Horner’s syndrome post tonsillectomy—a systematic review

Introduction

Tonsillectomy, the surgical removal of the palatine tonsils, is one of the most frequently performed procedures worldwide. Horner’s syndrome has been reported as a rare complication of tonsillectomy, with only sixteen cases report in world literature (1-17). Horner’s syndrome, also known as oculosympathetic palsy, was first described by Swiss ophthalmologist Johann Friedrich Horner in 1869 (18). The disruption of sympathetic innervation to the eye gives rise to the triad consisting of miosis, ptosis, and anhidrosis (18). Horner’s syndrome can be caused by a disorder to the primary (central), secondary (preganglionic), or tertiary (ganglionic and postganglionic) nerve pathways. Identifying the anatomical location of the lesion is crucial for guiding both diagnosis and management (18,19).

The superior cervical ganglion (SCG) is the largest and most rostral of the three cervical sympathetic ganglia, typically located at the level of the second and third cervical vertebrae (C2–C3) (18,19). It lies anterior to the longus capitis muscle, posterior to the carotid sheath, and medial to the internal carotid artery (19). This elongated structure, measuring approximately 2–3 cm, represents the fusion of the uppermost cervical sympathetic ganglia and serves as a critical relay for sympathetic innervation to the head and neck. The SCG receives preganglionic sympathetic fibers originating from the intermediolateral cell column of the spinal cord at levels T1–T3. These fibers ascend through the cervical sympathetic chain and synapse within the SCG, giving rise to multiple postganglionic pathways that influence various autonomic functions (18,19).

One of the most significant pathways involves the internal carotid nerve and plexus, through which postganglionic fibers travel alongside the internal carotid artery to supply sympathetic innervation to intracranial structures. These fibers contribute to the innervation of the eye, including the dilator pupillae muscle via the long ciliary nerves, and the lacrimal gland via the deep petrosal nerve. Dysfunction of this pathway can lead to Horner’s syndrome. Clinically, the proximity of the SCG to the palatine tonsil is particularly relevant. The postganglionic fibers, particularly those traveling along the carotid plexus and its branches, pass within approximately 1.5 cm of the palatine tonsil. This anatomical relationship may explain rare cases of sympathetic dysfunction following tonsillar procedures.

This systematic review aims to evaluate the association between Horner’s syndrome and tonsillectomy, identifying its incidence and underlying mechanisms as a rare but significant postoperative complication. A deeper understanding of this relationship may help refine surgical techniques, enhance postoperative monitoring, and ultimately improve patient safety and outcomes.

Methods

This two-part methodology includes a case report as well as systematic review. The study is reported according to the PRISMA reporting checklist (available at https://www.theajo.com/article/view/10.21037/ajo-24-65/rc) (20). The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s guardian for publication of this article and accompanying images. Ethical approval was not required for this study as it was conducted as a systematic review.

Case report

A 7-year-old female presented for an adenotonsillectomy and bilateral grommets for recurrent otitis media with effusions, speech and language delay, recurrent tonsillitis and sleep disordered breathing. She was an otherwise well child with no past medical or surgical history.

The myringotomy was performed, and bilateral Armstrong grommets were placed without complication. Following this a radiofrequency ablation extracapsular tonsillectomy and adenoidectomy was performed. During the tonsillectomy she was noted to have deep invaginated tonsil and active tonsillitis with increased inflammation of the tonsillar plane. Haemostasis was achieved and topical 0.5% bupivacaine-soaked gauze was briefly placed in the tonsillar fossa to aid with post-operative pain. The operation was completed without any intraoperative complications.

Immediately post operatively in recovery, she was noticed to have ptosis, miosis and anhidrosis on the left side. There was no other neurological deficit noted. Anaesthetics and paediatric consults were acquired to assisting the management of this patient. Given the patient was well with no other focal neurological deficit she was diagnosed with a Horner’s syndrome and was admitted overnight for monitoring. She was started on short course of 4 mg dexamethasone daily for 3 days and amoxicillin and clavulanic acid twice daily for 5 days. The Horner’s syndrome had completely resolved day 1 post operatively. She completed her steroids and antibiotic course and was followed up at 14 days day post operatively at which stage she had no further relapse of symptoms and was well.

