Seizure-associated venous air embolism during awake craniotomy in the supine position: A case report

Abstract

BACKGROUND

Venous air embolism (VAE) is a recognized complication of neurosurgical procedures, particularly in the sitting position, but may occur in any position where the surgical field is above the level of the heart. Its occurrence during awake craniotomy in the supine position is rare and diagnostically challenging due to limited monitoring and nonspecific clinical manifestations.

CASE SUMMARY

We report the case of a 22-year-old male undergoing awake craniotomy in supine position for resection of a right fronto-temporal low-grade glioma, identified on preoperative magnetic resonance imaging as a non-enhancing cortical lesion in close proximity to eloquent motor cortex, with functional magnetic resonance imaging demonstrating perilesional motor and supplementary motor area activation. Near the completion of tumor excision, the patient developed non-convulsive seizure activity followed by persistent coughing, dyspnea, chest tightness, tachypnoea, tachycardia, and hypoxemia. A new continuous precordial murmur was detected. VAE was suspected based on clinical findings. Immediate management included flooding the surgical field with saline, Trendelenburg positioning, administration of 100% oxygen with positive end-expiratory pressure, and supportive care. The patient improved rapidly, with normalization of oxygen saturation and vital parameters. Post-event transthoracic echocardiography revealed no cardiac dysfunction, while lung ultrasound demonstrated bilateral B-lines, consistent with pulmonary interstitial involvement.

CONCLUSION

VAE can occur during awake craniotomy even in the supine position, potentially precipitated by seizure-related deep inspiratory efforts. Given the nonspecific presentation and diagnostic limitations in awake neurosurgery, a high index of suspicion and prompt supportive management are essential to ensure favourable outcomes.

Key Words: Venous air embolism; Awake craniotomy; Seizure; Supine position; Neuroanesthesia; Case report

Core Tip: Venous air embolism (VAE), though classically associated with neurosurgical procedures in the sitting position, can also occur during awake craniotomy in the supine position and may present with subtle, nonspecific symptoms. In awake patients, seizure-related deep inspiratory efforts and transient negative intrathoracic pressure can facilitate air entrainment through exposed cerebral veins, particularly when the surgical field is positioned above the level of the heart. Overlap between seizure activity and the clinical manifestations of VAE can delay recognition in the absence of advanced monitoring. This case highlights the need for heightened vigilance, early clinical suspicion, and prompt supportive management to ensure favorable outcomes during awake craniotomy.

INTRODUCTION

Venous air embolism (VAE) refers to the entrainment of air into the venous circulation from exposed surgical sites, potentially leading to significant cardiopulmonary and neurological consequences[1]. While many episodes remain subclinical, clinically significant VAE has been most frequently reported during neurosurgical procedures performed in the sitting position, with an incidence ranging from 10% to 80%[1]. However, VAE may occur in any surgical position in which the operative field is above the level of the heart.

Awake craniotomy has become increasingly common for lesions involving eloquent cortical regions, allowing real-time neurological assessment. Despite its advantages, detection of VAE during awake craniotomy is particularly challenging due to limited monitoring modalities and the absence of invasive airway control[2,3]. Reports of VAE during awake craniotomy, especially in the supine position, are scarce, with only isolated cases described in the literature[2].

We describe a rare case of VAE occurring toward the end of tumor resection in a patient undergoing awake craniotomy in the supine position, likely precipitated by seizure-associated deep inspiratory efforts.

CASE PRESENTATION

Chief complaints

A 22-year-old male undergoing awake craniotomy in supine position for resection of a right fronto-temporal low-grade glioma. Intraoperatively, near the completion of tumor excision during awake craniotomy, the patient developed sudden dyspnea associated with persistent coughing, chest tightness, tachypnea, tachycardia, and a drop in oxygen saturation.

History of present illness

The patient was undergoing awake craniotomy in the supine position for resection of a right fronto-temporal glioma. Standard monitoring was in place, including electrocardiography, pulse oximetry, invasive arterial blood pressure monitoring, and capnography via nasal cannula. Supplemental oxygen was administered at 3 L/minute through nasal prongs. Sedation was provided using dexmedetomidine (loading dose of 1 μg/kg over 15 minutes followed by infusion at 0.5 μg/kg/hour) and fentanyl infusion at 1 μg/kg/hour. A scalp block was performed using 0.5% bupivacaine.

