- Email: [email protected]
Tension pneumocephalus and oxygen emboli from hydrogen peroxide irrigation
Case Reports / Journal of Clinical Neuroscience 21 (2014) 323–325
References 1. Aaronson DW, Rovner RN, Patterson R. Cough syncope: case presentation and review. J Allergy 1970;46:359–63. 2. O’Doherty DS. Tussive syncope and its relation to epilepsy. Neurology 1953;3:16–21. 3. Williams B. Cough headache due to craniospinal pressure dissociation. Arch Neurol 1980;37:226–30. 4. Williams B. Chronic herniation of the hindbrain. Ann R Coll Surg Engl 1981;63:9–17. 5. Prilipko O, Dehdashti AR, Zaim S, et al. Orthostatic intolerance and syncope associated with Chiari type I malformation. J Neurol Neurosurg Psychiatry 2005;76:1034–6. 6. Milhorat TH, Chou MW, Trinidad EM, et al. Chiari I malformation redefined: clinical and radiographic findings for 364 symptomatic patients. Neurosurgery 1999;44:1005–17. 7. Weig SG, Buckthal PE, Choi SK, et al. Recurrent syncope as the presenting symptom of Arnold-Chiari malformation. Neurology 1991;41:1673–4. 8. Guillon B, Robertson D. Chiari I malformation as a cause of orthostatic intolerance symptoms: a media myth? Am J Med 2001;111:546–52. 9. Nogués MA, Newman PK, Male VJ, et al. Cardiovascular reflexes in syringomyelia. Brain 1982;105:835–49. 10. List CF. Neurologic syndromes accompanying developmental anomalies of the occipital bone, atlas, and axis. Arch Neurol Psychiatry 1941;45:577–616. 11. Speer MC, Enterline DS, Mehltretter L, et al. Chiari type I malformation with or without syringomyelia: prevalence and genetics. J Genet Couns 2003;12:297–311. 12. Von Torklus D, Gehle W. The upper cervical spine. London: Butterworths; 1972. p. 21–53. 13. Wackenheim A. Roentogen diagnosis of the craniovertebral region. Berlin: Springer-Verlag; 1974. p. 353–79. 14. Caetano de Barros M, Farias W, Ataide L, et al. Basilar impression and ArnoldChiari malformation. A study of 66 cases. J Neurol Neurosurg Psychiatry 1968;31:596–605. 15. Menezes AH, Ryken TC. Abnormalities of the craniovertebral junction. In: Cheek AE, Marlin AE, MacLone DG, Reigel DH, Walker ML, editors. Pediatric neurosurgery. 3rd ed. Philadelphia: Saunders; 1994. p. 139–58. 16. Moore KL, Persaud TVN. The developing human: clinically oriented embryology. 6th ed. Philadelphia: WB Saunders; 1998. p. 405–26. 17. Di Lorenzo N, Fortuna A, Guidetti B. Craniovertebral junction malformations. Clinicoradiological findings, long-term results, and surgical indications in 63 cases. J Neurosurg 1982;57:603–8. 18. Mesiwala AH, Shaffrey CI, Gruss JS, et al. Atypical hemifacial microsomia associated with Chiari I malformation and syrinx: further evidence indicating that Chiari I malformation is a disorder of paraxial mesoderm. J Neurosurg 2001;95:1034–9.
