Horner’s syndrome as a complication of thoracic epidural analgesia
Authors:
J. Resler; O. Kráčmar; Z. Chovanec
Authors place of work:
I. chirurgická klinika LF MU a FN u sv. Anny v Brně
Published in the journal:
Cesk Slov Neurol N 2024; 87(6): 433-434
Category:
Dopisy redakci
doi:
https://doi.org/10.48095/cccsnn2024433
Dear Editor,
Horner's syndrome (HS), described as a combination of symptoms of ptosis, miosis, anhidrosis (sometimes also facial flush, conjunctival congestion or apparent enophthalmos), arises from a variety of causes. Rarely, it is also reported as a complication of neuroaxial blockade (NB). It was first described as such in 1972 [1]. We present a case of a 34-year-old patient with the development of right-sided HS in the postoperative period after pulmonary metastasectomy due to epidural analgesia (EA) at the Th5-6 level.
A 34-year-old man with a diagnosis of primary mediastinal germ-cell tumor after oncological and surgical (extirpation by sternotomy) treatment was indicated by the decision of a multidisciplinary thoracic oncology committee for surgical removal of a metachronous metastasis of the left lung. His neurological picture showed only chronic signs of polyneuropathic syndrome after chemotherapy in the form of paresthesias to acral pain in all limbs, and he was recently treated with Pregabalin Accord 150 mg 1-0-1 tbl p.o.
Immediately before the procedure, the patient received an epidural catheter through a medial approach and a loss of resistance technique through the Th4-5 intervertebral space. The catheter was removed for blood aspiration, reinserted to the Th5-6 level, and placed 5 cm into the epidural space using an 18G × 31/4 Tuohy needle. Verification with a test dose of 3 ml of 0.5% bupivacaine showed no signs of complication and subjectively caused no discomfort to the patient. After 55 min of induction of anesthesia, epidural analgesia was initiated with a mixture of 0.5% bupivacaine, sufentanil, and saline in a 2 : 1:2 ratio. An uncomplicated S9 metastasectomy was performed from the left posterolateral thoracotomy including lymphadenectomy of stations 5, 6, and 8-11. None of the procedures involved the right hemithorax, pulmonary apex, or pleural dome. In the postoperative period, EA was continued with administration of the indicated mixture at a rate of 5 ml/h.
Postoperatively, the patient reported minimal pain and no new neurological complaints. Clinical examination subsequently revealed ptosis of the right eyelid with a 2 mm drop against the contralateral eye slit and anisocoria with a 1 mm miosis on the right (Figure 1). Neurological examination confirmed right-sided HS. EA was firstly considered as the cause, followed by a positional lesion caused by perioperative oppression.
Based on the examination, the administration of EA was discontinued. CTA of the head and neck did not show a lesion explaining the new-onset HS; a spacious cisterna magna communicating with the IV cerebral ventricle and a Dandy-Walker variant of the posterior fossa were described as secondary findings. The epidural catheter was removed. Full recovery was achieved within 12 h. Thus, the cause was determined to be asymmetric iatrogenic sympathetic blockade during EA. Symptom resolution persisted into the dimissed 5th postoperative day and was confirmed at clinical follow-up on the 17th postoperative day (fig. 2).
Horner's syndrome is caused by a lesion anywhere along the trigeminal pathway hypothalamus - centrum ciliospinale (Budge's center) - ganglion cervicale superius - effector organs. A new-onset syndrome may refer to a serious cause, including a spinal cord lesion, neoplasm, or carotid arterial dissection. Martin cites tumor as the cause of 13% of newly diagnosed HS (3% of which is due to a previously undetected malignancy). A full 13% of the lesions detected were attributable to the central neuron, 44% were preganglionic, and 43% were caused by postganglionic lesions [2]. High NB can cause conduction disturbance on the second order neuron as it moves away from the spinal cord, thus it is a preganglionic lesion. Preganglionic sympathetic neurons for the eyelid, eye and face originate from the Budge centre at the C8-Th2 level and leave the spinal cord together with the ventral roots of the first four thoracic spinal nerves [1,2]. The main causes of high blockage include misapplication of anesthetic into the subarachnoid space and its incorrect dosage. HS is almost always transient in such cases, although its persistence is rarely encountered in the literature [3]. The most serious consequences of high blockade include respiratory insufficiency, arterial hypotension, cardiac arrest and impaired consciousness.
The cause of HS as a complication of NB may be due to variability in catheter placement, its insertion into the wrong compartment, misadministration of analgesic mixture or anatomical anomalies of the epidural space. HS is most frequently found in case reports related to obstetric analgesia, and rarely in thoracic catheterization, where it is often associated with accompanying neurological symptoms [4]. The course of HS as a complication of EA is predominantly benign and transient. Nevertheless, its occurrence needs to be paid close attention as it may highlight inadequate catheter insertion or management. The incidence ranges between 0.13 and 1.33% of NB [1].
