A case of cardiorespiratory collapse following bilateral sub-Tenon’s blocks from brainstem anaesthesia

Abstract

Sub-Tenon’s block has a superior safety profile and life-threatening complications such as cardiovascular collapse and brainstem anaesthesia are extremely rare. We report a case of cardiorespiratory collapse following bilateral sub-Tenon’s blocks at the conclusion of a laser photocoagulation procedure under general anaesthesia. The cause was most likely brainstem anaesthesia. We explore and discuss the likely mechanisms and other potential differential diagnoses. It highlights the importance of maintaining vigilance following an eye block. Attention should not falter upon completing a block or at the conclusion of a case, regardless of its type or safety profile. This case also illustrates how the presence of general anaesthesia may obscure and delay the diagnosis of brainstem anaesthesia.

Introduction

Sub-Tenon’s block is safe, ¹ effective, and fast becoming the most popular regional anaesthetic technique for ophthalmic surgery worldwide. Life-threatening complications such as cardiac collapse and brainstem anaesthesia are extremely rare. We report a case of brainstem anaesthesia following bilateral sub-Tenon’s blocks during a retinal photocoagulation procedure under general anaesthesia, ultimately leading to cardiorespiratory collapse. Written informed consent was obtained from the patient’s next of kin and the surgeons for the publication of this case report.

Case presentation

A 76-year-old, Caucasian female (weight 81 kg, height 1.54 m, body mass index 34.2 kg/m², American Society of Anesthesiologists physical status classification 3) presented for elective bilateral pan retinal photocoagulation for proliferative diabetic retinopathy. She had multiple medical comorbidities including a previous stroke, atrial fibrillation, hypertension, heart failure with preserved ejection fraction, peripheral vascular disease, mild to moderate pulmonary hypertension, peripheral vascular disease, type 2 diabetes mellitus, chronic kidney disease (stage 3b; estimated glomerular filtration rate 40 ml/min per m²) and anaemia. Her medications included apixaban, clopidogrel, insulin glargine, linagliptin, metformin, metoprolol, spironolactone, frusemide and iron polymaltose. She was allergic to penicillin (angioedema). She had undergone an uneventful MicroPulse laser procedure to her right eye six days earlier under a peribulbar block with ropivacaine 1% 4 ml containing hyaluronidase 75 U/ml.

Preoperatively, her blood pressure was 135/55 mmHg, her heart rate was 56/min and her oxygen saturation on pulse oximetry (SpO₂) was 100%. Her cardiorespiratory examination was unremarkable with no clinical signs of heart failure. Her electrocardiogram (ECG) showed atrial fibrillation. General anaesthesia was selected as the preferred anaesthetic technique because of the bilateral procedure, antithrombotic effects of apixaban and clopidogrel, and a likelihood of suboptimal tolerance to bilateral sub-Tenon’s blocks.

General anaesthesia was induced with an admixture of propofol 100 mg and lignocaine 20 mg. A size 3 Ambu® AuraGain™ laryngeal mask airway (Ambu, Ballerup, Denmark) was inserted. Anaesthesia was maintained with sevoflurane in oxygen and air mixture, targeting an age-adjusted end-tidal anaesthetic gas concentration of 0.7 minimum alveolar concentration (MAC). She was placed in assisted spontaneous ventilation with pressure support of 6 to 8 cmH₂O (Dräger Atlan® A350 XL, Dräger, Lubeck, Germany). No other medications, including opioids, were administered during the procedure.

The photocoagulation procedure took approximately 35 min. Her haemodynamic parameters were stable throughout with a dose of metaraminol 0.5 mg administered once to maintain systolic blood pressure above 100 mmHg. The case was otherwise uneventful until the end of the procedure. Upon completion of laser photocoagulation, bilateral sub-Tenon’s blocks were administered for postoperative analgesia by the surgeons. Following the application of topical 10% povidone-iodine, a speculum was applied to the eye, and a curved metallic sub-Tenon’s cannula (19G, 25 mm, Sterimedix Ltd, Worcestershire, United Kingdom) was introduced through an inferonasal incision.

The first block, administered by the specialist ophthalmologist, consisted of ropivacaine 1% 4 ml. The second block, performed by a trainee ophthalmologist immediately after the first block, consisted of lidocaine 2% 3 ml. The specialist demonstrated his technique for the first block and provided direct hands-on supervision of the second block. There were no other adjuvants (hyaluronidase, adrenaline) in the local anaesthetic solutions. Following the blocks, anaesthesia was maintained with sevoflurane at an age-adjusted MAC of 0.7 with the intention to transfer her to the post-anaesthesia care unit in the existing plane of anaesthesia with the laryngeal mask airway (LMA) still in place. The vital signs over the subsequent 3 min were unremarkable, consistent with the previous trend.

