|Year : 2007 | Volume
| Issue : 6 | Page : 531-533
Severe venous air embolism in a paediatric patient undergoing neurosurgical procedure
Naresh Dua1, Jayashree Sood2
1 MD, Consultant, Department of Anaesthesiology, Pain & Perioperative Medicine, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi-110 060, India
2 MD, FFARCS, PGDHHM, Senior Consultant & Chairperson, Department of Anaesthesiology, Pain & Perioperative Medicine, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi-110 060, India
|Date of Acceptance||22-Sep-2007|
|Date of Web Publication||20-Mar-2010|
Department of Anaesthesiology, Pain & Perioperative Medicine, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi-110 060
Source of Support: None, Conflict of Interest: None
Venous air embolism (VAE) is a well-recognized complication and twice much common in children undergoing neurosurgical operations. A case of catastrophic presentation of venous air embolism during perioperative period is hereby reported. Early detection by adequate vigilant monitoring techniques and appropriate management of VAE as well as massive blood transfusion to replace the severe blood loss made the successful outcome.
Keywords: Venous air embolism (VAE); Neuroanaesthesia; Sitting position
|How to cite this article:|
Dua N, Sood J. Severe venous air embolism in a paediatric patient undergoing neurosurgical procedure. Indian J Anaesth 2007;51:531-3
|How to cite this URL:|
Dua N, Sood J. Severe venous air embolism in a paediatric patient undergoing neurosurgical procedure. Indian J Anaesth [serial online] 2007 [cited 2021 Mar 8];51:531-3. Available from: https://www.ijaweb.org/text.asp?2007/51/6/531/61194
| Introduction|| |
Though venous air embolism (VAE) can occur in any position, it is a frequent occurrence in sitting position 25-40%  , in which operating site is above the level of heart.Although veins collapse in most situations preventing the further air aspiration but in tumor affected area veins are of large diameter and tortutous because of increased vascularity and may not collapse. Venous sinuses are non collapsible because of their dural attachments, walls of the diploic veins are fixed and thus the incidence of VAE is particularly high (45-50%) , . Despitethe availability ofsensitivemodes of monitoringsuch as precordial Doppler and end-expiratory CO 2 tension, VAE remains a serious complication and it is twice much common in children than adults ,,, .
| Case report|| |
A2-year-old male child weighing 11 kg was admitted to the hospital with progressive large swelling over right parietal and temporal region for one year. The size of the swelling was 5cm X 5cm X 6cm. Patient was diagnosed as right parietal tumour and was posted for craniotomy and tumour excision.
On preoperative examination, all the investigations were normal and had no significant past history of any illness or delayed milestones. The airway assessment was not pointing towards difficult intubation because of prominence of right parietal eminences. No premedication was given. The patient was pre-oxygenated for five minutes and anaesthesia was induced with 50% nitrous oxide and halothane 1-2% (inspired concentrations) in 50% oxygen and fentanyl 20 mcg intravenously. The muscular relaxation was facilitated with rocuronium 8 mg. The patient's trachea was intubated with a 5.0 mm internal diameter uncuffed tracheal tube. Anaesthesia was maintained with oxygen, nitrous oxide (50%:50%) and 1-2% inspired concentration of isoflurane, fentanyl and vecuronium bromide. Anaesthesia monitoring included ECG, ABP, SpO 2 , EtCO 2 , FiO 2 conc., respiratory rate, airway pressure, CVP, rectal temperature and urine output. Surgery was commenced under head-up (15°) position. The surgical incision was given. The skin and galea over the tumor was dissected. During dissection, sudden decrease in end tidal CO 2 was noted from 31 mm Hg to 15 mm Hg. In the mean time, the systolic arterial blood pressure also dropped from 90/40 mm Hg to 45/31 mm Hg and SpO 2 decreased from 100% to 81%. Immediately nitrous oxide was discontinued. Surgeons were duly informed. Flooding the surgical field with warm saline and sealing the sites of egress with bone wax, head down position were done to prevent further atmospheric air entrainment. To stabilize the vital parameters, fluids were rapidly transfused. Aspiration of air was tried through femoral vein catheter already placed but it was not successful. Despite all these efforts, patient was hypotensive to the extent of nonpalpable peripheral pulses and inconclusive arterial monitoring. Vasopressors (mephentermine and adrenaline 1in10,000;0.01mg.kg -1 ) were given in incremental doses repeatedly. Then, after 15 minutes, arterial blood pressure achieved to the extent of 60/40 mmHg. In the mean time, PaCO 2 increased gradually from 15 to 20 then finally 27 mmHg. Arterial blood gases measurement (ABG) was done and interpretation was metabolic acidosis along with dyselectrolytaemia (pH-7.21, PO 2 - 70mmHg, PCO 2 - 45mmHg, BE- - 8, HCO 3 - 16Meq/L, Ca - 0.71Meq/L, lactate 2.71mmoL/L). Metabolic and electrolyte correction was done according toABG. During that period, blood loss was in significant amount and transfusion started immediately with compatible blood to replace it. With the stabilization of vital parameters, the surgery was allowed to proceed. No murmur was found on chest auscultation. The vitals were HR-120/ min, ABP-92/60 mm of Hg, PCO 2 -30 mm of Hg, CVP7 cm of water. Near the completion of surgery, patient had haematuria. The blood transfusion was discontinued and sent for re-crossmatching. Frusemide 2mg intravenously was given to facilitate glomerular filtration. The patient was not reversed and shifted to the neurointensive care unit on ventilatory support. At the time of shifting, the vitals were as follows- HR-107/ min, B.P.-109/44 mm Hg, chest- bilateral clear, CVSS 1 S 2 normal and was kept on IPPV mode of ventilation with PEEP- 4cm of water. Total duration of surgery was 6 hrs and the blood loss during the surgery was 1.6 L approximately for which patient received 4 units (350ml) of fresh blood and 4 units of fresh frozen plasma. The administered fluids during the perioperative period were Isolyte-P 1 litre, NS/2 500ml. During the perioperative period, total urine output was 120 ml although it was almost nil for 1½ hrs during the event.