Symptomatology of HS in EA varies interindividually. Not always the whole basic triad is fully expressed, sometimes additional symptoms are observed. In 2018, Chambers and Bhatia analyzed 78 previously described cases of HS after NB. In 73 cases, ptosis and miosis were expressed simultaneously, in 24 cases anhidrosis. Among other symptoms, conjunctival congestion was present in 21 cases, onophthalmos and nasal obstruction in seven cases, and facial flush in five cases. Furthermore, HS was accompanied by ipsilateral motor or sensory disturbances of the upper limb, blurred vision, eye, head or neck pain, lacrimation or trigeminal nerve palsy, and in one case contralateral lesion of the nervus hypoglossus [1].
The asymmetric anaesthetic effect in epidural blockade has no clear cause. For example, slow injection or different density of local anaesthetics in combination with the patient's position, the presence of epidural septa or other mechanical obstructions have been suggested as possible reasons. The higher extent of sympathetic blockade may also be attributed to the fact that preganglionic sympathetic fibres show a higher sensitivity to local anaesthetic compared to nociceptive fibres [5]. More detailed examinations may demonstrate catheterization of the subdural space, even in the absence of alteration of consciousness or cardiac symptoms. According to Rabinovich et al, body mass index (BMI; BMI), patient position during administration, or catheter length did not influence the risk of developing HS. In contrast, the epidural block technique may have influenced the risk of developing HS [6].
The most likely cause of asymmetric action in EA is often suggested to be the placement of the catheter tip [7]. Even with proper insertion into the epidural space, the subsequent course of the catheter is not always straight; it may curl, change craniocaudal orientation, or even leave the epidural space through the intervertebral foramen. This may be due to the ruggedness of the epidural space and the presence of obstructions such as septa, fat pedicles, etc.[8] Even a correctly achieved position may not be static. Eide and Sorteberg described peroperative displacement of the epidural catheter by more than one vertebral level in 24% of catheterization cases during thoracic surgery [9]. Nakamura et al. report that further progression through the epidural space cannot be predicted beyond 2-3 cm from the entry [10].
According to current recommendations, the development of HS is not a clear indication for discontinuation of EA. However, it may refer to a more serious cause than EA or be an indication of other impending adverse effects of NB. Therefore, careful monitoring of the patient and individual consideration of the risks and benefits of continued analgesia are always necessary.
Grant support
Supported by the project MUNI/A/1619/2023.
Conflict of interest
The authors declare that they have no conflict of interest in relation to the subject of the study.
This is an unauthorised machine translation into English made using the DeepL Translate Pro translator. The editors do not guarantee that the content of the article corresponds fully to the original language version.
Zdroje
1. Chambers DJ, Bhatia K. Horner’s syndrome following obstetric neuraxial blockade – a systematic review of the literature. Int J Obstet Anesth 2018; 35 : 75–87. doi: 10.1016/j.ijoa.2018.03.005.
2. Martin TJ. Horner syndrome: a clinical review. ACS Chem Neurosci 2018; 9 (2): 177–186. doi: 10.1021/acschem neuro.7b00405.
3. Hered RW, Cummings RJ, Helffrich R. Persistent Horner‘s syndrome after spinal fusion and epidural analgesia. A case report. Spine (Phila Pa 1976) 1998; 23 (3): 387–390. doi: 10.1097/00007632-199802010-00021.
4. Park SY, Chun HR, Kim MG et al. Transient Horner‘s syndrome following thoracic epidural anesthesia for mastectomy: a prospective observational study. Can J Anaesth 2015; 62 (3): 252–257. doi: 10.1007/s12630-014-0284-9.
5. Heavner JE, de Jong RH. Lidocaine blocking concentrations for B - and C-nerve fibers. Anesthesiology 1974; 40 (3): 228–233. doi: 10.1097/00000542-197403000-00004.
6. Rabinovich A, Abedelhady R, Mazor M et al. Horner‘s syndrome following epidural analgesia during labor: report of six cases. Eur J Obstet Gynecol Reprod Biol 2010; 149 (2): 229–230. doi: 10.1016/j.ejogrb.2009.11.020.
7. Holzman RS. Unilateral Horner’s syndrome and brachial plexus anesthesia during lumbar epidural blockade. J Clin Anesth 2002; 14 (6): 464–466. doi: 10.1016/s0952-8180 (02) 00399-9.
8. Hermanides J, Hollmann MW, Stevens MF et al. Failed epidural: causes and management. Br J Anaesth 2012; 109 (2): 144–154. doi: 10.1093/bja/aes214.
9. Eide PK, Sorteberg W. Simultaneous measurements of intracranial pressure parameters in the epidural space and in brain parenchyma in patients with hydrocephalus. J Neurosurg 2010; 113 (6): 1317–1325. doi: 10.3171/2010.7.JNS10483.
10. Nakamura K, Sugita A, Sekiya S et al. Paths of thoracic epidural catheters in children undergoing the Nuss procedure for pectus excavatum repair. J Anesth 2022; 36 (3): 335–340. doi: 10.1007/s00540-022-03048-5.
Štítky
Dětská neurologie Neurochirurgie NeurologieČlánek vyšel v časopise
Česká a slovenská neurologie a neurochirurgie
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