Head Trauma

(Head injury)

THITINAN LIMCHOOPORNWIKUL
Overview
Initail approach
General management
Specific injuries
 Initail approach
Monroe-Kellie hypothesis-Volume within the skull remains constant
Cerebral perfusion pressure(CPP)=
Mean arterial pressure (MAP) – Intracranial pressure (ICP).
-Reduced CPP is the pathologic
force of concern during head injury.
Bleeding within skull raises the ICP.
Body will compromise by raising
the MAP
Cushing'sresponse-Seen in elevated ICP;
hypertenson, bradycardia, and
tachypnea.Demands decisive action.
-Compression/distortion of CN X

Hx will be very important in your

differential
Cushing'sresponse
Inital approach
-All head injuries are a C-spine injury until proven othenwise(5% )
-A: Ensure secure airway.Hypoxia is an independent risk factor for mortality,
·All pts should beput on 100%high flow O2 NRB mask
·Pts w/ GCS<8 or other indications should be intubated via orotracheal intubation
-B:All pts should be monitored w/ pulse oximetry and frequent checks of respiratory
status
·Pts who were intubated should get an ABG
-C: Maintain MAP>90 mmHg with fluids.Hypotension is an independent risk factor
for morbidity and mortality.
·Avoid glucose-containing Acids
·Watch carefully for Cushing's response(inc.BP,dec.HR,inc.RR)
-D: Obtain a GCS score on pt;this will help categorize the injury.
-Check pupil size: Anisocoria points to elevated ICP.Larger pupil is IL to lesion.
-If pt has altered mental status,assessfor possible reversible Causes
Inital approach
-Reversible causes can beremembered by how they're treated
(DONT forget how to treat reversible AMS causes) .
Dextrose-50 amp (hypoglyecemia)
Oxygen 100% NRB (hypoxemia)
Naloxone(narcotic OD-pinpoint pupils)
Thiamine w/ fluids (alcoholics)
Inital approach
-Orher considerations:
-Pts w/ significant head injury should be considered for seizure prophylaxis.
Phenytoin,fosphenvtoin,or carbamazepinemay be used.
-Post-traumatic convulsions should be treated promptly w/ lorazepam
-Narcotics and benzodiazepines may be started after initial exam
-Pts w/sx of elevated ICP should be given
mannitol and IV fluids; mainain serum osmolahy
below 320 mOsm
-Focused physical examination: Look for ecchymoses
(Battle sign, Raccoon sign.)Look for scalplaceration,
avulsions,palpate for fractures.Look for hemotympanum.
Check for primitive reflexes (namely, Babinski )
Glasgow Coma Scale

(E)+(V)+(M)=score/15
General management
-After initial approach,a head CTis warranted in all but the very few of
head injury pts.
-Indications: Loss of consciousness at injury,neurological deficit,
AMS,moderate to severe mechanism of injury,
suspected skull fracture on palpation
-Wll demonstrate facture(s) intracranial bleeding,
contusions, axonal injuries
-Traumalabsshould be ordered:
CBC,BMP,blood type,blood alcohol levels, toxicology
-Obtain a good history of the mechanism of injury and
any events surrounding it
-Do not removed any impaled object until the pt is in the OR
 Soft
Tissue
and
Scalp
injury
 Scalp injury
1. Scalp hematoma
①Caput succadaneum
②Subgaleal hematoma
③Cephalohematoma
2. Scalp laceration
3. Scalp avulsion
Scalp hematoma
①Caput succadaneum
-low volume of hematoma
-localization
-The surrounding is
harder than the central
-no fluctuation
②Subgaleal hematoma
-Not restricted by cranial suture
-Hematoma can spread to the whole head
-Soft touch
-Can have obvious wave motion
③Cephalohematoma
-Generally, it does not cross the cranial suture,
-The hematoma has higher tension.
-It can w/ skull fx.
 Management
①Caput succadaneum
Many do not need special treatment, can be absorbed
②Subgaleal hematoma
Pressure dressing （ Smaller ）
Drainage and Pressure dressing(Bigger)
③Cephalohematoma
if w/ skull fx avoid pressure dressing
 Scalp laceration

-The scalp is abundantly vascularized; it can bleed profusely.