323
19. Shapiro R, Robinson F. Anomalies of the craniovertebral border. Am J Roentgenol 1976;127:281–7. 20. MacRea DL, Barnum AS. Occipiltalization of the atlas. AJR Am J Roentgenol 1953;70:23–46. 21. Menezes AH, VanGilder JC. Anomalies of the craniovertebral junction. In: Youmans J, editor. Neurological surgery. 3rd ed. Philadelphia: Saunders; 1990. p. 1359–420. 22. Nishikawa M, Sakamoto H, Hakuba A, et al. Pathogenesis of Chiari malformation: a morphometric study of the posterior cranial fossa. J Neurosurg 1997;86:40–7. 23. Vega A, Quintana F, Berciano J. Basiochondrocranium anomalies in adult Chiari type I malformation: a morphometric study. J Neurol Sci 1990;99:137–45. 24. Berge JK, Bergman RA. Variations in size and in symmetry of foramina of the human skull. Clin Anat 2001;14:406–13. 25. Coin CG, Malkasian DR. Foramen magnum. In: Newton TH, Potts DG, editors. Radiology of the skull and brain: the skull. St. Louis: Mosby; 1971. p. 275–347. 26. Lang J. Clinical anatomy of the posterior cranial fossa and its foramina. New York: Thieme; 1991. p. 1–112. 27. Muthukumar N, Swaminathan R, Venkatesh G, et al. A morphometric analysis of the foramen magnum region as it relates to the transcondylar approach. Acta Neurochir (Wien) 2005;147:889–95. 28. Kagawa M, Jinnai T, Matsumoto Y, et al. Chiari I malformation accompanied by assimilation of the atlas, Klippel-Feil syndrome, and syringomyelia: case report. Surg Neurol 2006;65:497–502. 29. Botelho RV, Bittencourt LR, Rotta JM, et al. Prospective controlled study of sleep respiratory events in patients with craniovertebral junction malformation. J Neurosurg 2003;99:1004–9. 30. Dauvilliers Y, Stal V, Abril B, et al. Chiari malformation and sleep related breathing disorders. J Neurol Neurosurg Psychiatry 2007;78:1344–8. 31. Garland EM, Robertson D. Chiari I malformation as a cause of orthostatic intolerance symptoms: a media myth? Am J Med 2001;111:546–52. 32. Ireland PD, Mickelsen D, Rodenhouse TG, et al. Evaluation of the autonomic cardiovascular response in Arnold-Chiari deformities and cough syncope syndrome. Arch Neurol 1996;53:526–31. 33. Botelho RV, Bittencourt LR, Rotta JM, et al. Adult Chiari malformation and sleep apnea. Neurosurg Rev 2005;28:169–76. 34. Zolty P, Sanders MH, Pollack IF. Chiari malformation and sleep-disordered breathing: a review of diagnostic and management issues. Sleep 2000;23:637–43. 35. Flemons WW, Tsai W. Quality of life consequences of sleep-disordered breathing. J Allergy Clin Immunol 1997;99:S750–6. 36. Botelho RV, Bittencourt LR, Rotta JM, et al. The effects of posterior fossa decompressive surgery in adult patients with Chiari malformation and sleep apnea. J Neurosurg 2010;112:800–7.
doi:http://dx.doi.org/10.1016/j.jocn.2012.10.044
Tension pneumocephalus and oxygen emboli from hydrogen peroxide irrigation Christopher Huang a,⇑, Justin Pik b a b
Neurosurgery Department, Canberra Hospital, Yamba Drive, 3/7 Eldridge Crescent, Garran, ACT 2605, Australia Australian Capital Territory Neurospine Clinic, Deakin, ACT, Australia
a r t i c l e
i n f o
Article history: Received 29 August 2012 Accepted 31 October 2012
Keywords: Hydrogen peroxide Oxygen embolus Oxygen emboli Peroxynitrite Tension pneumocephalus
⇑ Corresponding author. Tel.: +61 2 6244 4080. E-mail address: [email protected] (C. Huang).
a b s t r a c t Hydrogen peroxide irrigation is commonly utilised in neurosurgical and non-neurosurgical procedures for its bacteriocidal and haemostatic effects, however it has been associated with devastating complications such as tension pneumocephalus, O2 embolism and even dysrhythmias. We report a patient who suffered hydrogen peroxide-related mortality due to widespread tension pneumocephalus and O2 emboli. Ó 2013 Elsevier Ltd. All rights reserved.
