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

2. Causes of ICPObstruction CSF flow and/or Mass effect: Hydrocephalus absorption : Malignancy Extensive meningeal disease (e.g., infectious, CVA with edema Cerebral contusionscarcinomatous, subdural or epidural hematomagranulomatous ) abscessSuperior sagittal sinus(decreased absorption) Diffuse Encephalopathies: Acute liver failureIncreased 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 traumaneed repeat head CT looking for ICP .Radiographic delay? Initial head CTs of 100 head injured traumapatients evaluated by group of 12radiologists : Sensitivity 83% , Specifity 78% 5. Invasive ICP measurments Gold standard External Ventricular Device Comlipcated/ invasive procedure Risks Infection, parenchymal injury , bleeding Bleeding diasthesis 6. Gold standard for ICPExternal Ventricular Device ( EVD ) 7. Papilledema Operator dependant Delayed manifestation: - 24 hrs May persist for several days to weeks after treatment 8. Papilledema ?Both are Normal 9. Outline Basic anatomy of the Optic nerve and its sheath How to measure ONSD? Rationale and evidence for using the ONSD for Increasedintracerebral pressure ( ICP ) Uses and rationale in different clinical settings : ESRD , ESLD ,HTN crises and altitude sickness 10. ONSD basic anatomy Optic Nerve: White matter tract direct extension of the CNS surroundedby CSF Sensitive to changes to CSF flow and intracerebral pressures( ICP ) 11. Intra-orbital CSFhIntracranial CSF 12. Optic Nerve 13. ONSD history British opthalmologistHayreh The mechanism of papiledema from increased ICP Placed inflatable balloons in the brain of monkeys 14. 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 highpressures showed a delay in regressionChanges in ONSD mimics changes in ICPActa Ophthalmol. 2011 Sep;89(6):e528-32. 15. 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 16. 3mmONSD 17. 3mmONSD 18. Lens Vitreous A-A 0.3cmB-B 0.62 cm 19. ONSD False Positive Emerg Med J 2007;24:251254. doi:10.1136/emj.2006.040931Volume status Emerg Med J 2007;24:251254. doi: 10.1136/emj.2006.040931 Abdullah SadikGirisgin, ErdalKalkan, SedatKocak, BasarCander, MehmetGul, Mustafa Semiz 20. Reproducible results 54 patients: 28 confirmed EICP via CT scan 26 no evidence of EICP 21. ONSD evidence based approach Most studies Trauma or neurosurgical patients 3 major studies on ONSD ( briefly ) 22. ONSD evidence Prospective study on 26 ED patients ONSD cutoff > 0.5 cmAll had CT scansEmer Med J published online August 15, 2010 ,Robert Major, Simon Girling and Adrian Boyleg 23. PPV100% NPV95%Sens 86%Sepcificity 99% forEICPONSD cutoff >5mm 24. ONSD evidence Small sample size Non-trauma GSC: 8 Compared to CT scan 25. Invasive and non-invasivecomparison76 patientsPulsatility index 26 Control 1832ModerateSevereInvasive ICPModerate Marshall score I and GSC > 8monitoringSevere Marshall score >I and GCS < 8 26. 76 patientsBrain CT injury scale No CT done Normal CT Abnormal CT 18% 82% ONSD cutoff 5.7mm 27. Non-invasive Invasive Monitoringmonitoring 28. ROC :0.93Sens : 74%Spec: 99%ONSD cutoff >5.7mmTheodorosSoldtos, Optic nerve sonography in thediagnosticEvaluation of adult brain injury, Critical care 2008;12R 67 29. Prospective Blind observationaltrial31 ICU patients with severe TBI GSC 5.7mm for EICP Sensitivity of around 93% Specificity: 96% 5-5.7mm Sensitivity is maintained however Specificitydeclines to 83% Screening tool Surrogate marker for EICP 33. ICP causesObstruction CSF flow and/or Diffuse Encephalopathies:absorption : ESLD ESRD HydrocephalusHypertensive Encephalopthy High Altitude cerebral edema Extensive meningeal disease granulo (e.g., infectious, carcinomatous, matous ) Mass effect: Superior sagittal sinus (decreased Malignancy absorption) CVA with edemaIncreased CSF production : Cerebral contusions Meningitis Subdural or epidural hematoma Subarachnoid hemorrhage, Abscess 34. Study Prospective observational/descriptive analysis Medicine patient admitted to general medicine floor , MICUESLD / 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 35. Hypothesis Absolute value of ONSD would be high among theencephalopathic group and would normalize aftertreatment Statistically significant change in ONSD pre and posttreatment 36. 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. 37. 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 24hrsafter treatment 38. ESLD and ICP Fulminant hepatic failure 80% EICP Ammonia and Manganese astrocyte edema Chronic ESLD EICP only in stage IV hepaticencephalopathy 39. N=24 NoEncephalopathyEncephalopathy N=10N=14Stage I Stage IIStage III Stage IV N=2N=5 N=3 N=0 40. Pretreament ESLD10Stage I ONSD in mm9 Stage II8 Stage III 765.7mm 54 32 1 N= 14 N=100Encephalopathy No EncephalopathyWith Encephalopathy 41. Post-treament ESLD10 Stage I ONSD in mm9Stage II8Stage III 7 Relative decrease 57%6 5.7mm 54 32 1 N= 14N= 100 Encephalopathy No Encephalopathy With Encephalopathy 42. Summary ESLDPretreatmentPost-treatment10 ONSD in mm10 Stage I 99Stage II 88 77Stage III 665.7mm 55 44 33 22 11 0 N= 8 0 N= 8N= 14 N= 14No EncephalopathyWith No WithEncephalopathy Encephalopathy Encephalopathy 43. ESRD and ICP Dialysis Dysequilibrium Syndrome Very high BUN > 110 44. Pretreatment ESRD PretreatmentPost-treatment10 ONSD in mm98 7 46 %decrease63% decrease654 32N= 13N= 4 1NoWith No With0 Encephalopathy EncephalopathyEncephalopathy Encephalopathy yes No1/9/02 45. 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? 46. 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 HTNencephalopathy not so much 47. HTN crisisPretreatmentPost-treatment10 ONSD in mm Encephalopathic9 5.2mm 7.2mm8 757% decrease 68% decrease654 32 N= 11 N= 5 1 Uncontrolled HTN emergency UncontrolledHTN emergency0HTNHTNyesNo 1/9/02 48. Data analysis Uncontrolled HTN had rather high ONSD subclinicalEICP Relative size decrease : 57% in Uncontrolled HTN 68% HTN emergency 49. High altitude sickness No data yet 14ers ONSD at base , peak , base Symptoms of Altitude sickness ONSD absolute value and change 50. 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 51. Thank you

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