Intracranial problems include injuries and increased ICP.
Majority of head injury deaths occur immediately from direct trauma or from massive hemorrhage and shock. Deaths occurring in a few hours are caused by progressive worsening of head injury or from internal bleeding. Note of changes in neuro status and surgery are critical in prevention of deaths at this point. Deaths 3 weeks or more after injury result from multisystem failure.
Can be like fainting all the way to unarousable, all ranges in between. Not a diagnosis or disease, but manifestation of many pathophysiologic processes: trauma, metabolic disturbances, mass lesions, infections. Care focuses on determining and correcting cause, maintaining function, protection from injury and hazards of immobility
Scalp is very vascular and bleeds freely when lacerated. Children may develop shock from briskly bleeding scalp wound. Head injuries are common in child abuse. Suspect abuse when no clear explanation of cause, if story is inconsistent with injury, or suggests child performed activity not age-appropriate. Pay attention to setting. If abuse suspected, follow procedures for your area. As a general rule, if you have an adult patient with a scalp injury who is in shock, look for another cause for shock (such as internal bleeding). However, do not underestimate blood loss from a scalp wound. Most bleeding from scalp can be easily controlled in field with direct pressure if your exam reveals no unstable fractures under wound.
IMAGE: Scalp laceration. Notice linear fracture on visible skull. Skull injuries can be linear nondisplaced fractures, depressed fractures, or compound fractures. Suspect an underlying skull fracture in adults who have a large contusion or darkened swelling of scalp. Very little can be done for skull fractures in field except to avoid placing direct pressure upon an obvious depressed or compound skull fracture. Open skull fractures should have wound dressed, but avoid excess pressure when controlling bleeding.
Basilar skull fracture indicated by any of following: Bleeding from ear or nose Clear or serosanguineous fluid running from nose or ear Swelling and/or discoloration behind ear (Battle’s sign) Swelling and discoloration around both eyes (raccoon eyes) Battle’s sign can occur from immediately following injury to within 1–2 hours postinjury. Raccoon eyes are a sign of anterior basilar skull fracture. Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation.
In a brain injury via acceleration, the skull moves directly away from the blow. The brain rapidly changes from a stationary to a moving state. The injury to the brain results in bruising from impact, as well as cellular damage due to the sudden change in motion.
When the brain becomes injured because of a sudden stop in motion, it is an injury of deceleration. An example is when the child’s head hits a car windshield. Here, the skull stops immediately, but the brain continues moving toward the point of impact resulting in cellular damage.
Coup and contracoup injuries, also referred to as cerebral contusion, result from a rapid, violent movement of the brain. In a coup injury, the brain is damaged at the impact site. In contracoup, the injury occurs on the side directly opposite the impact.
IMAGE: Knife impaled in skull. IMAGE: X-ray of gunshot to head. Tissue destruction is seen in light area. NOTE: Reference to Mechanism of Injury (from Scene Size-up lecture). Remember: Velocity injuries (missiles) cause additional damage due to the shock wave of expanding tissues (temporary cavity). Penetrating objects in skull should be secured in place (impaled object) and patient transported immediately. Unless there is a clear entrance and exit wound in a perfectly linear path, assume that bullet may have ricocheted and is lodged in neck near spinal cord.
Forces that can cause a skull fracture can also cause a brain injury. Treat brain injury with adequate oxygenation and maintain perfusion.
Major trauma includes contusions and lacerations, usually with closed injuries. Contusion frequently at site of fracture. Coup-contrecoup occurs because of mass movement of brain inside skull. Injury at site of direct impact of brain on skull and opposite side from injury.
Neurologic emergency, usually caused by fracture crossing a major artery in the dura. Arterial tear develops rapidly and under high pressure: unconscious at scene, brief lucid interval, decreased LOC. HA, N/V. acute arterial bleeding has these typical signs: unconscious at scene, regains consciousness briefly, then nonresponsive. May have venous or arterial origin. Subdural hematoma usually venous in origin, much slower to develop mass large enough to produce symptoms, may be acute, subacute, chronic. Chronic develops over weeks or months after minor head injury, peak incidence in 60s and 70s, brain atrophy causes tension on structures, may tear. Head trauma only 60-70% of cases. Intracerebral hematoma usually from rupture of vessels in frontal and temporal lobes at time of injury.
