Head Injury, Cranial Surgery and IICP

NUR 2549

Unconsciousness

An abnormal state in which client 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 client from injury

Etiology

Arousal State of being awake that depends on a group of

neurons in the brainstem Can maintain level of wakefulness even without

functioning cortex

From Human Physiology

RAS is located in brain stem

Etiology

Content part of consciousness Ability to reason, think and feel Also to react to stimulus with purpose and

awareness Controlled by cerebral hemispheres (higher

centers) Intellect and emotional function are also controlled

in the same area.

Major Reactions

Two reactions affecting cerebral metabolism occur: Cerebral ischemia /anoxia – brain isn’t getting

enough oxygen and compensatory mechanisms take place

Cerebral edema results because the brain compensates by dilating blood vessels trying to get more oxygen

Behavior

Document accurately what the client’s behavior is. Example: if the client opens eyes on command but not spontaneously, chart it as such. Be descriptive.

Glascow Coma Scale

Used to document assessment in three areas

Eyes Verbal response Motor response

Normal is 15 and less than 8 indicates coma

From Rehabilitation Nursing

From Rehabilitation Nursing

Other Assessment

Assess bodily function including respiratory, circulatory and elimination

Pupil checks – are pupils equal and how they react to light

Extremity strength Corneal reflex test

Intracranial Pressure

Monro-Kellie hypothesis (applies only to children with a rigid skull and not neonates) Skull is an enclosed space with three variables

Brain tissue Blood Cerebrospinal fluid

Intracranial Pressure

The skull cannot expand to allow for extra space occupying tissue or fluid

If one of the three components increases the other two must decrease in order to compensate

Intracranial Pressure

Other factors that influence intracranial pressure Arterial pressure Venous pressure Intraabdominal and intrathoracic pressure Posture Temperature Blood gases (left off handout)

Normal Intracranial Pressure

Pressure exerted by total volume from: Brain tissue Blood Cerebrospinal fluid Normal manometer reading – 80-180 Normal transducer reading – 0-15mm Hg

Cerebral Blood Flow

Amount of blood going through 100g of brain tissue in 1 minute – cerebral blood flow is 50ml/min per 100g

Brain uses 20% of the body’s oxygen Brain uses 25% of body’s glucose

Autoregulation of Cerebral Blood Flow Blood vessels alter their diameter to ensure a

constant cerebral blood flow Lower limit for MAP is 50mm Hg. Below this, cerebral flow decreases and there is risk

of ischemia Upper limit is MAP of 150mmHg. Above this the

cerebral blood vessels are maximally constricted. Blood vessels cannot constrict more to control high pressure. Blood brain barrier is disrupted and cerebral edema and ICP results

MAP= DBP + 1/3 Pulse Pressure

Cerebral Perfusion Pressure (CPP) Pressure needed to maintain blood flow to

the brain MAP-ICP=CPP Normal CPP is 60-100 CPP>100 is hyperperfusion and IICP CPP< 60 hypoperfusion CPP<30 incompatible with life

Elastance – stiffness of the brain High elasticity –high elastance ICP increases with

small increases in volume Low elasticity – brain compensates and ICP

stays stable

Compliance

Low compliance is same as high elastance High compliance – ICP remains stable Blood pressure

If MAP is low, blood vessels in brain dilate to bring in more blood

If MAP is high, blood vessels constrict to shunt away blood from brain

Metabolic Factors affecting cerebral blood flow

Oxygen tension – When oxygen tension (PaO2) falls below 50, cerebral arteries dilate to increase cerebral blood flow. If this fails to happen, the brain metabolism changes to anaerobic metabolism and lactic acid builds up

Carbon dioxide tension - If the blood becomes acidic, the blood vessels dilate to increase cerebral blood flow (increased CO2 and acidosis are potent vasodilators)

Metabolic Factors

Globally extreme cardiovascular changes (asystole) Pathophysiologic states (diabetic coma)

Focally Trauma and tumors

Stages of Increased ICP

Stage 1 – High compliance and low elastance. Autoregulation is functioning

Stage 2 – Compliance is lower and elastance is increased. An increase in volume places client at risk for IICP

Stage 3 – High elastance and low compliance. Small changes in volume will cause large increase in ICP

Stages of Increased ICP

Stage 4 – ICP rises to terminal levels with little increase in volume. Brain herniates leading to

REST IN PEACE

Increased Intracranial Pressure From an increase in cranial volume that

results from increase in one or more of the following: Brain tissue Blood Cerebrospinal fluid

Increased Intracranial Pressure Cerebral edema – regardless of cause,

increases tissue volume, can lead to IICP Types –

Vasogenic-most common (tumors, abscesses, ingested toxins)

Cytotoxic-local disruption of cell membranes (lesions or trauma)

Interstitial-uncontrolled hydrocephalus, hyponatremia

Complications of IICP

Inadequate cerebral perfusion Cerebral herniation

Brain shift : Lateral, downward, or both Irreversible Edema and ischemia further increased Compression of brainstem and cranial nerves

may be fatal Cerebellum and brainstem forced through

foramen magnum

Clinical Manifestations

Change in level of consciousness is the most sensitive and important indicator of neuro status

