HEAD TRAUMA

Will/Grundy EMS 2009 2nd Trimester May CME

OBJECTIVES
Understand the divisions of the brain and their main function. Understand the neurological assessment and the cranial nerve exam. Describe primary injury vs. secondary injuries. Describe the evolution of increased intracranial pressure and the treatment for the brain injured patient. Explain the Monro-Kellie Doctrine and autoregulatory system

NO PRESSURE

MENINGES
1) Dura Mater 2) Arachnoid 3) Pia Mater

DURA
Outermost layer Tough, fibrous Produces folds
Falx cerebri Tentorium cerebelli

Dura Mater creates Potential Space * Epidural space * Subdural space

Epidural Hemorrhage

Subdural Hemorrhage

ARACHNOID
Avascular connective tissue Fibrous cords (trabeculae) attached to the PIA mater Arachnoid Villi
Reabsorb CSF

Subrachnoid Space
Contains large blood vessel Contains CSF Expanded areas-Basilar cistern, Lumbar cistern

PIA
Thin, vascular Carries a rich supply of blood vessels Forms the choroid plexus Choroid plexus is found in the walls of the ventricles Choroid plexus produce CSF

Meninges of the Brain

CEREBRAL CORTEX

FRONTAL LOBE
Personality Behavior Voluntary motor function Motor speech (Brocas), Left side dominent Intellectual functions, problem solving Judgment; good/bad, right/wrong
Called the MOM portion of the Brain

PARIETAL LOBE
Primary sensory lobe; pain, pressure, vibration, touch Localization of stimuli Object recognition Position sense Sensory association

TEMPORAL LOBE

Primary auditory lobe Long term memory Emotions Cognitive speech (Wernickes); organize language, understand and respond to verbal input

Uncus discriminates smells

OCCIPITAL LOBE
Processing visual input

INTRACRANIAL DYNAMICS
Three substances in the cranial vault
Brain 80% Blood 12% CSF 8%

MONRO-KELLIE DOCTRINE
If one of these substances increase, then one or both of the other must therefore decrease to maintain normal pressure within the cranial vault

 Normal ICP = 5 to 10/15

Upper limits of 20 may be acceptable as long as CPP is adequate

Cerebral perfusion pressure (CPP) = 60 to 100

The pressure needed to perfuse the brain Ideal is 70 Calculated by subtracting ICP from MAP

Cerebral Blood Flow

Oxygen and glucose delivery are controlled by cerebral blood flow
A function of cerebral perfusion pressure (CPP) and resistance of the cerebral vascular bed CPP is determined by the mean arterial pressure (MAP) (the diastolic pressure plus one-third pulse pressure) minus intracranial pressure

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs Results in increased cerebral blood volume (increasing ICP) and further cerebral vasodilation

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs Results in increased cerebral blood volume (increasing ICP) and further cerebral vasodilation

Cerebral Blood Flow

Vascular tone in the normal brain is regulated by:
Carbon dioxide pressure (PCO2) Oxygen pressure (PO2) Autonomic and neurohumoral control

PCO2 has the greatest effect on intracerebral vascular diameter and subsequent resistance

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs Results in increased cerebral blood volume (increasing ICP) and further cerebral vasodilation

Cerebral Blood Flow

Vascular tone in the normal brain is regulated by:
Carbon dioxide pressure (PCO2) Oxygen pressure (PO2) Autonomic and neurohumoral control

PCO2 has the greatest effect on intracerebral vascular diameter and subsequent resistance

Intracranial Pressure (ICP)

Normal range is 0-15 torr When ICP rises above this level, the ability to maintain CPP is compromised
Cerebral blood flow is diminished

The body attempts to compensate for the decline in CPP by a rise in MAP
Further elevates ICP, and CSF is displaced to compensate for the expansion

If unresolved, the brain substance herniates

CAUSES OF INCREASED ICP

Defecation Coughing Airway obstruction Vomiting PEEP Suctioning Muscle exertion ROM Isometric Exercise Position changes Hypercapnia PCO2 >45 Stress Pain, noxious stimuli Seizures Hyperthermia Hip flexion Poor neck allignment

SIGNS & SYMPTOMS OF INCREASED ICP

Early Signs Change in LOC Change in pupils Decreased motor Worsening headache Change in speech Elevation in ICP monitoring There may be no change in vitals Late Signs Difficult to arouse Unequal pupils Posturing Change in respiratory pattern Abnormal reflexes Cardiac changes Loss of cranial nerves Cushings response

MEDICAL MANAGEMENT
Only 25% to 58% of the causes of increased ICP can be surgically treated.(Kinney) For those patients who are treated surgically, or those patients who have difficulty in their autoregulatory system, the aim is to reduce the ICP by medical means.

