Approach Considerations
Two techniques are commonly used for carotid endarterectomy (CEA): patch angioplasty and eversion CEA (eCEA). In the former, a longitudinal arteriotomy is made and then carried beyond the plaque both proximally and distally. This is typically followed by the use of a patch angioplasty closure; several randomized trials demonstrated that clinically relevant outcome measures favored patch closure over primary closure. [34, 35, 36, 37, 38]
In eCEA, the internal carotid artery (ICA) is obliquely transected at its origin at the carotid bifurcation, and the plaque is then extirpated through eversion and reimplantation of the ICA into the carotid bulb. Although eCEA was first described by DeBakey in the 1950s, it was not until the 1990s that it gained widespread use as a technique that shortens operating time, avoids use of prosthetic material, facilitates reconstruction of a kinked or coiled ICA, and lowers restenosis rates.
Incision
To minimize skin-edge bleeding, 0.5% bupivacaine mixed with epinephrine may be preoperatively infiltrated into the skin and subcutaneous tissue. Constant attention to hemostasis is critical throughout the procedure.
A vertical incision is most effective for exposure of the carotid sheath and the carotid vessels (from the distal common carotid artery [CCA] to the disease-free portion of the ICA and the proximal external carotid artery [ECA]) during eCEA. In addition, a vertical incision allows additional exposure of the carotid vasculature if necessary because it can readily be extended superiorly, toward the posterior belly of the digastric muscle.
The incision is created over the anterior border of the sternocleidomastoid muscle, along the line connecting the sternocleidoclavicular junction with the processus mastoideus (see the image below), and carried down to the carotid sheath. The great auricular nerve must be preserved superiorly; injury to this nerve leads to paresthesia of the ear.

The incision should be slightly curved posteriorly, toward the processus mastoideus, to avoid injury to the marginal mandibular branch of the facial nerve. Marginal mandibular nerve palsy leads to a cosmetic deficit (drooping at the corner of the mouth) as well as a functional deficit (drooling).
Exposure
Mobilization of sternocleidomastoid and dissection of carotid sheath
The skin incision is deepened through the subcutaneous fat and the platysma. The platysma is divided longitudinally. This yields access to the investing layer of deep cervical fascia, which is then incised along the anterior border of the sternocleidomastoid muscle (see the image below).

After the fascial incision, the medial border of the sternocleidomastoid muscle is mobilized along the entire length of the incision to expose the underlying carotid sheath (see the first image below). Dissection of the carotid sheath is carried low on the neck, along the medial aspect of the internal jugular vein (IJV). The initial incision of the carotid sheath should be performed carefully to avoid injury to the vagus nerve, which is located anterior to the carotid artery 10% of the time (see the second image below).

In most patients, the vagus nerve occupies the most posterior part of the carotid sheath. Although this nerve contains somatovisceral afferent and efferent neurons, the most important neurologic deficit associated with vagus nerve injury at the level of CEA is recurrent laryngeal nerve palsy. This deficit leads to ipsilateral vocal cord paralysis characterized by hoarseness, impaired phonation, and ineffective cough.
Identification and mobilization of carotid vessels
Once the carotid sheath is entered, the medial aspect of the IJV is exposed until the common facial vein is visualized. The common facial vein is a landmark for the carotid bifurcation in the vast majority of patients; it courses across the CCA and drains into the IJV. The facial vein is mobilized, suture-ligated, and divided (see the first image below). Once this has been done, the IJV is retracted laterally to yield clear exposure of the underlying CCA and ICA (see the second image below).


Next, the CCA is mobilized circumferentially and encircled with vessel loops. Circumferential exposure of the CCA is required only for the arterial segment where vessel loops are to be placed; great care must be taken posteriorly, where the vagus nerve is expected to be found in most patients (see the image below). To avoid injury to the vagus nerve, gaining and maintaining the dissection plane immediately external to the adventitia of the artery is critical.

To expose the carotid bifurcation, periarterial dissection of the surrounding tissues is continued superiorly. During the exposure of the carotid bifurcation and the carotid sinus, bradycardia may occur. Recognizing any significant alterations in heart rate and rhythm at this point in the procedure is critical because many patients with carotid artery stenosis have coexisting coronary artery disease.
If sinus bradycardia occurs, 1-2 mL of 1% lidocaine may be administered topically between the ICA and the ECA to block nerve conduction to the carotid sinus. Some surgeons routinely administer lidocaine at the time of bifurcation exposure to prevent sinus bradycardia.
The ECA lies superficial to the ICA and can easily be identified by its proximal branches (the superior thyroid artery and the ascending pharyngeal artery). The ECA is dissected free of surrounding tissue and encircled with a colored vessel loop (see the image below), as is the proximal superior thyroid artery. The ICA lies posterolaterally in the carotid sheath and is exposed superior to the carotid bifurcation.

