IL TRAUMA NEL GRANDE ANZIANO Inquadramento del

IL TRAUMA
NEL GRANDE ANZIANO
Inquadramento del problema
clinico nel trauma cranico
dott. Pasquale Caiazzo
Direttore U.O.S.C. Neurochirurgia
A.O.R.N. “Antonio Cardarelli “ Napoli
BACKGROUND
• Incidence as well as severity of head injuries is rising all over the world
due to rapid industrialization and more rapid modes of transport.
• Elderly people account for 12-15% of EU population
• 10-14% of all trauma victims are >65
• By the year 2030, twenty-percent of the population will be 65 years of
age or older.
• Individuals 85 years and older represent the fastest growing segment of
the world population.
• The elderly with head injuries do present differently from the rest of the
population.
• Most of the elderly patients may have one or more medical disorder that
may be obscured by the head injury
Severe head injury in elderly carries a grave prognosis
with a mortality of around 70%.
Associated morbidities (diabetes mellitus, coronary
artery disease) and associated spinal injury add to
the poor outcome.
Ventilator associated pneumonia with resultant
septicemia is the foremost postoperative cause of
death in severe head injury in the elderly.
Time interval between injury and intervention is critical. Earlier the intervention, better
is the outcome.
Mechanisms
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•
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Motor Vehicle Crashes (MVC)
Pedestrian vs. Motor Vehicle
Falls
Burns
Assaults
AUTO-PED
• 46% elderly trauma occurs at crosswalk
• Parking lots
FALLS AND THE ELDERLY
• Some studies indicate that the rate of injury begins to
increase by the age of 65
• In older individuals there are physical changes that make
their brains more vulnerable to injury and reduce their
chances of recovery (Patrick, 1996).
• Generally they take longer to recuperate, need more time
and effort to reach the same level of recovery that
younger individuals attain and often have a less positive
prognosis, recovery and outcome (Pilisuk & Feinberg,
1996).
FALLS ARE THE LEADING CAUSE OF BRAIN
INJURY IN THE ELDERLY
• Factors that contribute to this include:
– Medication and alcohol use
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–
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–
–
–
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–
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Other Medical Conditions
Visual Impairments
Osteoporosis
Depression
Sleep problems
High blood pressure
Diabetes
Parkinson’s
Orthopedic Problems
– Lack of Exercise
– Improper Footwear
– Environmental hazards
•
•
Falls in older adults are the leading cause of traumatic brain injury
Men have a higher rate of fatal falls (due to TBI)
FALLS ARE USUALLY MULTIFACTORIAL
Intrinsic Factors
Age changes
Chronic
conditions
Extrinsic Factors
Medications
related
FALLS
Footwear
Alcohol
Environmental
factors
LE weakness
Acquired Factors
Assistive device
HEAD INJURY
– Scalp
– Skull
– Brain
SCALP AND SKULL INJURIES
• Scalp lacerations
– Can bleed profusely
• Skull fractures
– Linear or depressed
• Linear is from a low velocity injury
– Simple, comminuted, or compound
• Simple with or without fragments is low velocity
• Comminuted is a direct blow, high momentum impact. The bone is
fragmented into many pieces.
• Compound fracture is a severe head injury. Usually a depressed
skull fracture with scalp laceration with a communicating pathway
into the intracranial cavity
– Closed or open
• Frontal fracture
– May see air in the forehead tissue, CSF coming out of their nose
• Orbital fracture
– Raccoon eyes, may have optic nerve injury
• Parietal fracture
– Facial paralysis
• Basilar fracture
– CSF out ears, nose, trouble hearing or tinnitus, facial paralysis,
conjugate gaze, vertigo. There is a tear in the dura so there is an
open pathway from nose/ear to brain!! Might give them
meningitis
Presence of skull fracture increases risk of intracranial bleeding
174 times compared to patients without a skull fracture
TRAUMATIC BRAIN INJURIES
 Concussion
 Epidural Hematoma
 Subdural Hematoma
 Subarachnoid hemorrhage
 Intracerebral Hematoma
 Intraventricular hemorrhage
 Shear injury / diffuse axonal injury
CONCUSSION
• Temporary loss of neurological functioning with no apparent
structural damage! May or may not have loss of consciousness
• May have amnesia
– Mild and Classic
• Mild – may lead to a period of reported or observed confusion,
memory lapse, possible loss of consciousness, can include a
seizure, HA, dizziness
• Classic – does result in a loss of consciousness, usually less
than 6 hours. Always accompanied by some degree of post
injury amnesia! No apparent structural damage on either one
of these guys
EPIDURAL HEMATOMA
– Results from bleeding between the dura and the
inner surface of the skull
– Neurologic emergency!!!
