Brainstem anesthesia during awake craniotomy: illustrative case

Yun Chen Graduate School, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
Departments of Anesthesiology

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Mei Sun Departments of Anesthesiology

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Hongmin Bai Neurosurgery, General Hospital of Southern Theatre Command of PLA, Guangzhou, Guangdong, China

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Ruixin Yang Neurosurgery, General Hospital of Southern Theatre Command of PLA, Guangzhou, Guangdong, China

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Huan He Departments of Anesthesiology

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BACKGROUND

Awake craniotomy (AC) is performed to remove the lesions near or in eloquent areas, during which the patients are alert and without any airway instrument. Apnea is a severe complication in AC. Here, the authors describe a case of sudden apnea induced by unexpected local anesthesia of the brainstem during AC.

OBSERVATIONS

A 42-year-old male underwent AC for a large, recurrent, bilateral frontal lobe mass and experienced transient apnea and loss of brainstem reflexes during the surgery. The patient recovered spontaneous breath rhythm just a few minutes after the removal of a lidocaine cotton pledget, which was found near the patient’s midbrain. Then the patient awoke and cooperated to finish the surgery.

LESSONS

The administration of a local anesthetic subdurally in AC is common but risky. The scouring action of cerebral spinal fluid can spread those agents and cause unexpected brainstem anesthesia. A lower concentration of the anesthetic and keeping away from the cistern can make it safer.

ABBREVIATIONS

AC = awake craniotomy; BIS = bispectral index; ECG = electrocardiography; MRI = magnetic resonance imaging

BACKGROUND

Awake craniotomy (AC) is performed to remove the lesions near or in eloquent areas, during which the patients are alert and without any airway instrument. Apnea is a severe complication in AC. Here, the authors describe a case of sudden apnea induced by unexpected local anesthesia of the brainstem during AC.

OBSERVATIONS

A 42-year-old male underwent AC for a large, recurrent, bilateral frontal lobe mass and experienced transient apnea and loss of brainstem reflexes during the surgery. The patient recovered spontaneous breath rhythm just a few minutes after the removal of a lidocaine cotton pledget, which was found near the patient’s midbrain. Then the patient awoke and cooperated to finish the surgery.

LESSONS

The administration of a local anesthetic subdurally in AC is common but risky. The scouring action of cerebral spinal fluid can spread those agents and cause unexpected brainstem anesthesia. A lower concentration of the anesthetic and keeping away from the cistern can make it safer.

ABBREVIATIONS

AC = awake craniotomy; BIS = bispectral index; ECG = electrocardiography; MRI = magnetic resonance imaging

Awake craniotomy (AC) aims to allow a maximal and safe resection of lesions near eloquent areas. Functional brain mapping is the core step of AC, during which the patients are awake and breathe spontaneously. Apnea uncommonly occurs during AC, but once it happens, patients’ lives are severely threatened. Here, we describe a case of brainstem anesthesia-caused apnea during AC to illustrate the performance of brainstem anesthesia and provide possible management strategies to prevent and handle such an emergency during AC.

Illustrative Case

A 42-year-old, 65-kg male was scheduled for AC for the resection of a recurrent, huge, bilateral frontal lobe mass. The patient had previously undergone a right frontotemporal insula glioma resection in our hospital 4 years earlier. Pathological examination had indicated a low-grade oligoastrocytoma, not otherwise specified, World Health Organization grade 2. Postoperatively, the patient received radiotherapy and regular imaging follow-up. The patient experienced tonic-clonic seizures 3 years after the surgery, and magnetic resonance imaging (MRI) indicated the recurrence. A suggested operation was refused by the patient and his family at that time, and seizure control was addressed with carbamazepine 200 mg twice a day; however, he still experienced on to two tonic-clonic seizures per month. Because of the poor seizure control, the patient went back to the hospital and requested the operation. Recently, cranial MRI revealed a 6 × 6 × 8 cm mass in the bilateral frontal lobes that showed weakly hyperintense on T2-weighted sequences and isointense on T1-weighted sequences, and heterogeneity enhanced with contrast. The lesion invaded a large area including almost all of the right anterior-interior frontal lobe, partial right temporal lobe, left anterior-inferior frontal lobe, hypothalamus, wall of the third ventricle, and rostrum and genu of the corpus callosum (Fig. 1A). The presenting symptoms of this patient included decreased physical strength of the left limbs, poor mental state, and impaired cognitive functions. Preoperative examinations showed normal electrocardiography (ECG) findings and no abnormalities on chest radiography and cardiac ultrasound. He had no hepatic, renal, or endocrine abnormalities.