Initial response of injured brain is to swell. Bruising or injury causes vasodilatation with increased blood flow to injured area, and thus an accumulation of blood that takes up space and exerts pressure on surrounding brain tissue. There is no extra space inside skull. Swelling of injured area increases intracerebral pressure and eventually decreases blood flow to brain that causes further brain injury. Increase in cerebral water (edema) does not occur immediately, but develops over hours. Only significant opening through which pressure can be released is foramen magnum at base, where brain stem becomes spinal cord.
Manifestations usually brief, patient usually discharged to notify if symptoms persist or behavior changes noted. Family should be taught to notify if decreased level of consciousness
Post-concussion syndrome: 2 weeks to 2 months after concussion. Persistent HA, lethargy, personality and behavior changes, short attention span, decrease short term memory, changes in intellectual ability. May be the beginning of a more serious, progressive problem.
LOC reflects the integrity of the brain as a whole, even subtle changes can be significant. Excess sleepiness can indicate increased ICP is developing. Evaluate LOC and compare with previous findings: include arousability, content of consciousness, speech. Determine the level of stimulus needed to arouse the patient (verbal, touch, shaking?) Content of consciousness: orientation Ability to follow commands: stick out your tongue, let go of my fingers Speech: clear, coherent, slurred, garbled, aphasic, incomprehensible sounds, no effort to speak Report changes immediately!
Brain itself is insensitive to pain. HA often continuous, but worse in the morning, straining or movement may exacerbate.
Nonspecific sign of IICP.
Compression of oculomotor nerve result in dilation of pupil, sluggish or no response to light, inability to move eye upward, ptosis of eyelid. A fixed, unilaterally dilated pupil indicates herniation of the brain. Signs of dysfunction of other cranial nerves are: blurred vision, diplopia, changes in extraocular eye movements.
Motor ability is controlled by nerve tracks originating in the frontal lobes of the brain, with fibers passing through the brain stem to the spinal cord before going to the muscles of the body. Distortion of brain tissue along these pathways can cause motor dysfunction. Patient may exhibit localization to painful stimulus or withdraw from it. Motor strength and tone are assessed in all 4 exxtremities. Decorticate posturing now called abnormal flexion, decerebrate posturing now called abnormal extension.
It may be difficult to identify IICP as cause of a coma, loss of consciousness confuses signs, makes it difficult to see the progress of IICP. Studies to identify the presence and cause of IICP. MRI and CT have revolutionized diagnosis of IICP, can differentiate many conditions that can cause IICP.
Because of confusion and ambiguity about terms describing altered states of consciousness, GCS developed in 1974. 3 areas assessed respond to definition of coma as inability to speak, obey commands, or open eyes with verbal or painful stimulus. Specific responses are given a number, can be graphed to see if patient is stable, improving, deteriorating. Nurse responsibility is to elicit the best response on each of the scales, higher scores mean higher level of brain functioning. Fully alert person is 15, 8 or less indicates coma. GCS is specific and structured, saves time by using number ratings rather than lengthy descriptions, can discriminate between different or changing states. GCS assess arousal aspect of consciousness.
Always assess circulation and respirations first! Other neuro assessments are pupillary checks, extremity strength testing, corneal reflex testing.
Mannitol is an osmotic diuretic, used to increase serum osmolarity so fluid is drawn into vascular space from interstitial space in cells, then excreted by kidneys. Has greatest effect on normal brain tissue, decreases bulk. Use in-line filter when administering mannitol because it tends to precipitate into crystals. Indwelling catheter necessary due to rapid diuresis, need for accurate monitoring, minimize patient activity. Anticipate effects in 5-15 minutes, lasting for several hours.
Drug therapy to reduce cerebral metabolism, decreases cerebral blood flow and ICP. High dose barbiturates (probably phenobarb) decrease metabolism, decrease ICP, reduce cerebral edema, produce more uniform blood supply to brain. May use Dilantin, seizures increase ICP. Infuse within 1 hour, tends to precipitate, don’t infuse with dextrose.