Before mobilization of the ICA, the hypoglossal nerve should be identified and preserved (see the image below). This can be facilitated by dividing the ansa cervicalis. The fibers of the ansa cervicalis diverge from the hypoglossal nerve as it crosses the ICA and descend superficial to the CCA and ICA to innervate the strap muscles. Division of the inferior or superior roots of the ansa cervicalis does not result in neurologic defects.

A suture tie placed on the divided ansa cervicalis serves as a retractor and allows the hypoglossal nerve to be moved or elevated without being injured. The hypoglossal nerve courses obliquely, just superior to the carotid bulb, and is tucked under the posterior belly of the digastric muscle. It runs in immediate proximity to the sternocleidomastoid branch of the occipital artery.
If the extent of the plaque and the course of the bifurcation necessitate additional distal exposure of the ICA, dissection of the sternocleidomastoid arterial branch of the occipital artery allows mobilization of the hypoglossal nerve superomedially for better rostral exposure. Injury to the hypoglossal nerve causes ipsilateral deviation of the tongue when the patient attempts to extrude the tongue, as well as difficulty with initiation of swallowing.
In very high dissections of the ICA, the glossopharyngeal nerve may be encountered as it parallels the course of the hypoglossal nerve superiorly. This nerve, located between the IJV and the ICA, passes superficial to the ICA and courses between the ICA and the ECA to enter the base of the tongue. It supplies sensation to the pharynx and innervates muscles that elevate the pharynx and larynx during swallowing. Injury to the glossopharyngeal nerve leads to impairment of swallowing.
The spinal accessory nerve runs lateral to the carotid sheath and innervates the trapezius and the sternocleidomastoid muscle. This nerve may be injured by excessive lateral retraction. Dysfunction of the accessory nerve is characterized by shoulder pain, winging of the scapula, and inability to shrug the shoulder.
Once the abovementioned nerves are identified and preserved, the ICA is mobilized well distal to the palpable atheromatous lesion, which can be visualized as a yellowish discoloration of the artery that feels firm and is less compressible than a healthy artery. Adequate mobilization can be confirmed by carefully palpating the normal arterial segment of the ICA above the lesion with a finger.
The same is done for the ECA to ensure that the superior thyroid artery branch is not injured. The superior laryngeal nerve is medial to the carotid sheath, and its external branch comes into proximity with the superior thyroid artery. Thus, dissection of the ECA and ligation of its proximal branches should stay close to the artery so as not to cause injury to the superior laryngeal nerve, which can lead to voice fatigue and alteration in sound quality with loss of high tones.
In patients who have a high carotid bifurcation or a lesion that extends relatively distally within the ICA, additional exposure can be obtained by carefully dissecting the periarterial tissues at the confluence of the ICA and the ECA. As noted (see above), the ascending pharyngeal artery can be located in this position.
This dissection enables further mobilization of the ICA because the tissue acts as a suspensory ligament for the carotid bifurcation. If necessary, additional distal exposure of the ICA can be obtained by mobilizing and dividing the posterior belly of the digastric muscle distally, the omohyoid muscle proximally, or both.
Particular care must be taken during exposure and manipulation of the carotid bifurcation and the bulb of the ICA because this is the location of the atheromatous lesion. Careful dissection of periarterial tissue and manipulation of the CCA, the ECA, and the ICA are vital for preventing plaque dislodgment with subsequent cerebral embolization; the lesion may be friable and contain atheromatous debris.
Determination of Safety of Cross-Clamping
Once the vessels have been exposed as described, a decision must be made regarding cerebral tolerance of carotid cross-clamping and, if necessary, the method of preserving adequate cerebral perfusion during carotid occlusion.
During periods of vulnerability to cerebral ischemia, including intraoperative arterial cross-clamping, collateral flow is critical for cerebral blood flow. The major pathways of collateral flow are the circle of Willis, the extracranial arterial anastomotic channels (eg, the contralateral ECA), and the leptomeningeal communications bridging watershed areas between major arteries.