Systematic review

Literature search and selection process

Three databases were searched, including PubMed, Medline and Embase on 1st July 2024 over a 1-month period. Search terms were “Horner’s syndrome” OR “oculosympathetic palsy” AND “tonsillectomy” which returned a total of 26 papers. There was no date limit assigned to the search criteria. If an article was in a language other than English, it was included if it was able to be translated.

Articles were included in this paper if they featured patients who had undergone tonsillectomy and subsequently developed Horner’s syndrome. Articles were excluded if: (I) they were review papers with no new cases; (II) patients underwent an operation other than a tonsillectomy; (III) animal studies; or (IV) cases were duplicates.

For inclusion and exclusion criteria, two authors reviewed all abstracts independently. Articles that met the inclusion and exclusion criteria were subsequently included in the study. A disagreement of abstracts resulted in a review by a third author to assess for acceptability into the study. This process is highlighted in Figure 1.

Figure 1 PRISMA flow chart illustrating the literature search and selection process.

Classification of cases and data collection

Once accepted into the study, the papers were reviewed by the study’s authors and critically appraised. Data was extracted from the paper, including patient demographics, surgical technique, use of local anaesthetics, the time of onset post-surgery, proposed mechanisms underlying the syndrome, treatment approaches, and patient outcomes.

Study risk of bias assessment

A structured, published and validated risk of bias tool using the Scottish Intercollegiate Guidelines Network (SIGN) checklist for systematic reviews and meta-analysis was used to ensure consistent and objective assessment of papers (21). The risk of bias was assessed in all included studies by individual and primary authors. The authors noted selection, confounding, detecting and attrition bias.

Data analysis

Descriptive analysis using Microsoft Excel Software was performed to assess patient demographics, surgical indications, dissection techniques, use of topical anaesthesia, clinical presentation, management, and recovery outcomes were compiled and analysed. Data analysis and Fischer’s exact were performed using Microsoft Excel Software.

Results

Study characteristics

The systematic review includes 17 cases of Horner’s syndrome following tonsillectomy from various studies spanning from 1933 to the current report and are outlined in Table 1. The included studies comprised retrospective studies, case series, and case reports, collectively representing Level III and IV evidence according to the Oxford Centre for Evidence-Based Medicine (OCEBM) (22). The patient demographics, surgical indications, dissection techniques, use of topical anaesthesia, clinical presentation, management, and recovery outcomes were compiled and analysed. These data are summarized in Table 2. The assessment of bias for each article is represented in Table 3.

Patient demographic

The ages of the patients ranged from 2 to 37 years, with a higher prevalence among females (10 out of 17 cases). Surgical indications varied, with recurrent tonsillitis being the most common, followed by sleep-disordered breathing including obstructive sleep apnoea and recurrent peritonsillar abscess. In several cases (8), the specific surgical indication was not stated.

Surgical technique

The surgical techniques employed in these cases were diverse. They included sharp dissection (5/16), combination cold steel dissection, snare, electrocautery (3/16), radiofrequency ablation (3/16) and monopolar dissection (1/16). A Fischer exact was performed to examine the relationship between non heat-based and heat-based surgical techniques on resolution rates. The relation between surgical techniques and resolution was not statistically significant [P=0.592, odds ratio (OR) =2.5, 95% confidence interval (CI): 0.253–24.72].

Topical anaesthesia

Several cases reported the use of topical anaesthesia, with agents including bupivacaine, novocaine, cocaine, lidocaine, and mepivacaine. However, there were variations between durations of action of these anaesthetic agents, as well as differences in their mode of administration (topically or infiltration). A Chi-squared test of independence was performed to examine the relationship between the use of topical anaesthesia and the resolution or persistence of Horner’s syndrome (with persistence being defined as more than 72 hours).

Fisher’s exact test revealed a statistically significant association between the use of local anesthetic being associated with resolution of Horner’s syndrome (P=0.041, OR =0.048, 95% CI: 0.0003–0.665). Additionally, a descriptive analysis of anaesthetic selection revealed no clear preference for a specific agent in cases complicated by Horner’s syndrome. Given the rarity of this condition, studying variations between anaesthetics is likely to be challenging.