Respiratory support Blood Pressure Management Osmotic diuretics Proper sedation Drainage of CSF

RESPIRATORY SUPPORT
Cerebral vessels are very sensitive to PaCO2 levels. As CO2 elevates (hypercapnia, acidemia), cerebral vessels dilate increasing cerebral blood flow and increasing ICP.

 Recommendations for proper ventilation

PaCO2 35 to 45 PO2 >60 PH 7.35 to 7.45

Recommendation for hyperventilation

Only to be done for short periods if patient has signs of herniation. This is a life saving measure only

BLOOD PRESSURE MANAGEMENT

Keep blood pressure normotensive to slightly hypertensive (This is for head trauma, not aneurysms) Hypotension causes cerebral ischemia Hypertension may aggravate cerebral edema and possibly bleeding Both will lead to an increase in ICP and thus a decrease in CPP

 Recommendations for altered BP

Hypotension treat fast treat now
Adequate fluid resuscitation

Hypertension doesnt usually happen with trauma, but it does with aneurysms

SEDATION
Sedation and paralytics are used to decrease the patients response to stimuli.
Decreases O2 demand Decreases metabolic demand Decreases ICP

Please avoid giving morphine to the brain injured patient. Although your patient may not be able to physically respond to you.they may still be able to hear and feel you.

Brain Trauma
A brain injury is a traumatic insult to the brain capable of producing physical, intellectual, emotional, social, and vocational change Categories of brain injury:
Mild diffuse injury Moderate diffuse injury Diffuse axonal injury Focal injury

Edema
Significant brain injuries may result in swelling of the brain tissue with or without associated hemorrhage Swelling results from humoral and metabolic responses to injury
Leads to a marked increase in intracranial pressure May lead to decreased cerebral perfusion or herniation

Ischemia
Can result from:
Vascular injuries Secondary vascular spasm Increased intracranial pressure Focal or more global infarcts can result

Hemorrhage
Can occur into or around brain tissue Epidural or subdural hematomas can compress underlying brain tissue or intraparenchymal hemorrhage Often associated with cerebral contusions and skull fractures

Classification of Skull Fractures

Linear fractures Basilar fractures Depressed fractures Open vault fractures

Skull Fractures - Complications

Cranial nerve injury Vascular involvement
Meningeal artery Dural sinuses

Infection Underlying brain injury Dural defects caused by depressed bone fragments

Linear Fractures
80% of all skull fractures Are not usually depressed Often occur without an overlying scalp laceration Generally have a low complication rate (as an isolated injury)

Linear Skull Fracture.

Depressed Skull Fractures

Usually result from a relatively small object striking the head at high speed
Commonly associated with scalp lacerations

Frontal and parietal bones most often affected

Depressed Skull Fracture.

Open-Vault Fractures
Result when there is direct communication between a scalp laceration and cerebral substance
Often associated with multisystem trauma and a high mortality rate May lead to infection (meningitis)

Prehospital management

Open Vault Fracture.

BASILAR SKULL FRACTURE

Base of the skull has irregular, sharp bony prominences. With a direct blow, strains occur
Compression Shearing Tension

 Basilar fractures occur at the base of the skull. They are very difficult to detect even with the use of x-rays. May be viewed best by CT with bone windows Diagnosis and treatment are based on patients clinical presentation.

