Horner's Syndrome after Carotid Endarterectomy: A Case Report and Review of Literature

Abstract

Horner's syndrome, characterized by ptosis, miosis, and anhidrosis, results from oculosympathetic complex injury, often due to trauma affecting the superior cervical ganglion. Although rare following carotid surgery, we present a case of Horner's syndrome after elective carotid endarterectomy (CEA). This report explores potential mechanism, including prolonged surgical retraction and hematoma formation, while reviewing similar cases in the literature. A 45-year-old woman presented with recurrent dizziness and progressive left-sided hearing impairment over 5 years. She also reported neck discomfort and experienced five episodes of amaurosis fugax in her left eye within 1 week. Computed tomography revealed occlusion of the right common and internal carotid artery (ICA), along with a 90% stenosis at the left common carotid bifurcation extending into the left ICA. Subsequently, an elective left CEA was performed. Within 24 hours postoperatively, she developed clinical signs of Horner's syndrome, including left-sided ptosis, miosis, anhidrosis, and concurrent facial nerve palsy. Notably, there was no evidence of hematoma formation or sensorimotor deficits. This case highlights the rare occurrence of Horner's syndrome as a postoperative complication of CEA. Surgeons should be mindful of anatomical variations and potential intraoperative mechanisms contributing to this complication to enhance prevention strategies. Recognizing this risk is essential for optimizing postoperative care and patient counseling.

Keywords

Horner's syndrome - carotid endarterectomy - postoperative complications

Introduction

Horner's syndrome is characterized by ptosis, miosis, and, in some cases, facial anhidrosis due to disruption of the sympathetic innervation to the eye. First documented in a soldier with neck injury, the condition results from damage to the superior cervical sympathetic ganglion or postganglionic oculosympathetic fibers.[1] This disruption impairs normal sympathetic functions, such as pupil dilation and heightened alertness, which are essential components of the “fight or flight” response.[2]

The superior cervical ganglion, located between the C8 and T2 vertebrae, lies posterior and superior to the carotid artery at the level of the digastric muscle. Postganglionic fibers from this ganglion travel along the internal, external, and common carotid arteries (CCAs). While Horner's syndrome is rarely reported after neck surgeries, its occurrence following carotid procedures is even less common.[3] Carotid endarterectomy (CEA), performed to remove arterial plaques and reduce the risk of stroke and transient ischemic attacks (TIAs), has minimal documented reports of Horner's syndrome. The precise mechanism remains unclear; however, proposed etiologies include excessive mobilization of the internal carotid artery (ICA) above the digastric muscle level resulting in damage to postganglionic fibers, prolonged intraoperative retraction leading to compression or injury of pre- or postganglionic fibers or the ganglion itself, and postoperative hematoma formation.[2] [4] [5]

In this context, we present a rare unusual iatrogenic complication following elective CEA, accompanied by cranial nerve injury, and provide a concise review of similar documented cases in the existing literature.

Case Description

A 45-year-old woman with a history of three miscarriages presented to the vascular surgery clinic with a 5-year history of vertigo and progressive left-sided hearing loss, a 3-year history of neck pain, and five recent episodes of transient monocular vision loss in her left eye over the past week. She denied any history of fever, weight loss, shortness of breath, palpitations, TIAs, or cerebrovascular accidents. She had no known comorbidities and reported no use of medications or recreational drugs.

On examination, she was alert, awake, and oriented. Pupillary responses to light were normal, and motor and sensory functions were intact. Decreased hearing was noted in the left ear, but the remainder of the cranial nerve examination was grossly unremarkable. She had initially been evaluated by a neurologist prior to presentation.

Baseline laboratory investigations were within normal limits. Initial neurological workup aimed at identifying an intracranial space-occupying lesion, such as a vestibular schwannoma, or cervical degenerative pathology. However, magnetic resonance imaging of the brain and cervical spine revealed no abnormalities.

