Razumovsky, Alexander

1,020 views
892 views

Published on

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
1,020
On SlideShare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
0
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Razumovsky, Alexander

  1. 1. SPECIFIC CLINICAL APPLICATIONS OFTRANSCRANIAL DOPPLERULTRASOUND FOR PATIENTS WITHWARTIME TRAUMATIC BRAIN INJURY RoccoArmonda, Teodoro Tigno, Sven Hochheimer, Frederick Stephens, Randy Bell, Alexander Vo, Meryl Severson, Robert Ecker, Alexander Razumovsky Presented for National Neurotrauma Symposium 2011 July 12, 2011
  2. 2. Disclosure R. Armonda, T. Tigno, S. Hochheimer, F. Stephens, R. Bell, A. Vo, M. Severson, R. Ecker – nothing to disclose A. Razumovsky is FTE for the private practice that currently is under contract with AMEDD
  3. 3. DisclaimerThe views expressed in this presentation arethose of the authors and do not reflect theofficial policy of the Department of the Army,Department of Defense, or U.S. Government.
  4. 4. TBI Civilian Battlefield Every 21 seconds, one person  Okie, NEJM, 2005: Among in the US sustains traumatic surviving soldiers wounded in brain injury (TBI) combat in Iraq and Afghanistan, TBI appears to account for a larger proportion of casualties than it has in other recent U.S. wars. According to the Joint Theater Trauma Registry, 22% had injuries to the head, face, or neck.
  5. 5. TBI: PathophysiologyPrimary Injury: - Contusions/Hemorrhages - Diffuse Axonal Injury (DAI)Secondary Injury (Intracranial) occurs hours to weeks/years after injury: - Blood Flow and Metabolic Changes - Cerebral Ischemia - Traumatic Hematomas - Cerebral Edema - Hydrocephalus - Increased Intracranial Pressure - PTSD?
  6. 6. WARTIME TRAUMATIC CEREBRAL VASOSPASM:RECENT REVIEW OF COMBAT CASUALTIES Armonda et al., Neurosurgery, 2006 The first study to analyze the effects of blast- related injury on the cerebral vasculature. This study showed that TCV occurred in a substantial number of patients with severe neurotrauma, and clinical outcomes were worse for those with this condition.
  7. 7. WARTIME TRAUMATIC CEREBRAL VASOSPASM: RECENTREVIEW OF COMBAT CASUALTIES Armonda et al., Neurosurgery, 2006 Based on this study, the authors recommend that an assessment of the cranial vasculature be made for all patients experiencing a severe closed or penetrating head injury from military-grade weaponry TCD used to perform the initial assessment and subsequent follow-up evaluation.
  8. 8. Multimodal Monitoring:Vasospasm/Ischemia/high ICP DetectionThe primary goal of  MAP  SaO2management for  ECGTBI is the  Et-CO2prevention of  CVP  Urine outputsecondary damage  ICPdue to neuronal  CBFV/TCDhypoxia and  PbO2hypoperfusion  cEEG  CT/MR Perfusion
  9. 9. Transcranial Doppler (TCD) Today, the use of the TCD to assess and monitor cerebral vasospasm and other cerebrovascular abnormalities, like intracranial hypertension, stroke, etc. is considered the minimum standard of care Physicians, including military - mainly neurologists and neurosurgeons, located at military and civil medical centers need immediate access to comprehensive TCD services in order to ensure the highest quality of neurology and neurosurgery care for civilians/warriors
  10. 10. Objectives Traumatic brain injury (TBI) is associated with the severest casualties from Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF). A consequences of neurotrauma are cerebral vasospasm and intracranial hypertension. From Oct. 1, 2008 AMEDD TBI program initiated TCD ultrasound service for TBI patients who were presented for care at the National Naval Medical Center and at the Walter Reed Army Medical Center. This prospective study evaluated all inpatient TCD studies related to battle injury from OIF and OEF.
  11. 11. MATERIAL &METHODS
