IL TRAUMANEL GRANDE ANZIANO

Inquadramento del problema clinico nel trauma cranico

dott. Pasquale CaiazzoDirettore 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

• 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

– 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

FALLS

Intrinsic Factors Extrinsic Factors

Age changes

Chronic conditions

Medications

LE weaknessEnvironmental factors

Footwear

Alcohol

Assistive deviceAcquired Factors

related

– Scalp

– Skull

– Brain

HEAD INJURY

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

• 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

CONCUSSION

– 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

EPIDURAL HEMATOMA

– Classic signs include• Initial period of unconsciousness• Brief lucid interval followed by

decrease in LOC• Headache• Nausea, vomiting• Focal findings

– 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

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

SUBACUTE 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

CHRONIC SUBDURAL HEMATOMA

Intracerebral and Subarachnoid Hematoma

– 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

SUBARACHNOID HEMORRAGE

– 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

INTRACEREBRAL HEMATOMA

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 SCALEGlasgow Coma Scale (GCS)Eye Opening Opens spontaneously 4

Responds to verbal command 3Responds to pain 2No eye opening 1

Verbal Oriented 5Disoriented 4Inappropriate words 3Incomprehensible speech 2No verbal response 1

Motor Obeys commands 6Localizes to pain 5Withdraws to pain 4Flexion to pain (Decorticate posturing) 3Extension to pain (Decerebrate posturing) 2No motor response 1

Current ClassificationGCS = 14-15 = Mild Head InjuryGCS = 9 – 13 = Moderate Head InjuryGCS < 9 = Severe Head Injury

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

• 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.

Warning Signs after Discharge

Inability to awaken the patientDecreased/Altered mental statusSevere or worsening headacheSomnolence or confusionRestlessness, Unsteadiness Seizure activityVisual difficultiesChange in behavior Vomiting, fever, neck stiffnessUrinary or bowel incontinenceWeakness or numbness

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 InsultsHypoxia (PaO2 < 60 mmHg)Hypotension (SBP < 90 mmHg)Anemia 2/2 Blood Loss (↓Oxygen Carrying Capacity)

Other Systemic InsultsSeizuresElectrolyte AbnormalitiesCoagulopathyInfectionHyperthermia

Intracranial InsultsIntracranial HypertensionExtra-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.