Trauma

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.

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• Objective
• Introduction
• Classification
• Signs and symptoms
• Investigations
• Management
• Complications
• Reference

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•To have a basic knowledge
about Head Trauma
• To Understand the assessment
& management principles of
patients with Head Trauma

4. Definion
Head injury:- Is an injury which occurs on scalp, skull and brain
tissue
Primary brain injury
The damage caused to the brain at the moment of impact.
 Concussion
 Diffuse axonal injury
 Contusion/laceration
Secondary brain injury
occurs at some time after the moment of impact and is often
preventable.
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5.  Head injury occurs with an incidence of
20–40 cases per 100 000 population per
year.
 It is the most common cause of death in
young adults(age 15–24 years)
 It is more common in males than females.
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6.  Road traffic accident
 65% of deaths following severe head injury
 Falls
 Assaults
 Injuries at work place, during sport, or at
home
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8.  Adult brain: 1200–1400 g
 15–20% of cardiac output.
 Cerebral Blood Flow(CBF)
 Adults-55/100gm/min
 Autoregulation- by adjusting resistance vessles
 CBF remains constant despite wide variations in the
Cerebral Perfusion Pressure(CPP).
CPP=MAP-ICP
 CBF maintained constant between MAP 60-
150mmhg.Beyond this limits CBF varies directly with CPP
 The partial pressure of arterial carbon dioxide (PaCO2) exert
a profound influence on CBF
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9.  Trauma
 Ischemia
 Hypercapnia
 Hypoxia
 Some anaesthetic agents
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10. Brain metabolism
 Brain oxygen consumption (CMRO2,
cerebral metabolic rate for oxygen) is
about 3.5 ml /100 g/min
 The brain relies on blood borne
glucose for 90% of its energy
requirements
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11. Cerebral blood flow and autoregulation
 Normal cerebral blood flow is approximately 55ml/100 g/min
 MAP of brain is between 50 and 150 mmHg.
 In head injury, mechanisms of cerebral authoregulation become
disordered.
 Cerebral blood flow fluctuates with MAP and the brain is more
vulnerable to hypotension.
CBF=CPP/CVR , Normal CPP=60-70 mmHg
CPP=MAP-ICP, Normal ICP= 5-10mmHg
MAP = SBP + 2 DBP
3
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Monroe-Kellie doctrine
The sum of the intra cranial volumes of blood, brain,
and other components (tumor, hematoma)is
constant, and that an increase in any one of these
must be compensated by an equal decrease in
another or else pressure will rise.

13. 1. Primary & secondary
2. Glasgow Coma Score
3. Skull fracture
4. Anatomy of bleeding
5. Closed & open
6. Coup & countercoup
7. Bone involved & types
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14. Primary brain injury
The damage caused to the brain at the moment of impact.
 Concussion
 Diffuse axonal injury
 Contusion/laceration
Secondary brain injury
 Occurs at some time after the moment of impact and is
often preventable.
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15.  Hypoxia: PO2 < 8 kPa
 Hypotension: SBP < 90 mmHg
 Raised ICP: ICP > 20 mmHg
 Low cerebral perfusion pressure (CPP): CPP < 60 mmHg
 Pyrexia
 Seizures
 Metabolic disturbance
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16. There are three types
1. Mild head injury: GCS 14 or 15
2. Moderate head injury: GCS 9–13
3. Severe head injury: GCS 3–8
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The GCS is composed of eye (E), verbal (V) and motor (M) responses
Eyes open Spontaneously 4
To verbal command 3
To painful stimulus 2
Do not open 1
Verbal Normal oriented conversation 5
Confused 4
Inappropriate/ words only 3
Sounds only 2
No sounds 1
Motor Obeys command 6
Localize pain 5
Withdrawal/flexion 4
Abnormal flexion (decorticate) 3
Extension (DE cerebrate) 2
No motor response 1