ANTERIOR BASILAR SKULL FRACTURE

Presentation Raccoon eyes Rhinorrhea Anosmia (damage to CN I, olfactory) Visual changes (damage to CN II, optic) Telecanthus

MIDDLE & POSTERIOR SKULL FRACTURES

Presentation Otorrhea Battles sign Facial nerve palsy (damage to CN VII) Hearing loss (damage to CN VIII)

Battle sign

Otorrhea

MONITOR
ABCs LOC Temp infection (meningitis) Pain Altered taste Altered smell Altered hearing Bruising may not develop for a few hours Drainage from nose or ears Signs and symptoms of increased ICP

 Halo sign Tests for CSF leak Place gauze near the area of drainage. Allow drainage to absorb into the pad. A yellow ring that appears around the bloody drainage would represent CSF.

TREATMENT OF BASILAR SKULL FRACTURES

Observe Treat clinical presentation Keep HOB up Use mustache dressing to absorb drainage Antibiotics Avoid
Coughing, sneezing, blowing nose

Do not use nasal cannula Do not use nasal gastric tube Do not suction nasotracheally Do not intubate nasotracheally

CEREBRAL CONTUSIONS
Bruising of the brain tissue that results from rapid acceleration-deceleration movement causing shearing of small vessels. Brain edema and mass effect can occur Coup injury-occurs directly below sit of impact Countercoup injury-occurs on opposite side of initial injury

CT with multiple cerebral contusions

Cerebral Contusion
Bruising of the brain around the cortex or deeper within the frontal (most common), temporal, or occipital lobes
Produces a structural change in the brain tissue Results in greater neurological deficits and abnormalities than are seen with concussion

Signs and symptoms Management

Cerebral contusions can be life threatening. If severe, diffuse cerebral edema (secondary injury) causes elevations in ICP.

EPIDURAL HEMATOMAS
Bleeding into the potential space, between dura and skull Usually associated with temporal bone fracture, resulting in laceration of the meningeal artery.

Because epidural hematomas are usually caused by an arterial bleed which expand quickly, your patient may require emergency surgery.

SIGNS & SYMPTOMS OF EPIDURAL HEMATOMAS

Characteristics
Brief loss of consciousness, followed by lucid interval Headache, increasing in severity Vomiting, due to increased ICP Seizure Contralateral hemiparesis, check pronator drift Ipsilateral pupil dilation (pressure of CN III)

SUBDURAL HEMATOMAS
Bleeding between the dura and arachnoid mater. Vast majority are caused by tearing of the bridging veins exp: CoupContrecoup Most common traumatic mass lesion Three classifications
Acute 48hrs Subacute 2-14days Chronic - >14days

 ACUTE Subdural Hematoma

Clinical presentation occurs within 48-72 hrs Gradual decrease LOC to coma Hemiparesis Hemiplegia s/s are associated with rapid expanding lesion causing increased ICP and brainstem compression

 SUBACUTE Subdural Hematoma

Clinical presentations occur within 2 days to 2 weeks Associated with moderate injury Bleeding is slower producing a steady decline in LOC
Subacute subdural hematoma with Sedimentation line

 CHRONIC Subdural Hematoma

Result from low-impact injuries-falls Symptoms occur 2 weeks to several months after injury s/s are vague, but progressive Headache Confusion Seizures hemiparesis High incidence in elderly and ETOH abuse

 Diagnosis and Treatment of Subdural Hematoma

Ct scan shows hypodensity as the injury gets older Small SDH may be treated medically because they frequently reabsorb Large SDH require surgical evacuation-craniotomy Burr holes

INTRACEREBRAL HEMATOMA
Bleeding develops within the brain parenchyma *Deep contusion *ruptured blood vessel May develop with other serious injuries
Contusions, lacerations Penetrating injuries Depressed skull fractures

 S/S of a intracerebral hematoma will depend on the location and extent of injury

SIGNS & SYMPTOMS OF ICH

Clinical presentation will depend on the location. They will resemble s/s of stroke Headache Decreased LOC to coma Contralateral hemiplegia Ipsilateral dilated pupil Speech deficits

 Treatment for ICH

Surgical repair of depressed fracture Removal of clot if possible

SUBARACHNOID & INTRAVENTRICULAR HEMORRHAGE

Arterial blood in the subarachnoid and intraventricular space
Trauma Aneurysm Arterial venous malformation (AVM)
Traumatic subarachnoid

