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Year : 2018  |  Volume : 62  |  Issue : 12  |  Page : 1002-1003  

Venous air embolism following application of Mayfield head clamp: A word of caution

1 Department of Neuroanaesthesiology and Critical Care, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India
2 Department of Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication10-Dec-2018

Correspondence Address:
Dr. Ankur Khandelwal
Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ija.IJA_477_18

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How to cite this article:
Khandelwal A, Gupta S, Prabhakar H, Burman S. Venous air embolism following application of Mayfield head clamp: A word of caution. Indian J Anaesth 2018;62:1002-3

How to cite this URL:
Khandelwal A, Gupta S, Prabhakar H, Burman S. Venous air embolism following application of Mayfield head clamp: A word of caution. Indian J Anaesth [serial online] 2018 [cited 2021 Jan 24];62:1002-3. Available from: https://www.ijaweb.org/text.asp?2018/62/12/1002/247122


The Mayfield head clamp is widely used for firmly stabilising the head during neurosurgical procedures. A number of complications associated with the use of Mayfield head clamp such as systemic and intracranial hypertension, dural laceration, skull fracture, epidural haematoma, frontal sinus fracture and cerebrospinal fluid leak, middle meningeal arteriovenous fistula (AVF) and venous air embolism (VAE) after removal of pins have been reported.[1],[2],[3],[4],[5] However, VAE has never been reported during or after application of pin headrest. We wish to report a case of a 65-year-old male (50 kg) with left petrous dural AVF and consequent brainstem oedema scheduled for AVF ligation surgery. Preoperatively, the patient had Glasgow Coma Scale of E4VtM6 (electively intubated due to obtunded airway reflexes) and stable haemodynamics [blood pressure (BP) - 136/75 mmHg, heart rate (HR) - 80/min, SpO2- 100% at FiO2- 0.5, sinus rhythm in electrocardiogram (ECG)]. Right subclavian central venous catheter (CVC, 7F, triple lumen) was present in situ. CVC was inserted in intensive care unit before the arrival of the patient in the operation theatre. Induction of anaesthesia was achieved with intravenous (iv) fentanyl 100 μg and propofol 100 mg. A loading dose of iv rocuronium 50 mg was used for neuromuscular blockade. Maintenance of anaesthesia was done with oxygen (O2) and nitrous oxide (N2O) in 1:1 ratio, sevoflurane (0.8 - 1 minimum alveolar concentration), fentanyl (1 μg/kg/h), and rocuronium (12 mg/h). At 10 min following induction, we recorded the following parameters: BP - 132/88 mmHg, HR - 92/min, EtCO2 - 29 mmHg, PaCO2- 34 mmHg, PaCO2–ETCO2 gradient 5 mmHg, SpO2- 100% at FiO2- 0.5 and sinus rhythm in ECG. For fixation of head, Mayfield three-pin head clamp was applied. However, its application impeded the lungs surgical operating area, and thus it was removed and placed again to create optimal area for surgery. After 4 mins, we noted a sudden decrease in EtCO2 (25 mmHg) associated with hypotension (73/48 mmHg) without major change in HR (95 beats/min) or SpO2 (99%). In the next 5 mins, EtCO2 dropped to 22 mmHg associated with severe hypotension (47/33 mmHg), atrial ectopic beats in ECG (HR 86–92 beats/min), PaCO2- 34 mmHg, SpO2- 98% at FiO2- 0.5 and PaCO2–EtCO2 gradient of 12 mmHg. We immediately informed the surgeon of a possible episode of VAE. At the same time, we discontinued N2O and ventilated the lungs with 100% O2, lowered the head end of the patient, administered intravenous fluids and titrated doses of mephentermine to stabilise BP. Meanwhile, we also aspirated around 25 mL of air from the distal port of CVC. Gradually, the vitals became stable over a period of 15 mins (BP - 108/64 mmHg, HR - 98/min, sinus rhythm, SpO2- 100% at FiO2- 0.5, EtCO2- 30 mmHg, PaCO2- 36 mmHg and PaCO2 - EtCO2 gradient 6 mmHg). Surgical sutures were applied at one of the initial pin sites which showed oozing of blood despite compression. Firm compression and dressing was applied on the other two sites. The surgery commenced thereafter. Except N2O, we continued the same maintenance anaesthetic regimen for the rest of the surgery. No further episodes of VAE were present either during surgery or after removal of pins after surgery. The trend of vital parameters is mentioned in [Table 1].
Table 1: Trend of vital parameters during the period of venous air embolism

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The above presentation could be a manifestation of systemic hypotension due to anaesthetic induction. However, the vital parameters at 10 min after induction were completely stable. Moreover, there was no pre-existing arrhythmia. Other probable causes include trigeminocardiac reflex (TCR) and exaggerated pre-existing brainstem oedema. However, the timing of pin application and consequent decrease in EtCO2 along with hypotension show a definite association with VAE. Moreover, aspiration of air from the CVC is highly suggestive of the diagnosis of VAE. Notably, HR did not change significantly from baseline and excludes TCR as a probable cause. The most probable reason for air entrainment and consequent VAE could have been pin-induced injury to the diploic veins at the initial pin sites. These veins drain the diploic space found in the vault of the skull and communicate to the cerebral sinuses by emissary veins. In our case, the head end of the patient was immediately elevated (around 30°) after initial pin application as a measure to reduce intracranial pressure. This could have created sub-atmospheric pressure aggravating the process of air entrainment from the initial pin sites. Again, the presence of N2O probably led to volume augmentation causing haemodynamic perturbations.

Thus, VAE should be considered as a differential diagnosis of haemodynamic perturbations during or after pin application.

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There are no conflicts of interest.

   References Top

Uyar AS, Yagmurdur H, Fidan Y, Topkaya C, Basar H. Dexmedetomidine attenuates the hemodynamic and neuroendocrinal responses to skull-pin head-holder application during craniotomy. J Neurosurg Anesthesiol. 2008; 20:174-9.  Back to cited text no. 1
Sade B, Mohr G. Depressed skull fracture and epidural haematoma: An unusual post-operative complication of pin headrest in an adult. Acta Neurochir (Wien). 2005; 147:101-3.  Back to cited text no. 2
Moumoulidis I, Fernandes H. CSF rhinorrhea secondary to use of a mayfield head clamp. Ear Nose Throat J. 2008; 87:E1-3.  Back to cited text no. 3
Inagawa T, Takeda T, Taguchi H, Kamiya K, Yamada T. Traumatic middle meningeal arteriovenous fistula caused by three-point skull fixation. Case report. J Neurosurg. 1984; 60:853-5.  Back to cited text no. 4
Prabhakar H, Ali Z, Bhagat H. Venous air embolism arising after removal of Mayfield skull clamp. J Neurosurg Anesthesio.l 2008; 20:158-9.  Back to cited text no. 5


  [Table 1]


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