplitude and pattern).
4. Measurement of cerebral blood ow (very
cumbersome, not practical).
5. Measurement of stump pressure (50 mmHg
acceptable, shunt required if lower).
The procedure begins with positioning, prep­aration, and draping of the elds. Head should be extended and turned away from the side of oper­ation. It is important not to hyperextend the neck. Elderly patient may have degenerative dis­ease of the spine. Hyperextension in these situa­tions may cause vascular (vertebral artery) and nerve compression. It is important to seal the operative area with impervious barrier to prevent any escape of oxygen into the eld from nasal cannula which if occurs can be a serious re haz­ard. The eld should be dried. Incision is oblique along the anterior border of sternomastoid. The external jugular vein coursing supercial to the muscle is ligated and divided. The muscle is retracted with retractors. Too aggressive retrac­tion and placing the retractor blades too deep may by itself cause stretch injury to recurrent laryngeal nerve. The common carotid artery is
exposed rst. Some of the tributaries of IJV will need ligation. Middle thyroid vein in the lower part of the neck and facial vein is generally at the level of carotid bifurcation. If nerves are seen coursing anterior to the carotid artery, the most common being Ansa cervicalis, gentle dissec­tion, and retraction are preferable to transection. Occasionally, the recurrent laryngeal nerve may course across the common carotid (nonrecurrent recurrent laryngeal nerve). The common carotid artery (CCA) is dissected rst and controlled with vessel loop. Keeping close to CCA, the dis­section proceeds cephalad, external carotid artery (ECA), and the very rst branch of it, superior thyroid is controlled with vessel loops. Care should be taken to avoid dissection or rough manipulation of the carotid bulb, since this is the area of disease and rough handling, can cause embolization of atheromatous debris. The inter­nal carotid artery (ICA) beyond the plaque should be dissected and controlled. Enough length of internal carotid should be dissected in case shunt is needed. It is important to identify the hypoglossal nerve which runs obliquely from lateral to medial about two inches cephalad to carotid bifurcation, however it can be lower. Once CCA, ECA, and ICA controlled, the patient is heparinized, adequacy of heparinization moni­tored with activated clotting time (ACT) which should be between 230 and 270 sec. ICA is clamped rst followed by ECA and CCA.Arteriotomy begins in healthy CCA below the diseased area and is extended into the bulb on a slightly lateral location (arteriotomy too medial on the bulb may result in distortion of the bulb when closed and extended anteriorly in ICA beyond the plaque). Endarterectomy is begun after developing an appropriate plane (ideally between the inner and outer media). The entire plaque is removed. The arteriotomy should extend beyond the ending of endarterectomy. No part of the plaque should be left behind (com­plete endarterectomy), particularly on the inter­nal carotid. If there is an intimal ledge, anchoring sutures may be used to tack the area to avoid dis­section when ow is restored. Endarterectomy from ECA is done by eversion technique. All the debris, shards, and bers are removed until the
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surface is smooth. The arteriotomy is closed with either a Dacron patch or bovine pericardial patch.
Unclamping Sequence (see diagram).
In order to prevent any embolization of par­ticulate matter and/or air, proper unclamping sequence should be followed. This has ve steps [36]
STEP 1. Unclamp the ICA and allow back bleed-
ing (last few stiches are kept loose to allow
this) STEP 2. Re-clamp the ICA at its origin STEP 3. Unclamp the ECA and let it bleed out STEP 4. Unclamp the CCA directing the blood to
ECA with ICA still clamped. Sutures are tied STEP 5. Unclamp the ICA
Heparin is neutralized with protamine sulfate. After assuring complete hemostasis, incision is closed in layers (Fig.21.12).

Eversion Endarterectomy

This is another technique popularized by the Albany group. In this technique, after dissection and clamping CCA, ECA, and ICA, the internal is transected obliquely from the carotid bulb.
Fig. 21.12 Carotid endarterectomy unclamping sequence
After creating proper endarterectomy plane, the ICA wall is gently rolled back (everted) to suf­cient length till the endpoint of the disease and plaque is removed. Similar maneuver is done on the common and external carotid. After comple­tion, the ICA is anastomosed to the bulb. The advantages of this procedure being, no patch is required. Disadvantage is that if the disease is extensive, eversion is technically difcult or inadequate. It is also harder to use a shunt if required. Eversion endarterectomy requires expe­rience and appropriate patient selection.

