WAR RELATED TRAUMATIC BRAIN INJURY

Transcription

1 WAR RELATED TRAUMATIC BRAIN INJURY Geoffrey Ling, M.D., Ph.D. Colonel, Medical Corps, US Army Professor and Vice-Chair, Neurology, USUHS Director, Neuro Critical Care, Walter Reed AMC Attending Physician, Anesthesiology & Critical Care Medicine, Johns Hopkins

2 Mechanisms of Traumatic Brain Injury Penetrating Injury Cause: Physical disruption of cells and fiber tracks, hemorrhaging, cell apoptosis Concussive Injury Cause: Mechanical loading leading to cell failure Hypoxia Cause: Lack of O 2 Explosive Blast Injury Cause: Mechanism of injury unknown

3 Blast Wave

4 Blast to Head

5 Blast Injury - Categories Four categories of blast injury: Primary Caused by the direct blast energy Crush injuries, lacerations, hemorrhage common Secondary Caused by projectiles and other hazards created by the blast Rubble, building fragments, shrapnel, etc. Tertiary Inertial injuries caused by personnel being propelled by the blast (being thrown) Quaternary Inhalation, burns, and anything else not described by first three

6 Blast TBI Wide spectrum of neurological Mild TBI effects have been described Subtle cognitive deficits, neurobehavior changes, mood and affect issues Both can occur together Moderate TBI Loss of consciousness, overt structural damage Severe TBI Severe neurological deficits, subarachnoid hemorrhage, vascular changes (acute and chronic)

7 Taxonomy of TBI Severity Mild no LOC or amnesia brief amnesia or LOC, or impaired alertness, memory postconcussive syndrome GCS Moderate LOC > 5 min, or focal neurologic deficit GCS 9-12 Severe GCS < 8

8 Mild TBI Pt suffered blast TBI from about 8 feet away Wearing helmet/armor No LOC but confusion/amnesia for at least 15min (Grade 2 concussion) CT: normal Persistent neuro cognitive deficits on Day #2 (transfer) Frontal lobe based tasks impaired (digit span, word list generation) Normal by Day 7, returned to duty

9 Moderate TBI Pt exposed to mortar explosion and struck by frag GCS 12 at scene, brought to CSH Ct: frag track w/ hematoma, no SAH

10 Moderate Injury to Brain Outcome Bifrontal craniotomy with debridement ICP monitor placed, treated with HTS TCDs increased flow velocities so ptient was treated Peaks at HD#7 and normal by HD#11 Discharge to home

11 Severe TBI Pt suffered TBI from hanging IED CT: L SDH, SAH, L temp fx, L orbital roof fx

12 Severe Blast TBI Outcome Initial Left hemi-craniectomy with SDH evac Partial frontal lobectomy (of herniated portion) ICP control with HTS CPP directed therapy Seizures but controlled Autonomic dysfunction syndrome controlled with propanolol and morphine Vasospasm successfully tx with HHH Followed commands by Day #7 Followed multi-step commands by Day #12 and extubated Transferred to civilian hospital on Day #14

13 TBI Management Learning from the war Evolving continuously

14 Mild TBI Good News Military Medical Care is leading the way Creation of the first large system-wide approach to concussion Concussion diagnostic tool being used widely in the field (including medics) MACE Clinical practice guidelines for care DoD-VA CPG mtbi/concussion 2009 guidelines Clinical guidelines for return to duty (or play) 3 strikes and you are out There is always room for improvement

15 In-Theater mtbi Treatment Developed by far forward providers MAJ Bell, 10 th MTN, FOB Shank, RC EAST LCDR Skipton, LT Nasky, Camp Leatherneck, RC South Mandatory mtbi screening with MACE All occupants of vehicle ahead and behind Dismounts within 100 meters Initial symptom management by unit level provider (medic) Persistent or concerning cases sent to battalion surgeon CT for most at CSH with return to FOB if negative Reconditioning center at FOB

16 Military Acute Concussion Evaluation (MACE) History and symptoms are represented by items I-VIII Available for free:

17 Standardized Assessment of Embedded in the MACE is the Standardized Assessment of Concussion (SAC), a widely used, validated, brief cognitive tool. Gross cognitive tool addressing 4 domains Orientation Immediate memory Concentration Memory recall Max score is 30 < 25 is significant Concussion (SAC) Available for free:

18 Mild TBI Treatment treating as we learn Writing Co-Chairs: Cifu, D, Labutta, R and Ling, GSF First, large system-wide approach to standardize management of concussion