FIG. 1
FIG. 1

A: Preoperative T2-weighted MRI series (left) and T1-weighted (right upper) and T1+contrast (right lower) images. B: T2-weighted MRI series acquired 24 hours after surgery, which showed the resection region near the midbrain.

Once the patient entered the operating room, an 18-gauge intravenous catheter was started in the patient’s left foot, while ECG, pulse oxygen saturation, blood pressure, and bispectral index (BIS) were monitored. According to his height, age, weight, and gender, the patient had an appropriate amount of target-controlled infusion of propofol and remifentanil aiming to target blood concentrations of 0.8 to 1.2 µg/mL and 1 to 2 ng/mL, respectively, to maintain the BIS at 60 to 80. Spontaneous breathing was preserved under mask oxygen inhalation with 100% oxygen while end-expiratory carbon dioxide was monitored. Next, internal jugular venipuncture and arterial puncture were performed.

The patient was placed supine, and the neurosurgeon performed scalp nerve block and incision infiltration anesthesia. Then the AC was performed. After removal of the skull flap, dural anesthesia was induced by infiltration with 2% lidocaine cotton pledgets, and the patient was awakened gradually by adjusting to maintain propofol at 0.2 to 0.5 µg/mL and remifentanil at 0.2 to 0.5 ng/mL. Then, the patient was awakened, and functional brain mapping followed. Neurosurgeons mapped the functional cortex and began to remove the tumor while monitoring the patient’s speaking and movement functions. Approximately 180 minutes after the beginning of the surgery, during the tumor removal, the patient suddenly did not respond to the call, and end-tidal carbon dioxide wave disappeared (Fig. 2A). The anesthesiologist examined the patient and found that he had lost his spontaneous respiratory rhythm and pupillary light reflex. Without hesitation, mask ventilation was immediately administered to control the airway and keep the vital signs stable. The operation was suspended at the anesthesiologist’s request; however, no abnormal conditions occurred in the surgical field. In addition, an arterial blood gas sample was sent, revealing pH 7.43, PaCO2 38 mm Hg. After ruling out an overdose of anesthetic drugs, the surgical field was screened and all cotton pledgets were removed. A lidocaine pledget infiltrating the anterior skull base was found near the midbrain (Fig. 2B). The patient recovered spontaneous breathing but with irregular rhythm in 10 minutes after removing the cotton pledgets. Approximately 30 minutes later, the patient’s consciousness recovered, and his respiratory rhythm became regular. Arterial blood gas results showed pH 7.408 and PaCO2 42 mm Hg.

FIG. 2
FIG. 2

A: The monitor showed the sudden disappearance of the end-tidal carbon dioxide wave. B: Sagittal and axial postoperative MRI, with the arrow indicating the location of lidocaine cotton pledget.

After that, the operation continued and was completed smoothly. The operation lasted for 7 hours, and the bleeding was approximately 800 mL. Two units of red blood cells and 400 mL of plasma were transfused. After the operation, the patient was aware and answered questions correctly. The patient returned to neurosurgical intensive care unit and was discharged from the hospital successfully.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

Observations

We describe a patient who underwent AC for the resection of a huge bilateral frontal lobe mass and suddenly experienced apnea with a loss of consciousness and brain reflection.

