Head Trauma Flashcards
Indications for EDH surgery:
Level:
1. EDH volume > 30cm3 should be evacuated regardless of GCS.
- EDH with all of the following characteristics can be managed nonsurgically with serial CT scans and close neurological observation in a neurosurgical centre:
a) volume < 30cm3
b) and thickness < 15mm
c) and midline shift (MLS) < 5mm (p.1110)
d) and GCS > 8
e) and no focal neurologic deficit
*The estimated volume of a lens = (1.6 to 2) × r2t = (0.4 to 0.5) × d2t ≈ (H × AP × T)/2 (that is 1/2 the products of the height times the length in the AP dimension times the thickness T).
EDH - general information:
Incidence: 1% of head trauma admissions (which is ≈ 50% of the incidence of acute subdural).
- male: female = 4:1
- 85% = arterial bleeding - middle meningeal artery
- 70% occur laterally over the hemispheres with their epicentre at the pterion
EDH - presentation:
“Textbook” presentation (< 10%-27%)
● brief posttraumatic loss of consciousness (LOC);
● followed by a “lucid interval” for several hours;
● obtundation, contralateral hemiparesis and ipsilateral pupillary dilatation;
60% of patients with EDH have a dilated pupil, 85% of which are ipsilateral
EDH - “PEDS”:
In peds, EDH should be suspected if there is a 10% drop in hematocrit after admission.
EDH - Kernohan’s phenomenon:
Shift of the brainstem away from the mass may produce compression of the opposite cerebral peduncle on tentorial notch which can produce ipsilateral hemiparesis (so called Kernohan’s phenomenon or Kernohan’s notch phenomenon
EDH - mortality:
Overall: 20–55%
Optimal diagnosis and treatment: 5–10% (12% in a recent CT era series)
Delayed epidural hematoma (DEDH) - definition:
EDH that is not present on the initial CT scan, but is found on subsequent CT.
9–10% of all EDHs
Posterior fossa epidural hematoma - characteristics:
- 5% of EDH
- More common in 1st two decades of life
- 84% have occipital skull fractures, only ≈ 3% of children with occipital skull fractures develop p-fossa EDH.
- Cerebellar signs are surprisingly lacking or subtle in most.
- Overall mortality is ≈ 26%
ASDH - receiving anticoagulation therapy - risk:
Receiving anticoagulation therapy increases the risk of ASDH 7-fold in males and 26-fold in females.
SDH - density changes on CT:
acute (1-3 days) - hyperdense
subacute (3 days to 2-3 weeks) - isodense
chronic (> 3 wks and < 3–4 mos) - hypodense
ASDH - indications for surgery:
- > 10mm or midline shift (MLS) > 5mm (on CT) => regardless of GCS
- < 10mm and MLS < 5mm:
a) GCS drops by ≥ 2 points from injury to admission
b) and/or the pupils are asymmetric or fixed and dilated
c) and/or ICP is > 20mm Hg - monitor ICP in all patients with ASDH and GCS < 9
ASDH - mortality range:
Mortality range: 50–90%
- 90–100% in patients on anticoagulants
Interhemispheric subdural hematoma - characteristics:
Subdural hematoma along the falx between the two cerebral hemispheres.
- may occur in children (possible child abuse)
- Spontaneous cases should be investigated for possible underlying aneurysm.
- Reported mortality: 25–42%.
Interhemispheric subdural hematoma - treatment:
Controversial. Small asymptomatic cases may be managed expectantly. Surgery should be considered
for progressive neurological deterioration with larger lesions. Approached through a parasagittal
craniotomy.
✖ Surgery for these lesions can be treacherous—there is risk of venous infarction and one often finds they are dealing with a superior sagittal sinus injury.
Infantile acute subdural hematoma - definition:
Def.: acute SDH in an infant due to minor head trauma without initial loss of consciousness
or cerebral contusion, possibly due to rupture of a bridging vein. The most common trauma is a fall
backwards from sitting or standing.
Infantile acute subdural hematoma - presentation:
The infants will often cry immediately and then (usually within minutes to 1 hour) develop a generalized seizure. Patients are usually < 2 yrs old (most are 6–12 mos, the age when they first begin to pull themselves up or walk).
Infantile acute subdural hematoma - treatment:
Minimally symptomatic cases (vomiting, irritability, no altered level of consciousness and no motor disturbance) with liquefied hematoma may be treated with percutaneous subdural tap, which may be repeated several times as needed.
Chronically persistent cases may require a subduroperitoneal shunt.
More symptomatic cases with high-density clot on CT require craniotomy.
Infantile acute subdural hematoma - mortality:
8% morbidity and mortality rate in one series.