May be pronounced or subtle Early signs may be nonspecific: restlessness,

irritability, generalized lethargy

Clinical Manifestations

Changes in vital signs-this is ominous sign This is a late sign – Cushing’s triad Increasing systolic blood pressure Pulse slowing and is bounding Irregular respiratory pattern May also have a change in temperature

Clinical Manifestations

Ocular signs Pupil changes are from pressure on third cranial

nerve Pupils become sluggish, unequal. This is

because of brain shift. May also be pressure on other cranial nerves

Clinical Manifestations

Decrease in motor function May have hemiparesis or hemiplegia May see posturing – either decorticate or

decerebrate Decerebrate – more serious from damage in

midbrain and brainstem Decorticate – from interruption of voluntary motor

tracts

Clinical Manifestations

Headache From compression on the walls of cranial nerves,

arteries and veins Worse in the morning Straining and movement makes worse

Clinical Manifestations

Vomiting NOT preceded by nausea- “unexpected” May be projectile

Diagnostic Tests

CT MRI Cerebral angiography EEG PET No lumbar puncture if there is ICP because sudden

release of pressure can cause brain to herniate ABG’s – keep O2 at 100% (Lewis 1615) and PCO2

as related to ICP (25-35)

Drug Therapy

Mannitol – Rapid short acting diuretic that decreases ICP. Decreases total brain water content

Watch fluids and electrolytes closely (I and O and labs)

Don’t give in cases of renal failure or if serum osmolality increased

Drug Therapy

Loop diuretics – reduce blood volume and tissue volume

Corticosteroids – Decadron most common steroid used. Watch for side effects. Should be on antacids or H2 receptor blockers to prevent ulcers.

Drug Therapy

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 client straining.

Skeletal muscle paralyzers may be used (Pavulon)

Antiseizure drugs - Dilantin

Nutrition

Clients need higher amounts of glucose to survive.

Will need nutritional support quickly. Watch sodium if on Mannitol – may need to

give additional salt. Also may need additional free water if

dehydrated – watch I and O closely. Give low CHO diet to help with CO2

Nutrition

Fluid balance is controversial Do not want too dry Keep normavolemic Give saline either .45% or normal saline – not

glucose to help prevent additional cerebral edema

Laboratory Work

ABGs regularly Electrolytes daily

Nursing Interventions

Airway and respiratory – suction only as needed and for 10 seconds at a time, only 2 passes. Give 100% O2 prior to suctioning.

Avoid abdominal distention – may need NG tube to decompress stomach

Sedate with care – if not on a vent, use sedation that will not interfere with respiration or mask any neuro changes

Nursing Interventions

Keep HOB elevated 30 degrees if BP is normal

If BP is low will need to put HOB flat Keep head in alignment to prevent cutting off

venous flow from the head Don’t elevate knees – this will increase

intrathoracic pressure Turn gently from side to side – if turning

raises ICP, client will need to stay on back

Nursing Interventions

If client is posturing frequently during care, will need to sedate first and then do only one thing at a time. Minimize stimulation

These clients can become agitated and combative – avoid over stimulating them

Restraining them will make them MORE AGITATED and RAISE THEIR ICP!

Nursing Interventions

Use minimal stimulation – perhaps one family member that is particularly calming – not the entire neighborhood can stay with client

Use a calm voice when talking to the client Calmly tell the client what you are going to do

when providing care NO TV IN ROOM Keep room darkened if needed

Nursing Interventions

Keep body temperature within normal limits Give ordered PRN antipyretics (probably

Tylenol) May need to use cooling blanket Do not use ice on client

Nursing Interventions

Hygiene – keep skin clean and dry. Watch for skin breakdown

May need to be on a special bed Keep mouth clean and moist May need eye drops to moisten eyes Families need a lot of support even after

client leaves ICU Client may benefit from rehab to help him

adapt and progress

Nursing Interventions

Prevent infection Protect from injury Avoid factors that increase ICP Psychological support

Pediatric Considerations

Open fontanels allow expansion of skull Neuro changes may be harder to detect

because child cannot communicate as well Cushing’s triad rarely seen in children Compare child’s behavior with their

developmental level

Pediatric Considerations

Assess for developmental differences and physical anomalies

Is child appropriate for age? Look for physical injuries such as bites,

bruises Use special Glascow coma scale for child

Pediatric Considerations

Allow parent to stay with child as much as possible

Avoid unnecessary stimulation Crying will increase ICP

Head Trauma

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

Head Trauma statistics

3 million/year in the U.S. Mortality rate is 19 per 100,000 MVAs and falls have decreased as causes Firearm-related head injury deaths have

increased

Head Trauma

Scalp lacerations – scalp has many blood vessels and will bleed profusely. Watch for infection