324
Case Reports / Journal of Clinical Neuroscience 21 (2014) 323–325
1. Introduction Hydrogen peroxide (H2O2) has been historically used mainly as a haemostatic agent after intracranial parenchyma resection.1 Its exact mechanism of haemostasis is unknown, but has been postulated to arise from a combination of its vasoconstrictive and vasoocclusive effects on blood vessels.2 In vitro studies have observed the tumouricidal properties of H2O2 on giant cell tumours and breast cancers,3 and recently on primary and metastatic brain tumours in humans and rats4 although its function as a tumouricidal agent is not widely accepted or utilised by neurosurgeons. Throughout the literature, there have been reports of various complications associated with the use of H2O2 irrigation. Haller et al.5 reported air embolism after H2O2 was used to irrigate a vulvular abscess and Morikawa et al.6 reported a similar incident when H2O2 irrigation was used in cervical spine surgery. Other cases have resulted in mortality7–9 and cardiac dysrhythmias from stimulation of the trigeminocardiac reflex.10
Fig. 2. Immediate postoperative axial CT scan showing widespread tension pneumocephalus in the surgical cavity, throughout the subarachnoid space, cisterns and Sylvian fissure bilaterally.
2. Case report A 65-year-old man presented with 5 weeks of increasing confusion, headaches, and nominal dysphasia. Subsequent CT scans and MRI of the brain observed a 2.6 cm left temporal lobe ringenhancing lesion with significant vasogenic oedema consistent with a high grade glioma (Fig. 1). The patient underwent preoperative assessment and was taken to theatre 6 days later. Mayfield fixation and intraoperative navigation (Medtronic StealthStation, Medtronic, Minneapolis, MN, USA) were used. A question mark incision was made over the left temporal region and a left temporal craniotomy was performed via free bone flap and the dura opening. The tumour was seen to be present through the temporal lobe cortex and slightly adherent to the dura. The left Sylvian fissure was widely split to expose the internal carotid artery and the optic nerve. A frozen section was obtained which revealed a highly malignant neoplasm. A formal temporal lobectomy was then performed. The procedure was performed without any intraoperative complication. The left third nerve, internal carotid artery and optic nerve were preserved. Diluted 3% H2O2 was used to secure intradural haemostasis and the wound was closed in layers with the bone replaced. The patient failed to wake postoperatively and developed bradycardia and hypertension as well as a dilated left pupil within an hour of the end of surgery. An urgent CT scan of the brain was performed showing changes suggestive of widespread tension pneumocephalus (Fig. 2). Air was observed in the subarachnoid space, the cisterns, both Sylvian fissures and over the left frontal lobe as well as in the surgical cavity. The patient was immediately taken back to the operating theatre and had the wound reopened. The surgical site was thoroughly
Fig. 3. Axial CT scan of the brain after the decompression showing resolution of the tension pneumocephalus.
irrigated and the wound closed again. Following the second operation, the patient developed a dilated right pupil in addition to the previously observed dilated left pupil. A subsequent CT scan 5 hours after the second operation (Fig. 3) showed resolution of the tension pneumocephalus, however the patient did not improve neurologically in the following 48 hours and mechanical ventilation was withdrawn. On post mortem examination there were widespread recent small infarcts of the cortical mantle, central grey and white matter,
Fig. 1. Preoperative MRI showing left temporal high grade glioma (left: axial, middle: coronal, right: sagittal).
Case Reports / Journal of Clinical Neuroscience 21 (2014) 323–325
cerebellum, midbrain, pons and medulla. Patchy damage of intrinsic intraneural small vessels with scattered microhaemorrhages was seen in the infarcted areas, and active axonal degeneration of some cranial nerves with patchy acute inflammatory cell infiltration and microhaemorrhages. No thrombotic or embolic occlusion of vessels was present. The formal coroner’s report stated that this was, ‘‘consistent with widespread failure of perfusion in the small vessel perforators of the anterior and middle cerebral arteries and the vertebrobasilar arterial system with the brunt being borne in the perforator territory of the basilar artery. The features are consistent with a widespread failure of perfusion. This could possibly have been due to an episode of vasoconstriction or occlusion by microvessels by evanescent O2 emboli as has been described by H2O2 irrigation. The possibility that a combination of tension pneumocephaly and the putative H2O2 irrigation may have had a summative effect producing the severe changes seen in this case should also be considered.’’