19 AAN RECOMMENDATIONS (single concussion) Grade 1 (mild) Remove from duty/work/play Examine immediately and at 5-minute intervals May return to duty/work if clear within 15 minutes Grade 2 (moderate) 1.Remove from duty for the rest of the day 2.Examine frequently for signs of CNS deterioration 3. Physician s neuro exam as soon as possible (within 24 hours) 4.Return to duty after 1 full asymptomatic week (after being cleared by physician) Grade 3 (severe) 1.Take to emergency department 2.Neurologic evaluation, including appropriate neuroimaging 3.Consider hospital admission Neurology 48: (1997)

20 AAN RECOMMENDATIONS (Repeated Concussion) Grade of Concussion Grade 1 (first) Grade 1 (second) Grade 2 (first) Grade 2 (second) Grade 3 (first) (brief LOC) Grade 3 (first) (long LOC) Grade 3 (second) Grade 3 (third) Return to Duty 15 min 1 week 1 week 2 weeks 1 week 2 weeks 1 month Consult neurologist Neurology 48: (1997)

21 Reconditioning Center Mandatory days taking a knee (rest and off patrol duty) but stay with unit at the front Symptom management Virtually 100% have h/a, many with sleep issues 5-days of symptom Rx therapy then as needed Education (daily 1-to-1 with provider) Cognitive exercises Sudoku, crosswords puzzles, Scrabble RTD (return to duty) if symptom free and off all meds at end of mandatory period If still symptomatic, then refer to CSH to neurologist

22 Military Management of Moderate-Severe TBI Good News The civilian medical care model for moderate to severe TBI has been adapted to in-theater use Neurosurgical advances have been made Decompressive hemicraniectomy Cerebral angiography for blast related vasospasm Intra-arterial nicardipine for blast related vasospasm Cranioplasty Hypertonic saline for ICP control Armonda et al, Neurosurg 59: 1215 (2006) Ling et al, J Neurotrauma 26: (2009)

23 Treatment begins on the battlefield Knuth, Letarte, Ling et al Brain Trauma Foundation (2005) Download available:

24 Pre-Hospital Guidelines for Management of TBI (Airway) Avoid hypoxia O 2 Sats > 90 or po 2 > 60mmHg Artificial airway for GCS < 8 Endotracheal tube (ET tube) or other Hyperventilation for cerebral herniation Not for ICP prophylaxis or routine use

25 Pre-Hospital Guidelines for Management of TBI (Circulation) Avoid hypotension Systolic BP > 90mmHg No specific resuscitation fluid is recommended Hypertonic saline has logistical advantages Hypertonic saline at < 500cc boluses is acceptable Use for ICP management is an option Mannitol for cerebral herniation if intravascular volume can be maintained

26 Pre-Hospital Guidelines for Management of TBI Determine GCS and pupil function as soon as possible Triage GCS 9 13 to CSH GCS < 14 should not return to duty until normalized Sedation and analgesia as needed for transport Analgesics in small doses with proper monitoring Antibiotics for penetrating TBI is an option

27 Moderate Severe TBI Guidelines for the management of severe traumatic brain injury The American Association of Neurological Surgeons J Neurotrauma 24 Suppl 1: p. S1-106 (2007) Download available: Explosive Blast Neurotrauma Ling, Bandak, Armonda, Grant and Ecklund Journal of Neurotrauma 26: (2009)

28 RAPID NEURO EXAM Mental Status: alert/oriented Glasgow Coma Score (GCS) Speech: naming common objects Cranial Nerves: pupils (midbrain), corneals (pons), gag, over-breathing ventilator (medulla) Visual Field (parietal, occipital, temporal) Motor (frontal) Sensory: light touch or pain (parietal) Reflexes: Babinski (CNS vs PNS)

29 Early Prognostic Signs Trauma Design: Retrospective study of adults and children Pts: 846 (668M:178F), MVA 50%, motorcycle 22%, falls 15% Outcome: 1 year GOS Results: GCS 8 (40% good recovery) to 3 (7%), death 8 (12% death) to 3 (73%), Pupils: Bilat abn (62% death, 5% PVS) vs normal (16% death, 0 PVS, 53% good). Conclude: Outcome assoc with GCS, pupils, body temp, age Jiang et al, J Neurotrauma 19: 869 (2002)

30 CT in Head Trauma Most useful imaging tool Identifies bony and soft tissue lesions Blood, edema, air Foreign bodies Weakness Acute blood may be low or iso dense in anemia or DIC Not as good as MRI for DAI, cortical contusion, posterior fossa pathology Miss fracture at vertex and traumatic aneurysms Zee and Go, Neuroimaging Clinics N Amer 8:525 (1998)

31 Indications for CT in TBI GCS < 15 Clinical evidence of basilar skull fx Depressed skull fx > 1 cm Penetrating injury Anisocoria or fixed and dilated pupils Neurological deficit Known bleeding diathesis or anticoagulant tx Prolonged LOC (> 5 min) Antegrade amnesia Zee and Go, Neuroimaging Clinics N Amer 8:525 (1998)