18.  A head injury may be classified according to the
type of injury that has occurred on skull.
 May be divided into
- Blunt or penetrating
- Vault or basal fracture
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19.  TBI in which the skull & Dura mater remain intact.
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20. When an object pierces the skull and breaches the Dura matter
 Low-velocity injuries such as those caused by stabbing
 High-velocity injuries such as gunshot injuries
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21. Roof of the skull
Open or closed
Linear or comminuted
Depressed or non-depressed
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22.  Anterior fossa
fracture
 Middle fossa fracture
 Posterior fossa
fracture
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23. Intracranial hematomas
 Epidural
 Subdural
 Subarachnoid
 Intra-paranchymal
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24. Mild head injury
• Headache
• Confusion
• Light headedness
• Dizziness
• Blurred vision or tired eyes
• Fatigue or lethargy
• A change in sleep patterns
• Behavioral or mood changes, and
• Trouble with memory, concentration, attention,
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25.  Repeated vomiting or nausea,
 Convulsions or seizures,
 Inability to awaken from sleep,
 Dilation of one or both pupils of the eyes,
 Slurred speech,
 Weakness or numbness in the extremities,
 Loss of coordination, and/or increased
confusion, restlessness,
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26.  Leaking cerebrospinal fluid (a clear fluid drainage
from nose, mouth or ear)
 Visible deformity or depression in the head or face;
 Wounds or bruises on the scalp or face.
 Basilar skull fractures, those that occur at the base of
the skull, are associated with
 Battle's sign,(bruising over mastoid)
 Hemotympanum, (or bleeding from ear)
 Cerebrospinal fluid rhinorrhea and otorrhea
"halo" sign also called the "ring" or "target" sign
beta-trace protein or beta-2 transferrin
 Bilateral per-orbital edema (raccoon eyes)
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27.  Routine lab exam
 X-Ray of head
 X-Ray of cervical spines
 CT-Scan – the first-line investigation
 EEG
 MRI
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28. 1. GCS<13 at any stage
2. GCS =13 or 14 at 2hours following injury
3. Suspected open or depressed #
4. Any sign of basal skull #
5. Post-traumatic seizures
6. Focal neurologic deficit
7. Post-traumatic amnesia of >30 minutes
8. Persistent vomiting
9. Mild head injury over the age of 65
10. On anti-Coagulants or coagulopathy
11. Significant mechanism of injury
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29.  Management of head injuries
 Triage well
 Early discharge if the criteria met
 Scalp wounds need closure
 Significant depressed fractures need elevating, antibiotics
and antiepileptic
 Skull base fractures may be associated with CSF leak.
Pneumococcus vaccination is valuable, but prophylactic
antibiotics are not usually indicated
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30.  ABC’s of life support
 Some patients with mild head injury are at
significant risk of intracranial hematoma and
require a CT scan
 CT scan if fulfills the criteria if not
 Discharge with Medical advice, when to return
to the emergency department.
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31.  GCS 15/15 with no focal deficits
 Normal CT brain if indicated
 Patient not under the influence of alcohol or drugs
 Patient accompanied by a responsible adult
 Verbal and written head injury advice:
 Seek medical attention if:
 Persistent/worsening headache despite analgesia
 Persistent vomiting
 Drowsiness
 Visual disturbance
 Limb weakness or numbness
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32.  The principal aim of treatment is the prevention of
secondary brain injury and this is best achieved
by the avoidance of hypoxia and hypotension.
 ABC’s of life support
 10-15% of head injury patients have Spine injury.
 Look for any other site of injury
 Other measures
 Surgical management
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33.  Comes after the management of life-threatening
conditions.
 The goal of critical care is designed to rapidly identify,
record, treat & prevent secondary brain injury.
 Occur within minutes, hours, or days after the primary
injury and can lead to further damage of nervous tissue,
contributing to permanent neurological dysfunction.
 Include hypoxia, hypotension, ICP, Seizure, hyperglycemia.
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34. 1)Prophylaxis against Cushing’s (stress) ulcers seen
in STBI
 antacid and/or H2 antagonist/ sucralfate / PPI
2) Aggressive control of fever (fever is a potent
stimulus to increase CBF
3) IV fluids:
 Isolated head injury: the choice is isotonic (e.g. NS + 20 m Eq KCl/L)
 Avoid hypotonic solutions (e.g. LR) which may impair cerebral
compliance
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35. 4)Avoid hypoxia (PaO2<60mm Hg or O2 sat <90%)
 Hypoxia may cause further ischemic brain injury
 Immediate goal – to maintain adequate cerebral
oxygenation
 maintain airway and ventilation
5) Avoid arterial hypotension - Strongly associated with poor
prognosis
 Maintain SBP>90mmhg &DBP> 60mmhg in order to keep CPP
>60mmhg
 2x mortality, 3x when hypoxia + hypotension
6) Control hypertension if present
 Nicardipine if not tachycardic
 Beta-blocker if tachycardic (labetalol, esmolol)
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36. 7)Prevent hyperglycemia: (aggravates cerebral edema)
usually present in head injury, may be exacerbated by
steroids
8) Intubation : for GCS≤8 or respiratory distress.
Give IV lidocaine first and antibiotics
9) light sedation: codeine 30–60 mg IM q 4 hrs, or
lorazepam 1–2mg IV q 4–6 hrs
10) Head Position- Keep head of bed at 30-45◦
 Enhancing venous outflow
 Promoting displacement of CSF
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37.  Monroe Kellie hypothesis
 Normal ICP varies with age.
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38. 1.Cerebral edema
2.Hyperemia
3.Trauma ass. Masses
a. Extra-axial bleedings
b.Haemorrhagic contusion
c.Foreign body
d.Depressed Skull Fracture
4.Hypoventilation
5.Increased muscle tone and valsalva maneuver
6.Sustained posttraumatic seizures (status
epilepticus)
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39.  A secondary increase in ICP is sometimes observed 3–10
days following the trauma, and may be associated with
a worse prognosis
 Possible causes include:
 Delayed hematoma formation
 Cerebral vasospasm
 Severe adult respiratory distress syndrome (ARDS)
with hypoventilation
 Delayed edema formation: more common in pediatric
patient
 Hyponatremia
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40. Goals of therapy
1.Keep ICP < 20mmhg
2.Keep CPP ≥70mmhg(i.e avoid hypotension)
Management Modalities
Surgical Rx
Any significant sub dural or epidural haematoma
Significant high contusions with mass effect
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41. 1) Heavy sedation and/or paralysis when necessary