-A scalp laceration often appears w/ a skull fracture;
carefully palpate the surrounding tisse and strongly
consider a CT
-Tx: Can be treated w/ staples or simple interrupted sutures;
be sure to look for any otherinjury and tx as needed
 Scalp avulsion

-Scalp avulsion is the most serious scalp injury

-A large scalp is avulsed from the subglacial aponeurosis or
together with the skull periosteum
-Prone to hemorrhagic shock
 Management

1. The flap has not been completely detached, and the blood supply is good,
suture in situ
2. Within 6 hours of being completely separated, the blood vessel should be
cut neatly, and the blood vessel should be anastomosed and the scalp will be
sutured.
3. The skin flap is severely damaged, and the periosteum can be grafted
4. The skull is exposed, and the skull is perforated to cultivate granulation
and then skin grafted
 Skull fractures
-Skull fractures should be suspected based on physical examination or on the
presence of scalp laceration
-The type of fracture is important for
determining how to manage the pt.
A head CT is necessary in determining
the type of fracture present.All pts w/
skull fractures should be admitted w/
strgeal consult.
 Skull fractures
-Types
-Closed fracture: Often associated w/ more serious intracranial problems
(hematoma, hemorrhage,etc.)which will show up on CT. These fractures
need no speciic tx themselves.
-Depressed fracture: Often associated w/ more serious intracranial
problems which will show up on CT. Increased risk of post-traumatic
Seizure and infection. Must go to OR
-Open fracture: Often associated w/ scalp lacerations and palpable
Inereased risk of iniection. Must go to OR
-Basilar fracture: Associated w/ periorbital (Racoon),retroauricular Batle
ecchymoses,otorrhea,hemotympanum,rhinorrhea,hearing loss
Traumatic
Brain
Injury
 Traumatic Brain Injury
-Extarnal force causes damagee to brain
(Mechanial,Thermal,Chemical,Eletrical,Rodiatian )
-Mechanism of injury
-Blunt
1.Acceleation : moving object make contact with head
(baseball bat hitting head)
2.Decelaration : moving head strikes stationary object
3.Accetleation-Decelelationa : rest-->moving-->rest
(motor vehicle accident)
4.Rotation: twist of brin in skull
(most common by sort of side impact to head)
5.Compression or Deformation: change in shape of skull cousing injury to brain
tissue
-Penetrating: When objuct has penetrated skull.
most common by gun,knives,Penetrating objects
 Primary brain injury
Concussion
For the lightest brain injury
It is characterized by temporary disturbance of consciousness
and forgetting of recent events after injury
Clinical manifestations and diagnosis
1. Transient loss of consciousness immediately after injury
2. Consciousness lasts for several seconds to several minutes,
usually less than half an hour
3. With pale complexion, changes in pupils, cold sweats, drop in blood pressure
4. Retrograde forgetting
(can't recall the situation at the time of injury and the recent situation before
injury)
5. No positive signs on nervous system examination
6. No abnormalities in brain CT
7. Lumbar puncture cerebrospinal fluid pressure is normal,
and the test is in the normal range
Treatment
1. No special treatment required
2. Bed rest for 5~7 days
3. Treat symptomatically such as sedation, analgesia, and elimination of fears as
appropriate
Brain contusion
Primary brain damage caused by violence to the head
Either focus on the brain tissue or hedging the injury
Clinical manifestations
1. Impairment of consciousness: it can occur immediately after injury,
and the duration varies
2. Headache, nausea, vomiting
3. Changes in vital sign: increased intracranial pressure caused by cerebral
edema to increase blood pressure, slower pulse, and slower breathing
4. Focal symptoms and signs: aphasia due to hemiplegia of the contralateral
limb due to injury to the motor area
Examination
1. Brain CT (the most meaningful and preferred examination)
Confounding of high and low density in local brain tissue
High density is hemorrhagic focus, low density is edema area
There may be ventricle compression, midline structure shift, etc.
2. Cerebrospinal fluid examination
Whether the cerebrospinal fluid contains blood can distinguish concussion
Draining bloody cerebrospinal fluid reduces symptoms
Severe increase in intracranial pressure is contraindicated for lumbar puncture
diagnosis
Impaired consciousness immediately after injury
Focal symptoms and signs, obvious headache, nausea, and vomiting
Patients with contusion and laceration of the frontal pole and temporal pole may
have no focal symptoms and signs, and CT diagnosis is required
Treatment
1. Observe closely the changes in the condition
2. General handling