3. Discussion H2O2 is a toxic reactive oxygen species and is normally kept at physiological levels in the body by catalase and the glutathione and glutathione peroxidise system. It permeates across the cell wall relatively well11 and also increases the permeability of endothelium. It is broken into H2O and O2 after exposure to catalase enzymes which are found in all cells, and up to 10 mL of O2 has been observed to be liberated from 1 mL of 3% H2O2.12,13 Further studies have also exhibited that excess H2O2 reacts with nitrous oxide to produce superoxide via multiple reactions, which in turn results in peroxynitite formation via other combination reactions with nitrous oxide.14 Peroxynitrite is a potent oxidant and increasing numbers of studies are beginning to witness the association between the production of this molecule and mitochondrial respiratory dysfunction after traumatic brain injury.15 Mut et al.13 showed that exposure to 15 mL of 3% H2O2 for 15 seconds resulted in formation of bubbles in the lumen of subpial arteries regardless of whether the pia layer was intact or not. They also discovered that there was clear peroxynitrite production around and in the vessels buried within the neuropil well below the intact pial layer, indicating that H2O2 diffuses passively and freely through the pia and the blood vessel wall. In the Mesiwala et al.4 study they reported brain parenchymal stromal vaculisation and degeneration of neurons, astrocytes and migrolia up to 1 mm beyond the tumour resection cavity in human brains, after treatment for 5 minutes with 3% H2O2 soaked cotton balls. In this patient, tension pneumocephalus throughout the brain was observed following irrigation of the tumour resection cavity with H2O2, most likely as a result of oxygen escape into the subdoi:http://dx.doi.org/10.1016/j.jocn.2012.10.044
325
arachnoid space. Although no obvious air was found to escape upon reopening the wound, the air could well have dissipated once the skin was open and during the craniotomy. The subsequent infarction may also have been the result of contributory insult from peroxynitrite formation secondary to the H2O2. To our knowledge, no patients with tension pneumocephalus throughout the cisterns have been previously reported secondary to H2O2 application. Three patients with tension pneumocephalus have been reported in the literature, two resulting from craniotomies16,17 and one of tension pneumocephalus in the posterior fossa from irrigation of an infected lumbar wound.18 This patient emphasises the potential of H2O2 to cause widespread neuronal damage distant from the site of application. Although H2O2 continues to be used for its haemostatic and bacteriocidal properties, consideration should be given to use of alternative haemostatic agents.
References 1. Epstein JA. Hydrogen peroxide for haemostasis. Neurosurgery 1987;20:63. 2. Szabo C, Ischiropoulos H, Radi R. Peroxynitrite: biochemistry, pathophysiology and development of therapeutics. Nat Rev Drug Discov 2007;6:662–80. 3. Nicholson NC, Ramp WK, Kneisl JS, et al. Hydrogen peroxide inhibits giant cell tumour metabolism in vitro. Clin Orthop Relat Res 1998;347:250–60. 4. Mesiwala AH, Farrell L, Santiago P, et al. The effects of hydrogen peroxide on brain and brain tumours. Surg Neurol 2003;59:398–407. 5. Haller G, Faltin-Traub E, Faltin D, et al. Oxygen embolism after hydrogen peroxide irrigation of a vulvular abscess. Br J Anaesth 2002;88:597–9. 6. Morikawa H, Mima H, Fujita J, et al. Oxygen embolism due to hydrogen peroxide irrigation during cervical spinal surgery. Can J Anaesth 1995;42:231–3. 7. Dubey PK, Singh AK. Venous oxygen embolism due to hydrogen peroxide ierrigation during posterior fossa surgery. J Neurosurg Anaesthesiol 2000;12:54–6. 8. Lopez LM, Traves N, Napal M. Fatal gas embolism during corrective scoliosis surgery using the posterior approach. Rev Esp Anestesiol Reanim 1999;46:267–70. 