The patient’s head was fixed in a Mayfield clamp with approximately 10° of neck flexion, and the head end of the operating table was elevated by about 20°. Sedation was discontinued during tumor resection to allow continuous neurological assessment. Intraoperative fine motor function was assessed using a structured task involving playing a mini piano, allowing real-time evaluation of motor coordination and dexterity (Figure 1).

Figure 1 Intraoperative photograph during awake craniotomy demonstrating real-time fine motor assessment using a mini piano for continuous evaluation of motor function.

Toward the end of tumor excision, the patient complained of facial paresthesia and dyspnea, raising concern for non-convulsive seizure activity. The surgical field was irrigated with cold saline, and intravenous midazolam 1 mg was administered. Over the next 5-10 minutes, the patient developed persistent coughing, increasing respiratory discomfort, and chest tightness. Oxygen saturation decreased from 98%-100% to 89%, accompanied by tachypnea and tachycardia. End-tidal carbon dioxide values decreased, although interpretation was limited due to displacement of the sampling cannula during coughing episodes. On auscultation, the lung fields were clear; however, a new, continuous, mild precordial murmur was detected. Arterial blood gas analysis demonstrated hypoxemia with a PaO₂ of 68 mmHg compared to a baseline of 102 mmHg.

History of past illness

The patient had a six-month history of progressive left-sided upper and lower limb weakness accompanied by recurrent focal seizures. He was diagnosed with a right fronto-temporal lobe glioma and was receiving antiepileptic therapy with phenytoin, levetiracetam, and lacosamide. There was no history of cardiovascular, respiratory, or metabolic disease. He had no prior surgeries and no known drug allergies.

Personal and family history

The patient was a non-smoker and did not consume alcohol or illicit substances. There was no history of recent infection or trauma. Family history was non-contributory, with no known hereditary neurological, cardiovascular, or pulmonary disorders.

Physical examination

Preoperatively, the patient was conscious, oriented, and cooperative. Vital signs were stable. Neurological examination revealed mild left-sided hemiparesis (Medical Research Council grade 4/5) with no cranial nerve deficits. Cardiovascular and respiratory examinations were unremarkable, and airway assessment was normal.

Laboratory examinations

Preoperative laboratory investigations, including complete blood count, serum electrolytes, renal and liver function tests, coagulation profile, electrocardiographic (ECG), and chest radiography, were within normal limits.

Imaging examinations

Preoperative magnetic resonance imaging (MRI) brain revealed a well-defined, irregular intra-axial lesion measuring approximately 3.8 cm × 3.2 cm × 3.7 cm involving the right fronto-temporal cortical region (Figure 2A). The lesion was hypointense on T1-weighted images and hyperintense on T2-weighted and fluid-attenuated inversion recovery sequences, with no diffusion restriction, hemorrhage, calcification, or significant post-contrast enhancement. There was no surrounding edema or mass effect. Imaging features were suggestive of a low-grade cortical neoplasm, such as diffuse neuroepithelial tumor or low-grade glioma.

Figure 2 Magnetic resonance imaging. A: Preoperative axial T1-weighted magnetic resonance imaging (MRI) of the brain demonstrating a hypointense right frontotemporal cortical lesion; B: Functional MRI motor cortex mapping using blood oxygen level–dependent sequences demonstrates perilesional activation of the motor cortex and the supplementary motor area during bilateral finger tapping.

Functional MRI of the brain was subsequently performed for preoperative motor cortex mapping using blood-oxygen-level-dependent sequences. Motor paradigms included bilateral finger tapping and bilateral foot tapping. During right and left finger tapping, few activation stripes were observed predominantly in the periphery of the lesion, with some activation extending within the lesion. Supplementary motor area activation was noted bilaterally (Figure 2B). During bilateral foot tapping, few activation stripes were again noted in the perilesional region, with predominant activation involving the right supplementary motor area. These findings indicated close proximity of eloquent motor cortical areas to the lesion, emphasizing the need for awake craniotomy with continuous neurological monitoring.

FINAL DIAGNOSIS

Intraoperative VAE during awake craniotomy in the supine position, likely precipitated by seizure-associated deep inspiratory efforts.

TREATMENT

Immediate management included flooding of the surgical field with saline, positioning the patient in the Trendelenburg position, administration of 100% oxygen via a tightly sealed face mask, and application of 5 cm H₂O positive end-expiratory pressure. Supportive measures were continued, and no invasive airway intervention was required. The patient showed rapid clinical improvement with normalization of oxygen saturation and vital parameters, allowing completion of the surgical procedure without further complications.

