Traumatic Brain Injury

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Types of forces

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Acceleration
Deceleration

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Primary Brain Injury

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caused by physical force, open or closed, severity categorized on GCS and LOC

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Open Head Injury (penetrating)

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most common, results in focal brain injury

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Fractures of teh skull

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Linear - simple clean break
Deressed - bone pressed into brain
Comminuted - depression of bond fragements into brain
Basilar - found at teh base of the skull

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Open Head Injuries can result in

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CSF leaking from nose and ears
Hemorrhage from internal carotid, infection, or damage to CN I, II, VII, VIII

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Closed Head Injury

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Blunt Trauma, dura mater remains intact and brain tissue is not exposed, biggest risk of increased ICP, focal or diffuse brain injuries

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Types of closed head injuries

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Concussion - brief loss of consciousness no permanent damage
Contusion - bruising of brain tissue.
Laceration - tearing of brain tissue or vesses, more serious than contusion, bleeding

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Coup

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Site of impact, primary injury

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Coutercoup

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Opposite site of injury, secondary injury

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Focal Brain Injury

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Grossly observable brain lesions, open or closed, Contusions, can lead to epidural, subdural and intracerebral hemorrhage, may be coup or coutercoup injury

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Contusion in the Brain Stem

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affects the respiratory and cardiac systems

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Priority NI for TBI

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Assess respiratory system and cardiac system

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Diffuse Brain Injury

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Blunt force to head, tearing, twisting or spraining neurons, associated with acceleration and deceleration injuries, may be associated with concussion

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Direct Blow

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By a stick, puck, ball hitting the head, fall where head hits ground

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Indirect Blow

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Brain crashes into their skull, moving player hits immovable object

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Complications of trauma pt

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Tissue perfusion problems
Respiratory problems
Anxiety
Unstable clotting factors
Malnutrition
Altered body image
Thromboembolism
Infection
Coping Problems

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Warning signs after head injury - first 24 hours

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Change in LOC, seizures, bleeding or watery drainage from nose or ears, pupils slow to react or unequal, blurred vision, loss of sensation to any extremity, slurred speech, vomiting

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Secondary Brain Injury

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Injury that is caused after initial injury

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Types of secondary brain injury

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Increased ICP
Hemorrhage
Loss of autoregulation
Hydrocephalus
Herniation

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Increased ICP

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Prevent ICP to minimilize neural damage, CNS nerves to do not regenerate after Wallerian Degeneration

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Types of Hemorrhage

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Epidural
Subdural
Subarachnoid
Intracerebral

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Epidural Hemorrhage

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Arterial bleeding in space between dura and the inner skull - very life threatening, short lucid time, increasingly symptomatic

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Subdural Hemorrhage

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Venous bleeding into space beneath dura and above arachnoid, nighest mortality, occurs more slowly

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Subdural Hemorrhage phases

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Acute - within 48 hrs
Subacute - occurs between 48 and 2 weeks
Chronic - after 2 weeks to several months

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Subarachnoid Hemorrhage

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Broken vessels between arachnoid and pia mater, can be from TBI, usually from aneurysm, Worst HA of their life

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Intracerebral Hemorrhage

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Tearing of small arteries and veins within brain or brain stem

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Loss of Auto regulation

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Alters blood flow, HTN increased blood flow and ICP
Hypoxemia dn hypercapnia cause vasodialation and increase ICP

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Hydrocephalus

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Abnormal increase in CSF through dialation of ventricles, or obstruction fo CSF pathway, increases ICP

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Herniation

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Don't want to have happen
Shift of brain tissue downward

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Type of herniation

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Uncal
Central
Cingulate
Cerebeller tonsillar

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Uncal herniation

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temporal area nd 3rd cranial nerve. Dialated and unresponsive pupils, ptosis, rapid deterioration

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Central herniation

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Downward shift of brain stem, pinpoint pupils and Cheyne-Stokes respirations

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Celebeller Tonsillar

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Respiratory or cardiovascular compromise or arrest

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History of TBI

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Loss of consciousness, when where, how, seizure, N/V

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Kernigs Sign

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Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

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Brudzinski's Neck sign

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Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.

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Clinical Presentation

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Baseline data, VS, neural
Early detection of change in status
Treat as if spinal cord injury intil MRI proves wrong
Airway breathing pattern assessment

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Psychosocial assessment

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Emotional changes
Disability
Aphasia
Change in personal or familydynamics
Care and monitoring necessary

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Lab Assessment

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for primary TBI none, CT MRI

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Lab Assessment for Secondary TBI

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ABG, CBC, Serum glucose, serum electrolytes and serum osmolarity

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Radiographic Assessment

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CT scan - primary what is problem
Radiography of cervical spine and skull bones - to check for fractures - keep support collar in place
MRI

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CT Scan

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ID space occupying lesions, hemorrhage, skull fractures, bran tissue shift

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MRI

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Diffuse axonal injury

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Doppler flow and cerebral angiogram

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integrity of blood vessels

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Evoked potentials

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Test the functioning of sensory pathways by CN tests

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IP monitoring device

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Intraentricular Catheter (IVC) is inserted into lateral ventricle, can test CSF or release CSF if ICP is increased

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Monitoring of TBI pt

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ICP, lab values, effectiveness of treatment, VS q 1-2 hrs, continuous cardiac monitoring