9. Lubnin AI, Sorokin VS. Gas embolism caused by erroneous intraventricular administration of hydrogen peroxide solution. Anaesteziol Reanimatol 1998;6:76–7. 10. Spiriev T, Prabhakar H, Sandu N, et al. Use of hydrogen peroxide in neurosurgery: case series of cardiovascular complications. JRSM Short Rep 2012;3:6. 11. Bienert GP, Schjoerring JK, Jahn TP. Membrane transport of hydrogen peroxide. Biochem Biophys Acta 2006;1758:994–1003. 12. Fuson RL, Kylstra JA, Hochstein P, et al. Intravenous hydrogen peroxide infusion as a means of extrapulmonary oxygenation. Clin Res 1967;15:74. 13. Mut M, Yemisci M, Gursoy-Ozdemire Y, et al. Hydrogen peroxide-induced stroke: elucidation of the mechanism in vivo. J Neurosurg 2009;110:94–100. 14. Koppenol WH, Moreno JJ, Pryor WA, et al. Peroxynitrite, a cloaked oxidant formed by nitric oxide and superoxide. Chem Res Toxicol 1992;5:834–42. 15. Singh IN, Sullivan PG, Hall ED. Peroxynitrite-mediated oxidative damage to brain mitcohondria: protective effects of peroxynitrite scavengers. J Neurosci Res 2007;85:2216–23. 16. Dolan EJ. Danger of use of hydrogen peroxide in stereotactic biopsies. Appl Neurophysiol 1987;50:237–8. 17. Zimmerman GA, Lipow KI. Pneumocephalus with neurological deficit from hydrogen peroxide irrigation. J Neurosurg 2004;100:1122. 18. Chhabra R, Pathak A, Ray P. Fatal posterior fossa pneumocephalus due to hydrogen peroxide irrigation of lumbar wound. Br J Neurosurg 2000;14:549–51.
References 1. Aaronson DW, Rovner RN, Patterson R. Cough syncope: case presentation and review. J Allergy 1970;46:359–63. 2. O’Doherty DS. Tussive syncope and its relation to epilepsy. Neurology 1953;3:16–21. 3. Williams B. Cough headache due to craniospinal pressure dissociation. Arch Neurol 1980;37:226–30. 4. Williams B. Chronic herniation of the hindbrain. Ann R Coll Surg Engl 1981;63:9–17. 5. Prilipko O, Dehdashti AR, Zaim S, et al. Orthostatic intolerance and syncope associated with Chiari type I malformation. J Neurol Neurosurg Psychiatry 2005;76:1034–6. 6. Milhorat TH, Chou MW, Trinidad EM, et al. Chiari I malformation redefined: clinical and radiographic findings for 364 symptomatic patients. Neurosurgery 1999;44:1005–17. 7. Weig SG, Buckthal PE, Choi SK, et al. Recurrent syncope as the presenting symptom of Arnold-Chiari malformation. Neurology 1991;41:1673–4. 8. Guillon B, Robertson D. Chiari I malformation as a cause of orthostatic intolerance symptoms: a media myth? Am J Med 2001;111:546–52. 9. Nogués MA, Newman PK, Male VJ, et al. Cardiovascular reflexes in syringomyelia. Brain 1982;105:835–49. 10. List CF. Neurologic syndromes accompanying developmental anomalies of the occipital bone, atlas, and axis. Arch Neurol Psychiatry 1941;45:577–616. 11. Speer MC, Enterline DS, Mehltretter L, et al. Chiari type I malformation with or without syringomyelia: prevalence and genetics. J Genet Couns 2003;12:297–311. 12. Von Torklus D, Gehle W. The upper cervical spine. London: Butterworths; 1972. p. 21–53. 13. Wackenheim A. Roentogen diagnosis of the craniovertebral region. Berlin: Springer-Verlag; 1974. p. 353–79. 14. Caetano de Barros M, Farias W, Ataide L, et al. Basilar impression and ArnoldChiari malformation. A study of 66 cases. J Neurol Neurosurg Psychiatry 1968;31:596–605. 15. Menezes AH, Ryken TC. Abnormalities of the craniovertebral junction. In: Cheek AE, Marlin AE, MacLone DG, Reigel DH, Walker ML, editors. Pediatric neurosurgery. 3rd ed. Philadelphia: Saunders; 1994. p. 139–58. 16. Moore KL, Persaud TVN. The developing human: clinically oriented embryology. 6th ed. Philadelphia: WB Saunders; 1998. p. 405–26. 17. Di Lorenzo N, Fortuna A, Guidetti B. Craniovertebral junction malformations. Clinicoradiological findings, long-term results, and surgical indications in 63 cases. J Neurosurg 1982;57:603–8. 18. Mesiwala AH, Shaffrey CI, Gruss JS, et al. Atypical hemifacial microsomia associated with Chiari I malformation and syrinx: further evidence indicating that Chiari I malformation is a disorder of paraxial mesoderm. J Neurosurg 2001;95:1034–9.