Given her episodes of transient monocular blindness, further evaluation for possible amaurosis fugax secondary to carotid stenosis, optic neuritis, or ophthalmologic pathology was pursued. Color Doppler ultrasonography of the carotid arteries demonstrated complete occlusion of the right CCA and ICA, along with 70 to 90% stenosis at the left carotid bulb due to an organized thrombus. Mild intimal-medial thickening was noted on the left side, with an elevated ICA/CCA peak systolic velocity ratio. Computed tomography angiography (CTA) confirmed nonopacification of the right CCA and collapse of the right ICA lumen, with ∼90% stenosis of the left ICA secondary to significant intimal-medial thickening. The vertebral arteries were patent, and no evidence of cerebral ischemia was identified. Transthoracic echocardiography subsequently demonstrated normal cardiac function.

A hypercoagulable workup was initiated ([Table 1]), and no abnormalities were detected. The initial hypercoagulable screening did not include antiphospholipid antibody (APLA) testing, which was subsequently recommended keeping in light the history of recurrent miscarriages. The patient, however, declined further testing due to financial constraints, particularly since the immediate management plan—consisting of dual antiplatelet therapy—would not have been altered by the result. She was counseled regarding the importance of APLA testing for long-term management and advised to undergo testing when feasible.

Table 1 Hypercoagulable blood panel

Investigation	Levels	Normal values	Unit
Homocysteine	4.65	5–12	µmol/L
Protein C	126	70–140	%
Antithrombin III	93	74–126	%
APC resistance	1.04	0.86–1.10
Protein S	83	56–121	%

Abbreviation: APC, activated protein C.

The patient was initiated on dual antiplatelet therapy with aspirin 75 mg daily and clopidogrel 75 mg daily. Because of high-grade symptomatic stenosis with transient blindness, she was scheduled for elective left CEA under general anesthesia within the same week.

Surgical exposure was achieved through a longitudinal incision along the anterior border of the left sternocleidomastoid muscle. Careful dissection was performed to isolate the carotid arteries. After placement of vascular clamps, an atheromatous plaque was removed from the common, internal, and external carotid arteries. Vascular reconstruction was accomplished using a bovine pericardial patch.

Postoperatively, within 24 hours, the patient developed left-sided facial nerve weakness (House–Brackmann Grade III) ([Fig. 1]), along with ipsilateral ptosis ([Fig. 2]), miosis, and hypohidrosis—clinical features consistent with Horner's syndrome, which was confirmed by ophthalmologic evaluation. No clinical evidence of neck hematoma was seen. No evidence of recurrent thrombosis was found on postoperative CTA. No specific treatment was administered, as the condition was expected to be transient. The patient was counseled regarding the prognosis.

Fig. 1 Left facial nerve weakness.

Fig. 2 Left ptosis.

At her 1-month follow-up visit, there was significant improvement in the ptosis, although mild residual facial weakness persisted. The events have been summarized in the form of flowchart in [Fig. 3].

Fig. 3 Flowchart summarizing the sequence of events leading to the diagnosis and management.

Discussion

In this report, we present a rare postoperative complication following elective CEA: the development of Horner's syndrome, characterized by the clinical triad of ptosis, miosis, and anhidrosis. This constellation of symptoms results from disruption of the oculosympathetic pathway, which comprises three sequential neurons. First-order neurons originate in the posterior hypothalamus and descend to the ciliospinal center of Budge (C8–T2). Second-order (preganglionic) neurons then exit the spinal cord, ascend through the cervical sympathetic chain, and synapse at the superior cervical ganglion, located near the carotid bifurcation. Third-order (postganglionic) fibers travel alongside the ICA to reach the eye and face, forming the internal carotid plexus. Disruption at any point along this course can result in Horner's syndrome.[6] [7]

In a study by Sabbagh et al, procedures involving the neck, chest, skull base, and paraspinal region were identified as the most common causes of Horner's syndrome, accounting for a significant proportion of cases, with cervical carotid dissection the next most common cause.[8] While Horner's syndrome has been reported following various neck procedures, its occurrence after CEA is rare. The close anatomical relationship between the superior cervical ganglion and the carotid artery poses a potential risk during surgical manipulation. In a 5-year retrospective study, Chisci et al reported a 1% incidence of Horner's syndrome in patients undergoing CEA, often transient and associated with true cranial nerve injuries. Factors associated with increased risk included prolonged operative time, diabetes, postoperative hematoma, and dual antiplatelet therapy.[5] A landmark analysis by Cunningham et al in the European Carotid Surgery Trial further highlights the incidence and risk factors for cranial nerve injury following CEA. Among 1,739 patients, 88 (5.1%) experienced cranial nerve injuries, of which 3.7% persisted at hospital discharge. Horner's syndrome was observed in three patients. At 4-month follow-up, only 0.5% of patients had residual deficits, which did not resolve subsequently. Crucially, the only independent predictor of cranial nerve injury was an operative duration exceeding two hours (hazard ratio 1.56, p < 0.0001), emphasizing the need for efficient and atraumatic dissection.[7] In our patient, Horner's syndrome was accompanied by postoperative facial nerve (cranial nerve VII) weakness.