Depending on the type of anesthesia used, several different modalities are available for assessing collateral cerebral circulation and the adequacy of cerebral perfusion. If the operation is performed under local anesthesia, trial occlusion is commonly used to determine the safety of temporary carotid clamping.
During the occlusion of the carotid arteries, the patient is continuously monitored for speech, cognitive, and motor function. The patient is asked to talk, answer questions, and move extremities on the side of the body contralateral to the lesion. Any alteration in speech or in cognitive or motor function is an absolute indication for shunt placement. It is estimated that adequate collateral circulation is present in 85-90% of patients; in the remaining 10-15%, an internal shunt is used.
If the operation is performed under general anesthesia, several methods can be used to assess the adequacy of collateral cerebral circulation. [39]
Intraoperative electroencephalographic (EEG) monitoring has been also used to assess cerebral perfusion; it is highly sensitive to changes in blood flow and can detect flow reductions of approximately 10-18 mL/g/min. [40] Although intraoperative EEG monitoring has been used at several centers with excellent results, it can be cumbersome because of the need to place electrodes preoperatively, the effect of general anesthesia on EEG tracing, and the expertise needed to interpret EEG results. [41]
Transcranial Doppler (TCD) ultrasonography (US) is used as well because it determines the middle cerebral artery velocity and pulsatility throughout the operation and is highly sensitive for microembolic signals suggestive of an active embolism. [42] Like EEG monitoring, TCD US also requires additional instrumentation that is placed before positioning, as well as additional personnel (to monitor the TCD results); consequently, it can be impractical and expensive.
Measurement of ICA stump pressure is the most widely accepted and commonly used method of evaluating collateral cerebral blood flow. After exposure of the carotid bifurcation and institution of weight-based heparinization (heparin 100 U/kg intravenously [IV]), a 22-gauge needle is connected to a pressure transducer via rigid pressure tubing. The ICA is occluded first, followed by the ECA and the CCA. The needle is inserted in the CCA and oriented axial to the artery, and the ICA is released.
The ICA stump pressure is then recorded. Because no antegrade pulsatile flow exists in the ICA, the pressures on the two sides of the carotid stenosis are equalized and are essentially equal to the pressure in the middle cerebral artery (MCA). Hence, this pressure is an indirect measurement of the perfusion pressure that is present on the ipsilateral side of the circle of Willis.
If the stump pressure is lower than 40 mm Hg, placement of an internal shunt is indicated. [43] The proper shunt and the appropriate instruments should be immediately available and should be promptly inserted to minimize cerebral hypoperfusion between carotid cross-clamping and shunt placement.
At the authors' institution, selective shunting is preferred to routine shunting for the following reasons:
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Shunts are indicated in only 10-15% of patients
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Shunts can cause intimal damage and secondary thromboembolism
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Shunts can prolong procedural times
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Shunts may interfere with access to the diseased arterial segments
In addition, Krul et al demonstrated that only 20% of intraoperative strokes are caused by hemodynamic failure and that most intraoperative cerebrovascular insults are caused by distal thromboembolic events. [44] On the other hand, proponents of routine shunting argue that routine delayed shunting is safe and effective, [45] that it allows unhurried operative performance, and that familiarity with shunt insertion makes it easier to operate around the shunt.
Data from a Cochrane overview of the relevant randomized trials did not demonstrate that either strategy is more efficient than the other. [46] Accordingly, the choice between selective and routine shunting may be left to the surgeon’s discretion. [47]
Removal of Plaque
Once proximal and distal control has been achieved, the ICA is obliquely detached from the CCA. Transection of the ICA is performed with a pair of Stephens scissors. The crook of the scissors is placed at the carotid bifurcation with the blades oriented inferolaterally so as to encircle the artery (see the first image below). The ICA is transected with a sharp, oblique and complete cut. This will yield exposure of the atheromatous plaque within the ICA (see the second image below).