 MSO4: 2–4mg/hr IV drip
 Fentanyl: 1–2ml IV q 1 hr (or 2–5 mcg/kg/hr IV drip)
 Sufentanil: 10–30 mcg test dose, then 0.05 -2 mcg/kg/hr
IV drip
 Midazolam : 2mg test dose, then 2–4mg/hr IV drip
 Propofol drip: 0.5 mg/kg test dose, then 20–75
mcg/kg/min IV drip avoid high dose propofol (do not
exceed 83 mcg/kg/min)
 “low dose” pentobarbital (adult: 100 mg IV q 4 hrs)
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42.  2) CSF drainage (when IVC is used): 3–5ml
 3) Osmotic therapy
 Mannitol=0.25–1 gm/kg bolus (over <20 min) followed by
0.25 gm/kg IVP (over 20 min) q 6 hrs
 May“alternate”with: furosemide 10–20 mg IV q 6 hrs
 Hypertonic saline= refractory to mannitol
 continuous 3% saline in fusion or as bolus of 10–20 ml of 23.4% saline
D/C after ≈ 72 hours
 Hold osmotic therapy if serum osmolarity is ≥320 mOsm/L
or SBP<100
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43.  4) Hyperventilation (HPV) to PaCO2=30–35 mmHg use only
for
 Short periods for acute neurologic deterioration
 Chronically for unresponsive to sedation, paralytics, CSF
drainage and osmotic therapy
 Avoid HPV during the first 24 hrs after injury
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44.  “Second tier” therapy for persistent ICP
 Repeating a head CT to rule out a surgical condition
 EEG to rule - outsubclinical status epilepticus
1)High dose barbiturate therapy : initiate if ICP
remains >20–25 mmHg
2)Hyperventilate to PaCO2=25–30 mm Hg
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45. 3) Hypothermia= reduce cerebral metabolism—dec in
CBV and ICP
 6–7% ↓ CMRO2 for every 1°C decrease in
temperature
 Neuroprotective-Decreases the release of excitotoxic
amino acids
 Monitored for a drop in cardiac index,
thrombocytopenia, elevated creatinine clearance, and
pancreatitis
4) Decompressive surgery
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46.  Early (≤ 7days) or late(>7days) after head trauma.
 Early = 30% of STBI.
May precipitate adverse events as a result of ↑ of
ICP, alterations in BP, changes in oxygenation, and
excess neurotransmitter release.
 Late PTS = within 2 years of head injury.
 Prophylactic AEDs= only to prevent early onset
PTS.
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47. 1.Acute subdural, epidural or intracerebral
hematoma
2.Open DSF with parenchymal injury
3.Seizure within the first 24hrs after injury
4.GCS<10
5.Penetrating brain injury
6.History of significant alcohol abuse
7.Cortical hemorrhagic contusion on CT
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48.  Drug of choice Phenytoin
 Should be started within the first 24hrs of
injury.
 AEDs must be tapered after 1 week.
 Might be used for more weeks in:
 Penetrating brain injury
 Prior seizure history
 Patients undergoing craniotomy
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49.  Nutrition support must be initiated within 24-48 hrs of
admission.
 Increase in energy expenditure in head injury.
 A balance must be maintained between the patient’s
metabolic needs and nutrition support
 The best indicator of nutritional adequacy is overall
clinical improvement.
 When wounds are healing, infection is resolving, and
patients are weaning off the ventilator.
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50.  STBI pts are prone to developing DVT(up to 25% ) b/c
 Prolonged bed rest
 Paralyzed limbs
 Long operating times of some procedures.
 Prophylaxis against DVT
1.General measures
 Passive range of motion
 Early ambulation
2.Mechanical techniques
 Pneumatic compression boots
 Electrical stimulation of calf muscles
 Rotating beds
3.Anti coagulation=heparin
7500 iu SC BID/TID may be started at admission or immediate
post op
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51. Principles
 Remove a compressive surface hematoma as
soon as possible.
 Conservative approach for hemorrhagic
contusions or intra-cerebral lesions
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52. Standard burr hole sites
 Frontal -8cm above the supra-ciliary ridge & 3cm from the midline
 Parietal -on the parietal eminence
 Temporal -1cm in front of the external auditory meatus, just above the
zygomatic arch
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54.  Laceration of the artery (mostly middle
meningeal)
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55.  Is a neurosurgical emergency
 It results from rupture of an artery, vein or venous sinus, in association
with a skull fracture
 Commonly the middle meningeal artery under the thin temporal bone
 A low energy injury mechanism, with brief loss of consciousness then
with subsequent lucid interval with headache, without any neurological
deficit
 Later rapid deterioration follows
 There is contralateral hemiparesis, reduced conscious level and
ipsilateral pupillary dilatation, the cardinal signs of brain compression
and herniation.
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56.  On CT, extradural hematomas appear as a lentiform
( ) hyper-dense lesion between skull and brain
 Areas of mixed density suggest active bleeding
 Mass effect may be evident, with compression of
surrounding brain and mid-line shift
 Immediate evacuation in deteriorating or comatose
patients or those with large bleeds
 Close observation with serial imaging in all cases
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58.  Although conservative management is often left to
clinical judgment, the "Guidelines for the Surgical
Management of TBI" recommended that patients who
exhibit an EDH that is
<30 mL,
<15-mm thick, and
<5-mm midline shift, without a focal neurological deficit
GCS >8
can be treated non-operatively.
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59.  Result from tearing of the bridging veins in subdural
space
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60.  It is a collection of blood between the brain & Dura
 It is due to injury to the cortical veins and blood gets collected in the
subdural space forming hematoma
 Hematoma is extensive and diffuse
 There is no lucid interval
 There is severe primary brain damage
 Hematoma may be of coup and countercoup type
 Loss of consciousness occurs immediately after trauma and is
progressive
 Convulsion is common
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61.  Hematoma is extensive and diffuse
 There is severe primary brain damage
 Hematoma may be of coup and counter-coup
type.
 Loss of consciousness occurs immediately after
trauma and is progressive.
 Convulsion is common.
 Features of raised ICP
 50 % mortality
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62.  Features of raised intracranial pressure
is obviously seen
 —high BP, bradycardia, vomiting
 Focal neurological deficits or
hemiparesis can occur
 CT scan shows concavo-convex lesion
50 % mortality
Treatment
 Antibiotics
 Anticonvulsants
 Mannitol
 Surgical decompression
is done by craniotomy
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63.  1 Cm thick
 5 mm shift
 The GCS score decreases by 2 or more
 Presents with fixed and dilated pupils
 ICP exceeds 20 mm Hg
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/ Craniectomy + duraplasty /

