|Year : 2016 | Volume
| Issue : 1 | Page : 139-141
Venous oxygen embolism after inadvertent subcutaneous injection of hydrogen peroxide
Kundan S Gosavi, Surbhi D Mundada MD , Senthil K Praveen Kumar
Department of Anaesthesia and Critical Care, Sir J.J. Group of Hospitals, Mumbai, Maharashtra, India
|Date of Submission||19-Nov-2014|
|Date of Acceptance||26-Feb-2015|
|Date of Web Publication||17-Mar-2016|
Surbhi D Mundada
Department of Anaesthesia and Critical Care, 6th Floor, Main Hospital Building, Grant Medical College and Sir J.J. Group of Hospitals, Byculla, Mumbai 400008, Maharashtra
Source of Support: None, Conflict of Interest: None
The hazards of hydrogen peroxide have been known for long time, but it is still widely used in our country for irrigation of wounds. We report a case of oxygen embolism when hydrogen peroxide was accidently infiltrated subcutaneously along with local anesthetic during spine surgery and was successfully managed. We discuss the possible mechanism for embolism and its management. We also want to emphasize on the importance of being vigilant and avoiding such mistakes.
Keywords: embolism, hydrogen peroxide, spine surgery, subcutaneous infiltration
|How to cite this article:|
Gosavi KS, Mundada SD, Praveen Kumar SK. Venous oxygen embolism after inadvertent subcutaneous injection of hydrogen peroxide. Ain-Shams J Anaesthesiol 2016;9:139-41
|How to cite this URL:|
Gosavi KS, Mundada SD, Praveen Kumar SK. Venous oxygen embolism after inadvertent subcutaneous injection of hydrogen peroxide. Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2023 Oct 2];9:139-41. Available from: http://www.asja.eg.net/text.asp?2016/9/1/139/178895
| Introduction|| |
Hydrogen peroxide (H 2 O 2 ), a chemical found in almost every operation theater, is often used for irrigation of wounds and sterilization by virtue of its antimicrobial and vasoconstricting properties. H 2 O 2 is a toxic reactive oxygen species, which is capable of forming highly toxic hydroxyl radicals through the Fenton's reaction , . Various complications have been reported by the use of H 2 O 2 during irrigation of wounds during various surgical procedures, ranging from a transient drop in end-tidal carbon dioxide (EtCO 2 )  to stroke  and cardiac arrest. We are reporting a case of transient venous embolism due to accidental subcutaneous infiltration of H 2 O 2 during spine surgery, which was managed successfully.
| Case report|| |
A 42-year-old woman, weighing 56 kg, was admitted with complaint of back pain and mild weakness of lower limbs. She was diagnosed to have lumbar disc protrusion at L3-L4 level and was posted for discectomy with instrumentation. Patient's history did not reveal any significant comorbid condition. General and systemic examination and investigations were also within normal limits. After obtaining written, valid, informed consent the patient was taken in the operation theatre.