Skull fracture types Linear Depressed Simple Comminuted Compound

Skull Fracture Locations Frontal Orbital fracture Temporal fracture Parietal fracture Posterior fossa fracture Basilar skull fracture

Occurs at base of the skull Watch for rhinorrhea and otorrhea Test fluid leaking from nose or ear for glucose and

watch for halo If the drainage is CSF then the fracture has crossed

the dura

Head Trauma

Check head injury client for bruising around eyes called raccoon eyes

Also look at hairline at nape of neck behind ear for bruising called Battle’s sign

Major complications of basilar skull fracture are infection and hematoma

Battle’s sign

Minor Head Trauma

Concussion – client may not lose consciousness

Will be a brief change in LOC, client may not remember the event and will have headache

Post-concussion syndrome is 2 weeks to 2 months after injury

Post Concussion Syndrome

Persistent headache Lethargy Personality changes Short attention span Decreased short-term memory When client is discharged after concussion

nurse should instruct family on what to watch for and when to call Dr.

Major Head Trauma

Contusion – bruising of brain tissue Has area of necrosis infarction and

hemorrhage Often from coup - contrecoup injury Seizures are common after contusion

Major Head Trauma

Lacerations Tearing of brain tissue Occurs with depressed skull fracture and

penetrating injuries May have bleeding into the brain structures-

intracerebral hemorrhage Very difficult to remove blood

Major Head Trauma

Epidural hematoma Comes from bleeding between dura and inner

surface of the skull Will be unconscious, then awake, and then

deteriorate Headache, nausea and vomiting Needs surgical intervention to prevent brain

herniation and death

Subdural Hematoma

Usually bleeding is from veins, so bleeding is GENERALLY slower than epidurals

CAN be from arteries and these require IMMEDIATE removal

Administration of anticoagulants is one of the causes of CHRONIC TYPES esp. in the elderly.

Diagnostic Studies

Skull xrays routine to r/o or identify fracture CT/MRI are best to determine trauma rapidly

Emergency Management-Initial Airway Stabilize cervical spine Oxygen administration IV access (2 large bore catheters), LR or NS Control external bleeding with pressure Assess for rhinorrhea, otorrhea, scalp

wounds Remove clothing

Emergency Management-Ongoing Maintain patient warmth Monitor VS, LOC, O2 sats, cardiac rhythm,

GCS, pupil size and reactivity Anticipate intubation if absent gag reflex Assume neck injury with head injury Administer fluids cautiously to prevent IICP

Rehab

Most head trauma requires rehab Some rehab units do coma management Client may have trouble swallowing and need

speech therapy Client may agitate easily and act out sexually May be a flight risk and have to be in a

locked ward until passes through the agitation phase

From Rehabilitation Nursing

FromRehabilitationNursing

Pediatric Client

Child is vulnerable to acceleration deceleration injuries because their neck is supple and moves around easily and the head is larger in proportion to their bodies

In a very young child the cranium may be able to expand enough to allow for some edema

Pediatric Client

Epidural hemorrhage is rare in children Subdural hemorrhage – from shaken baby

syndrome, falls Can result in quadriplegia, hyperthermia, bulging

fontanels Retinal hemorrhages Dizziness Unsteady gait

Elderly

At risk for head trauma from falls Be alert if client has fallen and is taking

anticoagulants

Cranial Surgery Brain tumor (benign or malignant) CNS infection Hydrocephalus Vascular abnormalities

Intracranial bleeding Aneurysm repair Arteriovenous malformation

Craniocerebral trauma Skull fractures

Epilepsy Intractable pain

Types of Cranial Surgery: Stereotactic Stereotactic: neurosurgery

Often computer assisted to precisely target area CT and MRI used to image targeted tissue Burr hole or bone flap for entry Can remove small tumors and abscesses, drain

hematomas, perform ablative procedures, repair AV malformation

Reduces damage to surrounding tissue

Types of Cranial Surgery: Craniotomy Location varies

Frontal Parietal Occipital Temporal Combination

Burr holes drilled, saw to remove bone flap Bone flap wired or sutured after surgery Drain may be placed to remove blood or fluid

Nursing Care: Pre-op

Compassion Uncertainty and fear about prognosis/complications

Teaching What can be expected Hair will be shaved Client will be in ICU after surgery

Nursing Care: Post-op

Prevent increased ICP!!! Maximum swelling occurs within 24-48 hours

Frequent assessment of neuro status x 48 hrs. Monitor fluids, electrolytes, osmolality closely

Detects changes in sodium regulation, onset of diabetes insipidus, severe hypovolemia

Positioning varies depending on procedure Assess dressing, drainage, incision Care to prevent wound infection

Nursing Care: ambulatory and home Rehab potential depends on reason for

surgery, post-op course of recovery, and client’s general health

Nursing considerations Foster independence for as long as possible to

highest degree possible Positioning, skin and mouth care, ROM exercises,

bowel and bladder care, adequate nutrition Potential recovery cannot be determined until

cerebral edema and IICP subside