1. Optic Nerve Sheath
Diameter ( ONSD )
in Increased
intracnial Pressures
( ICP )
A new tool in the Ultrasound Era

2. Causes of ICP
•Obstruction CSF flow and/or  Mass effect:
•Hydrocephalus
absorption :
 Malignancy
•Extensive meningeal
disease (e.g., infectious,
 CVA with edema
 Cerebral contusions
carcinomatous,  subdural or epidural hematoma
•
granulomatous )  abscess
Superior sagittal sinus
(decreased absorption)  Diffuse Encephalopathies:
 Acute liver failure
•Increased CSF production :  Hypertensive Encephalopthy
• Meningitis  High Altitude cerebral edema
•Subarachnoid hemorrhage,  Uremic Encephalopathy
 PseudotumorCerebri

3. Why look at ONSD?
 How do we currently assess EICP :
 Non-specific signs and symptoms
 Imaging CT scan/MRI
 Pulsatliity index
 Invasive monitoring
 Papilledema

4. CT and ICP
 Moving patients
 Repeat for head CT  one third of trauma
need repeat head CT looking for ICP .
Radiographic delay?
 Initial head CTs of 100 head injured trauma
patients evaluated by group of 12
radiologists :
 Sensitivity 83% , Specifity 78%

5. Invasive ICP measurments
 Gold standard External Ventricular Device
 Comlipcated/ invasive procedure
 Risks  Infection, parenchymal injury
, bleeding
 Bleeding diasthesis

7. Gold standard for ICP
External Ventricular Device ( EVD )

8. Papilledema
 Operator dependant
 Delayed manifestation: - 24 hrs
 May persist for several days to weeks after treatment

9. Papilledema ?
Both are Normal

11. Outline
 Basic anatomy of the Optic nerve and it’s sheath
 How to measure ONSD?
 Rationale and evidence for using the ONSD for Increased
intracerebral pressure ( ICP )
 Uses and rationale in different clinical settings :
 ESRD , ESLD ,HTN crises and altitude sickness

12. ONSD basic anatomy
 Optic Nerve:
 White matter tract direct extension of the CNS surrounded
by CSF
 Sensitive to changes to CSF flow and intracerebral pressures
( ICP )

13. Intra-orbital CSF
h
Intracranial CSF

14. Optic Nerve

15. ONSD history
 British opthalmologistHayreh
 The mechanism of papiledema from increased ICP
 Placed inflatable balloons in the brain of monkeys

19. Rapid response ONSD
 Hansen et al :
 Infused NS into CSF
 Changes in ONSD occurred within minutes
 Mean change of 1.97mm or around 83% increase
 Relieving pressure  rapid decrease in size
 Exception was with prolonged exposure to very high
pressures showed a delay in regression
Changes in ONSD mimics changes in ICP
Acta Ophthalmol. 2011 Sep;89(6):e528-32.

20. How do we measure the ONSD?
 3-7.5Mhz Probe
 Supine position at around 20 degrees phlebotactic axis
 Perpendicular axis at 3mm behind ON entry point
 2 reading on each eye
 Probe applied directly over the eyelid
 Cutoff 5mm or 5.7mm

21. 3mm
ONSD

22. 3mm
ONSD

23. Lens
Vitreous
A-A 0.3cm
B-B 0.62 cm

24. ONSD False Positive
 Emerg Med J 2007;24:251–254. doi:
10.1136/emj.2006.040931
Volume status
Emerg Med J 2007;24:251–254. doi: 10.1136/emj.2006.040931 Abdullah
SadikGirisgin, ErdalKalkan, SedatKocak, BasarCander, MehmetGul, Mustafa
Semiz

25. Reproducible results
 54 patients:
 28 confirmed EICP via CT scan
 26 no evidence of EICP

27. ONSD evidence based approach
 Most studies  Trauma or neurosurgical patients
 3 major studies on ONSD ( briefly )

28. ONSD evidence
 Prospective study on 26 ED patients
 ONSD cutoff > 0.5 cm
All had CT scans
Emer Med J published online August 15, 2010 ,Robert Major, Simon Girling and Adrian Boyleg

29. PPV100%
NPV95%
Sens 86%
Sepcificity 99% for
EICP
ONSD cutoff >5mm

30. ONSD evidence
 Small sample size
 Non-trauma  GSC: 8
 Compared to CT scan

31. Invasive and non-invasive
comparison
76 patients
Pulsatility index
26 Control 18 32
Moderate Severe
Invasive ICP
Moderate  Marshall score I and GSC > 8 monitoring
Severe  Marshall score >I and GCS < 8

32. 76 patients
Brain CT injury scale No CT done Normal CT Abnormal CT
18% 82%
ONSD cutoff 5.7mm

33. Non-invasive Invasive Monitoring
monitoring

34. ROC :0.93
Sens : 74%
Spec: 99%
ONSD cutoff >
5.7mm
TheodorosSoldtos, Optic nerve sonography in the
diagnostic
Evaluation of adult brain injury, Critical care 2008;12
R 67

35. Prospective Blind observational
trial
31 ICU patients with severe TBI
GSC<8
16 EICP 15 Normal ICP
All patients underwent invasive
ICP monitoring
Intensive Care Med (2007) 33:1704–1711, T. Geeraerts () · Y. Launey · L. Martin ·J. Pottecher
· B. Vigué · J. Duranteau ·D. Benhamou