– Venous or arterial origin
• 99.9% a tear in the middle meningial arterial artery, the
source of bleeding is arterial
– Classic signs include
• Initial period of
unconsciousness
• Brief lucid interval followed by
decrease in LOC
• Headache
• Nausea, vomiting
SUBDURAL HEMATOMA
– Occurs from bleeding between the
dura mater and arachnoid layer of
the meningeal covering of the brain
– Most common source is the veins
that drain the brain surface into the
sagittal sinus
• Since it’s venous it’s a slower bleed, but
still an emergency!
• Bleed from the small bridging veins that
connect the surface of the cortex to the
dural sinuses
• Associated with high mortality b/c of the
severe secondary injuries that are
associated with it. Often uncontrolled
rise in IC
SUBACUTE SUBDURAL HEMATOMA
• Occurs within 2 to 14 days of the injury
• After initial bleeding, subdural hematoma may
appear to enlarge over time
• Slow as shit bleed, it takes 2 – 14 days to start
causing problems. Or from small acute subdural
that they thought had stopped, but a little bit of
increased ICP re-pops the shiz
CHRONIC SUBDURAL HEMATOMA
• Develops over weeks or months after a
seemingly minor head injury
• Peak incidence in sixth and seventh decades of
life
• Presenting complaint often focal symptoms, not
signs of increased ICP
• Delay in diagnosis in older adults because
symptoms mimic those of vascular disease and
dementia
Intracerebral and Subarachnoid Hematoma
SUBARACHNOID HEMORRAGE
– Bleeding into the subarachnoid space
• Most common causes are subarachnoid
aneurysm, head trauma, or hypertension
• Mean age is 50, super bad, people die all the
time… Mortality is high, maybe because there
is usually something else going on in their
body that is messed up that lead them to
having the berry aneurysm and bleed in the
first place
INTRACEREBRAL HEMATOMA
– Occurs from bleeding
within the parenchyma
• Usually occurs within
the frontal and temporal
lobes
– Size and location of
hematoma determine
patient outcome
– Worse prognosis
• Twice as likely as other head
injured patients to suffer from
death, persistent vegetative
state or severe disability
DIFFUSE AXONAL INJURY (DAI)
– Widespread axonal damage occurring after a mild, moderate, or severe TBI
– Process takes approximately 12 to 24 hours
– Damage occurs around
• Axons in subcortical white matter of the cerebral hemispheres
• Basal ganglia
• Thalamus
• Brainstem
• Associated with prolonged coma, poorest prognosis of any other brain
injury we have. Usually come in in a coma already, they are posturing,
global cerebral edema, diagnosis is made with CT or MRI. Shearing type
thing, as the brain shears there are little tears. Then injury stops and
settles back down, doesn’t look like an injury on the initial scan, but as
time passes you being to see these little blood spots. Usually in white
matter associated with acceleration and deceleration injury.
• Coup/ContreCoup injury. Responsible for most cases of post traumatic
dementia, also in conjunction with hypoxic ischemic injury. Most
common cause of persistent vegetative state. Slight movements are
usually reflexes, but not always.
CLINICAL FEATURES
•
Confusion
– Characterized by three cardinal features
• Disturbance of vigilance and heightened distractibility
• Inability to maintain a coherent train of thought
• Inability to carry out a sequence of goal directed movements
•
Amnesia
– May be anterograde or retrograde
– Often characterized by repetitive questioning, inability to follow commands, inability to
retain information during medical evaluation
– Amnesia will decrease slowly over time and small amount of memory deficit remains
– No loss of biographical data
•
i.e. Name, etc. – typically the result of hysterical rxn or malingering
– Duration does correlate with severity and outcome of head injury
•
Loss of Consciousness
– Results from rotational forces at the junction of the upper midbrain and thalamus that
results in disruption of reticular neuron function and inability to maintain alertness
– Presence of LOC is not a predictor of long term neuropsychiatric sequelae of head injury
CLINICAL FEATURES
– Pupillary Size + Reactivity
• Fixed Dilated Pupil = Ipsilateral Intracranial Hematoma resulting in uncal herniation
• Bilateral Fixed + Dilated = Poor Brain Perfusion, bilateral uncal herniation or severe
hypoxia
– Indicative of very poor neurological outcome
– Neurological Posturing
• Decorticate Posturing = Upper extremity flexion with lower extremity extension
– Cortical Injury above the midbrain
• Decerebrate Posturing = Arm extension and internal rotation with wrist flexion
– Indicative of brainstem injury
– Very Poor predictor of outcome
Look for specific injury patterns
– Battle’s sign, CXF Otorrhea, CSF Rhinorrhea, Hemotympanum, peri-orbital Ecchymosis is
indicative of skull fracture and is concerning for underlying brain injury
GLASGOW COMA SCALE
Glasgow Coma Scale (GCS)
Eye Opening
Opens spontaneously
Responds to verbal command
Responds to pain
No eye opening
Verbal
Oriented
Disoriented
Inappropriate words
Incomprehensible speech
No verbal response
Motor
Obeys commands
Localizes to pain
Withdraws to pain
Flexion to pain (Decorticate posturing)
Extension to pain (Decerebrate posturing)
No motor response
Current Classification
GCS = 14-15 = Mild Head Injury
GCS = 9 – 13 = Moderate Head Injury
GCS < 9 = Severe Head Injury
4
3
2
1
5
4
3
2
1
6
5
4
3
2
1
SYMPTOMS OF BRAIN INJURY IN THE ELDERLY
• With the elderly it is essential to remember that some of
the symptoms of a brain injury may be the same
symptoms they are already experiencing from other
medical conditions.