323
19. Shapiro R, Robinson F. Anomalies of the craniovertebral border. Am J Roentgenol 1976;127:281–7. 20. MacRea DL, Barnum AS. Occipiltalization of the atlas. AJR Am J Roentgenol 1953;70:23–46. 21. Menezes AH, VanGilder JC. Anomalies of the craniovertebral junction. In: Youmans J, editor. Neurological surgery. 3rd ed. Philadelphia: Saunders; 1990. p. 1359–420. 22. Nishikawa M, Sakamoto H, Hakuba A, et al. Pathogenesis of Chiari malformation: a morphometric study of the posterior cranial fossa. J Neurosurg 1997;86:40–7. 23. Vega A, Quintana F, Berciano J. Basiochondrocranium anomalies in adult Chiari type I malformation: a morphometric study. J Neurol Sci 1990;99:137–45. 24. Berge JK, Bergman RA. Variations in size and in symmetry of foramina of the human skull. Clin Anat 2001;14:406–13. 25. Coin CG, Malkasian DR. Foramen magnum. In: Newton TH, Potts DG, editors. Radiology of the skull and brain: the skull. St. Louis: Mosby; 1971. p. 275–347. 26. Lang J. Clinical anatomy of the posterior cranial fossa and its foramina. New York: Thieme; 1991. p. 1–112. 27. Muthukumar N, Swaminathan R, Venkatesh G, et al. A morphometric analysis of the foramen magnum region as it relates to the transcondylar approach. Acta Neurochir (Wien) 2005;147:889–95. 28. Kagawa M, Jinnai T, Matsumoto Y, et al. Chiari I malformation accompanied by assimilation of the atlas, Klippel-Feil syndrome, and syringomyelia: case report. Surg Neurol 2006;65:497–502. 29. Botelho RV, Bittencourt LR, Rotta JM, et al. Prospective controlled study of sleep respiratory events in patients with craniovertebral junction malformation. J Neurosurg 2003;99:1004–9. 30. Dauvilliers Y, Stal V, Abril B, et al. Chiari malformation and sleep related breathing disorders. J Neurol Neurosurg Psychiatry 2007;78:1344–8. 31. Garland EM, Robertson D. Chiari I malformation as a cause of orthostatic intolerance symptoms: a media myth? Am J Med 2001;111:546–52. 32. Ireland PD, Mickelsen D, Rodenhouse TG, et al. Evaluation of the autonomic cardiovascular response in Arnold-Chiari deformities and cough syncope syndrome. Arch Neurol 1996;53:526–31. 33. Botelho RV, Bittencourt LR, Rotta JM, et al. Adult Chiari malformation and sleep apnea. Neurosurg Rev 2005;28:169–76. 34. Zolty P, Sanders MH, Pollack IF. Chiari malformation and sleep-disordered breathing: a review of diagnostic and management issues. Sleep 2000;23:637–43. 35. Flemons WW, Tsai W. Quality of life consequences of sleep-disordered breathing. J Allergy Clin Immunol 1997;99:S750–6. 36. Botelho RV, Bittencourt LR, Rotta JM, et al. The effects of posterior fossa decompressive surgery in adult patients with Chiari malformation and sleep apnea. J Neurosurg 2010;112:800–7.