32 Indications Based on Risk High Risk for intracranial pathology (need CT) Focal neurol signs, penetrating wound, depressed skull fx (palpable), impaired MS (no drugs, intoxicants) Moderate Risk (possible CT) Hx of changed MS, progressive h/a, sz, amnesia, clinical evid of basilar skull fx, serous facial injury, vomitting, multiple trauma, possible child abuse, < 2 y.o. Low Risk (no CT) Asymptomatic, headache, dizziness, scalp lac or hematoma Mirivs and Shanmuganathan, J Intens Care Med 9:305 (1994) Masters et al, New Engl J Med 316:84 (1987)

33 MRI in Head Trauma MRI is superior to CT for every pathology except skull fracture and acute subarachnoid hemorrhage Much superior for edema, DAI, contusions and hematomas (> 30% better for SDH and EDH), posterior fossa lesions Less advantageous Speed of study, ability to image bones, abdomen and chest at the same sitting Improved data does not impact clinical care Bruce, Child Nerv Syst 16: 755 (2000) Orrison et alm Am J Neurorad 15: 351 (1994) Zimmerman & Bilaniuk, Neuroimag Clin N Amer 4:349 (1994)

34 Indications for ICP Monitoring Severe TBI (GCS < 8) and abn CT Severe TBI and normal CT, if (>2): > 40 years old, uni or bilateral motor posturing, systolic BP < 90 mmhg Other clinical indications Marmarou et al, J Neurosurg 75:S59-S66 (1991) Gopinath et al, J N Nsurg Psy 57: (1994) Eisenberg et al, J Neurosurg 69:15-23 (1988)

35 ICP Threshold for Intervention In pts without craniectomy, an ICP threshold of 25 mmhg improved outcome. craniectomy pts, ICP threshold 15 mmhg Using logistic regression analysis of pts in the TBI Databank, 20 mmhg was found to correlate with best outcome. Eisenberg et al, J Neurosurg 69:15-23 (1988) Marmarou et al, J Neurosurg 75:S59-S66 (1991)

36 ICP Plateau or A Waves Sustained ICP elevation for min Associated with pathology Exacerbates ischemic state, prob cause for herniation Only observed in pathologic states

37 Brain Code Head of Bed to 30 o Hyperventilate to pco mmHg Mannitol (0.5gms/kg, i.v. slow push) Saline bullet (23% NaCl, 30cc) CSF drainage

38 Hyperventilation Paradox in TBI Aggressive hyperventilation (PaCO2<25 mmhg) can cause a rapid reduction in ICP a therapeutic goal HV can increase jugular venous desats assoc with poor outcome HV can incr AVdo 2 and decrease CBF potentially exacerbating ischemia

39 Hyperventilation Use in TBI For acute ICP management, begin with a PaCO2 goal of mmhg For recalcitrant ICP, advance PaCO2 goal to mmhg consider use of jugular bulb catheter, LiCox, etc Taper HV as soon as possible Chronic HV should be avoided, particularly in the first 24 Hrs

40 Mannitol Effectiveness in TBI Superior to barbiturate for control of ICP and CPP Significantly better survival Reduction of edema after low doses use as single bolus (not infusion) of 0.5-1gm/kg, i.v. Schwartz et al, Can J Neurol Sci 11: (1984) Nath & Galbraith, J Neurosurg 65:41-43 (1986)

41 Hypertonic Saline 0.9% to 3% to 23.4% NaCl solutions Shown to be effective in neurotrauma by shrinking brain and thus reduce ICP can do so and maintain intravascular volume Goal is to increase osmolarity not dehydrate May not be effective in stroke Bayir et al, Crit Care 31:S112 (2003) Qureshi and Suarez, Crit Care Med 28: 3301 (2000) Bhardwaj et al, Stroke 31: 1694 (2000) Munar et al, J Neurotrauma 17: 41 (2000)

42 Hypertonic Saline Emergency treatment for herniation Saline bullet = 30 bolus of 23.4% saline Can be repeated Up to 50% reduction of ICP 65% of pts below 20mmHg ICP Effect lasts for hours Potential toxicity ATN Suarez et al, Crit Care Med 26: 1118 (1998)

43 Hypertonic Saline Clinical Approach Establish central venous access Initiate therapy with 3% saline at 75 cc/hr (or higher if requiring fluid resuscitation) use 50% chloride/50% acetate to minimize risk of hyperchloremia Infuse to a goal Na (ex ) Check serum Na frequently (q 4-6 hrs) ballpark serum osm will be double serum Na

44 Hypertonic Saline Clinical Approach Reassess neuro exam, increase Na goal as needed (max: ) When goal is achieved, continue infusion with 0.9% saline (or 2% if Na drifts downward) Continue treatment until day 4 or 5 post-injury To stop, just d/c hypertonic saline infusion and allow pt to autotaper