64.  Inside the brain tissue
 Intra-ventricular
hemorrhage
 Inside the brain ventricle
 Common in premature infant
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65. Indications for evacuation
 GCS score 6- 8
 Frontal & temporal >20 ml
 Parietal >50 ml
 Midline shift 5mm
 Cisternae compression
 Posterior fossa with mass effect
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66.  Penetrating injury
 Superficial debridement and dural closure to prevent CSF
leak is generally recommended
 prophylactic broad-spectrum antibiotics (usually a
cephalosporin) to reduce incidence of infection
 Depressed fractures
 increased risk of infection and seizures
 Tetanus status should be determined
 Prophylactic antibiotics be given for five to seven days
 Anticonvulsants should also be used to reduce the risk of
seizures.
 Emergent elevation is recommended if there is a dural
tear, pneumocephalus, an underlying hematoma, or a
grossly contaminated wound.
 >1cm, 5 mm below the adjacent inner table, cosmetic
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67.  Meningitis & brain abscess
 CSF rhinorrhea & otorrhea
 Epilepsy
 Hydrocephalus
 Amnesia (PTA)
 Post concussional Sx
 Post traumatic encephalopathy
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68.  Greenberg Handbook of Neurosurgery 9th
edition.
 Atlas of Emergency Neurosurgery
 Advanced Trauma Life Support (ATLS),2018
 UptoDate 21.6
 Internate
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