  12. 12. Clinical Material Ninety patients (2 females) aged 18 to 50 years (mean 25.9 years) who had suffered wartime TBI injuries (with Glasgow Coma Scale scores ranging from 3 to 15) were investigated with daily TCD studies. A total of 567 TCD studies (mean 6.4 tests/patient, ranged from 1 to 30) were made after admission.
  13. 13. Clinical material TBI Number % M F TLA Cranioplasty Type/MechanismCHI 19 21.1 18 1 1 4CHI/IED 18 20 18 - 1 -PHI 33 36.6 32 1 2 10PHI/IED 20 22.2 19 - 1 4Total 90 88 2 5 18
  14. 14. TCD Protocol Comprehensive TCD protocol and well published diagnostic criteria for vasospasm and abnormally high intracranial pressure (ICP) applied in all cases
  15. 15. TCD Criteria for diagnosis of vasospasmMean CBFV MCA/ICA ratio Interpretation (cm/s) (Lindegaard Ratio)<100 <3 Nonspecific100-140 3-6 Mild140-200 3-6 Moderate>200 >6 Severe
  16. 16. Typical morphology of TCD wave-form MCA (M1 and M2 segm)  OA ICA (C1, C3 and C4 segm) ACA (A1 segm) PCA (P1, P2 segm) VA’s and BA  High peripheral resistance/High PI Low peripheral resistance/Low PI
  17. 17. TCD wave-form changes with development of intracranial hypertensionNormal ICP
  18. 18. TCD criteria for abnormally high ICP We are judging quantitative and qualitative TCD wave form morphology changes These changes usually will be obvious after ICP will be more 30 mm Hg However, one condition must be full filled if you would be using TCD wave from changes to predict intracranial hypertension: MAP, cardiac output and PaCO2 are normal and not different significantly compared to the previous day PI more than 1.2 in two or more vessels
  19. 19. RESULTS:POSTTRAUMATICVASOSPASM
  20. 20. Posttraumatic Vasospasm 57 patients or 63% demonstrated different degree TCD signs of vasospasm
  21. 21. TCD signs of Vasospasm (in %) bytype of TBI80 7570 68.4605040 36.8 Mild (%) 35.7 31.5 Mod (%) 2930 23.5 Severe (%)20 17.6 14.3 15.710 5.2 5.2 0 PHI PHI/IED CHI CHI/IED
  22. 22. TCD signs of anterior circulation vasospasm by TBI type 300 250 200 CBFV 150 Mild(cm/sec) Moderate 100 Severe 50 0 PHI PHI/IED CHI CHI/IED
  23. 23. TCD signs of posterior circulationvasospasm by TBI type 180 160 140 120 100 CBFV Mild(cm/sec) 80 Moderate 60 Severe 40 20 0 PHI PHI/IED CHI CHI/IED
  24. 24. 25 yo, closed TBI, no SAH TLA TLACBFV(cm/sec) TLA Calendar
  25. 25. 25 yo, CHI, no SAHBefore TLA After TLACBFV 120 cm/s CBFV 57 cm/s
  26. 26. 25 yo, CHI, no SAHCBFV 112 cm/s CBFV 89 cm/s
  27. 27. 23 y/o patient, s/p IED blast injury with penetrating fragments300 RIGHT LEFT MC250 AC200 SevereVSP ICA150 Moderate VSP VA BA100 Mild VSP MA 50 Hc TLA TLA ICP 0 Pa
  28. 28. 23 y/o patient, s/p IED blast injury with penetratingfragments. TCD before and one hour after TLALeft MCA 205 cm/sec; PI 0.8 Right MCA CBFV 195 cm/sec; PI 0.5Left MCA CBFV 69 cm/sec; PI 1.7 Right MCA CBFV 66 cm/sec; PI 1.4
  29. 29. Role of TCD for post TBI vasospasm Posttraumatic vasospasm is a significant event in a high proportion of patients after severe TBI, close TCD monitoring is recommended for the treatment of such patients The presence and temporal profile of CBFV’s in all available vessels must be detected and serially monitored
  30. 30. Role of TCD for post TBI vasospasm The pattern of CBFV’s elevation may indicate the need to follow patient carefully for evidence of deficits related to specific vascular territory TCD waveform appearance either regionally, or globally may be clinically significant
  31. 31. Role of TCD for post TBI vasospasm Vasospasm following TBI is a very important source of morbidity and mortality. Too often, the first sign is a neurologic deficit, which may be too late to reverse. TCD assists in the clinical decision-making regarding further diagnostic evaluation and therapeutic interventions. As TCD-defined vasospasm preceded the neurological deficit in 64%, earlier intervention might reduce the incidence of vasospasm-related stroke in military/civilian hospitals with similar practice patterns
