Transcript TBI and Stroke
Traumatic Brain Injury
Galen V. Henderson, M.D.
Brigham and Women ’ s Hospital Harvard Medical School
Outline
• • • • • • • Epidemiology Concussion Types of hemorrhages with TBI Treatment of intracranial HTN Penetrating injuries Surgical decompression Intracranial monitoring vs. neuro exam and cerebraling
TBI in the United States
52,000 Deaths 275,000 Hospitalizations At least 1.7 million TBIs occur in the United States each year.* 1,365,000 Emergency Department Visits ??? Receiving Other Medical Care or No Care * Average annual numbers, 1995-2001
Causes of Death in US, 2012
(37/100,000)
Causes of Death in US, 2012
Age > 65: Accidents are #9 cause of death; rate 94.5/100,000
Classification of Head (Brain) Injury
Minimal Glasgow Coma Scale GCS 15 Mild GCS 14-15 Moderate GCS 9-13 Severe GCS < 8 Best Motor Response: Obeys Localizes pain Flexion withdrawal 6 5 4 Flexion abnormal (decorticate rigidity) Extension (decerebrate rigidity) 2 No response Best Verbal Response: Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response Eye Opening: Spontaneously 1 5 4 3 2 1 To verbal stimuli To pain Never 4 3 2 1 3-15 3
Concussion
Immediate and transient loss of consciousness accompanied by a brief period of amnesia after a blow to the head. 128/100,000 population in the US The clinical status of the momentary sensation of being "starstruck," or dazed, after head injury without a brief period of loss of consciousness is uncertain, but it is generally considered the mildest form of concussion.
Young children have the highest rates.
Sports and bicycle accidents account for the majority of cases among 5- to 14-year-olds Falls and vehicular accidents are the most common causes of concussion in adults.
Ropper A, Gorson K. N Engl J Med 2007;356:166 172 Mechanism of Concussion
Symptoms of post-concussive syndrome
Somatic Symptoms Persistent low grade headache Dizziness Vertigo Fatigability Insomnia Nausea/vomiting Mood Anxiety Depression Irritability Cognitive Deficits Slow thinking Poor attention and concentration Impaired memory
Control
fMRI and symptom severity
Chen JK, Johnston KM, Collie A, McCrory P, Ptito A.
J Neurol Neurosurg Psychiatry
2007; 78(11): 1231-1238.
Low PCS Moderate PCS High PCS
1 0.4
0.3
0.2
0.1
0 * * 2 1 2 0.5
0.4
0.3
0.2
0.1
0 Control group Low PCS group Moderate PCS group High PCS group
Spectrum of Pathologic Features and Outcomes of Traumatic Brain Injury DeKosky ST et al. N Engl J Med 2010;363:1293-1296.
Epidural Hemorrhage
Occurs in about 3% of head injuries Acute presentation; 40% have lucid interval with delayed (hrs) LOC 90% have skull fx; 85% of these are temporal Children get EDHs without fx Elderly rarely get EDHs – dura firmly adherent Amount of blood seen in fatal EDHs is 100-150ml
Source of blood Torn meningeal vessels Torn dural sinus Diploic veins Marrow sinusoids
Epidural Hemorrhage
Hyperdense Bi-Concave Limited by sutures (unless fracture crossed suture line)
Subdural Hemorrhage
Acute to subacute presentation Associated with severe trauma (except in elderly and especially those with coagulopathy) Associated with non-traumatic events (hypertensive hemorrhage or ruptured AVM with SAH/SDH Source of blood Torn bridging veins Laceration of cortical vessels Expanding contusion hematoma
Acute SDH
50% associated with a skull fx (not always at site of SDH) Most lethal form of SDH; 40-60% mortality rate Frequently associated with other forms of injury (DAI, contusions etc.)
Acute SDH
Amount of blood which is “ significant ” depends on pt age and rate of accumulation Infants: few mls Toddlers: 30-50 ml Children and adults: 150-200 ml
Subarachnoid Hemorrhage
Traumatic Most common cause Seen in almost any significant injury (+/- impact) In areas of contusions, lacerations, penetrating injuries Under SDHs where traction on bridging veins tears arachnoid vessels Non-traumatic Ruptured aneurysm/vascular malformation Torn/dissection of vertebral artery
Acceleration/Deceleration
Brain: SDH Diffuse vascular injury Traumatic axonal injury Contusional Tears Eye: Retinal hemorrhages, Optic nerve sheath hemorrhage Spine: Stretching
Gunshot Wounds
Damage is dependent on energy of missile which is dependent on the velocity Tissue damage Permanent track of bullet Temporary cavity which follows bullet Low-velocity bullet: 4-5 x bullet size Hi-velocity bullet: up to 15 times bullet size Secondary missiles (bone fragments)
Gunshot Wounds
Low Velocity Bullets (most civilian handguns) Most often do not exit skull Ricochet off inner table to form secondary track Exhaust energy and come to rest in brain High Velocity Bullets or Shotgun at close/contact range Most often exit skull producing massive fractures Large temporary cavity Often thrusts much of brain out of head
DON
’
T FORGET TO PROTECT THE C-SPINE !!