SIGNS & SYMPTOMS

Sudden severe headache Decreased LOC or comatose EKG changes s/s of meningeal irritation Nuchal rigidity Photophobia Blurred vision N/V Fever Backache Non-traumatic subarachnoid hemorrhage Aneurysm

 TREATMENT FOR SAH & IVH Determine cause of injury

CT Angiography

Once cause is determined then treatment can be determined

Emergent ICP Possible surgery Intensive medical management Intensive clinical monitoring

Mild Diffuse Injury (Concussion)

A fully reversible brain injury that does not result in structural damage to the brain Causes Signs and symptoms Management

Moderate Diffuse Injury

Moderate injuries are those that result in minute petechial bruising of brain tissue
Involvement of the brainstem and reticular activating system lead to unconsciousness

Signs and symptoms Management

Diffuse Axonal Injury (DAI)

Severest form of brain injury
Results from brain movement within the skull secondary to acceleration or deceleration forces

DAI may be classified as mild, moderate, or severe

Diffuse Axonal Injury

Mild DAI
Associated with coma of 6 to 24 hours

Moderate DAI
More common Distinguished by coma lasting more than 24 hours and abnormal posturing

SEVERE DAI
Severe DAI (formerly known as brainstem injury)
Involves severe mechanical shearing of many axons in both cerebral hemispheres extending to the brainstem

Focal Injury
Focal injuries are specific, grossly observable brain lesions Included in this category are lesions that result from:
Skull fracture Contusion Edema with associated increased ICP Ischemia Hemorrhage

IMPALEMENT & PENETRATING INJURIES

Bullets or other projectiles destroy brain tissue along their path injuries to multiple brain structures and vessels can occur.

 Treatment of projectile injuries

May require emergent surgery Intense medical management Intense clinical monitoring

 Treatment for impaled objects

DO NOT remove object Determine injury Surgery Intense medical management Intense clinical monitoring

Most common complication of penetrating injuries is infection

Prophylactic antibiotics

With any injury to the brain look for signs and symptoms of increased intracranial pressure. Treatment will depend on the type of injury. The goal being to decrease intracranial pressure and decrease secondary injury, through surgical techniques, or medical treatments.

NEURO ASSESSEMENT
BASELINE ASSESSMENT IS OF GREAT IMPORTANCE TO DETERMINE THE HISTORY OF THE PRESENT ILLNESS AND TO ACT AS A GUIDE FOR FURTHER SERIAL ASSESSMENTS

LEVEL OF CONSCIOUSNESS
Glasgow coma score
Under 8, patient is considered comatose/AIRWAY Reasons for coma A=ALCOHOL E=EPILEPSY I=INSULIN O=OPIATES U=URATES T=TRAUMA I=INFECTION P=POISON P=PSYCH S=SHOCK

 Best eye opening

Degree of stimulus required to awaken the patinet
Verbal Tactile Deep stimulus/Painful

Best verbal response

Assessment of the eloquent brain (speech center)

Best motor response

Assess how a patient interprets information and reacts to it

PUPIL RESPONSE
Size
Small Pinpoint Large Dilated Unequal

Shape
Round Keyhole Irregular Ovoid

Reaction to light
Direct light reflex Consensual light reaction Brisk, fixed, Hippus, sluggish, Anisocoria

VITAL SIGNS
The blood pressure and heart rate are assessed to determine if adequate cerebral tissue perfusion requirements are being meet. Keep MAP ~ 80 Keep in mind that the ICP will be subtracted from the MAP to obtain the Cerebral Perfusion Pressure (CPP)

 Cushings Triad
Late sign of increased ICP
Increase in SBP Widened pulse pressure Bradycardia Irregular respirations

What does this mean IMPENDING HERNIATION

TEMPERATURE
Keep the patient Normothermic to mildly hypothermic As temperature rises the need for increased oxygen requirements and metabolic demands double--bad news for a head trauma

RESPIRATIONS
Cheyne-Stoke
Earliest and most common alteration in respiratory pattern Result of hemispheric compression

 Posturing
Indicates interruption of corticospinal pathways at the internal capsule, midbrain or upper pons.