Other reports have highlighted similar postoperative occurrences. Allen and Meyer documented six cases of Horner's syndrome following neck surgery, with only one linked to CEA.[3] Perry et al described the delayed onset of Horner's syndrome at 48 hours postoperatively, while experimental models in rabbits have shown its development at 72 hours following superior cervical ganglion ischemia.[2] In our patient, the complication was noted 24 hours after surgery. Hidayat et al also reported Horner's syndrome post-CEA, attributing it to a technically difficult dissection around the carotid artery.[4]

Interestingly, Horner's syndrome has also been documented following carotid artery stenting—a less invasive procedure—primarily due to postprocedural hematoma compressing the sympathetic chain or due to immediate expansion of the ICA.[9] [10] [11]

Our patient developed symptoms 24 hours postoperatively. The overall surgery duration was more than 2 hours. Intraoperatively, a challenging dissection due to inflammation and adhesions necessitated forceful mobilization and prolonged retraction of the carotid artery, likely contributing to compression or injury of the cervical sympathetic chain. The brief ischemia time of 2 minutes makes ischemic insult an unlikely cause. Therefore, mechanical traction or pressure during surgery appears to be the most plausible mechanism.

In the evaluation of postoperative Horner's syndrome, it is critical to consider and exclude other potential etiologies beyond surgical injury. Central causes such as brain stem infarction or demyelinating disease were unlikely in this case, as the patient exhibited no additional neurological deficits and remained alert with intact motor and sensory function. Postganglionic causes, including ICA dissection, typically present with pain, neurological symptoms, or radiological evidence, none of which were observed.[12] Neoplastic etiologies, such as Pancoast tumors, were ruled out based on the absence of respiratory symptoms and unremarkable chest imaging. Although the patient's history of recurrent miscarriages raised suspicion for an underlying autoimmune condition such as APLA syndrome, there were no clinical signs of systemic vasculitis (e.g., fever, rash, arthralgia), and the patient declined further serological testing due to financial limitations. Taken together, the temporal correlation with surgery, absence of systemic findings, and intraoperative factors strongly suggest mechanical injury to the cervical sympathetic chain as the most plausible cause.

Fortunately, most cases of Horner's syndrome following CEA resolve without specific intervention. Our patient showed partial resolution of ptosis by 1 month postoperatively. This case highlights several critical points: the importance of maintaining anatomical awareness during carotid surgery, minimizing traction and retraction around the sympathetic chain, monitoring for postoperative signs of cranial nerve injury, and educating patients about potential transient complications. Understanding the typically self-limiting nature of Horner's syndrome can help avoid unnecessary diagnostic investigations and guide appropriate postoperative care and reassurance.

Conclusion

This case of Horner's syndrome with associated cranial nerve injury following CEA highlights the need for heightened surgical awareness of vulnerable anatomical structures, particularly around the carotid bifurcation where the cervical sympathetic chain is susceptible to traction or compression. Although Horner's syndrome is a rare and usually transient complication, thorough preoperative counseling and recognition of its self-limiting nature can help alleviate patient anxiety, avoid unnecessary investigations, and enhance postoperative care.

Conflict of Interest

None declared.

Authors' Contributions

N.S. was responsible for planning the manuscript, taking consent from the family, critically revising the manuscript and providing intellectual output, and giving final approval of the manuscript. F.S. was responsible for the preparation of the manuscript draft, adding pictures and table, and giving final approval of the manuscript. S.M. was responsible for the preparation of the case in the manuscript draft and giving final approval of the manuscript. F.S. was responsible for critically revising the manuscript, providing editorial input, and giving final approval of the manuscript.

Ethical Approval

Consent and institutional ethical approval have been obtained.

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Publication History

Article published online:
25 June 2025