Clinical presentation

Horner’s syndrome typically presented immediately postoperatively, with symptoms including ptosis, miosis, and anhidrosis. The onset of symptoms varied, but most cases showed symptoms either immediately or within a few hours after surgery. A Chi-squared test of independence was performed to examine the relationship between the use of topical anaesthesia and timing of presentation. The relation was not statistically significant with Fischer’s exact (P=1, OR =0.667, 95% CI: 0.047–9.472). Similarly, Fischer’s exact was used to assess relationship between surgical technique (non-heat and heat-based) and timing of onset. The relation was not statistically significant (P=1, OR =1.5, 95% CI: 0.071–31.576).

Management and outcomes

The management strategies for Horner’s syndrome post-tonsillectomy varied across the cases. Treatments included antibiotics and stress dose steroids. There was insufficient data to complete a Chi-squared test to assess the relationship between treatment with steroids and outcomes. Short-term outcomes varied, with some patients experiencing resolution of symptoms within 24 hours, while others had persistent symptoms. Long-term follow-up showed that in 10 (59%) cases, Horner’s syndrome persisted for months to years postoperatively.

Discussion

The tonsillectomy is one of the most common ENT procedures worldwide and is performed for a wide range of indications including recurrent tonsillitis, sleep-disordered breathing, and recurrent peritonsillar abscess (23). While it is generally considered safe, several postoperative complications can arise, including bleeding, infection, and anaesthesia-related issues (8,23). Interestingly, cases of Horner’s syndrome post tonsillectomy have immerged as a rare complication of this procedure.

In our case we presented a young female patient who underwent a tonsillectomy for recurrent tonsillitis and sleep-disordered breathing who developed a left Horner’s syndrome post operatively. As discussed throughout the literature a wide range of techniques were used for tonsillectomy including sharp dissection, combination cold steel dissection, snare, electrocautery, radiofrequency ablation and monopolar dissection, with 9 cases utilising local anaesthetics. In our case, we utilised radiofrequency ablation and local anaesthetics. Interestingly, our case had rapid resolution of Horner’s syndrome within 1 day postoperatively. This is in contrast with the literature with ~60% of case persisting several months to years post operatively.

The aetiology of Horner’s syndrome in the context of tonsillectomy can be attributed to several mechanisms (18). These theories stem from the understanding of the anatomical relationship between the tonsil and the postganglionic fibres which are highlighted in Figure 2.

Figure 2 Anatomical relationship between palatine tonsil and sympathetic ganglion.

The first theory includes the potential for local anaesthetics, particularly when used in large volumes or high concentrations, to diffuse across into the cervical sympathetic chain causing a temporary oculosympathetic palsy (3-5). In our review there was a statistically significant relationship between the use of local anaesthetics and recovery time. Suggesting that in cases where local anaesthetic is the cause then a full recovery should be expected.

However, not all cases in which local anaesthetic was utilised recovered (1,10). Therefore, a second theory is hypothesised that the cervical plexus branches, which are within close proximity to the tonsil bed, are injured directly during dissection or by the transfer of heat from diathermy or radiofrequency tools.

When encountered with Horner’s syndrome post operatively we recommend a thorough diagnostic work up including history, examination and diagnostic testing with assistance from an ophthalmologist. The assessment of Horner’s syndrome post-tonsillectomy begins with a detailed history to identify potential causes or precipitating factors such as surgical technique, duration, infection and can determine the onset and progression of symptoms. The history can also help the clinician identify symptoms to localize the Horner’s syndrome to the primary, secondary, or tertiary nerve pathways (18,19).

A thorough ophthalmic and neurological examination is then performed to confirm the diagnosis and rule out other potential causes. The aim is to identify characteristic signs of the syndrome, which includes ipsilateral ptosis (less than 2 mm), due to loss of innervation to superior tarsal muscle (Muller’s muscle), anhidrosis and miosis with worsening anisocoria in darkness and auditory stimulation of the sympathetic nervous system. A “dilation lag” whereby a more obvious anisocoria is present in the first 5 seconds after lights are turned off and reduces after 10–15 seconds, particularly useful in subtle cases (18,19).