In I.C.U., hematuria continued for 14 hrs, and then it gradually declined. After meeting the extubation criteria, the patient was extubated next morning. The post extubation period and postoperative stay of patient in hospital was uneventful. Patient was discharged on 11 th postoperative day of surgery. The re-crossmatching report was found compatible with transfusion. On biopsy of tumour, histologically it was found neurofibroma.
| Discussion|| |
Venous air embolism (VAE) , is a well-recognized complication in neurosurgical, cardiovascular, obstetrics, orthopaedic and transplantation surgery. It is twice much common in children than adults ,,, . The incidence is as high as 45-50% in posterior fossa surgery , . While a large share of VAE occurs at the commencement of surgery (78.7%), still 18% of embolic phenomena are reported at the end of surgery, probably associated with reopening of injured vein when retractors are removed  . For the prevention of VAE various methods have been described such as use of MAST suits, application of PEEP  , inflatable cervical torniquet and positive pressure at the end of procedure  but none seems to be a full proof method  .
For venous air embolism to occur, there must be a communication between the vascular lumen and the source of gas as well as a pressure gradient favoring ingress of the gas into the vessel. In this case, the veins were too much dilated and tortuous over the tumour; so, during the operative procedure after dissecting the skin and galea, the veins were held open to the atmosphere allowing copious air entry to cause VAE. Early detection by vigilant monitoring and appropriate management made the outcome favourable. The immediate intervention in the form of putting off N 2 O, maintenance of PEEP, change of posture, flooding the surgical field and replacing the acute losses were done to stabilize the haemodynamic parameters.
In this case, massive blood transfusion was done to replace severe blood loss. While hypothermia  , hypocalcemia  due to citrate overload in stored blood, coagulation abnormalities  and acid base disturbances are known complications of massive blood transfusion. Keeping all these abnormalities in mind,ABGs were done at regular intervals and acid base and electrolyte correction were done accordingly well in time. In this case, hematuria was present for few hours but gradually diminished itself.
In conclusion, VAE is much common in children as compared to adults who are more haemodynamically compromised. So, immediate detection and vigorous management with all the measures are required for successful outcome.
| References|| |
|1.||Orebaugh SL. Venous air embolism; clinical and experimental considerations. Crit Care Med 1992; 20: 1169-77. |
|2.||Black S, Ockert DB, Oliver WC. Cucchiara RF. Outcome following posterior fossa craniectomy in the sitting position Vs horizontal position. Anesthesiology 1988; 69: 49-56. |
|3.||Young ML, Smith DS, Murtagh F, et al. Comparison of surgical & anesthetic complications in neurosurgical patients experiencing venous air embolism in the sitting position. Neurosurgery 1986; 18: 157-61. |
|4.||Cucchiara RF, Bowers B. Air embolism in children undergoing suboccipital craniotomy. Anesthesiology 1982; 57: 338-9. |
|5.||Meyer PG, Cuttaree H, Charron B, Jarreau MM, Perie AC, Sainte, Rose C. Prevention of venous air embolism in paediatric neurosurgical procedures performed in the sitting position by combined use of MAST suit and PEEP. Br J Anaesth. 1994; 73: 795-800. |
|6.||LubninAlu, Oskanova Mlu. Prevention of air embolism in neurosurgical patients operated on in a sitting posture: a comparative study of 3 methods. Anesteziol Reanimatol 1994;5:22-6. |
|7.||Sharma A, Uppal R. Catastrophic presentation of venous air embolism - a case report. Indian J Anaesth 2002;46:403-4. |
|8.||Stehling L. Fluid replacement in massive transfusion. Massive Transfusion AABB1994; 1. |
|9.||Dzik WH, Kirkley SA. Citrate toxicity during massive transfusion. Transfus Med Rev 1988; 2:76. |
|10.||Lundsgaard-Hansen P. Treatment of acute blood loss. Vox Sang 1992; 63:241 |