doi:http://dx.doi.org/10.1016/j.jocn.2012.10.044
Tension pneumocephalus and oxygen emboli from hydrogen peroxide irrigation Christopher Huang a,⇑, Justin Pik b a b
Neurosurgery Department, Canberra Hospital, Yamba Drive, 3/7 Eldridge Crescent, Garran, ACT 2605, Australia Australian Capital Territory Neurospine Clinic, Deakin, ACT, Australia
a r t i c l e
i n f o
Article history: Received 29 August 2012 Accepted 31 October 2012
Keywords: Hydrogen peroxide Oxygen embolus Oxygen emboli Peroxynitrite Tension pneumocephalus
⇑ Corresponding author. Tel.: +61 2 6244 4080. E-mail address: [email protected] (C. Huang).
a b s t r a c t Hydrogen peroxide irrigation is commonly utilised in neurosurgical and non-neurosurgical procedures for its bacteriocidal and haemostatic effects, however it has been associated with devastating complications such as tension pneumocephalus, O2 embolism and even dysrhythmias. We report a patient who suffered hydrogen peroxide-related mortality due to widespread tension pneumocephalus and O2 emboli. Ó 2013 Elsevier Ltd. All rights reserved.
324
Case Reports / Journal of Clinical Neuroscience 21 (2014) 323–325
1. Introduction Hydrogen peroxide (H2O2) has been historically used mainly as a haemostatic agent after intracranial parenchyma resection.1 Its exact mechanism of haemostasis is unknown, but has been postulated to arise from a combination of its vasoconstrictive and vasoocclusive effects on blood vessels.2 In vitro studies have observed the tumouricidal properties of H2O2 on giant cell tumours and breast cancers,3 and recently on primary and metastatic brain tumours in humans and rats4 although its function as a tumouricidal agent is not widely accepted or utilised by neurosurgeons. Throughout the literature, there have been reports of various complications associated with the use of H2O2 irrigation. Haller et al.5 reported air embolism after H2O2 was used to irrigate a vulvular abscess and Morikawa et al.6 reported a similar incident when H2O2 irrigation was used in cervical spine surgery. Other cases have resulted in mortality7–9 and cardiac dysrhythmias from stimulation of the trigeminocardiac reflex.10
Fig. 2. Immediate postoperative axial CT scan showing widespread tension pneumocephalus in the surgical cavity, throughout the subarachnoid space, cisterns and Sylvian fissure bilaterally.
2. Case report A 65-year-old man presented with 5 weeks of increasing confusion, headaches, and nominal dysphasia. Subsequent CT scans and MRI of the brain observed a 2.6 cm left temporal lobe ringenhancing lesion with significant vasogenic oedema consistent with a high grade glioma (Fig. 1). The patient underwent preoperative assessment and was taken to theatre 6 days later. Mayfield fixation and intraoperative navigation (Medtronic StealthStation, Medtronic, Minneapolis, MN, USA) were used. A question mark incision was made over the left temporal region and a left temporal craniotomy was performed via free bone flap and the dura opening. The tumour was seen to be present through the temporal lobe cortex and slightly adherent to the dura. The left Sylvian fissure was widely split to expose the internal carotid artery and the optic nerve. A frozen section was obtained which revealed a highly malignant neoplasm. A formal temporal lobectomy was then performed. The procedure was performed without any intraoperative complication. The left third nerve, internal carotid artery and optic nerve were preserved. Diluted 3% H2O2 was used to secure intradural haemostasis and the wound was closed in layers with the bone replaced. The patient failed to wake postoperatively and developed bradycardia and hypertension as well as a dilated left pupil within an hour of the end of surgery. An urgent CT scan of the brain was performed showing changes suggestive of widespread tension pneumocephalus (Fig. 2). Air was observed in the subarachnoid space, the cisterns, both Sylvian fissures and over the left frontal lobe as well as in the surgical cavity. The patient was immediately taken back to the operating theatre and had the wound reopened. The surgical site was thoroughly
Fig. 3. Axial CT scan of the brain after the decompression showing resolution of the tension pneumocephalus.