The head of the bed is raised 15°~30° awake, lying on the side in a coma
Keep the airway open
Nutritional support
Find the cause of agitation (pain, urinary retention, high intracranial pressure, etc.) and deal with it
Combined use of anti-epilepsy drugs in patients with epilepsy
Central hyperthermia can be treated with sub-hibernation
Brain protection (barbiturates, ganglioside e, acetoglutamine, etc.)
3. Prevent brain edema and brain swelling (mannitol, etc.)
4. Indications for surgical treatment (solve intracranial hypertension and clear hematoma)
①Secondary cerebral edema is severe, dehydration treatment is ineffective,
and the condition is aggravated
②There is no significant relief of intracranial pressure after the removal of intracranial hematoma
③Brain herniation
5. Surgical method
Cerebral contusion and laceration removal, frontal or temporal pole resection
Decompressive craniectomy
Diffuse axonal injury
The head is subjected to external rotating force, which is caused by shear stress
It is characterized by swelling and rupture of the nerve axon in the central area
of ​the skull
Difficulty in treatment, poor prognosis
Primary brainstem injury is considered the most severe diffuse axonal injury
Clinical manifestations
1. Impairment of consciousness
Prolonged severe disturbance of consciousness immediately after injury
(typical clinical manifestations)
2. Changes in pupils and eye movements
Some patients have unilateral or bilateral dilated pupils
Patients with extensive injuries may have both eyes deviated in the
same direction, staring downwards, and separated eyeballs
Examination
CT: high-density imaging of the corpus callosum, upper brain stem,
internal capsule and basal ganglia
Generally not accompanied by peripheral edema or other damage
MRI (highest diagnostic sensitivity):
T1 high signal, T2 low signal at the acute stage of tissue tearing and
hemorrhage
Acute non-hemorrhagic tissue tear T1 low signal, T2 high signal
Diagnostic criteria
1. Sustained coma after injury (>6h)
2. CT showed tearing or normal brain tissue
3. Normal intracranial pressure but poor clinical condition
4. Persistent vegetative state after injury without clear brain structure abnormalities
5. Diffuse brain atrophy after trauma
6. Autopsy showed characteristic pathological changes in brain tissue
Treatment
1. High fatality rate and disability rate, no breakthrough in clinical treatment
2. Respiratory management, hyperventilation and oxygen inhalation
3. Low temperature
4. Calcium antagonist
5. Dehydration
6. Barbiturates
7. Combined with intracranial hematoma or severe cerebral edema, Sx
intracranial hematoma
It is the most common and serious secondary lesion in craniocerebral injury
If not treated in time, brain herniation can be caused by
increased intracranial pressure
Classification
1. According to the time of symptom
① Acute hematoma (within 3 days)
②Subacute hematoma (after 3 days to within 3 weeks)
③Chronic hematoma (more than 3 weeks)
2. According to the location
①Epidural hematoma
②Subdural hematoma
③Intracerebral hematoma
Epidural hematoma
Formation mechanism
1. The main source of epidural Epidural hematoma
Middle meningeal artery and venous sinus rupture
2. Main formation mechanism
Direct violence caused skull fracture to tear blood vessels
Clinical manifestations
1. Impairment of consciousness
Primary brain damage is mild (waking → coma)
Slightly severe primary brain damage (coma→waking (intermediate waking period)→coma)
Primary brain damage is severe (progressive increase in coma after injury)
2. Increased intracranial pressure: headache, nausea, vomiting, increased blood pressure,
slower breathing and pulse
3. Pupil changes
4. Neuro signs
CT manifestations of epidural hematoma
1. Double convex lens or arcuate high density between the inner plate of skull and dura mater
2. May be accompanied by ventricle compression, midline shift, and cerebral edema
Diagnosis
1. History of head trauma
2. Wake up after injury and then fall into a coma,
Or there is an intermediate waking period of
consciousness disorder process
3. Head CT
Epidural hematoma treatment
1. Indications for surgery
Signs and symptoms of markedly high intracranial pressure
CT shows an epidural hematoma with obvious brain tissue compression
Falx cerebri ＞ 30ml ， Tentorium cerebelli ＞ 20mL (bleeding volume=0.524
(length×width×height))
Tentorium cerebelli ＞ 10mL
2. Surgical method
Bone flap or bone window craniotomy for hematoma removal + proper hemostasis
Subdural hematoma
Mechanism
1. Acute and subacute subdural hematoma source: cerebral cortical vascular rupture
2. Occurrence mechanism: most of them are hedging injuries
3. The bleeding source and pathogenesis of chronic subdural hematoma are still unclear