Severity of brain injury - stratification:
Minimal:
- GCS 15 pt
- No LOC
- No amnesia
Mild:
- GCS 14 pt
OR
- GCS 15 pt + LOC < 5 min + impaired alertness or memory
Moderate:
- GCS 9-13 pt
OR
- LOC >= 5 min
OR
- focal neurologic deficit
Severe:
- GCS 3-8 pt (CRITICAL GCS 3-4 pt)
Clinical signs of IC-HTN:
Clinical signs of IC-HTN:
1 - pupillary dilatation (unilateral or bilateral)
2 - asymmetric pupillary reaction to light
3 - decerebrate or decorticate posturing (usually contralateral to blown pupil)
4 - progressive deterioration of the neurologic exam not attributable to extracranial factors
Practice guideline: BP and oxygenation
Level II: monitor BP and avoid hypotension (SBP < 90mm Hg)
Level III: monitor oxygenation and avoid hypoxia (PaO2 < 60mm Hg or O2 saturation < 90%)
Practice guideline: Early sedation and paralysis
Level III: sedation and neuromuscular blockade (NMB) can help transport the head-injured
patient, but they interfere with the neuro exam
Level III: NMB should be used when sedation alone is inadequate
Practice guideline: Intubation—indications
Level III: secure the airway (usually by endotracheal intubation) in patients with GCS ≤ 8 who are
unable to maintain their airway or who remain hypoxic despite supplemental O2
Practice guideline: Antibiotics for intubation
Level II: periprocedural antibiotics for endotracheal intubation reduce the risk of pneumonia, but do
not alter length of stay or mortality
Practice guideline: Early/prophylactic hyperventilation
Level II: prophylactic hyperventilation (PaCO2 ≤ 25mm Hg) is not recommended
Level III
● hyperventilation (HPV) before ICP monitoring is established should be reserved as a temporizing
measure for patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes
● HPV should be avoided during the first 24 hrs after TBI (when CBF is often dangerously decreased)
Practice guideline: Early use of mannitol
Level III: the use of mannitol before ICP monitoring is established should be reserved for patients
who are adequately volume-resuscitated with signs of transtentorial herniation or
progressive neurologic deterioration not attributable to extracranial causes
Mannitol - indications in E/R:
- evidence of intracranial hypertension
- evidence of mass effect (focal deficit, e.g., hemiparesis)
- sudden deterioration prior to CT (including pupillary dilatation)
- after CT, if a lesion that is associated with increased ICP is identified
- after CT, if going to O.R.
- to assess “salvageability”: in patient with no evidence of brainstem function, look for return of
brainstem reflexes
Mannitol - Contraindications:
- prophylactic administration is not recommended due to its volume-depleting effect.
- hypotension or hypovolemia: hypotension can negatively influence outcome. Therefore, when
intracranial hypertension (IC-HTN) is present, first utilize sedation and/or paralysis, and CSF
drainage. If further measures are needed, fluid resuscitate the patient before administering mannitol.
Use hyperventilation in hypovolemic patients until mannitol can be given - relative contraindication: mannitol may slightly impede normal coagulation
- CHF: before causing diuresis, mannitol transiently increases intravascular volume. Use with caution
in CHF, may need to pre-treat with furosemide (Lasix®)
Mannitol after TBI - dosage:
bolus with 0.25–1 gm/kg over < 20 min (for average adult: ≈ 350 ml of 20% solution). Peak effect
occurs in ≈ 20 minutes
Practice guideline: Prophylactic antiseizure medications after TBI
Level II: prophylactic phenytoin, carbamazepine, phenobarbital, or valproate do not prevent late PTS
Level II: ASMs (e.g., phenytoin, valproate, or carbamazepine) may be used to decrease the
incidence of early PTS (within 7 days of TBI) in patients at high risk of seizures after TBI however, this does not improve outcome
Conditions with increased risk of posttraumatic seizures:
Conditions with increased risk of posttraumatic seizures:
1. acute subdural, epidural, or intracerebral hematoma (SDH, EDH or ICH)
2. open-depressed skull fracture with parenchymal injury
3. seizure within the first 24 hrs after injury
4. Glasgow Coma Scale score < 10
5. penetrating brain injury
6. history of significant alcohol abuse
7. ± cortical (hemorrhagic) contusion on CT
Noncontrast head CT for patients ≥ 16 years age with GCS = 14-15 following non-penetrating TBI are
indicated only if one or more of the following is present
Level I: For patients with LOC or posttraumatic amnesia
● headache
● vomiting
● age > 60 years
● intoxication (alcohol or drugs)
● short-term memory deficits
● physical signs of trauma above the clavicle
● posttraumatic seizure
● GCS < 15
● focal neurologic deficit
● coagulopathy (including anticoagulants/antiplatelet drugs)
Level II: For patients without LOC or posttraumatic amnesia
● focal neurologic deficit
● vomiting
● severe headache
● age ≥ 65 years
● signs of basal skull fracture (includes hemotympanum, “raccoon’s eyes” (p. 1065), CSF rhinorrhea
or otorrhea, Battle’s sign (p. 1065))
● GCS < 15
● coagulopathy (including anticoagulants/antiplatelet drugs
● dangerous mechanism of injury: pedestrian hit by motor vehicle, ejection from automobile, fall
from height > 3 feet or > 5 stairs