Must meet nutritional needs, regardless of state of consciousness or health. Early enteral feeding following brain injury improves outcomes. Patient with IICP is in hypermetabolic and hypercatabolic state, needs glucose for metabolism of injured brain. Need nutritional replacements within 3 days after injury. May need added salt, minerals, free water to meet fluid needs. Malnutrition promotes continued cerebral edema!
Controversy about whether patients should be in state of moderate dehydration: may be effective to reduce cerebral, fluids restricted to 65-75% of normal. But---hypovolemia may result in decreased CO and BP, may have impact on cerebral perfusion and oxygen delivery to brain, dehydrated patients do not respond well to vasoactive drugs. May use 5% dextrose in water for piggyback meds, .45% or .9% NS for IV solution
Base ventilatory support on basis of gases, be aware if moderate hyperventilation is desired. Disturbances have adverse effect on ICP. Especially monitor: glucose, sodium, potassium, osmolality.
Dr Mohamed EL Hady.
Senior Neurosurgeon Specialist
K S H
Any trauma to the
Head trauma includes an alteration in
Common major trauma
4 million people experience head trauma
Severe head injury is most frequent cause of trauma death
At Risk population
Males 15-24 males 2x as likely as women
Usually signifies craniocerebral trauma
Includes alteration in consciousness
High potential for poor outcome
Death at injury
Death within 2 hours after injury
Death 3 weeks after injury
State depends on intact cerebral
Reticular activating system (RAS) in the brain
stem midbrain hypothalamus and thalamus
Impairment on conscious level occurs due to
any lesions in the cerebral hemispheres or in
An abnormal state in which patient is
unaware of self or environment
Can be for very short time to long term coma
Care is designed to
Determine the cause
Maintain bodily functions
Support vital functions
Protect patient from injury
Different Types of Injury
• Highly vascular, bleeds briskly
Shock: child may develop
Shock: adult another cause
No unstable fracture:
direct pressure, dressings
Unstable fracture: dressings, avoid
10Head Trauma -
• Linear nondisplaced
• Large contusion or darkened swelling
• Dressing, avoid excess pressure
• Before operating
11Head Trauma -
Trauma must be extreme to cause fracture
Basilar Skull Fracture
May tear dura
Permit CSF to drain
through an external
May mediate rise of ICP
Evaluate for“Halo” sign
Mechanism of injury
Non- missile or closed head injury
Acceleration – decelaration
Coup - counter coup
o Direct blow to the head
o Skull moves away from force
o Brain rapidly accelerates from stationary to
in- motion state causing cellular damage
o Head impacts to a stationary object (e.g., car
o Moving skull stops motion almost immediately
o However, brain, floating in
cerebral spinal fluid (CSF),
briefly continues moving
in skull towards direction
of impact, resulting in
significant forces that
Injury resulting from
movement of brain is
called coup and
contracoup. This action
is also referred to as a
o Coup: an injury
beneath the skull
at the area of
injury occurs on
the opposite side
of the area that
Direct Brain Injury Types
Injury at site of
Mechanism of injury
Missile or penetrating
Head Trauma - 26
Forces that cause skull fracture
can also cause brain injury.
As defined by the National Head Injury
“a traumatic insult to the brain capable of
producing physical , intellectual, emotional,
social and vocational changes.”