Decortication>>>Decerebration>>>Flaccidity
DECORTICATION

DECEREBRATION

Assessment and Evaluation

Prehospital management of the head-injured patient is determined by:
Mechanism and severity of injury Patient's level of consciousness Associated injuries

Airway and ventilation Circulation Neurological examination Fluid therapy

Code 16
SECONDARY PATIENT ASSESSMENT 1. 2. 3. 4. 5. 6. 7.

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ROUTINE TRAUMA CARE

Vital Signs GCS scoring parameters Systematic head to toe assessment Medications Allergies Reassure patient, provide comfort and loosen tight clothing Evaluate cardiac rhythm, if indicated. (All ALS patients do not necessarily require continuous ECG monitoring or transmission of a strip to the hospital.) 8. Contact hospital as soon as patients condition permits. Transmit assessment information and await orders. If no radio contact can be established or patients condition requires immediate treatment, refer to appropriate SMO and begin intervention immediately. 9. Recheck vitals and other pertinent signs at least every 15 minutes and record, noting times. If unstable vital signs/sustained hypotension (SBP <90 on two separate readings 5 minutes apart), vital signs should be taken and recorded every 5 minutes. 10. All patients, who, in the judgment of prehospital personnel, would benefit from care derived from a Trauma Center, should be transported accordingly (Refer to FIELD TRIAGE PROTOCOLS CODE 14). If unable to ventilate, transport to nearest hospital.

NOTE TO PREHOSPITAL PROVIDERS: In a combative or uncooperative patient, the requirement to initiate initial routine trauma care, as written, may be altered or waived in favor of rapidly transporting the patient for definitive care. Document the patients actions or behaviors which interfered with the performance of any assessments and/or interventions.

OUTLINE FOR RADIO REPORT (Transmit using as few words as possible) 1. Name and vehicle number of provider 2. Requested destination, closest hospital, and estimated time of arrival 3. Age, sex, and approximate weight of patient 4. Chief Complaint, to include symptoms and degree of distress 5. History of present illness/injury 6. Pertinent Medical History: - Allergies -Medications -Past History of Current Illness -Last Meal -Events surrounding incident 7. Clinical condition: -Focused and detailed patient assessment findings 8. Treatment initiated and Response

Code 18
SUSPECTED SPINAL CORD INJURY SPINAL IMMOBILIZATION Mechanism:
Suspected Deceleration Injuries, Motor Vehicle Crashes, Falls, etc.

Spine pain/tenderness or complaint of neck/spine pain No Physical findings suggesting neck and/or back injury No Other painful injury identified (Distracting Injury) No Decreased or altered level of consciousness No Motor/Sensory Exam Patient is Calm Cooperative Alert Ambulatory without pain No apparent distress No suspected intoxication Reliable patient exam
Reviewed Reviewed Reviewed Effective 05/01/08 06/01/06 05/01/04 05/01/98

Yes

Yes

Yes

Yes Abnormal?

Having an acute stress reaction Suspected of being intoxicated Have symptoms of brain injury Acting inappropriately Having difficulty communicating, such as, speaks a foreign language, deaf, etc.

NO IMMOBILIZATION NEEDED

IMMOBILIZE

Code 19
HEAD TRAUMA/UNCONSCIOUS PATIENT
100% OXYGEN Assist ventilations as needed Vomiting precautions Immobilize C-spine Routine Trauma Care
Yes

ALERT?

No

UNRESPONSIVE TO VOICE AND PAIN

TRANSPORT Pupil(s) dilated Signs of increased intracranial pressure and/or Glasgow Coma Score 8 or less Sedate -Refer to MEDICATION ASSISTED INTUBATION CODE 75a, if indicated ET intubation with in-line manual stabilization ACCELERATED TRANSPORT
Revised 05/01/08 Reviewed 06/01/06 Revised 05/01/04 Effective 05/01/98 ALS

NOTE TO PREHOSPITAL PROVIDERS: 1. Do not delay transport time with multiple intubation attempts. 2. If unequal or fixed pupils and/or posturing, ventilate at 20 breaths/min.