Clinical Care- Closed head injury (including aneurysm) Flashcards
overview/definition of a concussion
Concussion is cognitive impairment brought on by diffuse brain injury after exposure to impact forces.
With or W/O LOC
Mildest subset of TBI
who is the most accident prone population?
young men (15-34), male, and drunk are most accident prone
pathophysiology of concussions
during accelerate, force is applied to brain and it creates shear force at white/grey matter junction.
severe enough may rupture axons. mild damage leads to swelling and inflammation.
what is the term for when an injury is present at site of impact as well as opposite side from rebound motion?
“coup-contrecoup”
Hallmarks of concussion
confusion and amnesia
clinical features of concussions
w/ or w/o LOC
may be immediate or delayed
lack of recall is red flag
early SX of concussion (min to hours)
headache, dizziness, vertigo, imbalance, nausea, vomiting
Delayed SX (hours to days)
mood/cognitive disturbance, light/noise sensitivity, sleep disturbance
COMMON signs of concussion
1) Vacant stare (befuddled facial expression)
2) Delayed verbal expression (slower to answer questions)
3) Inability to focus attention (easily distracted)
4) Disorientation (walking in the wrong direction, not A&O)
5) Slurred or incoherent speech (making disjointed statements)
6) Gross observable incoordination (stumbling)
7) Emotionality out of proportion to circumstances (appearing distraught, crying for no apparent reason)
8) Memory deficits (exhibited by patient repeatedly asking the same question that has already been answered or inability to memorize and return three of three words and three of three objects for five minutes)
LESS common sign of concussions?
1) Seizures
a) If seizures occur within one week of head injury, much more likely to be related to TBI than epilepsy
b) Occur in 5% of TBI patients, more common with severe injury
what is defined as a complicated concussion?
any concussion with concomitant hemorrhage. may preset as acute, subacute or chronic.
usually arterial in origin.
Acute evaluation of a concussion
HX and MACE w/ in 48 hrs
focus on neuro exam to detail extent of damage (more cognitive sx means more severe)
facial fractures are concerning for occult injury
management of concussions
Direct observation for 24 hrs
awake pt every 2 hrs.
low level of activity for 24 hrs.
No Alcohol, sedatives, or pain relievers other than NSAIDS for 48 hrs.
Immediate Referral/MEDEVAC for concussion
(a) Inability to awaken the patient
(b) Severe or worsening headaches
(c) Somnolence or confusion
(d) Restlessness, unsteadiness, or seizures
(e) Difficulties with vision
(f) Vomiting, fever, or stiff neck
(g) Urinary or bowel incontinence
(h) Weakness or numbness involving body part
5 possible complications of concussion
Second impact syndrome post concussion syndrome posttraumatic headaches sleep disturbances Chronic traumatic encephalopathy
what is second impact syndrome?
cerebral swelling that can develop in setting of a second concussion
2nd concussion when still symptomatic from 1st.
rare, potentially fatal
what is post concussion syndrome?
Headache, dizziness, cognitive impairment, psych symptoms that develop in
the first few days after mild TBI and resolve in weeks to months
what is chronic traumatic encephalopathy (CTE)?
1) Repeated concussions can lead to cumulative neuropsychologic deficits
a) Behavior changes, personality changes, depression, increased suicidality
b) Parkinsonism
c) Speech and gait abnormalities
Cranial traumas are likely to be what kind of fracture?
linear fractures, less risk for underlying damage
clinical features of a skull fracture
if open, look for CSF leakage
high likelihood of infection
scalp will bleed, must be cleaned
presence of tissue swelling, hematoma, palpable fracture, crepitus
thin areas of the skull
temporal region
nasal sinuses
what does it mean that force must be large for skull fracture
large impact or small area.
signs of basilar skull fracture
battle sign "racoon" eyes hemotympanum CSF rhinorrhea/otorrhea cranial nerve deficits
Acute management of skull fracture
- orogastric tube may be more appropriate than nasogastric
- watch for signs of swelling
- other fracture care as needed
- oxygen, C Spine, MEDEVAC ASAP
- serial neuro
- IV fluid
signs of ICP
decreased mental status
dilated pupils or anisocoria
papilledema
Cushing’s Triad (bradycardia, hypertension, respiratory irregularity)
if signs show rapid increase of ICP or herniation what are our actions
open airway
elevate head of bed
ventilate, avoid hyperbarbia
iv fluids (NS or LR) DO NOT USE GLUCOSE OF HYPOTONIC SOLUTIONS.
management of ICP
osmotic therapy (mannitol: 1g/kg 15-20% solution, repeat .25-.5 g/kg every 6-8 hrs OR 7.5% Hypertonic NaCL 250cc bolus)
consider hyperventilation as last resort.
if seizure, diazepam (10mg IV q10min max dose of 30mg)
3 major types of ICH sites
epidural hematoma
subdural hematoma
subarachnoid hematoma
Epidural Hemorrhage - Pathophysiology
85% of the time, skull fracture leads to arterial injury
Middle meningeal artery commonly affected
Normally the epidural space is a potential space, with the dura tightly attached to the skull, Under arterial pressure, the dura slowly peels away and a blood pocket forms
how will a epidural hemorrhage present?
immediate LOC
“Lucid interval” with recovery of consciousness, after a period of hours increasing headache with deteriorating neuro function
may see seizure, coma, anisocoria, respiratory collapse
what is the acute management of someone with epidural hematoma
oxygenation, GCS <8, intubate
neurosurgical consultation
monitor for increased ICP/herniation
complications of epidural hematoma
coma
respiratory depression
death unless treated surgically
disposition of epidural hematomas
MEDEVAC ASAP
who is more at risk for subdural hemorrhage?
elderly, alcoholics, anticoagulated at risk
may occur without impact, dismal prognosis
what’s happening during a subdural hematoma?
Acceleration in the lateral direction tears bridging veins draining the brain blood to the dural sinuses
Lower pressure blood, but more actual rather than potential space
clinical manifestation of a subdural hematoma
(a) May or may not have history of head trauma
(b) Acute subdural hematoma presents 1-2 days after onset
1) May have lucid interval after injury
(c) Chronic subdural hematoma presents 15 days or more after onset
(d) Insidious onset of headaches, light headedness, cognitive
impairment, apathy, somnolence are typical symptoms
patient management of subdural hematoma
managed same as epidural
SAH hemorrhage epidemiology
over 80% are usually rupture of aneurysm
high pressure bleeding into the subarachnoid space
SAH clinical presentation
Hallmark-thunderclap, worst headache of my life
sudden onset of headache, possible meningeal irritation
patient may have been doing something strenuous to increase intrathoracic pressure
some activities like cocaine, amphetamines, smoking, hypertension, alcohol use (all put stress on Cardio system)
treatment of SAH
rest
analgesia with tylenol
avoid anticoagulation drugs
MEDEVAC
Complications of SAH
Rebleeding (7%) only eliminated by treating underlying cause
Cerebral ischemia (30-40%) either by loss of blood flow or vasospasm
Increase ICP (54%) includes due to increase blood volume and swelling from inflammation
Seizures (7%), Hyponatremia, Cardiac arrhythmia