• These individuals must be closely monitored
• Subtle changes must be noted as well as exaggeration of
already existing symptoms.
• Symptoms may be worsened by medications
• Blood thinners may be especially problematic.
• Alcohol may increase these symptoms and could possibly
lead to seizures.
MANAGEMENT
• Mild Head Injury
• Moderate and Severe Head Injury
MILD HEAD INJURY MANAGEMENT
– Symptomatic treatment and prevention of secondary injury
– Appropriate management of Risk factors for intracranial
hematoma
• Coagulopathy, Drug/Alcohol Intoxication, Previous neurosurgical
procedures, Pre-trauma epilepsy or older age (> 60 y/o)
– All patients with mild traumatic brain injury should be
observed for 24 hours after that injury
MILD HEAD INJURY MANAGEMENT
• Discharge Instructions
– Appropriate follow-up instructions should be
provided both verbally and written instructions.
– No need to awaken patient q 2 hours
– Patients who return to ED due to persistent
symptoms should undergo careful repeat
neurological evaluation but little data supports
repeat CT Scanning
Warning Signs after Discharge
Inability to awaken the patient
Decreased/Altered mental status
Severe or worsening headache
Somnolence or confusion
Restlessness, Unsteadiness
Seizure activity
Visual difficulties
Change in behavior
Vomiting, fever, neck stiffness
Urinary or bowel incontinence
Weakness or numbness
• Return to Play Guidelines
– Patients should return to sporting activities in a step-wise fashion that
emphasizes physical and cognitive rest
– Patients should not return to sporting events if they are still symptomatic
– There are many commonly used tools for assessing a players ability to return
to sporting events.
MOD. SEVERE HEAD INJURY MANAGEMENT
• General Principles
– All moderate and severe head injured patients should undergo CT imaging
– Stabilization and prevention of secondary insults is mainstay of treatment
Systemic Insults
Hypoxia (PaO2 < 60 mmHg)
Hypotension (SBP < 90 mmHg)
Anemia 2/2 Blood Loss (↓Oxygen Carrying Capacity)
Other Systemic Insults
Seizures
Electrolyte Abnormalities
Coagulopathy
Infection
Hyperthermia
Intracranial Insults
Intracranial Hypertension
Extra-axial Lesions
Cerebral Edema (Peaks
at 24-48 hrs post injury)
MOD. SEVERE HEAD INJURY MANAGEMENT
• Airway Management
– Prevention of hypoxia and hypoventilation key to preventing secondary
insults
– Patients with GCS < 9, should have endotracheal airway placed
• Special attention should be paid to maintaining cervical spinal
immobilization
• Sedation
• ICP/CPP management
– Osmolar therapy
– Hypertonic saline
• Decompressive craniotomy
• Induced coma
• Hypothermia
• Antiseizures prophilaxis
SEQUELAE OF HEAD INJURY
•
Post Concussive Syndrome
– Constellation of symptoms that develops within 4 weeks of the injury and may
persist for months (90% at 1 month, 25% at 1 year)
– Treatment is with analgesia, anti-depressents and anti-emetics
•
Post-traumatic Epilepsy
– Seizure activity > 7 days from traumatic injury
– Head trauma is cause of long term epilepsy in 3% of patients with epilepsy
– Incidence is highest in patients with compound skull fracture, intracranial
hemorrhage or presence of early acute symptomatic seizure (presence of all 3
factors increases risk by 50-80%)
– Cannot be prevented with prophylactic use of antiepileptics
•
Persistent Vegetative State
– Rare complication of severe head injury, first described in 1972 by Jennett and Plum
– Disruption of cerebral cognitive function with sparing of brainstem function
– No awareness of themselves or environment and cannot interact with others but will
maintain normal sleep-wake cycle
– Recovery is rare if symptoms persist for > 3 months, no recovery documented after
12 months of symptoms
CONCLUSION
• The best cure for brain injury is prevention.
Older people in particular should take decisive
action to minimize the risk of a fall that could
result in a TBI. However should a fall occur,
immediate medical attention should be
sought, including screening for TBI.