– Has reached epidemic proportions due to motor vehicle accidents
Other causes include:
– Falls, assaults, sports injuries
– Two thirds of patients are under 30 yrs, most are males.
Head injuries often cause damage to the brain from bleeding or swelling which results in increased intracranial pressure.
– The cranial skull contains three components: brain , blood, and cerebrospinal fluid (CSF)
– The cranial skull is a closed system, and if one of the three components increases in volume, at least one of the other two must decrease in volume, or the pressure increases. Any bleeding or swelling within the skull increases the volume of contents within the skull and therefore causes increased intracranial pressure.
– Normal ICP is 10 – 20 mm Hg
Increased ICP – PathophysiologyIf the pressure increases enough, it can cause displacement of the brain through or against the rigid structures of the skull. This causes restriction of blood flow to the brain , decreasing oxygen delivery and waste removal. Cells in the brain become anoxic and cannot metabolize properly, producing ischemia, infraction, irreversible brain damage, and eventually brain death.
Depends on the severity and anatomic location of the underlying brain injury. Localized pain usually suggests that a fracture is present. Fracture of the cranial skull may or may not produce swelling in the region of the fracture. But frequently produce hemorrhage. Therefore, an x-ray is needed for diagnosis.
Early signs of Increased ICP
Earliest sign is change in LOC
– Slowing of speech, delay in responding to questions
– Restlessness, Confusion
– Pupillary changes
– Weakness in one extremity
– constant, aggravated by movement, increasing in intensity
Late signs of increased ICP
– LOC deteriorates to comatose
– Bradycardia, fluctuating to tachycardia
– Decreased respiratory rate
– Altered respiratory pattern ( Cheyne-Stokes)
– BP and temperature rises
– Widening pulse pressure ( difference between systolic and diastolic pressure)
– Projectile vomiting
– Decorticate or decerebrate posturing, followed by bilateral flaccidity
– Loss of brainstem reflexes (pupils, corneal, gag, swallowing ) are ominous signs
– Most serious brain injury
– Collection of blood
– Epidural (between the skull and the dura ) this can result from a skull fracture that causes a rupture or laceration in the artery between the skull and the dura
– Subdural (between the dura and the brain ) this can cause from trauma, but can also occur as a result of rupture of an aneurysm
– Intracerebral (into the substance of the brain) result from: systemic hypertension rupture of aneurysm – intracranial tumors – when force is exerted to the head e.g. bullet wound
Management of Increased ICP
– True emergency requiring prompt treatment
– Monitor ICP
– Intraventricular catheter, subarachnoid bolt, epidural catheter
– Reduce Cerebral Edema
– Osmotic diuretics (mannitol)
– Corticosteroids ( dexamethasone)
Maintain cerebral perfusion
– Maintain cardiac output with fluids and dobutamine
– Reduce CSF and blood volume
– Drain CSF
– Hyperventilation – results in vasoconstriction
– Fever increases cerebral metabolism and edema
– Antipyretics, cooling blanket
– Avoid shivering which increases ICP
Reduce metabolic demands
– Barbiturates decrease ICP
– Muscle relaxants to paralyze patient
Scalp – trauma causes abrasion, contusion, laceration or hematoma beneath the layers of tissue of the scalp.
Skull Fracture- break in the continuity of the skull caused by forceful trauma.
Classified as linear, depressed or basilar.
Skull fracture may be open or closed
Open – tear in the dura
Closed – dura is intact
Closed – damage to brain tissue, but no opening through skull and dura.
Open – occurs when object penetrates the skull, enters the brain – opens the scalp, skull, dura to enter the brain.
– Minor Injury – client rapidly regains mental function.
– Concussion – temporary loss of neurologic function with brief loss of consciousness few seconds to few minutes
Contusion – bruising and hemorrhaging at brain surface – unconsciousness for more than a few seconds to few minutes.
– Loss of neurological function – paralysis, speech and visual disturbances
– Increased ICP – brain compression
– Intracranial Hemorrhage – hematomas (collection of blood) that develops within the cranial vault – most serious of brain injuries.
– Hematoma – epidural (above the dura)
subdural (below the dura)
Intracerebral (within the dura)
Based on physical and neurological examination,
Treatment of increased ICP
– Supportive measures –
– Ventilatory Support
– Fluid and Electrolyte maintenance
– Nutritional support
– Pain and Anxiety management.
– History of Trauma
– Time, cause, direction and force of the blow
– Loss of consciousness, duration
Assess LOC – Glasgow Coma Scale
– Response to verbal commands or tactile stimuli
– Pupillary response to light
– Motor Function
– Monitor for signs of increased ICP
– Move extremities, hand grasp, pedal push, speech
Ineffective airway clearance related to accumulation of secretions and decreased LOC
Maintain patient airway
– Suction carefully
– Discourage coughing (causes increase in ICP)
– Elevate HOB 30 degrees
– Guard against aspiration
– Monitor ABGs to assess ventilation
Ineffective breathing pattern related to neurological dysfunction
Monitor constantly for respiratory irregularities
– Cheyne Stokes, hyperventilation,
HOB 30 degrees
Position patient lateral or semi prone
Altered cerebral tissue perfusion related to increased intracranial pressure
Position patient to reduce ICP :
– head in midline position to promote venous drainage
– Elevate HOB 30 degrees
– Avoid extreme rotation or flexion of neck
– Avoid extreme hip flexion
– Stool Softeners
– High Fibre diet
Space Nursing activities
Maintain calm atmosphere, reduce stimuli
Risk for fluid volume deficit related to dehydration procedures and decreased LOC
– Brain damage can produce metabolic and hormonal dysfunctions
Monitor intake and output
Monitor IV fluids carefully
Monitor urine for acetone, osmolality
Record daily weights
Altered nutrition related to metabolic changes, inadequate intake.
Start enteral feedings when patient stabilized
– NG feeding unless CSF rhinorrhea
– Elevate HOB 30 degrees
– Aspirate for residual before feeding to prevent distention and aspiration
– Use pump to regulate feeds
Risk for injury related to disorientation, restlessness and brain damage.
Assess for cause of restlessness
– Often present as patient emerges from coma
– May be due to hypoxia, fever, pain, full bladder
Use padded side rails or wrap hands in mitts
– Avoid restraints as straining against them increases ICP
Minimize environmental stimuli
– Low lights, limit visitors, speak calmly
– Orient patient frequently
Risk for altered body temperature related to damage to temperature -regulating mechanism
Monitor temperature every 4 hrs.
– Can be increased as result of:
Damage to hypothalmus
Cerebral irritation from hemorrhage
Reduce temperature with acetaminophen and cooling blankets
If infection suspected –
– Culture potential sites
– Start antibiotics
Potential for impaired skin integrity related to bed rest, immobility, unconsciousness
Assess all body surfaces every 8 hrs.
Turn every 2-4 hrs
Provide skincare every 4 hrs
Assist patient to chair (if possible)