Head injury

Head Trauma

Wayne Triner, DO, MPH, FACEPProfessor, Emergency Medicine

Albany Medical College & State University at Albany

New Zealand TBI

All TBI 790 / 100,000 py

Mod to Severe 41 / 100,000 py 1.2 x risk Maori 2-5 x risk in rural

the incidence of TBI per 100 000 people per year (790 cases), especially mild TBI (749 cases), in New Zealand was substantially greater than in other high-income countries. in Europe (47–453 cases) and North America (51–618 cases).

TBI FactoidsUnited States 2007

Pathophysiology

Primary Direct tissue injury

Secondary Cerebral

perfusion/edema Vasoregulation Tissue ischemia Herniation

Cerebral Blood Flow

Cerebral Blood FlowCBF ~ CPP – CVP

Cerebral Perfusion PressureCPP = MAP – ICP

CBF ~ (MAP – ICP) - CVP

The Range of TBI

Mild GCS > 12

Moderate GCS 12-8

Severe GCS < 8

Head Injury StratificationGlasgow Coma Score

Eye Opening 4=Spontaneous 3=To voice 2=To pain 1=None

Verbal 5=Normal conversation 4=Disoriented conversation 3=Words, but not coherent 2=No words......only sounds 1=None

Motor 6=Normal 5=Localizes to pain

4=Withdraws to pain 3=Decorticate posture 2=Decerebrate 1=None

Mild GCS > 12

Moderate GCS 12-8

Severe GCS < 8

Mild TBI

GCS 13-15 < 30 minute LOC Non-focal exam

Mild TBI:Is there a problem?

Short term Mood and cognitive

disturbances Validation Variable rate of CT

abnormalities

Long term Depression Dementia Parkinson’s Cognitive deficits

Mild TBI:Who to CT

The goal being identification of significant conditions amenable

to intervention

Critical Questions;Which patients with mild TBI need a head CT?

LEVEL I RECOMMENDATIONA noncontrast head CT is indicated in head trauma patients with loss of consciousness or pos- traumatic amnesia only if one of the following is present: headache, vomiting, age > 60 years, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicle, posttraumatic seizure, GCS < 15, focal deficit or coagulopathy.

LEVEL II RECOMMENDATIONA noncontrast head CT should be considered in head trauma patients with no loss of consciousness or post-traumatic amnesia if there is focal deficit, vomiting, severe headache, age > 65 years, signs of basilar skull Fx, GCS < 15, coagulopathy or dangerous mechanism (ejection from vehicle, pedestrian struck, fall of more than 3 ft or 5 stairs)

Clinical Policy: Neuroimaging and Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute

SettingACEP 2008

Understand the Intent and Concepts

Understand the risk factors Age Small brains Inability to fully evaluate Propensity for bleeding Mechanism and evidence of trauma

Recognize neurological abnormalities HA, vomiting, focal deficits

What works to improve outcomes in minor TBI?

Recommendations “Neuro rest”

Proven ?????

Concussion and Sports:return to play guidelines(second impact syndrome)

Moderate to Severe TBI (GCS 3 – 12)

ABCs Limit secondary brain injury Preservation of CBF Issues of coagulation

Reversal of coagulopathies▪ F VIIa▪ Prothrombin complex concentrate▪ Vit K and FFP

Management of Severe Head Trauma

“Evidence based” Standards, Guidelines and Options• Preserve oxygenation

(at all costs)• Avoidance of hypotension

(SBP < 90)• Euventilation

Hyperventilation

Rapid reduction in ICP

3 compartment model

Below pCO2 < 23, CBF < 20 ml/100g/min

Severe TBI;Proven Management Strategies

Preserve oxygenation (at all costs) Issues of airway management▪ Pre-hospital ETT▪ Neuro-protective RSI▪ Laryngeal manipulation▪ Hypotension▪ ICP management

Severe TBI;Proven Management Strategies

Avoidance of hypotension (SBP < 90) Preserve CBF Control of cerebral edema▪ Brief hyperventilation

Hyperosmolar therapy

Hyperosmolar Therapy

Recommendations; Level II

▪ Mannitol is effective for the control of raised intracranial pressure at doses of 0.25 to 1 g/kg. Hypotension (SBP < 90) should be avoided

Level III▪ Restrict mannitol use prior to ICP monitoring

to patients with signs of transtentorial herniation or deteriorating mental status not attributable to other causes

Mechanism of Action Blood rheology

▪ immediate plasma volume expansion

Osmotic redistribution Hypertonic Saline

23.4% 50 ml

Indications for hyperosmolar therapy: impending herniation

Typically uncus herniating across tentorum CN III compression▪ pupillary dilitation▪ 80% ipsilateral to side of structural lesion

Pyramidal tract compression▪ Contralateral weakness▪ 80% contralateral to side of structural lesion

Rapid deterioration of mental status Cushing’s reflex

Hypothermia

No Level I or II recommendations Level III:

No change in all-cause mortality 46% improved chance of favorable

outcome (GOS 4-5) Some evidence of improved outcome

with > 48 hours of cooling

Traumatic SAH

Most common CT finding in TBI

Often occurs in concert with other imaging abnormalities

Neuro deficits reflect parenchymal injury and generally not a vascular insult

Epidural Hematoma

High Mortality Rate Association with Skull Fracture

Subdural Hematoma

Acute Higher Mortality

Rate Than EDH underlying brain

injury co-morbidity

Chronic Subacute

Cerebral (Parenchymal) Contusions

Presence of contusion does not independently predict outcome

Cerebral Edema

• Cisterns• Gray – White

Interface

Indications For Surgical Intervention

Decompressable lesion with neuro findings SDH, EDH, very few contusions Traumatic SAH is not decompressable

and not an indication for aneurysm screening

Indications of increasing ICP Deteriorating mental status Herniation syndromes

Decompressive craniectomy

Intracranial Pressure Monitoring

Cerebral edema Monitoring

GCS < 8 and Abnormal Head CT

GCS < 8 and Normal Head CT with... ▪ age > 40▪ posturing▪ hypotension

ICP determination early detection of

mass lesions limit potentially

harmful therapies determination of

prognosis CSF drainage*

Penetrating Head Trauma

All about GCS GSW injury reflect patterns of

ballistics

Basilar Skull Fracture

Issues in management Hearing Antibiotics Disposition

Severe TBI Prognosis

1 Fearnside MR, Cook RJ, McDougall P, et al.: The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical, and CT variables. Br J Neurosurg 7:267-279, 1993.2 Braakman R: Interactions between factors determining prognosis in populations of patients with severe head injury. In Frowein RA, Wilcke O, Karimi-Nejad A, et al. Advances in Neurosurgery: Head Injuries-Tumors of the Cerebellar Region. Springer-Verlag, Berlin: 12-15, 1978.3 Phuenpathom N, Choomuang M, Ratanalert S: Outcome and outcome prediction in acute subdural hematoma. Surg Neurol 40:22-25, 1993

Age

Strong factor in determining outcome from severe TBI

This holds true even after correcting for co-morbid conditions.

The Cutting Edge

TBI Biomarkers Need for imaging Validation Prognostication

Intervention Hypothermia Progesterone Reduction of oxidative stress

Useful Resources