Approximately 3 min after the second sub-Tenon’s injection, the patient’s haemodynamic parameters became unstable. Initially her blood pressure dropped to 86/42 mmHg, followed by a reduction in both tidal volume and respiratory rate. Her SpO₂ quickly fell to 91% along with reduction in her end-tidal carbon dioxide level. Her heart rate then dropped from 60 to 40/min. The ECG monitoring (Lead II) revealed a rapidly slowing heart rhythm with an irregularly irregular narrow complex bradycardia on a background of chronic atrial fibrillation. Notably, there were no ECG patterns suggestive of other critical arrhythmias such as ventricular tachycardia, ventricular fibrillation or asystole. As ephedrine was locked in secured storage and not readily available, metaraminol boluses were administered to restore her blood pressure, without success. She was also switched to manual bag ventilation.

In the following few minutes, there was complete cardiorespiratory collapse. Her blood pressure dropped to 35/20 mmHg, then became unrecordable. Her heart rate dropped to 30/min. Even with manual ventilation, her SpO₂ fell below 69%.

She was ventilated with 100% oxygen; sevoflurane was switched off and emergency response activated. Two boluses of adrenaline 10 µg were administered in quick succession without improvement. A further 50 µg of adrenaline was administered, which led to rapid improvement in all her haemodynamic parameters, eliminating the need to commence chest compressions. Her femoral pulse became palpable, blood pressure recordable and oxygen saturation improved.

A radial arterial line and a second intravenous cannula were inserted, and 1 l of Hartmann’s solution was administered. Her immediate arterial blood gas (ABG) showed pH 7.09, pO₂ 224 mmHg, pCO₂ 59.4 mmHg and lactate 6.6 mmol/. Her haemoglobin was 104 g/l and blood glucose level was 21.7 mmol/l. The ECG showed atrial fibrillation with no new ischaemic changes.

It was concerning that she remained unconscious for a total of 30–35 min when all the general anaesthetic agents were withdrawn. After her condition was stabilised, attention shifted to the possible causes and further management strategies, including discussions on whether to provide sedation and pursue further investigations such as a computed tomography scan of the brain. Amidst these reflections, the patient began showing signs of neurological improvement. She started moving her left upper limb, followed by left lower limb and rest of the body in quick succession. Soon she regained consciousness, opened her eyes spontaneously and responded to verbal commands. The LMA was then removed. Her subsequent ABG showed significant improvement, with pH 7.23, pO₂ 326 mmHg, pCO₂ 43.2 mmHg and lactate 4.3 mmol/l. A provisional diagnosis of brainstem block was made.

Postoperatively, she underwent further investigations. Cardiac telemetry recorded only bradyarrhythmia and occasional premature ventricular complexes. Transthoracic echocardiography revealed normal left ventricular size and systolic function with no significant valve disease and mild pulmonary hypertension. Her blood tests were similarly unremarkable. Serial troponins T were 52 ng/l (at 3 h), 79 ng/l (at 5 h) and 40 ng/l (at 22 h) (reference range <15 ng/l). These changes were subsequently considered as inconsequential by the cardiologist. Serial tryptase was 10.1 μg/l (at 4 h), 10.3 μg/l (at 24 h) (reference range 0–11.4 μg/l). A 1-h tryptase level was requested but was unfortunately not taken.

Discussion

Sub-Tenon’s block, with its superior safety profile, has gained increasing popularity in many countries. ² The risk of sight- or life-threatening complications is extremely rare. The incidence of central nervous system spread was estimated to be 0.023% in sub-Tenon’s block comparing with 0.02% in peribulbar block.^3,4

There have been two cases of transient loss of consciousness with no cardiac involvement after sub-Tenon’s block attributed to brainstem anaesthesia.^3,5 There have been two case reports of cardiac arrest after sub-Tenon’s block, both in the presence of significant cardiac comorbidities. The mechanism was thought to be local anaesthetic toxicity from rapid absorption through a carotid-cavernous fistula in one case while a sole cardiac cause was thought to be the reason for the second case although the possibility of brainstem anaesthesia could not be excluded.^6,7 Both of these cardiac arrest cases reported fatal outcomes. Our patient had major cardiorespiratory collapse, responded to intravenous adrenaline, and did not require chest compressions. Despite having many significant medical comorbidities, she made a full recovery.

The precise mechanism of brainstem anaesthesia following sub-Tenon’s block remains unclear. Three mechanisms have been proposed: a perforation could occur during the dissecting in sub-Tenon’s space, allowing local anaesthetic to cross the optic nerve sheath; ³ the posterior sub-Tenon’s space is a lymph space in continuation with the optic nerve so injectate could enter the subarachnoid space though the optic nerve sheath; ⁸ and accidental perforation of sub-Tenon’s capsule could lead to local anaesthetic traversing into the intraconal space, through the orbital foramen and into the central nervous system. ⁸

Sub-Tenon’s block can be administered using either a metallic or a plastic cannula. The rigidity of the metallic cannula facilitates insertion but there is potential increased risk of globe perforation, periorbital haemorrhage and central spread of local anaesthetic solution. A flexible plastic cannula is perceived as having reduced risk of these complications. ⁹ Since the precise mechanism of brainstem anaesthesia after sub-Tenon’s block is unclear, we are therefore unable to pinpoint the exact cause in our case. It has been recommended that the sub-Tenon’s cannula tip should be advanced just passing the equator of the globe and very posterior placement should be avoided. ² We postulate that one of the sub-Tenon’s cannulae might have been placed too far posterior, leading to the local anaesthetic traversing into the central nervous system. Considering the rarity of such a life-threatening complication, the probability of this occurring twice consecutively by two different proceduralists is extremely unlikely.