Focal brain injury
Bruises on the brain
Contusion – bruising of brain tissue
Has area of necrosis infarction and
Often from coup - contrecoup injury
Seizures are common after contusion
Focal brain injury
•Blood between skull and
•period of lucency
•present in 1% of all
Focal brain injury
Comes from bleeding between dura and inner
surface of the skull
Will be unconscious, then awake, and then
deteriorate ( lucid interval )
Headache, nausea and vomiting
Needs surgical intervention to prevent brain
herniation and death
Focal brain injury
> Between the dura mater and the piaarachnoid mater
> Occurring in approximately 30% of severe head injuries
- - - Usually bleeding is from veins, so bleeding is
GENERALLY slower than epidurals
CAN be from arteries and these require
Administration of anticoagulants is one of the
causes of CHRONIC TYPES esp. in the
Focal brain injury
Can even appear 24 hours
following initial insult
Traumatic Subarachnoid Hemorrhage
Most common CT finding in moderate to severe
If isolated head injury, may present with
headache, photophobia and meningismus
The outcome depends on the Size of bleed
Timing of CT
Nimodipine reduces death and disability by 55%
Signs & Symptoms
of Brain Injury
Changes in pupil
Pathophysiology of Changes
Frontal Lobe Injury
Alterations in personality
Occipital Lobe Injury
Reduce mental status or Amnesia
Unable to recall events before injury
Unable to recall events after trauma
Hemiplegia, Weakness or Seizures
Signs & Symptoms
of Brain Injury
Minor Head Trauma
Concussion –patient may not lose
Will be a brief change in LOC, patient may
not remember the event and will have
Post-concussion syndrome is 2 weeks to 2
months after injury
Post Concussion Syndrome
Short attention span
Decreased short-term memory
When patient is discharged after concussion
nurse should instruct family on what to watch
for and when to call Dr.
Clinical Manifestations of head injury
Change in level of consciousness is the
most sensitive and important indicator of
May be pronounced or subtle
Early signs may be nonspecific: restlessness,
irritability, generalized lethargy
From compression on the walls of cranial nerves,
arteries and veins
Worse in the morning
Straining and movement makes worse
NOT preceded by nausea- “unexpected”
May be projectile
Pupil changes are from pressure on third cranial
Pupils become sluggish, unequal. This is
because of brain shift. May also be pressure on
other cranial nerves
Decrease in motor function
May have hemi paresis or hemiplegia
May see posturing – either decorticate or
Decerebrate – more serious from damage in
midbrain and brainstem
Decorticate – from interruption of voluntary motor
Transcranial Doppler studies
Looking for vasospasm
No lumbar puncture if there is IICP because sudden
release of pressure can cause brain to herniate
ABG’s – keep O2 at 100% and PCO2 as related to
Cervical spine x-ray
You must see from 1 – 7 to see that they have no
Glasgow Coma Scale (GCS)
Glasgow coma scale
First described in 1974 by Graham Teasdale
and Bryan J. Jennett
Lancet 1974, 2:81
Glascow Coma Scale
Used to document assessment in three areas
Normal is 15 and less than 8 indicates coma
Principles of emergency management
First priority is -
Stabilize cervical spine
Limited time for initial evaluation of neurological
Treatment of hemorrhagic shock takes
precedence over neurosurgical procedures
Stabilize cervical spine
IV access (2 large bore catheters), LR or NS
Control external bleeding with pressure
Assess for rhinorrhea, otorrhea, scalp
Secondary Trauma Survey
After patient relatively stable
Look for coexisting other organ injuries
Complete neurological examination
Severity of head injury classified by GCS
Mannitol – Rapid short acting diuretic that
decreases ICP. Decreases total brain water
Watch fluids and electrolytes closely
Don’t give in cases of renal failure or if serum
Barbiturates – causes decrease in
metabolism and ICP. Causes reduction in
cerebral edema and blood flow to brain.
Watch for hangover effects and drowsiness. Side
effects make it harder to check LOC. Watch for
constipation – do not want patient straining.
Skeletal muscle paralyses may be used (Pavulon)
Antiseizure drugs - Dilantin
Prevent secondary injury in the brain
Surgery if necessary
Patient need higher amounts of glucose to
Will need nutritional support quickly.
Watch sodium if on Mannitol – may need to
give additional salt.
Also may need additional free water if
Fluid balance is controversial
Do not want too dry
Give saline either .45% or normal saline – not
glucose to help prevent additional cerebral
Most head trauma requires rehab
Some rehab units do coma management
Patient may have trouble swallowing and
need speech therapy
Patient may agitate easily and act out
May be a flight risk and have to be in a
locked ward until passes through the
At risk for head trauma from falls
Be alert if patient has fallen and is taking