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Optic Nerve Sheath Diameter ( ONSD )
in Increased intracnial Pressures
( ICP ) A new tool in the Ultrasound Era
Causes of ICP
Mass effect:
Malignancy
CVA with edema
Cerebral contusions
subdural or epidural hematoma
abscess
Diffuse Encephalopathies:
Acute liver failure
Hypertensive Encephalopthy
High Altitude cerebral edema
Uremic Encephalopathy
PseudotumorCerebri
•Obstruction CSF flow and/or absorption :
•Hydrocephalus
•Extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous )
•Superior sagittal sinus (decreased absorption)
•Increased CSF production :
•Meningitis
•Subarachnoid hemorrhage,
Why look at ONSD?
How do we currently assess EICP :
Non-specific signs and symptoms
Imaging CT scan/MRI
Pulsatliity index
Invasive monitoring
Papilledema
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%
Invasive ICP measurments
Gold standard External Ventricular Device
Comlipcated/ invasive procedure
Risks Infection, parenchymal injury , bleeding
Bleeding diasthesis
Gold standard for ICPExternal Ventricular Device ( EVD )
Papilledema
Operator dependant
Delayed manifestation: - 24 hrs
May persist for several days to weeks after treatment
Papilledema ?
Both are Normal
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
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 )
Intracranial CSF
Intra-orbital CSF
h
Optic Nerve
ONSD history
British opthalmologistHayreh
The mechanism of papiledema from increased ICP
Placed inflatable balloons in the brain of monkeys
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
Acta Ophthalmol. 2011 Sep;89(6):e528-32.
Changes in ONSD mimics changes in ICP
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
3mm
ONSD
3mm
ONSD
Lens
Vitreous
A-A 0.3cm
B-B 0.62 cm
ONSD False Positive
Emerg Med J 2007;24:251–254. doi: 10.1136/emj.2006.040931
Emerg Med J 2007;24:251–254. doi: 10.1136/emj.2006.040931 Abdullah SadikGirisgin, ErdalKalkan, SedatKocak, BasarCander, MehmetGul, Mustafa Semiz
Volume status
Reproducible results
54 patients:
28 confirmed EICP via CT scan
26 no evidence of EICP
ONSD evidence based approach
Most studies Trauma or neurosurgical patients
3 major studies on ONSD ( briefly )
ONSD evidence
Prospective study on 26 ED patients
ONSD cutoff > 0.5 cm
Emer Med J published online August 15, 2010 ,Robert Major, Simon Girling and Adrian Boyleg
All had CT scans
Sens 86% Sepcificity 99% for EICP
ONSD cutoff >5mm
PPV100%NPV95%
ONSD evidence
Small sample size
Non-trauma GSC: 8
Compared to CT scan
Invasive and non-invasive comparison
76 patients
26 Control 18Moderate
32Severe
Moderate Marshall score I and GSC > 8Severe Marshall score >I and GCS < 8
Pulsatility index
Invasive ICP monitoring
76 patients
Brain CT injury scale No CT done Normal CT Abnormal CT18% 82%
ONSD cutoff 5.7mm
Non-invasive monitoring
Invasive Monitoring
TheodorosSoldtos, Optic nerve sonography in the diagnostic Evaluation of adult brain injury, Critical care 2008;12 R 67
ROC :0.93Sens : 74%Spec: 99%
ONSD cutoff > 5.7mm
Intensive Care Med (2007) 33:1704–1711, T. Geeraerts () · Y. Launey · L. Martin ·J. Pottecher· B. Vigué · J. Duranteau ·D. Benhamou
31 ICU patients with severe TBIGSC<8
16 EICP 15 Normal ICP
Prospective Blind observational trial
All patients underwent invasive ICP monitoring
5.7 mm
Thomas Geerats M.D, Ultrasonography of Optic nerveSheath may be useful in detecting raised ICP After head trauma. Intensive care Medicine 2007, 33:1704-1711
ROC: 0.96Sens: 91%Spec: 94%
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
Diffuse Encephalopathies: ESLDESRDHypertensive EncephalopthyHigh Altitude cerebral edema
Obstruction CSF flow and/or absorption :
•Hydrocephalus
•Extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous )
•Superior sagittal sinus (decreased absorption)
Increased CSF production :
•Meningitis
•Subarachnoid hemorrhage,
Mass effect:•Malignancy
•CVA with edema
•Cerebral contusions
•Subdural or epidural hematoma
•Abscess
ICP causes
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/sencephalopathy pre-treatment /24hrs post-treatment
Convenience sample
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
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.
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
ESLD and ICP
Fulminant hepatic failure 80% EICP
Ammonia and Manganese astrocyte edema
Chronic ESLD EICP only in stage IV hepatic encephalopathy
N=24
N=10
Stage I
N=2
Stage II
N=5
Stage III
N=3
Stage IV
N=0
N=14
EncephalopathyNo
Encephalopathy
Pretreament ESLD
0
1
2
3
4
5
6
7
8
9
10
No Encephalopathy With Encephalopathy
N= 14 N=10
Encephalopathy
ONSD in mm
5.7mm
•Stage I•Stage II•Stage III
Post-treament ESLD
0
1
2
3
4
5
6
7
8
9
10
No Encephalopathy With Encephalopathy
N= 14 N= 10
Encephalopathy
ONSD in mm
5.7mm
•Stage I•Stage II•Stage III
Relative decrease 57%
Summary ESLD
0
1
2
3
4
5
6
7
8
9
10
No Encephalopathy With Encephalopathy
N= 14 N= 8
ONSD in mm
5.7mm
•Stage I•Stage II•Stage III
0
1
2
3
4
5
6
7
8
9
10
No Encephalopathy
With Encephalopathy
N= 14 N= 8
Pretreatment Post-treatment
ESRD and ICP
Dialysis Dysequilibrium Syndrome
Very high BUN > 110
Pretreatment ESRD
0
1
2
3
4
5
6
7
8
9
10
yes No 1/9/02
No Encephalopathy
WithEncephalopathy
ONSD in mm
N= 4N= 13
No Encephalopathy
WithEncephalopathy
Pretreatment Post-treatment
46 %decrease 63% decrease
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?
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
HTN crisis
0
1
2
3
4
5
6
7
8
9
10
yes No 1/9/02
Uncontrolled HTN
HTN emergency
ONSD in mm
N= 5N= 11
Pretreatment Post-treatment
Uncontrolled HTN
HTN emergency
Encephalopathic
57% decrease 68% decrease
7.2mm5.2mm
Data analysis
Uncontrolled HTN had rather high ONSD subclinicalEICP
Relative size decrease :
57% in Uncontrolled HTN
68% HTN emergency
High altitude sickness
No data yet
14er’sONSD at base , peak , base
Symptoms of Altitude sickness
ONSD absolute value and change
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
Thank you