The proximal part of the arteriotomy is “fish-mouthed.” Under direct vision, the plaque is reached with a DeBakey forceps. With gentle and constant downward traction on the plaque, the outer arterial layer of the ICA is peeled back to deliver the plaque (see the image below). Eversion is maintained, with forceps holding the edges of the transected artery, until the distal endpoints of the plaque are fully visualized within the ICA. This facilitates manipulation of the transected arterial end and subsequent anastomosis of the proximal ICA with the CCA.

After extraction of the atheromatous plaque (see the first image below), the everted edges, as well as the lumen of the proximal ICA, are carefully inspected for residual debris and well irrigated with the heparinized saline (see the second image below).

After the plaque has been removed from the ICA, attention is directed to the CCA. The optimal plane of dissection lies between the intima and the circular fibers of the media. This endarterectomy plane allows a smooth distal tapering of the endpoint. Once the proper endarterectomy plane of the CCA is established (see the image below), dissection is continued circumferentially about the artery.

To complete the circumferential mobilization of the plaque, a spatula is passed behind the plaque to isolate it from the adventitial plane on the opposite side of the artery (see the image below). The distal end of the plaque is transected with scissors placed perpendicular to the direction of the artery. Gentle traction is placed on the plaque with a forceps, and the plaque is removed from the CCA with a spatula in an upward direction (ie, toward the bifurcation).

After removal of plaque from the ICA and the CCA, attention is directed to the ECA. The plaque is separated from around the orifice of the ECA and held with forceps. With the clamp or a forceps, careful traction is applied to the plaque in the direction of the bifurcation. The distal ECA is gently pushed toward the orifice, and plaque is removed to a good distal endpoint. The lumen and edges of the CCA and ECA are thoroughly inspected for residual atheromatous plaques and debris and irrigated with heparinized normal saline (see the image below).
Anastomosis
A double-armed continuous 6-0 polypropylene suture is used for the anastomosis (see the first image below). Creation of the end-to-side anastomosis begins with the stitch at the distal end of the artery, with one arm placed through the transected ICA and the other through the bifurcation (see the second image below). This is anchor-tied.

The front wall of the anastomosis is completed in the same manner as the back wall (see the first image below)—that is, from the distal end to the proximal end (see the second image below).
The suture should pass through all layers of the arterial wall, with particular care taken to include the intima so as to avoid creation and development of an intimal flap. [48] The suture must be carefully pulled and held taut continuously to prevent suture-line bleeding and facilitate adequate closure. The end-to-side anastomosis makes narrowing the arterial lumen at the suture line very difficult, and this lowers the restenosis rate.
Before the arterial closure is completed, the clamps are released one by one to flush out any residual debris (see the image below). To minimize the possibility of cerebral embolization with residual debris, the ECA circulation is restored first. The clamp on the ICA is removed last.

Finally, intraoperative duplex US is performed to verify the technical results of the procedure and to assess the patency of the carotid vasculature with the newly created anastomosis (see the image below).
Closure
Before closure is begun, a No. 19 Blake drain is placed through a separate stab incision, and the wound is well irrigated with normal saline (see the image below). After hemostasis is secured, the wound is closed in two layers with a continuous absorbable suture.
The only deep layer that is approximated is the platysma, closure of which is accomplished with 2-0 monofilament absorbable suture (see the first image below). For closure of the skin, a subcuticular technique with 4-0 monofilament absorbable suture is used because it provides skin closure with excellent cosmetic results (see the second image below).

