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Complications - Dolichoarteriopathy – Severe kinking with luminal narrowing type I/III of the right internal carotid artery

  1. Intraoperative complications

    Perioperative stroke

    The rate of perioperative strokes after carotid endarterectomy is 1%–3%, in specialized centers <1%. 

    1. Clamping ischemia of CCA in deficient intracranial collateral circulation (circle of Willis)

    • alert patient (regional anesthesia): neurologic symptoms such as unconsciousness, loss of speech, paralysis, agitation
    • sleeping patient (general anesthesia):  e.g. non-pulsating, dark red arterial return, significant changes in EEG or SSEP (somatosensory evoked potentials) to below 50% of baseline despite adequate blood pressure, significant decrease in velocity in the middle cerebral artery
    • Recommendation: Before clamping the CCA administer intravenous heparin 3,000 IU - 5,000 IU (weight-adapted)
    • -> Insert a lumen-adapted shunt from the common carotid into the internal carotid artery

    2. Inadequate reconstruction with flow turbulence

    • Caused by: Remaining plaque, elongations, stenotic kinking, distal step in eversion carotid endarterectomy (ECEA)
    • Result: turbulent flow activates coagulation (platelet clotting)
    • may lead to perioperative strokes and early occlusion
    • Prevention: technically flawless reconstruction, supplementary anticoagulation with intravenous heparin 3,000 IU–5,000 IU prevents thrombus formation
    • Intraoperative angiography for quality assurance
    • -> operative revision/mechanical recanalization
    • -> Immediate postoperative intraarterial lysis if cerebral bleeding is reliably ruled out (imaging!); immediate postoperative systemic lysis is contraindicated

    3. Embolization by mobilizing plaque material during the dissection phase

    • Prevention: subtle no-touch dissection
    • -> operative revision/mechanical recanalization,  possibly by endovascular technique

    4. Inadequate flushing of all afferent and efferent vessels to rinse out stasis clots

    • -> operative revision/mechanical recanalization

    5. Intimal clamping damage in severe sclerosis of the afferent common carotid artery

    • Local dissection stays undetected
    • May result  in thromboembolism
    • -> operative revision/mechanical recanalization
  2. Postoperative complications

    Hematoma/secondary bleeding
    • According to NASCET trial in 7.1% of all carotid endarterectomies, with 3.9% mild (no revision), 3% moderate (revision) and 0.3% as the most severe complication with lasting deficit or fatal outcome
    • hypertensive blood pressure situations during the recovery and early postoperative period increase the risk of secondary bleeding -> Intense monitoring for at least 8 - 12 hours
    • Intubation complicated or impossible due to airway obstruction; therefore, immediate hematoma relief (if necessary, at point-of-care with temporary manual hemostasis, then intubation and revision surgery).
    • Warning signs: Inspiratory stridor, dumpy or nasal speech, dysphagia
    • Incidence about 1%
    • Deep infections <0.5%
    • Treatment of early and late superficial/deep infections of the soft tissues of the neck follows the usual standards
    • Open and drain putrid infections early, targeted antibiosis according to antibiogram
    Wound infection
    Nerve lesions

    1. Skin nerves

    • According to literature, injury rates for skin nerves in the immediate postoperative phase up to 69% and permanently up to 26%
    • Sensory regeneration possibly, but may take months
    • Regeneration prognosis for protopathic sensitivity (pain and temperature sensation) more favorable, since these fibers terminate blindly in the subcutis
    • Persistent neuropathic pain after skin nerve lesion is quite rare

    2. Cranial nerves

    • Incidence about 5%–15%
    • Mostly temporary or often reversible within one year
    • Treatment: Corticosteroids

    Nervous injuries in the region of approach to the carotid artery

    Nerve

    Special aspects

    Deficit

    Transverse cervical nerve

    • Almost always crosses the surgical field in oblique longitudinal skin incisions and must be transected
    • cutaneous anesthesia of submandibular anterior region of the neck

    Great auricular nerve

    • Anesthesia of the earlobe, inferior and lateral auricle, skin around the jaw angle

    Deep ansa cervicalis

    • Highly variable (thickness, number of branches)
    • Well-developed branches coursing anteriad must sometimes be severed
    • Often clinically silent, no symptoms
    • Dysfunction of the external laryngeal muscles (globus sensation, dysphonia)
    • Impaired stability of the cervical spine

    Vagus nerve (X)

    • Transection in the native surgical field can always be avoided
    • But: Pressure injury by retractors and when clamping out the carotid artery
    • Rr. pharyngei -> Paresis of the soft palate with dysphagia and weakened pharyngeal reflex
    • Superior/inferior laryngeal nerve -> Impairment/loss of ipsilateral vocal cord function, voice hoarse, weak, rapidly fatigued