If the diagnosis remains unclear after the initial assessment, pharmacological testing can be performed. Apraclonidine 0.5%, an α-2 adrenergic agonist with weak α-1 activity, is often used initially. The test is performed by placing a drop of apraclonidine 0.5% in both eyes and again at 5 minutes (24). If the anisocoria reverses (pupil reversal) with the smaller affected pupil becoming larger than the contralateral pupil at the end of 45 minutes, the test is considered positive. This is due to denervation hypersensitivity in patients with Horner’s syndrome as the upregulation of postsynaptic α-1 adrenergic receptors result in an increased sympathetic response (see Figure 3). However, if the test is negative in a patient with Horner’s syndrome of onset within 2 weeks, this could indicate that denervation hypersensitivity has not yet occurred. In this situation, it is recommended to use a 10% cocaine hydrochloride eye drop test, particularly in cases where imaging is challenging due to factors such as the child’s age, the need for general anaesthesia, or limited accessibility (25). A drop is placed in both eyes and the test is deemed positive if the affected pupil does not dilate as well as the normal eye with anisocoria of at least 0.8 mm after 45 minutes (exaggerating anisocoria). This is due to the lack of sympathetic outflow in patients with Horner’s syndrome, which leads to a reduced pupil dilation (24).

Figure 3 The diagnostic tests for Horner’s syndrome utilising apraclonidine and cocaine eye drops.

Cocaine testing is also preferred in infants and young children due to the risks of respiratory depression with adrenergic receptor agonists such as apraclonidine (25). However, given apraclonidine is readily available, has a clear positive end point, and higher sensitivity, it is the preferred first-line diagnostic pharmacological test for Horner’s syndrome (24). Hydroxyamphetamine 1% eye drops has also been used previously to distinguish between pre- and post-ganglionic Horner’s syndrome. However, given that most patients inevitably require imaging to uncover the underlying cause, this test is only mentioned for historical reasons (18,24,25).

Management strategies for Horner’s syndrome vary depending on the severity and duration of symptoms. Short-term management may involve the administration of short course of steroids and antibiotics to reduce inflammation and treat any underlying infection. In cases where Horner’s syndrome persists or when the clinical presentation raises suspicion of an underlying pathology, further imaging of the cervical ganglion with computed tomography (CT) or magnetic reason imaging (MRI) modalities are warranted (19). Persistent symptoms may indicate a more serious underlying cause, such as a tumour, vascular anomaly, or other structural abnormalities affecting the sympathetic pathway.

Recommendations for surgical techniques emphasize the importance of careful dissection to avoid damage to the cervical sympathetic chain. The use of minimally invasive techniques and cautious application of electrocautery and radiofrequency energy can help reduce this risk. When using topical anaesthesia, it is important to administer an appropriate volume and dose while being mindful of the potential for diffusion or inadvertent injection into adjacent structures, such as the carotid sheath. Postoperative monitoring should include vigilant observation for symptoms of Horner’s syndrome, allowing for early detection and management.

The limitations of this study include the retrospective nature of the data collection and the variability in reporting standards across different studies. The infrequent occurrence of Horner’s syndrome post-tonsillectomy also limits the generalisability of the findings. Some cases had incomplete data complications and outcomes making data analysis less reliable. Intricate details regarding management strategies to address complications were limited reducing the transferability of information to those wanting to learn relevant non-operative and operative techniques.

Conclusions

In conclusion, while Horner’s syndrome is a rare complication of tonsillectomy, its potential occurrence necessitates awareness among surgeons. Although numbers were small, Horner’s syndrome caused by topical anaesthesia was associated with recovery. This review also showed that a high percentage of cases were also persistent. This author encourages surgeons to report their post-operative complications of Horner’s syndrome, as further studies are needed to provide more comprehensive guidelines and enhance our understanding of this condition.

Acknowledgments

Our abstract has been presented at the ASOHNS ASM 2025, 28–30 March 2025, ICC Sydney, NSW.

Footnote

Reporting Checklist: The authors have completed the PRISMA reporting checklist. Available at https://www.theajo.com/article/view/10.21037/10.21037/ajo-24-65/rc

Data Sharing Statement: Available at https://www.theajo.com/article/view/10.21037/ajo-24-65/dss

Peer Review File: Available at https://www.theajo.com/article/view/10.21037/ajo-24-65/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://www.theajo.com/article/view/10.21037/ajo-24-65/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s guardian for publication of this article and accompanying images. This study did not require ethics as it was a systemic review.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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