Retrobulbar block is a technique of ophthalmic surgical anesthesia in which local anesthetic is injected into the intraconal space (retrobulbar space within the cone) behind the eye. It has the advantage of simultaneously achieving painlessness of the surgical field and akinesia of the eye.
Since Koller’s report of ophthalmic local anesthesia using cocaine in 1884, it has long been the gold standard for ophthalmic surgery. However, due to the invasiveness of the technique and the risk of complications, extraconal injection (peribulbar anesthesia, sub-Tenon’s anesthesia) is now positioned as the standard technique, and the use of retrobulbar block varies by facility and surgical procedure.
The incidence of serious systemic complications from ophthalmic local and regional anesthesia is reported to be 3.4 per 10,000, most of which are brainstem anesthesia, subarachnoid block, and convulsions due to spread of local anesthetic into the optic nerve sheath.
Retrobulbar Block
Injection site: Intraconal space
Quality of anesthesia: Strong and reliable painlessness and akinesia
Risk of globe perforation: Slightly higher
Risk of brainstem anesthesia: Possible due to optic nerve sheath puncture
Cochrane comparison: No difference in efficacy compared to peribulbar anesthesia
Peribulbar Anesthesia
Injection site: Extraconal space
Quality of anesthesia: Slightly weaker (supplemental injection may be needed)
Risk of globe perforation: Lower than retrobulbar
Chemosis: More common than retrobulbar
Eyelid hematoma: Less common than retrobulbar
In ophthalmic surgery, local anesthesia (retrobulbar/peribulbar) has the advantage of avoiding general anesthesia-related complications (e.g., aspiration, airway issues). However, retrobulbar anesthesia carries its own risk of serious complications such as brainstem anesthesia. The optimal method should be chosen in collaboration with an anesthesiologist, considering the patient’s overall condition, surgical procedure, and surgeon’s expertise.
Normal response when retrobulbar anesthesia is properly administered:
Symptoms when complications occur:
In a case of a 91-year-old woman reported by Sanchez et al., the following findings appeared approximately 2 minutes after injection of 5 mL (2.5 mL of 1% ropivacaine + 2.5 mL of 2% lidocaine) for retrobulbar anesthesia. 1)
BIS value 40–50 and EEG findings with delta wave predominance were observed. Head CT and blood tests were normal; the patient was extubated after 4 hours and discharged after 48 hours without neurological sequelae. 1)
In a case of a man in his 60s reported by Thomasius et al. (23G blunt needle 32 mm, mepivacaine 2% 2.5 mL + bupivacaine 0.5% 2.5 mL + hyaluronidase), hypertension (270/166 mmHg), tachycardia (130 bpm), and loss of spontaneous breathing occurred. Head CT showed intracranial emphysema and left frontal basal hematoma, confirming dural injury. After ICU management, vitrectomy was performed under general anesthesia the next day. 2)
In a case of a 72-year-old woman reported by Nanda et al. (31G blunt needle 25 mm, 0.5% bupivacaine 5 mL, for repair of globe rupture), a steady increase in ETCO2 and apnea appeared 7 minutes after injection, leading to a diagnosis of brainstem anesthesia. The patient was extubated after 1.5 hours and recovered. 3)
Operator-related factors
Anatomical factors
Drug and technique factors
Patient-related factors
In intra-arterial injection, a grand mal-like seizure typically appears as the first symptom within seconds to minutes after injection. In contrast, brainstem anesthesia presents with impaired consciousness, apnea, and circulatory changes 5 to 50 minutes (average 20.5 minutes) after injection. 3) The key differentiating point is that seizures are the main symptom in intra-arterial injection, whereas loss of consciousness and apnea are prominent in brainstem anesthesia.
The following should be evaluated before performing retrobulbar anesthesia:
If the following symptoms appear after retrobulbar anesthesia, brainstem anesthesia should be suspected first:
Differential diagnoses: oversedation (excluded by minimal sedative use), stroke (excluded by imaging or complete recovery), intra-arterial injection (presence of seizures).
The incidence of central nervous system complications is reported to be 0.27–0.79%. In a study of 6,000 retrobulbar blocks, 16 cases (0.26%) of CNS signs and 1 case (0.02%) of cardiac arrest were identified. 2) The frequency of respiratory depression is reported to be approximately 0.03%. 2)
Basic Technique
Recommended Anesthetics
Precautions
Treatment of brainstem anesthesia is primarily supportive, awaiting spontaneous recovery.
Acute management (ABCDE approach)
Prognosis for recovery
In most cases, symptoms completely resolve within a few hours as the anesthetic clears from the central nervous system. 1)2)3) For local anesthetic-induced central nervous system toxicity, lipid emulsion therapy (20% lipid emulsion: 1 mg/kg bolus followed by 15 mL/kg/h continuous infusion) is considered effective. 3)
The main mechanisms of brainstem anesthesia are broadly divided into the following two.
Mechanism 1: Optic nerve sheath puncture → spread into the subarachnoid space
The optic nerve is surrounded by three sheaths: dura mater, arachnoid mater, and pia mater. The subarachnoid space is continuous with the intracranial subarachnoid space. If the retrobulbar needle accidentally punctures the optic nerve sheath, the injected local anesthetic spreads via the subarachnoid space to the brainstem and diencephalon. Symptoms via this mechanism appear 5–50 minutes (mean 20.5 minutes) after injection. 3)
Mechanism 2: Intra-arterial injection → retrograde intracranial flow
In accidental injection into the ophthalmic artery, the local anesthetic flows retrogradely into the internal carotid artery and then to cerebral vessels, reaching the thalamus and midbrain. Symptoms via this mechanism appear within seconds to minutes, often with generalized convulsions resembling a grand mal seizure as the initial symptom.
Course of brainstem anesthesia
When local anesthetic reaches the brainstem, first, sympathetic hyperactivity due to parasympathetic blockade occurs (tachycardia, hypertension, bilateral mydriasis), followed by suppression of consciousness and respiratory centers, leading to coma and central apnea. As the local anesthetic is metabolized and redistributed, symptoms gradually resolve, and in most cases, all symptoms disappear within about 4 hours. 1)
When a head CT is performed for suspected brainstem anesthesia, abnormal findings are usually not observed. If there is dural injury (Thomasius case), intracranial emphysema may be confirmed. 2)
A method in which anesthetic is injected while confirming the needle tip position in real time using ultrasound (echo). Research is progressing as it may avoid accidental puncture of the optic nerve sheath or blood vessels. However, accurate understanding of intraorbital ultrasound anatomy and specialized equipment are required, and it is not yet standardized.
Sub-Tenon anesthesia, which has a much lower risk of globe perforation and optic nerve sheath puncture compared to retrobulbar and peribulbar anesthesia, is becoming more widespread as the first choice in many cataract and vitrectomy facilities. The frequency of retrobulbar anesthesia use is expected to decline further.
Case reports have accumulated that 20% lipid emulsion (1 mg/kg bolus → 15 mL/kg/h continuous) is life-saving for systemic toxicity of local anesthetics. 3) It is positioned as an adjunctive therapy when brainstem anesthesia becomes severe, but evidence for its efficacy against brainstem anesthesia (subarachnoid spread) is insufficient.
