336 traumatic and penetrating head injury

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Traumatic and penetrating head injuries Youmans Chapter 336 Bizhan Aarabi, Rocco Armonda,Randy S. Bell, Frederick L. Stephenstle 24/05/59

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Page 1: 336 Traumatic and penetrating head injury

Traumatic and penetrating head injuriesYoumans Chapter 336Bizhan Aarabi, Rocco Armonda,Randy S. Bell, Frederick L. Stephenstle 24/05/59

Page 2: 336 Traumatic and penetrating head injury

Outline• Ballistic• Pathogenesis• Clinical finding• Management• Complication• Prognosis

Page 3: 336 Traumatic and penetrating head injury

Ballistics

• Three component– Interior ballistics

• Projectile to gun barrel– Exterior ballistics

• Projectile’s behavior in medium, air• Shape, caliber, weight, initial velocity, ballistic coefficient

– Terminal ballistics• Projectile impact on target

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Pathogenesis• Juxtamissile pressure : affects the brain tissue immediately in

the path of a projectile• Longitudinal strong shock waves : start immediately after

impact of the projectile with brain tissue and travel in spheres ahead of the projectile

• Ordinary pressure waves : projectile transfers its kinetic energy to the surrounding brain tissue and produces a temporary cavity

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Pathology

Page 6: 336 Traumatic and penetrating head injury
Page 7: 336 Traumatic and penetrating head injury

Clinical finding

• Demographic– Male, Homicide, Suicide, Accident

• Level of consciousness– Focal deficit, Unconsciousness, Consciousness

• Brainstem function– Abnormal pupillary response to light, corneal and doll’s eye

reflexes, cold calorics, cough and gag reflexes– Reflect damage by either brain shift secondary to a

temporary cavity resulting from ordinary pressure waves– Uncontrollable intracranial hypertension secondary to

swelling or hematomas

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Clinical finding• Focal deficits

– CN injuries– Sensorimotor aphasia

• Mild Traumatic Brain Injury, Blast, and Posttraumatic Stress Disorder– High-frequency (0.5 to 1.5 kHz) low-amplitude stress

waves damage the blood-brain barrier– Low-frequency (<0.5 kHz) high-amplitude shear waves

damage the gray-white matter junction– The result is brain edema, cellular necrosis and apoptosis,

cytoskeletal damage, diffuse axonal injury, and neuronal

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Management

• Imaging Studies• Medical Management• Surgical Management

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Imaging Studies

• CT scan– Injury Profile

• entry site and trajectory of the fragment into the brain• terminal ballistics (perforating, penetrating, and tangential)• involvement of the paranasal sinuses, orbits, skull base, and

mastoids• missile track,number of tracks and ricochet• presence or absence of intracranial hematomas • brain edema and ischemia and brainstem involvement is defined

by CT

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Imaging Studies• CT scan– Vascular Injury Profile

• subarachnoid hemorrhage and delayed traumatic intracerebral hematomas

– Involvement of Air Sinuses and Mastoid Air Cells• CFS leakage

– Surgical Planning– Retained Fragments– Deep Infections– Prognosticating Tool

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Imaging Studies• Conventional Angiography– “gold standard” for the diagnosis of major vascular injuries

and vasospasm

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Medical Management

• Prehospital rescue, intubation, oxygenation, ventilation, volume resuscitation

• Broad-spectrum antibiotics• Anticonvulsants

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Surgical Management

• Débridement and Repair of the Scalp– Staphylococci with or without gram-negative organisms

(coliform bacteria,Aerobacter aerogenes, Klebsiella species, and Acinetobacter species)

– Plastic surgeon– Tripod incisions are not favored– Sutures are not to be removed for up to 2 weeks.

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Surgical Management

• Craniectomy versus Craniotomy– Recommendation is craniotomy and débridement of the

skull with replacement of the bone to avoid the future need for cranioplasty

• Débridement and Watertight Closure of the Dura Mater

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Surgical Management

• Débridement of Devitalized Brain• Débridement of Retained Fragments• Repair of the Skull Base

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Complication

• Vascular Injuries with Gunshot Wounds to the Head– incidence of TICA : 3 -40 %– Urgent to detect : delayed traumatic intracerebral

hematoma, new stroke, persistent coma, death– Risk factor : orbitofaciocraniocerebral injuries, injuries

near the pterion, and patients harboring intracranial hematomas

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Page 19: 336 Traumatic and penetrating head injury

Complication• Intracranial Infections– Acinetobacter

• Posttraumatic Epilepsy– 34% and 50% of victims of PBI become epileptic when

monitored for 2 to 15 years– phenytoin, carbamazepine, and valproate are effective in

preventing early posttraumatic seizures in patients with closed head injury, but these medications do not prevent long-term epileptic seizures