We believe, given the rapid onset after sub-Tenon’s blocks, the clinical course of deterioration and subsequent rapid recovery, the most likely cause in our patient was brainstem anaesthesia from the sub-Tenon’s block(s). In unanaesthetised patients, there are symptoms and signs that may indicate brainstem block, including amaurosis and non-reactive pupil in the contralateral eye. However, our patient was anaesthetised with bilateral sub-Tenon’s blocks and adrenaline was administered during resuscitation, which complicated the clinical picture and delayed the diagnosis of brainstem anaesthesia. This case emphasises the crucial importance of maintaining vigilance following an eye block, regardless of its type or risk profile. Attention should not wane upon completing a block or at the conclusion of a case.

Many medications are increasingly being locked up in secured storage nowadays to combat substance abuse. Such practice has its disadvantages as these agents are not readily available for use, which may hinder emergency circumstances like our case. Ephedrine was locked up in accordance with our local hospital policy, therefore it was not immediately available for use during resuscitation. We had instead used metaraminol and adrenaline because they were readily available on the anaesthetic drug trolley. Timely access to all resuscitation agents would be ideal. However, as her haemodynamic parameters did not improve with metaraminol boluses and small doses of adrenaline, we postulate that ephedrine may not have altered the course of her resuscitation.

It is prudent to exclude other potential causes of sudden cardiorespiratory collapse at the end of the procedure. There are many differential diagnoses, including vasovagal response, oculocardiac reflex, anaphylaxis, local anaesthetic toxicity, acute right heart decompensation resulting from pulmonary hypertension and massive pulmonary embolus.

Pressure and manipulation on the eye, through stimulation of vagal-mediated afferent tracts on the ophthalmic division of the trigeminal nerve, can induce oculocardiac reflex leading to bradycardia, various cardiac arrhythmias and even cardiac standstill, as well as apnoea.^10,11 This reflex is often seen in strabismus surgery, especially in children, during traction on extraocular muscle. Other orbital stimuli, such as injection during regional ophthalmic block, can also trigger this reflex. ¹² An oculocardiac reflex is unlikely to be the cause of cardiorespiratory collapse in our patient. The onset of the reflex is often prompt and cessation of ocular stimuli usually restores normal heart rhythm.^13,14 In our case, the bradycardia was more gradual and it persisted despite removal of ocular stimuli.

Another possibility for cardiorespiratory collapse is anaphylaxis. Hyaluronidase was not administered in our case. The agents used, including povidone-iodine, lignocaine, ropivacaine, propofol and sevoflurane, have a low incidence of anaphylaxis according to a large audit on perioperative anaphylaxis. ¹⁵ In addition, a very low score (<8) using the consensus clinical scoring system and our laboratory investigations also did not support this diagnosis. ¹⁶

Local anaesthetic systemic toxicity is another differential diagnosis. It has been reported in procedures involving peribulbar and retrobulbar blocks.^17,18 This is, however, unlikely to be the mechanism in our patient for many reasons. Vascular puncture is less likely with blunt dissection in a sub-Tenon’s block, the local anaesthetic dose administered was well below the toxic limit and the neurological recovery pattern seen in our patient was more consistent with brainstem anaesthesia.

Acute right heart failure from worsening of pre-existing pulmonary hypertension could possibly lead to cardiovascular collapse. Pain, hypercapnia and high ventilatory pressures are known to precipitate acute right heart failure. ¹⁹ However, at the time of clinical deterioration in our patient, the end-tidal carbon dioxide was stable, the painful stimuli from the operation had stopped and the airway pressure monitoring parameters were within normal limits. In addition, her transthoracic echocardiography showed only mild pulmonary hypertension.

Massive pulmonary embolus was another possibility. Our patient was active and mobile prior to the procedure, her antiplatelet and antithrombotic agents were not suspended preoperatively, and the rapid clinical improvement afterward made this diagnosis extremely unlikely.

Conclusion

In conclusion, we present a case of acute cardiorespiratory collapse following bilateral sub-Tenon’s blocks under general anaesthesia, most likely due to brainstem anaesthesia. Our case underscores the importance of vigilance following all eye blocks, irrespective of when it is given or who administers it. Despite the superior safety profile of sub-Tenon’s block, our case serves as a reminder that attention should not falter. This case further demonstrates how symptoms and signs of brainstem anaesthesia may be masked by the presence of general anaesthesia, necessitating heightened awareness.