Measurement of Optic Nerve Sheath Diameter for the Assessment of Risk of Raised Intracranial Pressure

Measurement of Optic Nerve Sheath Diameter for the Assessment of Risk of Raised Intracranial Pressure

Benhamou Dan, Geeraerts Thomas, Menon David K

European Neurological Review, 2009;4(1):50-2

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Abstract
Raised intracranial pressure (ICP) is associated with poor outcome after brain injury, but is difficult to detect without invasive devices. As a part of the central nervous system, the optic nerve is surrounded by a dural sheath, and the subarachnoid space surrounding the optic nerve is subject to the same pressure changes as the intracranial compartment. Distension of the optic nerve sheath reflects an increase in cerebrospinal fluid (CSF) pressure and can be used to estimate the risk of raised ICP. Ocular sonography or brain magnetic resonance imaging (MRI) enables valid measurement of the distension of the dural sheath surrounding the optic nerve. An optic nerve sheath diameter greater than 5.8mm is likely to be associated with raised ICP. This non-invasive estimate of ICP may detect patients at risk, help make decisions regarding the placement of invasive ICP devices and allow the selection of patients for transfer to specialist centres.

Keywords
Intracranial pressure, neurocritical care, ocular sonography, optic nerve sheath diameter, traumatic brain injury

Disclosure: Thomas Geeraerts is supported by grants from the Société Française d’Anesthésie et de Réanimation (SFAR) and Journées d’Enseignement Post -Universitaire d’Anesthésie-Réanimation (JEPU)-Novo Nordisk. David K Menon is supported by grants from the Medical Research Council, UK, Royal College of Anaesthetists, Wellcome Trust, the Evelyn Trust and Queens’ College Cambridge. Dan Benhamou has no conflicts of interest to declare.
Received: 22 October 2008 Accepted: 16 February 2009
Correspondence: Thomas Geeraerts, University Department of Anaesthesia, Addenbrooke’s Hospital and University of Cambridge, Cambridge CB2 2QQ, UK. E: thgeeraerts@hotmail.com

Raised intracranial pressure (ICP) is frequent and is associated with poor outcome after brain injury, and also after liver failure, acute ischaemic stroke, cerebral venous thrombosis, meningitis and encephalitis.1–5 However, the early detection of raised ICP can be difficult when invasive devices are not available. Clinical signs of raised ICP are not specific and are often difficult to interpret. In sedated patients, clinical signs of raised ICP frequently appear late, when ischaemic brain injury is already established.6 The gold standard method for ICP measurement is based on the use of invasive devices such as intraventricular drain or intraparenchymal probes. Nevertheless, invasive ICP monitoring is not routinely used in many centres – principally because of the lack of availability of neurosurgeons – or may be contraindicated in cases of coagulation disorders. The worst attitude would be to ignore the danger of raised ICP in these patients and to run an unacceptable risk of cerebra ischaemia. In these situations, a non-invasive estimation of the risk of raised ICP may be clinically valuable.

Anatomical Background
The optic nerve, as part of the central nervous system, is surrounded by a dural sheath. The intraorbital subarachnoid space surrounding the optic nerve is subject to the same pressure changes as the intracranial compartment.7–10 The retrobulbar part of the perioptic subarachnoid space is distensible and can therefore inflate if pressure increases. Hayreh showed in monkeys and humans that the subarachnoid spaces surrounding the optic nerve communicate with the intracranial cavity, and that changes in cerebrospinal fluid (CSF) pressure can be transmitted along the optic nerve sheath.11 He also showed that oedema of the optic disc (papilloedema) requires a few days to develop and resolve, making it less useful when acute changes in ICP are suspected.11 Papilloedema thus appears more as a delayed consequence of chronic CSF accumulation i the retrobulbar optic nerve dural sheath due to raised CSF pressure in the cranial cavity. Direct assessment of such CSF accumulation by measuring optic nerve sheath diameter (ONSD) may provide an earlier and more reactive measure of intracranial hypertension. In cadavers, the ONSD displays predominantly anterior enlargement following injection into the orbital perineural subarachnoid space.12 In humans, following an intrathecal lumbar infusion of Ringer’s solution, ONSD dilation reaches a maximum at peak CSF pressure, strongly suggesting a close relationship between CSF pressure and dilation of the orbital perineural subarachnoid space.

