Head and Neck Flashcards
Altered Head Injured Patient. Start with trauma primary survey
ABCDE
D=Disability, caused by the injury?
E=Exposure, take the pts cloths off.
Pupil eval
Miosis?
one pupil larger then other?
Mydirasis?
Miosis=OPIATES. PONTINE LESION
One pupil bigger then the other?=LEFT HEMATOMA- HERNIATION OR OCULAR GLOBE TRAUMA, commonly stroke, brain or optic tumor, brain aneurysm, MS.
Mydriasis=INCREASED ICP WITH POOR CEREBRAL PERFUSION, DRUG EFFECT, BILATERAL HERNIATION, SEVERE HYPOXIA
Evaluation and Management of the Head injured Patient
The Glasgow Coma Scale
Standardized evaluation of neurological status
Reproducible - can be performed by multiple examiners at different levels of care
Predictive of morbidity/mortality
Glasgow Coma Scale
Eye opening
4: Spontaneous eye opening.
3: Eye opening in response to speech – that is, any speech or shout.
2: Eye opening in response to pain.
1: No eye opening.
GCS continued
Best Verbal Response
5: Oriented - patient knows who and where they are, and why, and the year, season and month.
4: Confused conversation - patient responds in conversational manner, with some disorientation and confusion.
3: Inappropriate speech - random or exclamatory speech, with no conversational exchange.
2: Incomprehensible speech - no words uttered, only moaning.
1: No verbal response.
GCS continued
Best Motor Response
6: Carrying out request (‘obeying command’) - patient does simple things you ask.
5: Localising response to pain.
4: Withdrawal to pain - pulls limb away from painful stimulus.
3: Flexor response to pain - pressure on nail bed causes abnormal flexion of limbs (decorticate posture).
2: Extensor posturing to pain - stimulus causes limb extension (decerebrate posture).
1: No response to pain.
GCS Interpretation
A.V.P.U. Alert, or responsive to Verbal stimuli, or to Painfull stimuli, or Unresponsive
Trauma eval. Secondary survey and AMPLE history
A -> Allergies
M -> Medications (especiallyanticoagulants/anti-platelets)
P -> Past medical history
L -> Last meal (especially if surgery is indicated emergently)
E -> Events (what happened just before..?)
VITALS SIGNS ARE VITAL!!!!
Epidural Hematoma=Definition, sx’s
Transient loss of consciousness; lucent interval
Laceration of dural vessels from skull fracture (91%), usually the middle meningeal artery
3rd nerve palsy (sign of cerebral herniation)
Somnolence 24-96 hrs after accident
Epidural Hematoma=Etiology
Hematoma expands
Increased ICP, decreased CBF
Herniation, ipsilateral CN-3 dysfunction and contralateral paralysis or posturing
Subdural Hematoma
Incidence: 5% of head trauma patients
Age: infants and elderly (large subarachnoid space with freedom to move)
Cause: damage to subdural veins (“bridging veins”)
Acute Subdural Hematoma:
Manifests hours after injury
Hyperdense (<1 week); isodense (1-3 weeks); hypodense (3-4 weeks)
Underlying brain injury (50%)
Worse long term prognosis than epidural hematoma
Subdural Hematoma=Etiology
May be acute, like epidural hematoma
May have delayed course, days to weeks
Increased ICP, edema, herniation
ETOH increases cerebral edema by increasing the permeability of the blood brain barrier
Subdural Hematoma=different types
Chronic Subdural Hematoma:
Following minor injury, rarely parenchymal injury
Convex configuration
Interhemispheric Subdural Hematoma:
Usually posterior
Most common acute finding in child abuse
(whiplash injury)
Sub-Arachnoid Hemorrhage
Bleeding from small vessels at site of coup or contrecoup injury
Bleeding under arachnoid, spreads in CSF
Vasoactive substances in blood contribute to ischemia and altered level of consciousness
Sub-Arachnoid Hemorrhage=etiology
Often occurring directly beneath an external injury
Can also occur as a contrecoup injury
Direct rupture of intrinsic cerebral vessels.
Whats the Battle sign?
Ecchymiosis behind the ear.
Its a late sign
Whats Hemotympanum?
Blood behind the tympanic membrane.
What are Raccoon eyes?
Blood behind the eye lids?
Basal Skull Fracture
Caused by deceleration injury or occipital trauma
4% of serious head injuries
Seldom fatal (except for race car drivers)
Separation of suture between temporal and occipital bones
May involve orbits or sphenoid bone, or fracture near foramen magnum
Basal Skull Fracture
Damage to Cranial nerves III, VII or CSF otorrhea, CSF rhinorrhea (danger of meningitis!) Battle’s sign Racoon eyes Hematotympanum
Treatment of the seriously head injured patient
Seizure prevention: IV Phenytoin
Prevent fever
Control bleeding, transfuse to HCT>30
Antibiotics for penetrating injury or basal skull fracture
Early neurosurgical consultation: ventriculostomy, craniotomy
Treatment of the seriously head injured patient
Treat hypotension, resucitate to MAP>90 (SBP 120-140 with NS. Pressors as needed. N.B. isolated head injury is unlikely to be hypotensive on initial presentation, so look for other injuries!
Control excessive hypertension. Labetolol to reduce BP 20-30%
Treat hypoxia, intubate and ventilate (increased CO2 dilates vessels and lowers cpp)
Sedate if needed (not ketamine)
Treatment of the seriously head injured patient
Treat increased ICP (target <20, cpp70- 80)
Raise head of bed to 30 degrees
IV mannitol boluses once euvolemic
(serum osmolality 280-300)
Hyperventilate PCO2 to 26-30? Consider only if other measures ineffective
Steroids not proven to have benefit in head trauma
Head injury, Disposition
GCS of 15 with resolved symptoms:, dispo to home with vigilant family members and return preacautions
GCS of 14-15 (ie: “mild” injuries)
Admit for observation. Neurological exams every 1-4 four hours. IV fluids, analgesia, anti-emetics.
Repeat head CT if worsening pain, vomiting or adverse change in level of consciousness
GCS of 9-13 (ie: “moderate” injuries)
Admit to ICU. Neurological exams every 1-2 hours.
NPO
Repeat head CT six hours after admission or promptly if pt worsens
If pt is immobile, DVT prevention may be warranted.