36. 5.7 mm

37. ROC: 0.96
Sens: 91%
Spec: 94%
Thomas Geerats M.D, Ultrasonography of Optic
nerve
Sheath may be useful in detecting raised ICP
After head trauma. Intensive care Medicine
2007, 33:1704-1711

38. ONSD evidence conclusion
 Cutoff> 5.7mm for EICP 
 Sensitivity of around 93%
 Specificity: 96%
 5-5.7mm  Sensitivity is maintained however Specificity
declines to 83%
 Screening tool
 Surrogate marker for EICP

39. ICP causes
Obstruction CSF flow and/or Diffuse Encephalopathies:
absorption : ESLD
ESRD
•Hydrocephalus Hypertensive Encephalopthy
High Altitude cerebral edema
•Extensive meningeal disease granulo
(e.g., infectious, carcinomatous,
matous ) Mass effect:
•Superior sagittal sinus (decreased •Malignancy
absorption) •CVA with edema
Increased CSF production : •Cerebral contusions
•Meningitis •Subdural or epidural hematoma
•Subarachnoid hemorrhage, •Abscess

40. Study
 Prospective observational/descriptive analysis
 Medicine patient admitted to general medicine floor , MICU
ESLD / ESRD / HTN crisis
 No head / ocular trauma
 No other cause for EICP
 Comparing ONSD diameter of non-encephalopathy v/s
encephalopathy pre-treatment /24hrs post-treatment
 Convenience sample

41. Hypothesis
 Absolute value of ONSD would be high among the
encephalopathic group and would normalize after
treatment
 Statistically significant change in ONSD pre and post
treatment

42. Definitions
 EICP: - > 20 mmHg, If invasive monitoring available .
 Radiographic evidence of raised ICP as determined by
CT
 ONSD : cut-off of 5.7 mm to define enlarged ONSD ,
 ESLD and Uremia straightforward
 HTN encephalopathy ? Unclear and vague definition.

43. Method
 7-12 MHz while patient is at 20 degree angle
 2 measurements from each eye ( for a total of 4 per patient
)
 Measurements will be taken both prior and within 24hrs
after treatment

44. ESLD and ICP
 Fulminant hepatic failure  80% EICP
 Ammonia and Manganese astrocyte edema
 Chronic ESLD  EICP only in stage IV hepatic
encephalopathy

45. N=24
No
Encephalopathy Encephalopathy
N=10 N=14
Stage I Stage II Stage III Stage IV
N=2 N=5 N=3 N=0

46. Pretreament ESLD
10 •Stage I
ONSD in mm
9 •Stage II
8 •Stage III
7
6
5.7mm
5
4
3
2
1
N= 14 N=10
0
Encephalopathy
No Encephalopathy With Encephalopathy

47. Post-treament ESLD
10
•Stage I
ONSD in mm
9 •Stage II
8 •Stage III
7
Relative decrease 57%
6
5.7mm
5
4
3
2
1
N= 14 N= 10
0
Encephalopathy
No Encephalopathy With Encephalopathy

48. Summary ESLD
Pretreatment Post-treatment
10 ONSD in mm 10 •Stage I
9 9
•Stage II
8 8
7 7
•Stage III
6 6 5.7mm
5 5
4 4
3 3
2 2
1 1
0 N= 8 0 N= 8
N= 14 N= 14
No Encephalopathy With No With
Encephalopathy Encephalopathy Encephalopathy

49. ESRD and ICP
 Dialysis Dysequilibrium Syndrome
 Very high BUN > 110

50. Pretreatment ESRD
Pretreatment Post-treatment
10
ONSD in mm
9
8
7
46 %decrease 63% decrease
6
5
4
3
2
N= 13 N= 4
1
No With No With
0
Encephalopathy Encephalopathy Encephalopathy Encephalopathy
yes No 1/9/02

51. Data analysis
 Relative decrease in ONSD in both groups was significant
 NO encephalopathy: - 46%
 With Encephalopathy: - 63%
 Other etiologies for increase ONSD :
 Volume status
 HTN
 Utility in predicting DDS?

52. HTN crisis
 Most common manifestation are neurologic :
 44% with HTN emergency have neurologic manifestations
 16% HTN encephalopathy
 Clinically subtle
 Pathophysiology Breakthrough autoregulation
 CT head to r/o CVA helpful however in HTN
encephalopathy not so much

55. HTN crisis
Pretreatment Post-treatment
10
ONSD in mm Encephalopathic
9
5.2mm 7.2mm
8
7
57% decrease 68% decrease
6
5
4
3
2
N= 11 N= 5
1
Uncontrolled HTN emergency Uncontrolled HTN emergency
0
HTN HTN
yes No 1/9/02

56. Data analysis
 Uncontrolled HTN had rather high ONSD subclinical
EICP
 Relative size decrease :
 57% in Uncontrolled HTN
 68% HTN emergency

57. High altitude sickness
 No data yet
 14er’s ONSD at base , peak , base
 Symptoms of Altitude sickness
 ONSD absolute value and change

58. Conclusion
 ONSD: Reliable surrogate marker for EICP
 Quick bedside evaluation that competes with CT scans
 Reproducible results easy to learn
 Large area of research
 Downfalls: - Etiology

59. Thank you