Apnea was found at the first in this case. The causes of apnea can be related to muscle relaxant residual, overdose of sedative and analgesic drugs, hypothermia, hypocarbia, surgical traction, and compression of the mass.1–3 Monitored anesthesia care, which was administered in this case, does not use muscle relaxants and will be maintained by propofol and remifentanil only. The blood concentration of propofol and remifentanil was too low to lead to apnea. Moreover, hypothermia and hypocarbia were excluded. Of note, both of these situations are easy to correct and will not induce the absence of brainstem reflexes.

Therefore, the absence of brainstem reflexes inspired us to think of brainstem anesthesia. A cotton piece was found near the midbrain during the combing process, the patient quickly recovered, and the operation was continued. This result confirmed our conjecture. However, midbrain anesthesia can cause loss of consciousness, the disappearance of the pupillary light reflex, and a change of respiratory rhythm but does not cause apnea. The spontaneous breathing rhythm center is located in the ventral medulla oblongata; a block above the midbrain plane can lead to loss of arbitrary breath but does not lead to the absence of spontaneous breath. Therefore, we hypothesized that the medullary anesthesia was caused by the spread of a local anesthetic.

At that time, the neurosurgeons were dealing with the tumor near the initial part of middle cerebral artery (M1) and tentorial incisure. To release the intolerable pain caused by artery and dura traction, patients are generally treated with 2% lidocaine cotton pledgets infiltration of the vascular wall and the dura surface. As we now see, the lidocaine cotton pledget was close to the lateral of the basal cisterns, and the arachnoids of the mesial temporal lobe were removed during the resection. At this time, the flushing of cerebrospinal fluid is likely to bring the lidocaine in the cotton pledgets into the basal cisterns, resulting in anesthesia of multiple cranial nerves and ventral medulla, and eventually inducing the loss of spontaneous respiratory rhythm and brainstem reflexes, as well as consciousness.

Brainstem anesthesia is commonly observed in ophthalmic surgery and is caused by unexpected intrathecal injection.4 Brainstem anesthesia in ophthalmic surgery has an incidence of 0.79%5 and can lead to relatively long-term (usually a few hours) brainstem suppression such as disturbance of consciousness, respiratory depression, arrhythmia, and even cardiac arrest.6 In this case, the patient returned to spontaneous breath shortly after removal of the cotton pledgets. This may have been related to the low dose of lidocaine in the cotton pledget and the short time the pads were in place.7 When brainstem anesthesia occurs, the airway should be artificially controlled, such as through endotracheal intubation or laryngeal mask and mechanical ventilation, and vital signs should be maintained immediately while the trigger is removed, if possible. Therefore, a lateral position is preferred rather than a supine position in AC, for more easily establishing airway control and less airway-related risks, such as glossoptosis and aspiration. Fortunately, although the supine position was used, the patient in our case had a fairly satisfactory saturation of pulse oxygen without an artificial airway, which may have been due to a slight functional suppression of the medulla oblongata.

Analgesia is one of the core techniques in AC anesthesia. A long-term scalp nerve block ensured analgesia of the scalp during the awake phase. However, analgesia of the dura was still a challenge. In addition to lidocaine pledget infiltration of the dura, direct dural injection may be a good method for avoiding pain. But the skull base dura injection is not easy to perform. Furthermore, pain during the awake phase was caused not only by traction of the dura, but also by traction of the middle and small artery and pia. At present, to prevent the pain caused by artery traction, lidocaine pledget infiltration was the only way during the awake phase. It is reported that the pain caused by mechanical stimulation to the dura of the skull base and dura of the falx cerebri is mainly the sensory territories of the V1 and V3 branches of the trigeminal nerve, while the pain caused by mechanical stimulation to the pia and the small cerebral vessels is the sensory territories of the V1 branch.8 Thus, trigeminal nerve block may also be a feasible approach in the future and may be a promising technique for awake phase analgesia.

Lessons

The concentration and location of the lidocaine cotton pledgets may be the most likely cause of brainstem anesthesia in AC. Lidocaine pads should be placed away from the cerebral cisterns, especially the suprasellar cisterns, ambient cisterns, and basal cisterns to avoid the spread of local anesthetic drugs due to cerebrospinal fluid washout. Moreover, the lateral position may be a proper way to control the airway anesthesiologist in this emergency situation.