Complications

Every surgical procedure has complications, but hazards can be disastrous and thus safeguards during carotid endarterectomy are a must [39]. The goal is to minimize the incidence and under ideal situation, it should reach near zero. Some of the complications unique and specic to carotid endarterectomy are as follows:
1. Bleeding: Bleeding can happen after any operative procedure. When happens after CEA, it can have catastrophic consequences. Even moderate hematoma in the neck can cause venous compression, which results in laryngeal edema manifested initially by hoarseness and stridor soon after. This is a surgical emergency. It is important to remove the neck staples/sutures and sutures of the underlying layer to decompress the hematoma by bedside in PACU while preparations are made to return to OR.As soon as the hema­toma is evacuated and the neck decompressed, patient will immediately feel better. The grave mistake is to attempt intubation of a patient in respiratory distress and stridor. Because of the laryngeal edema, the entrance to trachea will be pinhole, the anesthesiologist will not be able to intubate and aggressive attempts to intubate without rst decompressing the neck will result in increasing anxiety on part of the patient, further anoxia and cardiac arrest.
2. Hypotension: Hypotension is seen in more than half of patients soon after the operation.
21 Surgical Decision-Making in Vascular Surgery: Practical Approaches to New Innovative Techniques…
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This is explained on the basis of irritability and alteration of the carotid baroreceptors which are a group of highly specialized cells located at the carotid bifurcation when stimu­lated baroreceptors cause hypotension and bradycardia. This is seen immediately or soon after the patient goes to Post Anesthesia Care Unit (PACU). It is important for the PACU nurse and other staff to be aware of this phe­nomenon. Unlike all other surgical proce­dures, where post-operative hypotension may indicate hypovolemia and calls for uid bolus or blood, post-carotid endarterectomy hypotension needs pressor agents. The most commonly used agent is phenylephrine (Neosynephrine) given as a drip with dose titrated to keep systolic blood pressure around 110–129mmHg. Hypotension generally lasts for about 4–6hours as the body’s autoregula­tion sets in by that time. If hypotension is not recognized or acted upon immediately, there is potential for the endarterectomized segment to thrombose with disastrous consequences. Hence the need for all CEA patients to be monitored for 6–8hours in PACU.
3. Hypertension and Cerebral Hyper-perfusion Syndrome: Patients who have history of hypertension should be monitored in PACU and also afterwards to assure good control of blood pressure to normal range. Hypertension may facilitate bleeding at fresh surgical site. If that happens, measures described above should be followed in addition to controlling the blood pressure. In patients who had sig­nicantly compromised blood ow before operation (high grade stenosis of one carotid with total occlusion of contralateral carotid), intraoperative, peri-operative, and postopera­tive hypertension can lead to cerebral hyper­perfusion syndrome. This is analogous to swelling of the limb and development of com­partment syndrome which occurs after resto­ration of blood ow in situations of acute and profound limb ischemia. There is vasodilata­tion of the cerebral vascular bed in response to severely reduced ow. After CEA, there is sudden ooding of the brain with increased ow and if there is element of hypertension,
this can lead to trans-vascular escape of uid, cerebral edema, microhemorrhages and even intracerebral hemorrhage This is a serious complication with an incidence of about 0.5% of carotid endarterectomy cases, resulting in high morbidity and mortality [37]. Cerebral hyper-perfusion syndrome can happen within a few hours after surgery to a week or 10 days if patient has uncontrolled hypertension. Typically, patient complains of severe head­ache on the side of operation may have sei­zures or neurologic decits similar to stroke [40]. Emergent CT scan, strict control of hypertension, barbiturates, and antiseizure drugs form the treatment strategy. Elective CEA should be postponed in patients with uncontrolled hypertension until their blood pressure is appropriately treated.
4. Nerve injury: Both cranial and other nerve injuries can happen in carotid operations4. The hypoglossal, vagus, and glossopharyn­geal nerves are in close proximity to the artery. The recurrent laryngeal nerve is the most common to be injured. This can happen by excessive stretch by self-retaining retrac­tors, or direct injury can occur by electrocau­tery, or transection during dissection CCA and ECA.Hoarseness and difculty swallow­ing saliva can occur if there is paralysis of ipsilateral vocal cord. This is very disabling in addition to medicolegal implications. Otolaryngology consult should be sought early for proper evaluation of extent of dis­ability and for intervention. Minor recurrent laryngeal nerve trauma will recover in a few weeks. The other nerve prone to injury is hypoglossal nerve which crosses from lateral to medial side. In most cases, it is about an inch or two higher cephalad to the carotid bifurcation. In some, it can cross lower, closer to carotid bifurcation. Transection can result in tongue deviated to the side of injury and affects the movement of tongue and ability to chew the food. Bilateral hypoglossal nerve injury results in paralysis of the tongue, caus­ing obstruction of oropharyngeal area. Patient will require tracheostomy. Careful history should be taken in any patient who has had
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CEA in the past who requires endarterectomy on the opposite side. In cases where hypoglos­sal or recurrent laryngeal nerve injury appears to have occurred, preoperative ENT evalua­tion is important. Injury to glossopharyngeal is rare, since it is not generally seen during carotid endarterectomy. However, in those situations where the bifurcation is high, or the disease is extensive that longer segment of ICA needs to be exposed, care should be taken to avoid injury to this nerve that courses ante­rior to ICA.Even clamp trauma to this nerve can cause signicant pharyngeal dysfunction causing difculty on swallowing. The recov­ery also is slow and some patients may require feeding tube or even PEG for feeding for 3–5weeks which is the time it takes for the muscles of deglutition to recover. The other nerve prone for injury is the cervical and man­dibular branch of the facial nerve. These can be injured when the neck incision extends higher than usual or from vigorous retraction by self-retaining retractors when the nerve gets compressed between the retractor blade and the mandible causes deviation of the angle of the mouth on the ipsilateral side. This is a signicant complication because of cos-
metic deformity. Injury to ansa cervicalis gen­erally does not result in any sequalae. Very rarely, the spinal accessory nerve can be injured (it courses across sternocleidomastoid muscle high) resulting in difculty in raising the shoulder. Hence it is important for the operating surgeon to be knowledgeable of relation of carotid artery to all the nerves and possible anatomic variations (Fig.21.13).
5. Neurologic decit after CEA: This is perhaps the most devastating to the patient and the sur­geon. Neurologic decit immediately after CEA is most likely due to technical factors and warrants immediate action. If the patient wakes up in the operating room with a neuro­logic decit, the incision should be opened for direct inspection of the carotid artery. The arteriotomy should be reopened to directly inspect if there is an intimal ap, residual plaque, clamp trauma or platelet thrombi, etc., all of which should be addressed. Intraoperative duplex scan of the artery will be helpful. If no technical problems noted, then embolization of the plaque material/ath­eromatous debris to the brain is the most probable cause. This calls for urgent CT to rule out a bleed and consultation with neuro-
Fig. 21.13 Relation of nerves of the face and neck to carotid artery-surgical considerations
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interventional experts. They have the ability to intervene and retrieve clot and debris from intracranial branches of ICA.All stroke cen­ters have neuro- intervention specialists.

