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LETTER TO EDITOR |
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Venous air embolism during meningomyelocele repair surgery in prone position
Sunil Kumar Routaray1, Sudhansu Sekhar Nayak2, Ankur Khandelwal3
1 Department Of Anaesthesiology & Critical Care, Rajiv Gandhi Cancer Institute & Research Centre, Sector 5, Rohini New Delhi, India
2 Department Of Anaesthesiology, ABVIMS & RML Hospital, New Delhi, India
3 Department Of Anaesthesiology and Critical Care, Sharda University School of Medical Sciences and Research, Greater Noida, Uttar Pradesh, India
| Date of Submission | 07-Feb-2022 |
| Date of Acceptance | 22-Mar-2022 |
| Date of Web Publication | 15-Oct-2022 |
Correspondence Address:
Sudhansu Sekhar Nayak,
Department of Anaesthesiology, ABVIMS & RML Hospital, New Delhi
India
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/jpn.JPN_27_22
Sir,
Literature pertaining to the occurrence of venous air embolism (VAE) during pediatric meningomyelocele (MMC) repair surgery in prone position is limited. We managed a case of intraoperative occurrence of VAE in a child posted for cervical MMC repair surgery.
An 8 month, 14 kg male child presented with history of swelling at the back of the neck since birth which was progressively increasing in size. MRI of the brain and spine revealed hydrocephalus with cervical MMC extending from C5-7 level. The child was planned for right occipital ventriculoperitoneal (VP) shunt and MMC repair surgery. Induction of anesthesia was done with fentanyl (1 mcg/kg), propofol (2 mg/kg) and rocuronium (0.8 mg/kg). His airway was secured with a cuffed endotracheal tube (3 mm ID). Surgery was performed in the prone position. Anesthesia was maintained with a mixture of oxygen and air (FiO2=0.5), propofol (75 mcg/kg/min) and fentanyl (1 mcg/kg/hr). The child was monitored with the electrocardiogram (ECG), pulse oximetry (SpO2), invasive blood pressure, end tidal carbon dioxide concentration (EtCO2), temperature and evoked potential (EP) monitoring. Intraoperatively, after the surgical site hemostasis and during the closure of the duramater, there was a sudden and sustained decrease in EtCO2 from 37 to 19 mm Hg. SpO2 dropped to 69% from 98% associated with tachycardia (190 beats/min from 135 beats/min) and hypotension (65/40 mm Hg from 88/58 mm Hg). Clinically, VAE was suspected. An arterial blood gas analysis was done which showed PaCO2 (35 mm Hg) and EtCO2 (19 mm Hg) gradient of 16 mm Hg. Immediately, the surgeon was informed of the VAE episode. The surgical field was flooded with saline. Simultaneously, we ventilated the lungs with 100% oxygen. The head end of the table was transiently lowered by 30⁰. Hemodynamics were maintained with bolus of intravenous fluids (50 ml) and mephentermine (1 mg incremental dose). Gradually, EtCO2 started increasing and reached up to 32 mm Hg. Other vital parameters also normalised. Intraoperatively, blood loss was around 70ml. The remaining part of the surgery was completed uneventfully. The patient was electively ventilated postoperatively. Extubation of the trachea was done on the postoperative day (POD-1). Thereafter, the child remained hemodynamically stable and was discharged on POD-6 in stable condition.
The incidence of VAE ranges between 16% and 86% in neurosurgical cases.[1] Incidence is higher in surgeries performed in sitting or semi-sitting positions. However, it can also occur in lateral, prone and supine position surgeries.[1],[2] Incidence of VAE is lower in pediatric neurosurgical patients than adults due to higher dural sinus pressure (DSP).[3] VAE occurs when a bolus of air is forced into an open vein due to the atmospheric pressure exceeding venous pressure. Contributing factors are presence of direct communication between air and non-collapsible veins and a pressure gradient favouring the air entry. Many veins of the vertebral venous plexuses (VVP) are valveless, so the venous pressure depends solely on the position relative to the level of the heart. Considerable gravitational gradient can exist between the right side of the heart and the VVP and the site of surgery in the prone position.[4] Large quantities of air may enter the venous system with a gravitational gradient as small as 5.0 cm2.[5] Hypovolemia further exaggerates air entrainment through the open epidural veins. Acute loss of cerebrospinal fluid (CSF) can lower the DSP leading to risk of air entry through open venous sinuses. In our case, prone position created a negative pressure gradient and excision of cervical MMC resulted in the loss of CSF which might have lowered the DSP. Also, the insertion of VP shunt just prior to MMC excision caused additional decrease in CSF volume. Moreover, spontaneous respiration attempts can also increase the gravitational gradient and hence the risk of air entrainment. Our patient did not receive muscle relaxant during maintenance of anesthesia due to EP monitoring. All these factors could have contributed for air entry into epidural veins causing VAE. Nevertheless, VAE was detected promptly and managed properly without any serious complications. A high index of clinical suspicion and close monitoring of VAE is needed, in order to promptly diagnose this condition and initiate appropriate therapy.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
| 1. | Giraldo M, Lopera LM, Arango M. Venous air embolism in neurosurgery. Rev Colomb Anestesiol 2015;43:40-4.  |
| 2. | 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. [Full text] |
| 3. | Harrison EA, Mackersie A, McEwan A, Facer E. The sitting position for neurosurgery in children: A review of 16 years’ experience. Br J Anaesth 2002;88:12-7. |
| 4. | Elouardi Y, Zarrouki Y, Darouich H, Khallouki M. Fatal venous air embolism during lumbar spondylolisthesis surgery. Indian J Anaesth 2021;65:171-3. [Full text] |
| 5. | Wills J, Schwend RM, Paterson A, Albin MS. Intraoperative visible bubbling of air may be the first sign of venous air embolism during posterior surgery for scoliosis. Spine (Phila Pa 1976) 2005;30:E629-35. |
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