Hemopericardium Liver lacerations
FACTORS CAUSING SECONDARY BRAIN INJURY
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HYPERCAPNEA THE 4 H
’
s
• • •
HYPOXIA ( PaO 2 < 60 mmHg; SpO 2 < 90%) SYSTEMIC HYPOTENSION ( < 90 mmHg )
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INTRACRANIAL HYPERTENSION
OTHER FACTORS CAUSING SECONDARY BRAIN INJURY
ISCHEMIA
VASOSPASM
SEIZURES
LOSS OF AUTOREGULATION
Intracranial HTN Treatment Modalities
Insert ICP monitor General goals: Maintain ICP < 20 mm Hg and CPP > 70 mm Hg For ICP > 20-25 mm Hg for > 5 minutes Drain CSF via ventriculostomy Elevate head of bed Osmotherapy Sedation, agitation and fever control Hyperventilation Pressor therapy to maintain MAP and ensure CPP For refractory intracranial HTN Phenobarbital/Hypothermia/Decompressive craniotomy
Osmolality of IV fluids
Fluid
5% Dextrose Lactated ringers Plasma 5% Albumin Normal Saline 0.9% 25% Albumin 6% Hetastarch 2% Normal Saline 3% Normal Saline 25% Mannitol 7.5% Normal Saline 23.4% Normal Saline
Osmolality (mOsm/kg)
252 250-260 285 290 308 310 310 682 1025 1375 2400 8008
Surgical Treatment of Intracranial HTN
Original Article Decompressive Craniectomy in Diffuse Traumatic Brain Injury
D. James Cooper, M.D., Jeffrey V. Rosenfeld, M.D., Lynnette Murray, B.App.Sci., Yaseen M. Arabi, M.D., Andrew R. Davies, M.B., B.S., Paul D'Urso, Ph.D., Thomas Kossmann, M.D., Jennie Ponsford, Ph.D., Ian Seppelt, M.B., B.S., Peter Reilly, M.D., Rory Wolfe, Ph.D., for the DECRA Trial Investigators and the Australian and New Zealand Intensive Care Society Clinical Trials Group N Engl J Med Volume 364(16):1493-1502 April 21, 2011
Study Overview
• Patients with severe traumatic brain injury and refractory intracranial hypertension were randomly assigned to either decompressive craniectomy or standard care.
• Craniectomy was associated with a significant reduction in intracranial pressure but worse outcomes.
Cooper DJ et al. N Engl J Med 2011;364:1493-1502 .
Cooper DJ et al. N Engl J Med 2011;364:1493-1502 .
Original Article A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury
Randall M. Chesnut, M.D., Nancy Temkin, Ph.D., Nancy Carney, Ph.D., Sureyya Dikmen, Ph.D., Carlos Rondina, M.D., Walter Videtta, M.D., Gustavo Petroni, M.D., Silvia Lujan, M.D., Jim Pridgeon, M.H.A., Jason Barber, M.S., Joan Machamer, M.A., Kelley Chaddock, B.A., Juanita M. Celix, M.D., Marianna Cherner, Ph.D., and Terence Hendrix, B.A.
N Engl J Med Volume 367(26):2471-2481 December 27, 2012
Study Overview
• In this randomized trial involving 324 patients with severe traumatic brain injury in Bolivia and Ecuador, guideline based management with intracranial pressure monitoring was not superior to management based on imaging and clinical assessments.
Cumulative Survival Rate According to Study Group.
Chesnut RM et al. N Engl J Med 2012;367:2471-2481
EEG MAP CPP ICP Exam TCD Cellular Metabolism
Summary
• • • • • • • Epidemiology Concussion Types of hemorrhages with TBI Treatment of intracranial HTN Penetrating injuries Surgical decompression Intracranial monitoring vs. neuro exam and cerebral imaging