  32. 32. Role of TCD for post TBI vasospasm• TCD can easily identify onset and time-course of posttraumatic vasospasm and augments neurological examination after TBI• TCD can evaluate effect of treatment, especially after endovascular interventions• When performed in isolation, the contribution of TCD to improving patient outcome has not been established in the prospective studies. Nevertheless, TCD has become a regularly employed tool in neurocritical care
  33. 33. RESULTS: TCD &INTRACRANIALHYPERTENSION
  34. 34. Presence of ICH (%) 57 58 52 50 PHI PHI/IED CHI CHI/IED
  35. 35. PI ICP CBFV 50 0 100 150 200 250 300 23-Jun 24-Jun 25-Jun 26-Jun 27-Jun 28-Jun 29-Jun 30-Jun 1-Jul 2-Jul 3-Jul 4-Jul 5-Jul 6-Jul RIGHT 6-Jul 7-Jul 8-Jul 9-Jul 10-Jul 11-Jul 12-Jul Patient with GSW 13-Jul 14-Jul 15-Jul 16-Jul 17-Jul 18-Jul PI x 100 for demonstration 19-Jul 20-Jul 21-JulCALENDAR 23-Jun 24-Jun 25-Jun 26-Jun 27-Jun 28-Jun 29-Jun LEFT 30-Jun 1-Jul 2-Jul 3-Jul 4-Jul 5-Jul 6-Jul 6-Jul 7-Jul 8-Jul 9-Jul 10-Jul 11-Jul 12-Jul 13-Jul 14-Jul 15-Jul 16-Jul 17-Jul 18-Jul 19-Jul 20-Jul 21-Jul ICP MCA PI Trend shows almost direct inverse relationship between CBFV and PI, MCA CBFV
  36. 36. PI ICP CBFV 250 100 0 50 350 200 150 300 27-Nov 29-Nov 1-Dec 3-Dec RIGHT 5-Dec 7-Dec 9-Dec 11-Dec 13-Dec 14-Dec 16-Dec 18-Dec 20-Dec 22-Dec 5-Jan 27-Nov 29-Nov 1-Dec CALENDAR 3-Dec 5-Dec 7-Dec 9-Dec LEFT 11-Dec 13-Dec 14-Dec 16-Dec 18-Dec 20-Dec 22-Dec 5-Jan 23 yo, PHI due to the IED (r =-0.7) ICPPI x 100 for demonstration MCA PI MCA M1
  37. 37. TCD role for intracranial hypertension evaluation TCD wave-form changes indicates abnormally high ICP, especially after 30 to 35 mm Hg TCD changes may alarm Neuro-ICU personnel and may indicate malfunctioning of ICP probe Abnormally globally decreased pattern of the CBFV’s in parallel with increased PI’s indicate onset of diffuse intracranial hypertension Sudden onset of asymmetrical CBFV’s and PI’s changes may indicate potential mid-line shift TCD quantitative and qualitative analysis must be taken into account for evaluation of intracranial hypertension
  38. 38. CONCLUSION
  39. 39. TCD signs of VSP & high ICP TBI Type Post TBI High ICP/% VSP/% CHI 13/14.4 12/13.3 CHI/IED 12/13.3 9/10 PHI 21/23.3 16/17.7 PHI/IED 11/12.2 12/13.3 Total 57/63.3 49/54.4
  40. 40. TCD is a Critical Tool in Critical Care The value of TCD in clinical practice is well established, especially to measure and grade vasospasm following SAH and TBI Based on AHA Guidelines and many years of clinical practice TCD is a tool employed by the Neurosurgeon, Neurointensivist and Neurologist in the management of vasospasm Based on high frequency of posttraumatic vasospasm and intracranial hypertension TCD testing must be utilized for management of patient with wartime TBI
  41. 41. TCD is a Critical Tool in Critical Care The use of TCD at hospital admission allows identification of patients with brain hypoperfusion due to the vasospasm and/or intracranial hypertension. In such high-risk patients, early TCD goal-directed therapy can restore normal cerebral perfusion and might then potentially help in reducing the extent of secondary brain injury. TCD could provide information about abnormally high ICP/brain death In the future incorporation of TCD data may facilitate more injury- and time-specific therapies for wartime or civilian TBI patients
  42. 42. Limitations Retrospective data analysis IRB protocol pending Complete data analysis and correlation with clinical, imaging data and outcome will be done after IRB approval
  43. 43. The European Brain InjuryConsortium:Nemo solus satis sapit: nobody knowsenough alone.Acta Neurochir (Wien).1997;139(9):797-803 QUESTIONS?

×