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Positioning of PT with TBI

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avoid extreme felxion of neck, logroll client, elevate HOB 30 degress to enhance drainage, preventing increased ICP

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Neuro assessment

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every 1-2 hours

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Pupil response

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Every 1-2 hours with neural eheck, gives the test info regarding extent of bleeding or injury, best every 90 minutes to help with REM sleep

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Drainage from nose or ear

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Collect drainage on white cloth to measure, CSF has bglucose but nasal drainage does not. Halo around blood spot may be CSF

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Hyperventilation

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Avoided as cerebral perfusion can be compromised, only if acute neurologic detioration for brief periods

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Precautions

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Avoid coughing
Seizure precautions

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Barbituate Coma

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Uncoltrollable Increases in ICP
Pentobarbital sodium
Decreases metabolic edemands of the brain stabilizing cell membranes, decreasing gasogenic edema, and providing a uniform blood supply.

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Barbituate Coma

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Requires ventilator and ICP monitoring

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Complications of Barbituate Coma

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Cardiac Dysrhythmias, hypotension, F&E Imbalances

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Mannitol

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osmotic diuretic used to treat cerbral edema nd increased ICP by drawng fluid out of brain tissue

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How to give mannitol

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Bolus

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How do you know mannitol is working

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mental status improves

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Lasix

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Enhances mannitol therapy, reduces edema, blood volume and production of CSF

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Fentanyl or codiene

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decrease agitation with ventilator clients

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Barbituates (neuromuscular blocking agents)

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decrease cerebral metabolism associated with agitation

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Anticonvulsants

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help prevent seizures

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Antipyuretic

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Reduce fever

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Fluid and Electrolyte Intervention

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I&O monitoring every hour, usually fluid restriction, acute renal failure

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Acute Renal Failure

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minotor serum osmolarity daily, monitory diuretics, F/C necessary

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Diabetes Insipidus and SIADH

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TBI pt at risk from damage or compressed pituitary gland or hypothalamus

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SIADH

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Can also occur from hypothalamic dysfunction as it regulates serum osmolality

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Pulmonary managemetn

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Increased and thickened secretions, suctioning, observe client for increasing ICP when suctioning

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Behavioral Management

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Hand mitts
Restraints used sparingly
monitor frequently (every hour)
Dim lighting and quiet environment

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Sensory and perceptual alterations

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Changes in senses, at risk for falling, chicking, diorientation, loss of memory, orient client frequently, assure them they are safe, cue within environment (large faced clock, sumple calendar)

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Immobility

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anti-thrombotic compression boots, prophylactic anticoagulants, ROM every 2-3 hrs, prevent foot-drop, anti-contracture devices

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Nutrition management

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daily weight
daily serum albumin
ability to chew or swallow
Supplemental milkshakes if conscious and able to swallow
Eneral feeding

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Signs of dehydration

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Skin tenting
Dry mucus membranes
Low urine output

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Daily Weight

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Best indication of fluid depletion or overload

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Craniotomy for uncontrolled ICP

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All interventions does not decrease ICP, remove ischemic and or tips of temporal lobes to allow for brain expansion without further compromise. Also used to remove epidural and subdural hematomas

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Post op Craniotomy

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Assess q30 for 4 then q hour until stable for 24 hours, then vitals every 2-4

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Post Op Assessment

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Breathing and respiratory status, Strict I&O (1500 ml/day), ROM every 2-3 hrs, compression boots

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Positioning post op

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doctor orders position, start flat and gradually increase HOB to 30 degrees, position on non-affected side, no nick or hop flexion, keep head midline, neutral position

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Monitor Craniotomy dressing

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Check every 2 hours, mark drainage one each shift for comparison, reinforce dressing prn, document amoutn, color, halo,

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What is typical wound drainage

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30 ml per shift
Report if > 50 ml to physician

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Glascow Coma Score

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scored between 3 and 15, 3 is the worst, 15 is the best

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Best Eye Response

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4 eyes open spontaneously
3 eyes open to verbal command
2 eyes open to pain
1 no eye opening

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Best Berbal response

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5 oriented
4 confused
3 inappropriate words
2 incomprehensible sounds
1 no verbal response

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Best Motor Response

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6 obeys commands
5 localizing pain
4 withdrawal from pain
3 flexion to pain
2 extension to pain
1 no motor response

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Glascow Coma Scale Evaluated

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13 - 15 mild
9 - 12 moderate
3 - 8 severe
<8 pts are in a coma

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Types of aphasia

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Naming severe - may not be able to name common or high frequency objects (key)
Naming Mild - May only have difficulty naming low frequency objects or parts

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Aphasia

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Disorder of higher cortical function

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Aphasia refers to

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an acquired abnormality of language, usually from focal brain lesion

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Type of Aphasia is dependent on

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location of lesion

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How to est Aphasia

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test fluency, comprehension, and repetition

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Common in all types of aphasia

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Difficulty writing, difficulty naming

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How to test language

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fluency, repetition, comprehension, naming, reading, writing

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Brocas Aphasia

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Impaired fluency and repitition, compresension is intact

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Wernickes Aphasia

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Fluency in tact, repitition and comprehension are impaired

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Visual Neglect

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Lack of attention paid to one hemisphere, failure to id on the left, usually caused by lesions on right frontal or parietal lobes, may fail to recognize left side of pictruresk arm, plate, or dress/shave on left.