Conclusion

Carotid endarterectomy has been a time-tested operation for symptomatic carotid disease and in select asymptomatic patients. With meticulous attention to every detail like proper patient selec­tion, appropriate indication, tailoring the type of anesthesia to patient’s medical status, neuromon­itoring, good surgical technique, and postopera­tive care by trained team guided by clinical pathway protocols, this procedure can be per­formed with stroke and death rates of 1% or lower. Acknowledging the vital importance of teamwork and practicing it as a habit has bene­ted patients enormously. This indeed is testa­ment to modern surgery.
Advanced Peripheral Arterial Techniques forLimb Salvage: Role ofIntravascular Lithotripsy

Introduction

Peripheral artery disease (PAD) is an important cause of cardiovascular morbidity and mortality, affecting over 230 million people worldwide [4146]. Vascular calcication is a common fea­ture in patients with PAD, especially in the set-
ting of diabetes mellitus and/or end-stage renal disease, leading to poor prognosis and increased risk of major amputation. To date, limited thera­peutic options are available to address severely calcied PAD including atherectomy and cutting balloons [4246]. However, these devices have not been effective in plaque modication and vessel expansion as the presence of vascular cal­cication can interfere with the delivery of endo­vascular therapies, where it is responsible for suboptimal vessel expansion and increased risk of vascular complications including dissection and perforation. Consequently, there are higher use of provisional stents and increased risk of suboptimal stent-related restenosis. Moreover, although atherectomy has been shown to improve luminal diameter and reduce the need for bailout stenting, vascular complications such as distal atheroembolization remain a signicant chal­lenge [4749].
Derived from renal lithotripsy, intravascular lithotripsy (IVL) is a novel technique that uses high-energy ultrasound waves to improve plaque modication and vessel compliance (Fig. 21.14) [50]. It uses pulsatile sonic pressure waves that pass through soft tissue and selectively interact strongly with high-density calcium, producing sig­nicant shear stresses that have the ability to frac­ture the calcium. Furthermore, it is designed to modify both intimal and medial calcium across a wide range of vascular applications to increase ves­sel compliance, restore vessel mobility, and pro­vide new versatile treatment options for patients.
The Shockwave Medical Peripheral IVL System (Shockwave Medical, Fremont, CA)
Fig. 21.14 Mechanism of action of the peripheral intravascular lithotripsy. Reproduced with permission from Shockwave Medical