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Keywords:
Intracranial pressure, neurocritical care, ocular sonography, optic nerve sheath diameter, traumatic brain injury, intracranial hypertension, intracranial pressure monitoring, cerebral perfusion pressure, intracranial pressure value, cerebral venous thrombosis, raised intracranial pressure, transcranial doppler ultrasound, optic nerve sheath decompression, acute intracranial hypertension, intracranial hypertension therapy,

References:
  1. Becker DP, Miller JD, Ward JD, et al., J Neurosurg, 1977;47:491–502.
  2. Marshall LF, Smith RW, Shapiro HM, J Neurosurg, 1979;50:26–30.
  3. Ware AJ, D’Agostino AN, Combes B, Gastroenterology, 1971;61:877–84.
  4. Newton CR, Crawley J, Sowumni A, et al., Arch Dis Child, 1997;76:219–26.
  5. Vahedi K, Hofmeijer J, Juettler E, et al., Lancet Neurol, 2007;6:215–22.
  6. Ghajar J, Lancet, 2000;356:923–9.
  7. Liu D, Kahn M, Am J Ophthalmol, 1993;116:548–56.
  8. Villain MA, Candon E, Arnaud B, et al., J Fr Ophtalmol, 2003;26:191–7.
  9. Hayreh SS, Doc Ophthalmol, 1968;24:289–411.
  10. Lichtenstein D, L’echographie générale en réanimation, Paris, Berlin, New York: Springer-Verlag, 1992;115.
  11. Hayreh SS, Br J Ophthalmol, 1964;48:522–43.
  12. Hansen HC, Helmke K, Surg Radiol Anat, 1996;18:323–8.
  13. Munk PL, Vellet AD, Levin M, et al., Am J Roentgenol, 1991;157:1079–86.
  14. Williamson TH, Harris A, Surv Ophthalmol, 1996;40: 255–67.
  15. Barnett SB, Ter Haar GR, Ziskin MC, et al., Ultrasound Med Biol, 2000;26:355–66.
  16. Berges O, Koskas P, Lafitte F, Piekarski JD, J Radiol, 2006;87:345–53.
  17. Hansen HC, Helmke K, J Neurosurg, 1997;87:34–40.
  18. Newman WD, Hollman AS, Dutton GN, Carachi R, Br J Ophthalmol, 2002;86:1109–13.
  19. Blaivas M, Theodoro D, Sierzenski PR, Acad Emerg Med, 2003;10:376–81.
  20. Helmke K, Burdelski M, Hansen HC, Transplantation, 2000;70:392–5.
  21. Tayal VS, Neulander M, Norton HJ, et al., Ann Emerg Med, 2007;508–14.
  22. Soldatos T, Karakitsos D, Chatzimichail K, et al., Crit Care, 2008;12:R67.
  23. Kimberly HH, Shah S, Marill K, Noble V, Acad Emerg Med, 2008;15:201–4.
  24. Geeraerts T, Merceron S, Benhamou D, et al., Intensive Care Med, 2008;34:2062–7.
  25. Geeraerts T, Launey Y, Martin L, et al., Intensive Care Med, 2007;33:1704–11.
  26. Ballantyne SA, O’Neill G, Hamilton R, Hollman AS, Eur J Ultrasound, 2002;15:145–9.
  27. Mashima Y, Oshitari K, Imamura Y, et al., Arch Ophthalmol, 1996;114:1197–1203.
  28. Lambert SR, Johnson TE, Hoyt CS, Arch Ophthalmol, 1986;104:1509–12.
  29. Gass A, Barker GJ, Riordan-Eva P, et al., Neuroradiology, 1996;38:769–73.
  30. Brodsky MC, Vaphiades M, Ophthalmology, 1998;105:1686–93.
  31. Agid R, Farb RI, Willinsky RA, et al., Neuroradiology, 2006;48:521–7.
  32. Watanabe A, Horikoshi T, Uchida M, et al., AJNR Am J Neuroradiol, 2008;29:863–4.
  33. Geeraerts T, Newcombe VFJ, Coles JP, et al., Crit Care, 2008;12:R114.

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