    Hypoglossal nerve (XII)

    • Thickness and position relative to carotid bifurcation vary
    • Usually easily identifiable
    • Extensive atraumatic exposure without deficits is possible
    • But: Extremely sensitive to pressure (e.g. retractors)
    • Lingual deviation to the ipsilateral (paretic) side
    • Problems with chewing (especially impaired bolus preparation for swallowing), swallowing and speaking
    • Chronic injury: Tongue atrophy

    Facial nerve (VII)

    • In carotid surgery, only the segment within the parotid gland is important

    Lesions of the extratemporal parts that are relevant for the vascular surgeon:

    • Ipsilateral paresis of the facial muscles
    • most likely impacted is the marginal mandibular branch -> impairment of the facial expression of the lower lip
    • Lower lip drawn to unaffected side
    • Baring of lower incisors no longer possible

    Accessory nerve (XI)

    • Regarding the approach to the carotid artery only the external branch is of interest
    • It is not exposed in the surgical field during regular dissection
    • Pressure lesions caused by retractors possible, but rare
    • Ipsilateral partial paralysis in the descending pars of the trapezius muscle and the sternocleidomastoid muscle
    • Drooping shoulder
    • Rotation of head to contralateral side weakened
    • Elevation of the arm above horizontal limited
    • Suggested winged scapula
    • Chronic course: Muscular atrophy with asymmetric outline
    • Workload dependent shoulder pain

    Glossopharyngeal nerve (IX)

    • Courses outside the field of the usual carotid operation mediad of the branches of the external carotid artery
    • Can only be reached when dissecting close to the base of the skull
    • Ipsilateral loss of taste ("bitter" quality) in the posterior third of the tongue
    • sensitive disorders (loss of tactile sensation) at base of tongue, at tonsils and in pharynx
    • Weakened ipsilateral pharyngeal reflex, dysphagia

    Cervical sympathetic nerve

    • Sympathetic fibers of the carotid plexus accompanying the internal carotid artery craniad
    • Careful dissection (including at the base of the skull) helps to avoid injuries
    • Horner syndrome (mild ptosis, miosis and enophthalmus)
    • Impaired tear and saliva secretion
    • Reduced sweat secretion in the face, with additional lesion of the caudal cervical ganglia also affecting the entire upper quadrants of the body
    • Impaired vasomotor activity -> hyperthermia and reddening of the skin areas noted above  
    • Loss of piloreaction (bristling of hairs as reflexive response to cold or stroking, "goosebumps")

    Preventing nerve injuries

    • Confident mastery of the anatomy
    • Identification and exposure of nerve structures in the surgical field by careful dissection.
    • Anticipate atypical anatomical variants and dissect them meticulously
    • Do not coagulate perineural bleeders
    • Avoid nerve injury from retractors
    • Rare neurologic complication after CEA or ICA stenting (incidence: 0.4%–3%), also resulting from clamping/declamping
    • Presents on postoperative day 5–7, peaking on day 5
    • Typical triad: Severe headaches, seizures, intracranial bleeding
    • Intracranial bleeding of 0.8%–1.8%, mortality of 40%–60 % (!)
    • Pathophysiology: Loss of intracerebral blood flow autoregulation
    • Outcome:
    Hyperperfusion syndrome

            → Stenosis-related primary hypoperfusion leads to reactive maximum vasodilation of intracerebral vessels downstream

            → After normal perfusion has been restored by CEA or stent: transmural edematous transudation due to capillary leaks -> cerebral edema, possibly also intracranial bleeding

    • Risk factors:  

             ◊ Marked postoperative hypertension

             ◊ High-grade contralateral stenosis or occlusion of the ICA

             ◊ History of ischemia and contralateral CEA within the last 3 months

             ◊ Also: Significant correlation between the clamp-time and postoperatively measured ipsilateral hyperperfusion

    • Prevention:

             ◊ Avoiding postoperative blood pressure spikes, requires appropriate monitoring

    • Treatment:

             ◊ Marked lowering of blood pressure

             ◊ Anticonvulsants

             ◊ Antiedematous treatment of brain edema

             ◊ Intubation/mechanical ventilation

    Recurrent stenosis
    • Incidence about 1% per year
    • Causes:

            ◊ Progressive arteriosclerosis

            ◊ Surgical technique:  Eversion CEA, CEA + patch, stent-PTA; patch type (vein, plastic, homologous patch material)

    • Treatment:

             ◊ Indication: Symptomatic or ICA stenosis >80%

             ◊ Surgical; endovascular: In surgical recurrent stenosis stent-PTA possible

    Pseudoaneurysm
    • Rare after CEA; usually years after implantation of plastic materials
    • Treatment: Vein patch