In the operation theater, monitoring was started by connecting ECG, pulse oxymeter, and noninvasive blood pressure (BP). She had a heart rate of 82/min and a BP of 126/72 mmHg. An intravenous line was secured, and she was premedicated with glycopyrrolate 0.2 mg, ondansetron 4 mg, midazolam 1 mg, and fentanyl 120 mcg intravenously. After preoxygenation, she was induced with propofol 120 mg and rocuronium 30 mg. The patient was intubated with 7.5 No. flexometallic endotracheal tube. EtCO 2 monitor was attached to confirm tracheal placement of endotracheal tube and was continued throughout the surgery. Anesthesia was maintained with N 2 O+O 2 and sevoflurane on circle absorber system. Air entry was bilaterally equal. An additional wide bore intravenous line and a central venous catheter was secured through antecubital vein using a Cavafix (Certo 358, 16 G diameter, 45 cm length; B Braun (Melsungen, Germany)). The patient was made to lie in prone position. Bilateral equal air entry and free abdominal movements were confirmed. All pressure points were padded properly. Assistant nurse was told to prepare the local anesthetic (LA) infiltration solution as follows: 10 ml of 2% lignocaine with adrenaline 1 : 100 000 diluted to 20 ml with normal saline. After marking and scrubbing the incision site surgeons infiltrated half of the incision site with 10 ml LA after negative aspiration. We focused our attention on the monitors. As the surgeon was loading the remaining 10 ml of LA, we noted a whitish blood-mixed froth from previous puncture sites. The assistant nurse was asked to check if she had provided the proper LA solution. While she was rechecking the bowls, there was a sharp fall in EtCO 2 from 32 to 20. The shape of capnogram was normal. SpO 2 was 95% and BP was 106/68 mmHg. We put off N 2 O immediately, keeping 100% O 2 , and checked breathing circuit for any fault. Peak inspiratory pressure was 20 cm of water. Even hand ventilation with reservoir bag revealed nothing. Lung auscultation was normal with equal air entry. This continued until 5 min; EtCo 2 then dropped to 15, retaining a normal shape. SpO 2 was still 95%. The nurse admitted that she might have diluted LA with H 2 O 2 instead of saline, which was kept in another bowl as per her trolley preparation protocol. We tried to auscultate the cardiac region for mill-wheel murmur but could not confirm it due to prone position. Suddenly, SpO 2 dropped from 90% EtCO 2 to 12. As heart rate, BP, and ECG were stable during this period, we did not turn the patient supine. We immediately started aspiration from central venous line. The operation theater table was tilted to left side to obtain right side up position. Intravenous fluid was pushed. Meanwhile, the surgeon made a deep incision on the marked site and gave a thorough saline wash. This released a lot of gas bubbles trapped beneath the skin and in muscles that were waiting to enter the circulation. Almost 70-80 ml frothy fluid was aspirated from the central line. EtCO 2 increased to 28 in few seconds and SpO 2 improved to 99%. The gas stopped appearing in syringe after this. Gradually, patient's EtCO 2 returned to 36 and SpO 2 was 100% and remained stable throughout thereafter. Surgeons were then allowed to proceed with the surgery. Rest of the surgery was uneventful. At the end of surgery, the patient was reversed and extubated on the table. She was monitored for 2 h in recovery, during which a transthoracic echocardiography was performed to see residual emboli in the heart or pulmonary vasculature, but there were none. Postoperative period was also normal and the patient was discharged after 8 days.
| Discussion|| |
H 2 O 2 was first produced by the French chemist Louis-Jaques Thenard in 1818 and has been used clinically since the 1850s. H 2 O 2 is broken down to oxygen and water by the glutathione/glutathione peroxidase system and the enzyme catalase. A total volume of 1 ml of 3% H 2 O 2 solution will produce 10 ml of oxygen  .
H 2 O 2 embolism has been reported in various procedures, which include cementing in orthopedic surgery  , enema  irrigation of wounds in general and gynecological surgeries, spine surgery  , and even neurosurgery , . Shock, coma, stroke, arrhythmias, cardiac arrest, and even death have been reported, which indicate seriousness of the complication. High heat of decomposition of H 2 O 2 probably favors tissue disruption, vasodilatation, and enables O 2 bubbles to penetrate the vasculature, especially in close cavities , . In prone position, the abdomen hangs freely, and the reduced hydrostatic pressure in the vena cava, as well as in the epidural veins, favors penetration of gas in vessels  . In our case subcutaneous tissue behaved similar to a closed space rich in vasculature favoring rapid entry of gas into circulation, and prone position also added to the effect. H 2 O 2 can produce gas bubbles in circulation, which then clogs the right atrium and pulmonary vasculature. If massive (5-8 ml/kg of air), it can cause stroke and cardiac ischemia in healthy patients, although even as little as 0.5 ml of air is reported to cause serious damage to the heart and brain secondary to coronary and cerebral oxygen embolism by paradoxical embolism through patent foramen ovale  . Its manifestation was transient in our case as we promptly aspirated the gas through a central venous catheter; surgical incision and wash caused rapid escape of trapped gas. Moreover, transfer of oxygen from H 2 O 2 to hemoglobin is known to be highly effective to remove the gas.