Acknowledgments

This work was supported by Science and Technology Projects in Guangzhou. The authors thank Qunlin Wu for technical assistance with anesthesia from the Department of Anesthesiology.

Author Contributions

Conception and design: Sun. Acquisition of data: Chen, Bai. Analysis and interpretation of data: He. Drafting the article: Chen. Critically revising the article: He, Yang. Approved the final version of the manuscript on behalf of all authors: He. Administrative/technical/material support: Bai. Study supervision: Yang.

References

  • 1

    Nelson RY, Bretz B, Egan TD Prolonged apnea after remifentanil. J Clin Anesth. 2007;19(1):6063.

  • 2

    Saganuwan SA Chemistry and effects of brainstem acting drugs. Cent Nerv Syst Agents Med Chem. 2019;19(3):180186.

  • 3

    Gaspari RJ, Paydarfar D Dichlorvos-induced central apnea: effects of selective brainstem exposure in the rat. Neurotoxicology. 2011;32(2):206214.

  • 4

    Sadler A, McLeod G, McHardy PG, Wilkinson T Ultrasound detection of iatrogenic injury during peribulbar eye block: a cadaveric study. Reg Anesth Pain Med. 2020;45(9):740743.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Ahmad S, Ahmad A Complications of ophthalmologic nerve blocks: a review. J Clin Anesth. 2003;15(7):564569.

  • 6

    Gunja N, Varshney K Brainstem anaesthesia after retrobulbar block: a rare cause of coma presenting to the emergency department. Emerg Med Australas. 2006;18(1):8385.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Kinoshita H, Kawahito S The clinically relevant concentration of local anesthetics is a matter of consideration in the in vitro study. Anesth Analg. 2020;131(2):e86.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Fontaine D, Almairac F, Santucci S, et al. Dural and pial pain-sensitive structures in humans: new inputs from awake craniotomies. Brain. 2018;141(4):10401048.

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  • FIG. 1

    A: Preoperative T2-weighted MRI series (left) and T1-weighted (right upper) and T1+contrast (right lower) images. B: T2-weighted MRI series acquired 24 hours after surgery, which showed the resection region near the midbrain.

  • FIG. 2

    A: The monitor showed the sudden disappearance of the end-tidal carbon dioxide wave. B: Sagittal and axial postoperative MRI, with the arrow indicating the location of lidocaine cotton pledget.

  • 1

    Nelson RY, Bretz B, Egan TD Prolonged apnea after remifentanil. J Clin Anesth. 2007;19(1):6063.

  • 2

    Saganuwan SA Chemistry and effects of brainstem acting drugs. Cent Nerv Syst Agents Med Chem. 2019;19(3):180186.

  • 3

    Gaspari RJ, Paydarfar D Dichlorvos-induced central apnea: effects of selective brainstem exposure in the rat. Neurotoxicology. 2011;32(2):206214.

  • 4

    Sadler A, McLeod G, McHardy PG, Wilkinson T Ultrasound detection of iatrogenic injury during peribulbar eye block: a cadaveric study. Reg Anesth Pain Med. 2020;45(9):740743.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Ahmad S, Ahmad A Complications of ophthalmologic nerve blocks: a review. J Clin Anesth. 2003;15(7):564569.

  • 6

    Gunja N, Varshney K Brainstem anaesthesia after retrobulbar block: a rare cause of coma presenting to the emergency department. Emerg Med Australas. 2006;18(1):8385.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Kinoshita H, Kawahito S The clinically relevant concentration of local anesthetics is a matter of consideration in the in vitro study. Anesth Analg. 2020;131(2):e86.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Fontaine D, Almairac F, Santucci S, et al. Dural and pial pain-sensitive structures in humans: new inputs from awake craniotomies. Brain. 2018;141(4):10401048.

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