irrigated and the wound closed again. Following the second operation, the patient developed a dilated right pupil in addition to the previously observed dilated left pupil. A subsequent CT scan 5 hours after the second operation (Fig. 3) showed resolution of the tension pneumocephalus, however the patient did not improve neurologically in the following 48 hours and mechanical ventilation was withdrawn. On post mortem examination there were widespread recent small infarcts of the cortical mantle, central grey and white matter,
Fig. 1. Preoperative MRI showing left temporal high grade glioma (left: axial, middle: coronal, right: sagittal).
Case Reports / Journal of Clinical Neuroscience 21 (2014) 323–325
cerebellum, midbrain, pons and medulla. Patchy damage of intrinsic intraneural small vessels with scattered microhaemorrhages was seen in the infarcted areas, and active axonal degeneration of some cranial nerves with patchy acute inflammatory cell infiltration and microhaemorrhages. No thrombotic or embolic occlusion of vessels was present. The formal coroner’s report stated that this was, ‘‘consistent with widespread failure of perfusion in the small vessel perforators of the anterior and middle cerebral arteries and the vertebrobasilar arterial system with the brunt being borne in the perforator territory of the basilar artery. The features are consistent with a widespread failure of perfusion. This could possibly have been due to an episode of vasoconstriction or occlusion by microvessels by evanescent O2 emboli as has been described by H2O2 irrigation. The possibility that a combination of tension pneumocephaly and the putative H2O2 irrigation may have had a summative effect producing the severe changes seen in this case should also be considered.’’
3. Discussion H2O2 is a toxic reactive oxygen species and is normally kept at physiological levels in the body by catalase and the glutathione and glutathione peroxidise system. It permeates across the cell wall relatively well11 and also increases the permeability of endothelium. It is broken into H2O and O2 after exposure to catalase enzymes which are found in all cells, and up to 10 mL of O2 has been observed to be liberated from 1 mL of 3% H2O2.12,13 Further studies have also exhibited that excess H2O2 reacts with nitrous oxide to produce superoxide via multiple reactions, which in turn results in peroxynitite formation via other combination reactions with nitrous oxide.14 Peroxynitrite is a potent oxidant and increasing numbers of studies are beginning to witness the association between the production of this molecule and mitochondrial respiratory dysfunction after traumatic brain injury.15 Mut et al.13 showed that exposure to 15 mL of 3% H2O2 for 15 seconds resulted in formation of bubbles in the lumen of subpial arteries regardless of whether the pia layer was intact or not. They also discovered that there was clear peroxynitrite production around and in the vessels buried within the neuropil well below the intact pial layer, indicating that H2O2 diffuses passively and freely through the pia and the blood vessel wall. In the Mesiwala et al.4 study they reported brain parenchymal stromal vaculisation and degeneration of neurons, astrocytes and migrolia up to 1 mm beyond the tumour resection cavity in human brains, after treatment for 5 minutes with 3% H2O2 soaked cotton balls. In this patient, tension pneumocephalus throughout the brain was observed following irrigation of the tumour resection cavity with H2O2, most likely as a result of oxygen escape into the subdoi:http://dx.doi.org/10.1016/j.jocn.2012.10.044
325
arachnoid space. Although no obvious air was found to escape upon reopening the wound, the air could well have dissipated once the skin was open and during the craniotomy. The subsequent infarction may also have been the result of contributory insult from peroxynitrite formation secondary to the H2O2. To our knowledge, no patients with tension pneumocephalus throughout the cisterns have been previously reported secondary to H2O2 application. Three patients with tension pneumocephalus have been reported in the literature, two resulting from craniotomies16,17 and one of tension pneumocephalus in the posterior fossa from irrigation of an infected lumbar wound.18 This patient emphasises the potential of H2O2 to cause widespread neuronal damage distant from the site of application. Although H2O2 continues to be used for its haemostatic and bacteriocidal properties, consideration should be given to use of alternative haemostatic agents.
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