Doppler echocardiography is the most sensitive indicator of any gas embolism, but we do not routinely use it in neurosurgical cases. Hence, fall in EtCo 2 and SpO 2 remains good clinical indicators of venous air embolism (VAE). The mill-wheel heart murmur is considered to be a relatively late sign of VAE, with moderate volumes of gas in the right ventricle (>5 ml/kg/min).
Management of oxygen embolism is similar to VAE, which includes giving 100% oxygen, trendelenburg position, positive intrathoracic pressure, increasing central venous pressure, aspiration of gas through central line, and cardiopulmonary resuscitation if needed  . Nitrous needs to be put off in such cases as it can rapidly expand the gas bubbles, but whether to ventilate the patient with 100% oxygen is of questionable value, as this will diminish the concentration gradient across the alveoli in oxygen embolism cases. However, it is still recommended, as the cause of hypoxia is not clear initially and as O 2 may have other routes of elimination and metabolism , . There are reports stating successful use of hyperbaric oxygen in these cases , .
| Conclusion|| |
Despite knowing the hazards of H 2 O 2 , it is still being rampantly used in many institutions as antiseptic and hemostatic agent and thus is still present on our surgical trolley. Accidental mixing or confusion with LA, although a rare mistake, has happened in our operation theater. However, fortunately for us the patient recovered. We must take care that LA is aspirated and kept in syringe separately and not mixed with other syringes. Whenever possible the anesthetist should read and give the agent to the staff and not rely on the staff or operation theater helper for this purpose. We must also monitor the vitals vigilantly during infiltration and irrigation of wounds.
| Acknowledgements|| |
Conflicts of interest
| References|| |
Watt BE, Proudfoot AT, Vale JA. Hydrogen peroxide poisoning. Toxicol Rev 2004; 23:51-57.
Bienert GP, Schjoerring JK, Jahn TP. Membrane transport of hydrogen peroxide. Biochim Biophys Acta 2006; 1758:994-1003.
Sehgal RS, Sharma B, Sood J. Venous embolism with oxygen following wound irrigation. J Anaesthesiol Clin Pharmacol 2012; 29:547-548.
Mut M, Yemisci M, Gursoy-Ozdemir Y, Ture U. Hydrogen peroxide-induced stroke: elucidation of the mechanism in vivo
. J Neurosurg 2009; 110:94-100.
Neff SP, Zulueta L, Miller R. Hydrogen peroxide: an unusual cause of arterial and venous gas embolism. Anaesthesia 1996; 51:683-684.
Ackland DC, Yap V, Ackland ML, Williams JF, de Steiger R. Pulse-lavage brushing followed by hydrogen peroxide-gauze packing for bone-bed preparation in cemented total hip arthroplasty total hip arthroplasty; a bovine model. J Orthop Surg (Hong Kong) 2009; 17:296-300.
Volonte F, Gervaz P, Poletti PA, Morel P. Portal vein gas embolism following oxygen peroxide enema. Colorectal Dis 2010; 12:e335-e336.
Dubey PK, Singh AK. Venous oxygen embolism due to hydrogen peroxide irrigation during posterior fossa surgery. J Neurosurg Anesthesiol 2000; 12:54-56.
Miranda P, Cabrera A, Esparza J, Jerez A. An oxygen embolism after hydrogen peroxide scalp infiltration. Case illustration. J Neurosurg 2006; 104:152.
Lagneaux D, Lecomte J. Embolism induced by rat by hydrogen peroxide. Path Biol 1981; 29:279-283.
Haller G, Faltin-Traub E, Faltin D, Kern C. Oxygen embolism after hydrogen peroxide irrigation of a vulvar abscess. Br J Anaesth 2002; 88:597-599.
Chhabra R, Pathak A, Ray P. Fatal posterior fossa pneumocephalus due to hydrogen peroxide irrigation of lumbar wound. Br J Neurosurg 2000; 14:549-551.