OUTCOME AND FOLLOW-UP

Post-event transthoracic echocardiography demonstrated no evidence of cardiac dysfunction. Lung ultrasound revealed bilateral B-lines, consistent with pulmonary interstitial involvement secondary to VAE. The patient remained hemodynamically stable postoperatively, with no neurological deterioration or respiratory sequelae. He was monitored in the neurosurgical intensive care unit and discharged with no residual cardiopulmonary complications attributable to the intraoperative event.

DISCUSSION

VAE is a well-recognized complication of neurosurgical procedures, particularly when performed in the sitting position, where a favorable pressure gradient between the surgical field and the right atrium facilitates air entrainment[1]. Nevertheless, VAE can occur in any surgical position in which the operative site is elevated above the level of the heart, including the supine position, especially in the presence of additional predisposing factors. Reports of VAE during awake craniotomy remain rare. In awake patients, spontaneous deep inspiratory efforts can generate negative intrathoracic pressure that is transmitted to central and cerebral venous structures, thereby increasing the likelihood of air entrainment through exposed venous channels[3].

VAE can present with highly variable and nonspecific clinical signs, especially when advanced monitoring is limited during awake procedures. The clinical presentation may include sudden dyspnea, coughing, desaturation, chest discomfort, nausea, and hypotension, and a mill-wheel murmur may be appreciated on auscultation in some cases[2,4,5].

The diagnosis of VAE is based on clinical suspicion supported by physiological and imaging modalities. Capnography is widely available and a sudden decrease in end-tidal carbon dioxide (EtCO₂), particularly > 5 mmHg and when associated with hypotension or desaturation, is highly suggestive of clinically significant VAE; however, its sensitivity is limited for small or subclinical air entrainment. Precordial Doppler ultrasonography is the most sensitive non-invasive monitoring technique and can detect very small volumes of intracardiac air (approximately 0.05 mL/kg), often preceding changes in EtCO₂ or hemodynamics, though its specificity is operator dependent. Transesophageal echocardiography is considered the most sensitive diagnostic modality overall, capable of detecting air volumes as low as 0.02 mL/kg and identifying paradoxical air embolism in the presence of a patent foramen ovale[1,4,6].

Despite the availability of multiple monitoring modalities, no single technique offers uniformly high sensitivity and specificity across all clinical scenarios. In practice, a multimodal approach, integrating vigilant clinical observation with trends in end-tidal CO₂, and adjunctive use of precordial Doppler or transesophageal echocardiography when feasible, provides the highest diagnostic yield.

In the present case, seizure-associated dyspnea and deep inspiratory efforts likely led to transient reductions in cerebral venous pressure, promoting venous air entrainment. This risk may have been further exacerbated by head elevation relative to the heart. Recognition of VAE was relatively delayed due to clinical overlap between seizure-related symptoms and the nonspecific signs of air embolism, compounded by the limited sensitivity of conventional intraoperative monitoring techniques typically employed during awake craniotomy.

Pulmonary air embolism can produce a spectrum of physiological effects, including sympathetic activation, pulmonary vasoconstriction, ventilation-perfusion mismatch, and hypoxemia[7,8]. Beyond these immediate effects, endothelial activation and inflammatory responses may increase pulmonary capillary permeability, leading to interstitial pulmonary edema, as documented in previous reports[8-10]. Collectively, these mechanisms provide a plausible explanation for the hypoxemia and ultrasound findings observed in the present patient.

The clinical severity of VAE is primarily determined by both the volume and rate of air entrainment. While small volumes of air may remain clinically insignificant, rapid introduction of larger volumes can markedly reduce cardiac output, resulting in hemodynamic instability and characteristic ECG changes[3]. In the current case, the absence of hypotension and significant ECG abnormalities, despite tachycardia and hypoxemia, suggests limited volume or a slow rate of air entrainment, consistent with prior observations[1].

This case underscores the importance of maintaining high clinical vigilance for atypical presentations of VAE during awake neurosurgical procedures. Symptoms such as persistent coughing, unexplained dyspnea, chest discomfort, or sudden hypoxemia in an awake patient should prompt consideration of VAE, even when overt hemodynamic deterioration is not evident.

CONCLUSION

VAE can occur during awake craniotomy even in the supine position and may be precipitated by seizure-associated alterations in respiratory mechanics, including deep inspiratory efforts. Because clinical manifestations are often subtle and nonspecific in awake patients, diagnosis may be delayed. A high index of suspicion and prompt institution of supportive measures are essential to prevent progression and ensure favorable outcomes.