45 Pharmacologic Coma TBI Pharmacologic coma may be considered for pts in whom intracranial hypertension remains refractory to maximal medical and neurosurgical interventions Basic Premise absolute ICP control improves outcome

46 Pharmacologic Coma in TBI Improved survival when used to treat recalcitrant intracranial hypertension in hemodynamically salvageable severe TBI pts. Patient selection is crucial pts who failed other ICP therapy pts with adequate cardiovasc fxn pts w/ intact autoregulation pts without diffuse injury Nordstrom et al, J Neurosurg 68: Lobato et al, J Neurosurg 68:

47 Malignant ICP Up to 15% of TBI pts will not respond to either maximal medical or neurosurgical intervention. Mortality in these pts approaches 100% Miller et al, J Neurosurg 54: (1981) Narayan et al, J Neurosurg 56: (1982)

48 Cerebral Perfusion Pressure in TBI CPP=MAP-ICP Prospective studies have shown 50% increase in survival 50% increase in good outcome No increase in ICP or adverse clinical outcomes by actively maintaining CPP Marion et al, J Neurosurg 75: (1993) Marshall et al, J Neurosurg 73:S28-S36 (1991)

49 TBI and Hemorrhagic Shock

50 Cerebral Perfusion Pressure in TBI CPP Goal > 60mmHg Retrospective studies have shown that there is 20% increased mortality for each incremental decrease of 10 mmhg For CPP < 60 mmhg greater than 33% of the time, 100% mortality Changaris et al, J Trauma 27: (1987) Ling and Neal, J Neuro Crit Care 2: (2005)

51 Resuscitation Whole blood Crystalloid with hypertonic fluids Saline is hypertonic Stop the bleeding fviia Use in TBI is being studied Known efficacy in hemorrhagic stroke Plasma Platelets

52 Adrenergic Receptors and Cerebral Vessels α receptors are on the outside of cerebral vessels no β receptors in cerebral vessels DA receptors are on the lumenal/inside of cerebral vessels Faraci and Heistad, Circ Res 66:8-17 (1990)

53 Vasopressors (when ICP is an issue) Acceptable Phenylephrine Use with caution Dopamine Norepinephrine Vasopressin

54 AEDs for Early Post-traumatic Seizures Phenytoin or carbamazepine are effective in preventing early post-traumatic seizures. Treat only for first 7 days post injury Temkin et al, NEJM 323:497 (1990) Glotzner et al, Neurochir 26:66-79 (1983) Manaka et al, JpnJ Psych Neuro 46: (1992) Amer Acad Phys Med Rehab Arch Phys Med 79: 594 (1998)

55 AEDs for Late Post-traumatic Seizures Phenytoin, carbamazepine, valproic acid and phenobarbital therapies did not significantly reduce the rate of late PTS Temkin et al, NEJM 323:497 (1990) Glotzner et al, Neurochir 26:66-79 (1983) Manaka et al, JpnJ Psych Neuro 46: (1992) Temkin et al, J Neurosurg 91: (1999)

56 Fever and Hypothermia Fever increases metabolic demand and worsen outcome Fever Acetominophen Cooling blankets Hypothermia Not yet Standard of Care No clinical evidence yet to support its use Most effective therapy in preclinical studies though

57 Pharmacologic Therapy Not Routinely Recommended Sedation interferes with neurologic exam and thus treatment Neuromuscular Blockade assoc w/ incr length of stay, incr incidence of pneumonia and sepsis no improvement in outcome Hsiang et al, Crit Care Med 22: (1994)

58 Steroids Use in TBI The use of steroids is not recommended for either improving outcome or reducing ICP. Brain Trauma Foundation Guidelines (2002)

59 Nutritional Support in TBI In first 2 weeks, pts are hypermetabolic TBI pts lose approx 15% of body wt/week from nitrogen loss 30% wt loss increases mortality

60 Nutritional Support Replace 140% of resting metabolism expenditure in nonparalyzed brain injured pts Use formulas containing at least 15% calories as protein by 7 th day after TBI Enteral feeds are preferable less hyperglycemia, less infxn, cheaper jejunal feeding may be superior Beware the free water content

61 Delayed Vasospasm of Blast TBI Prevalence of 47% Onset Subclinical: 2-3 days post injury Clinically evident: days after Treatment Endovascular Medical Armonda et al, Neurosurg 59: 1215 (2006) ACA SHUNTING with SEVERE L ICA VASOSPASM

62 Hemicraniectomy Surgical intervention for moderate to severe blast TBI Early hemicraniectomy as blast brain becomes hyperemic and edematous very quickly (few hours) ICP treatment and local cooling effect Ling et al, J Neurotrauma (2009)

63 Conclusion In adversity there is opportunity Learning as we treat. Clinical management of TBI is advancing as we continue to learn from the best teachers --- our patients. 63