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Underlying etiology of carotid artery stenosis is formation of atheromatous plaque at bifurcation of common carotid artery and in origins of internal carotid artery.
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A. Simplified flow patterns at carotid bifurcation demonstrate complex reversal of flow along posterior wall of carotid sinus. This region is most vulnerable to plaque development. B. Established plaque at carotid bifurcation. C. Soft, central necrotic core with overlying thin fibrous cap. This area is prone to plaque rupture. D. Disruption of fibrous cap allows necrotic cellular debris and lipid material from central core to enter lumen of internal carotid artery, thus becoming atherogenic emboli. Patient may experience symptoms (transient ischemia, stroke, or amaurosis fugax) or remain asymptomatic, depending on site of lodgment and extent of tissue compromise. E. Empty necrotic core becomes deep ulcer in plaque. Walls of ulcer are highly thrombogenic and reactive with platelets. This leads to thromboembolism in internal carotid artery circulation.
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North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. Convention for describing carotid stenosis is to compare lumen diameter at most narrow point to diameter of internal carotid artery in normal segment several centimeters distal to stenosis.
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A. Arterial flow (red) is displayed in internal carotid artery (ICA) and common carotid artery (CCA). Sampling for flow velocities and spectral waveform analysis is carried out in center stream of ICA, and waveform is shown below. Peak systolic and end-diastolic velocities are measured on representative wave. B. Same general area is being interrogated in diseased ICA. Lumen appears to narrow, and red color becomes variegated and lighter. Arterial flow is sampled in area of maximal disturbance and narrowing, and resultant waveform is displayed below.
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Representative image of extracranial circulation obtained with CT angiography and 3-dimensional reconstruction. Arrow points to stenosis in left internal carotid artery.
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Patient is placed in supine position with hyperextension of neck. Head is rotated 15-20° away from operating side to face contralateral to side of lesion. This maneuver is used to move mandible superiorly, to expose mediolateral aspect of neck, and to open up angle of access to anterior neck triangles at side of lesion.
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Operating area is cordoned off with 4 sterile drapes. It is essential to incorporate ear lobe and mastoid process (superiorly), neck midline (medially), and sternoclavicular joint (inferiorly) into surgical field.
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Incision is created over anterior border of sternocleidomastoid muscle, along line connecting sternocleidoclavicular junction with processus mastoideus, preserving great auricular nerve superiorly and carried down to carotid sheath. This is the position of the incision for optimal exposure of common carotid artery, internal carotid artery, and external carotid artery.
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Skin incision is deepened through subcutaneous fat and platysma. Platysma is divided longitudinally. This gains access to investing layer of deep cervical fascia, which is incised along anterior border of sternocleidomastoid muscle.
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Sternocleidomastoid muscle is retracted posteriorly to expose carotid sheath.
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Dissection of carotid sheath is carried low on neck, along medial aspect of internal jugular vein. Initial incision of carotid sheath should be performed carefully to avoid injury to vagus nerve, which is located anterior to carotid artery 10% of time.
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Facial vein is landmark for carotid bifurcation in vast majority of patients. It courses across common carotid artery and drains into internal jugular vein. Facial vein is mobilized, suture-ligated, and divided.
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After division of common facial vein, internal jugular vein is retracted laterally to yield clear exposure of underlying common carotid artery and internal carotid artery.
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Circumferential exposure of common carotid artery is required only for arterial segment where vessel loops are to be placed; great care must be taken posteriorly, where vagus nerve is anticipated to be encountered in majority of patients.
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External carotid artery is dissected free of surrounding tissue and encircled with colored vessel loop, as is proximal superior thyroid artery. Internal carotid artery lies posterolaterally in carotid sheath.
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Common facial vein branch of internal jugular vein marks site of carotid bifurcation. After division of facial vein, internal jugular vein is retracted posteriorly to expose carotid bifurcation. Before mobilization of internal carotid artery, hypoglossal nerve should be identified and preserved.
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Transection of internal carotid artery (ICA) is performed with pair of Stephens scissors. Crook of scissors is placed at carotid bifurcation with blades oriented inferolaterally to encircle artery. ICA is transected with sharp, oblique, and complete cut.
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Transection of internal carotid artery (ICA) will lead to exposure of atheromatous plaque within ICA lumen.
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Under direct vision, plaque is reached with DeBakey forceps. With gentle and constant downward traction on plaque (top), outer arterial layer of internal carotid artery (ICA) is peeled back (everted) to deliver plaque (middle). Eversion should be maintained with forceps holding edges of transected artery constantly (bottom). This will allow facilitated manipulation of transected arterial end and subsequent anastomosis of proximal ICA with common carotid artery.
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Extraction of atheromatous plaque from internal carotid artery.
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After extraction of atheromatous plaque, everted edges, as well as lumen of proximal internal carotid artery, are carefully inspected for residual debris and well irrigated with heparinized saline.
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After plaque extraction from internal carotid artery, attention is directed to common carotid artery and external carotid artery. Optimal plane of dissection lies between intima and circular fibers of media. This endarterectomy plane allows smooth distal tapering of endpoint.
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Spatula is passed behind plaque to isolate it from adventitial plane on opposite side of common carotid artery.
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After plaque extraction, lumen and edges of common carotid artery and external carotid artery are thoroughly inspected for residual atheromatous plaques and any debris and generously irrigated with normal saline.
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Double-armed continuous 6-0 polypropylene suture is used for end-to-side anastomosis.
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Creation of end-to-side anastomosis (using "heel first, toe last" technique) begins with stitch at proximal end of the artery (heel), with one arm penetrating through transected internal carotid artery and other arm through proximal bifurcation.
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Back wall of anastomosis is completed with continuous suture ending in internal carotid artery.
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Front wall of anastomosis is completed in same manner as back wall, from distal to proximal.
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Before completion of arterial closure, each clamp is released individually to flush out any residual debris.
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Newly created anastomosis. Duplex ultrasonography is performed to verify technical result of procedure and to assess patency of carotid vasculature.
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Before closure is begun, Blake drain is placed through separate stab incision.
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Only deep layer to be approximated is platysma. Platysma is closed with 2-0 monofilament absorbable suture.
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For closure of skin, subcuticular technique with 4-0 monofilament absorbable suture is used; this provides skin closure with excellent cosmetic results.