Clinical manifestations of acute and subacute subdural hematoma
1. Impairment of consciousness
Patients with acute complex hematoma with brain contusion and laceration are mostly persistent
coma or coma progressively worsening
Subacute or simple hematoma can have intermediate lucid interval
2. Increased intracranial pressure: headache, nausea, vomiting and changes in vital signs
3. Pupil changes
4. Neuro signs
Clinical manifestations of chronic subdural hematoma
1. The disease progresses slowly, and the course of the disease is longer,
mostly one month, but several months
2. Classification of clinical manifestations
①Symptoms of increased intracranial pressure are the
main symptoms, lack of localized symptoms
②The main symptoms of the lesion, such as hemiplegia,
aphasia, localized epilepsy, etc.
③Mainly intellectual and mental disorders, dizziness, tinnitus,
memory loss, etc.
CT manifestations of acute and subacute subdural hematoma
1. Crescent shaped high-density or mixed-density shadows between
the brain surface and the skull
2. May be accompanied by brain contusion and laceration and displacement of the midline
brain under pressure
CT manifestations of chronic subdural hematoma
Crescent shaped low-density or iso-density shadow on the brain surface
Diagnosis of acute and subacute subdural hematoma
1. History of head trauma, impaired consciousness and gradually worsened after the injury,
accompanied by intracranial hypertension
2. Head CT can be diagnosed
Diagnosis of chronic subdural hematoma
1. The elderly have a recent history of mild head trauma
2. Chronic intracranial hypertension symptoms, intellectual and mental abnormalities or
focal symptoms
3. Head CT or MRI can be diagnosed
Treatment
1. The treatment principle of acute and subacute subdural hematoma
is the same as that of epidural hematoma
2. Treatment of chronic subdural hematoma
Surgery as soon as possible if the symptoms are obvious,
the first choice for drainage
Intracerebral hematoma
Rarely, the incidence in closed head injury is about 0.5%-1.0%
Often co-exists with frontal and temporal concussion brain contusions when the occipital is exerted
Mechanism
1. Superficial hematoma: It is usually caused by the rupture of the cerebral cortex blood vessel that
is constricted and often coexists with subdural hematoma
2. Deep hematoma: caused by the rupture of deep blood vessels in the brain, there may be contusion
and laceration on the brain surface
Clinical manifestations and diagnosis
1. Often accompanied by brain contusion and laceration, the symptoms are similar to those
of brain contusion and laceration. Consciousness disorder
Manifestations of intracranial hypertension
Focal brain symptoms
2. Need brain CT to diagnose
CT findings of intracerebral hematoma
Round or irregular high-density shadows in the white matter near the brain contusion
or deep brain
Treatment
The treatment principle is the same as that of subdural hematoma
Debone flap or craniotomy to remove hematoma
Clear the combined presence of subdural hematoma and obvious contusion and
erosion of brain tissue
 Secondary brain injury
-Secondary brain injury occurs after the primary mechanisms of
injury have run their course
-Those "physiological variables" are not all associated with the primary brain injury,
as one can see:
Increased ICP
Hypotension
Hypoxia
Hypercapnea/hypocapnea
Hypoglycaemia and hyperglycaemia
Hyponatremia and hypernatremia
Hyperthermia
Seizures
-Prevention
Normoxia:
keep the PaO2 above 60 mmHg
Low normocapnia:
keep the PaCO2 between 35-40 mmHg
Normotension:
measure the MAP, and keep the systolic above 90mmHg
Intracranial Pressure monitoring:
keep it under 20mmHg
Cerebral perfusion pressure:
keep it 60-70mmHg
Cerebral oxygenation monitoring:
keep the SjO2 >50%, and PbrO2 >55mmHg
-Prevention
Managing increased intracranial pressure for which there is a variety of strategies:
Draining the EVD ( about 20ml/hr, max)
Positioning the head straight
Removing the C-spine collar
Sedation :
Propofol sedation to decrease distress and thus decrease ICP
Barbiturate coma if other methods of lowering ICP have failed
Analgesia to prevent increased ICP in response to suctioning and
routine care
Paralysis
Osmotherapy
Controversial measures
Decompressive craniectomy
Hypothermia
Dexamethasone
-Prevention
Decreasing cerebral oxygen demand:
Sedation
Propofol sedation to decrease distress and thus decrease ICP
Barbiturate coma if medical and surgical methods of lowering ICP have failed
Analgesia - opioid selection is irrelevant, but opiate boluses increase ICP
Seizure prophylaxis is infrequently indicated, and the course is 7 days only
Controversial measures:
Decompressive Craniectomy
Hypothermia
Tranexamic acid