2. Management of Head injury.
Introduction
death 18-40 age groups .
WHO---300 people per day .. on Africa’s roads.
falls, road traffic accidents and assaults, with young men
and children the most affected.
In the UK, around one million people per year attend
Emergency Departments due to head injury.
Mild head injury makes up around 90% of all cases (GCS
13-15), moderate 5% (GCS 9- 12) and severe head injury 5% (GCS
≤8).
3. a major cause of long-term disability and economic
loss to society.
needs immediate management of head-injured
patients.
The primary injury is due to irreversible
mechanical injury.
secondary injury which leads to cerebral ischaemia, results
from raised intracranial pressure (ICP), hypotension,
hypoxia, anaemia, seizures, hypoglycaemia and
hyperthermia.
Prevention and correct management .
4. PATHOPHYSIOLOGY
1. Haemorrhagic contusions
usually affecting grey matter of temporal and frontal
lobes. They account for 3% of severe head injuries.
The CT image …. ‘salt and pepper’ appearance due to
interspersed haemorrhage and oedema.
Contusions are better with MRI scans.
2. Intracerebral haematomas usually affect the white
matter or basal ganglia and are the cause of delayed
neurological deterioration in 8–19% of patients admitted
with severe HI.
Haematoma is differentiated from contusion by
demarcation between normal and injured brain.
The prognosis is usually good unless there is a marked
mass effect.
5. 3. Subdural haematomas (SDH) are due to tearing of
cortical veins between the dura and pia arachnoid and
appear crescent-shaped on CT scan occurring most
commonly in the inferior frontal and anterior temporal
lobes.
acute (< 3–4 days old and appearing hyperdense on CT
imaging).
subacute (4–20 days old, isodense).
chronic (> 20 days old, hypodense) and are
predisposed with increasing age, alcoholism,
coagulopathy, epilepsy and in those with ventricular
shunts.
A poor outcome is more likely if SDH is bilateral,
accumulates rapidly, or there is a > 4 hour delay in
surgical management of acute SDH. Increased patient age
and underlying brain contusion also lead to poor
outcome.
6. Acute subdural haemorrhage
This type of injury is often caused
following forceful acceleration-
deceleration events.
Blood is seen on CT between the dura and
the brain. Rapid neurosurgical
intervention is often required,
necessitating rapid transfer. On
CT scan the border of the haematoma
next to brain tissue is typically concave
towards the midline.
Figure : CT scan showing large left
frontoparietal
subdural haematoma (A), with
midline shift and compression of the left
lateral ventricle.
10. 4. Extradural haematomas (EDH)
biconvex lenticular lesions between the skull and
dura.
Most (90%) are associated with skull fractures and
due to injury of the middle meningeal artery and
therefore affect the parietal and parieto-temporal
areas.
The remainder is due to venous sinus laceration.
Underlying brain contusion is less common than
with SDH.
Outcome depends on the level of consciousness at
the time of surgery with mortality approaching 20%
if unconscious.
11. 5. Diffuse axonal injury (DAI)
50–60% of severe head injuries and is characterised by small bilateral non-
haemorrhagic lesions affecting the lobar white matter, corpus callosum and
upper brainstem.
They are classified as mild (coma for 6–24 hours), moderate (> 24 hours
coma without decerebrate posturing) and severe (> 24 hours coma with
decerebrate posturing).
Outcome is usually poor with the mortality for severe DAI
approaching 50%.
6. Traumatic arterial and venous injuries
(e.g. dissection, fistula formation, pseudoaneurysm) are diagnosed by
angiography. These injuries may be associated with subarachnoid
haemorrhage and secondary vasospasm.
7.Traumatic subarachnoid haemorrhage
This is the most common type of intracranial haemorrhage. Blood is seen in
the CSF and subarachnoid space. It is often caused by tearing of small
subarachnoid blood vessels.
Vasospasm may complicate traumatic subarachnoid haemorrhage and the
amount of blood is related to the patient’s GCS and outcome.
12. Principles of management
The main aim
to maintain adequate cerebral blood flow (CBF) and to avoid cerebral
ischaemia and hypoxia.
CPP = MAP – ICP.
Increase (compliance).
Decrease ICP.
13. The main mechanisms of maintaining CPP are to ensure adequate
MAP (by the use of fluids and vasopressors) to prevent excessive rises
in ICP .
*In normal individuals the ICP is 0-15mmHg and this is largely
determined by autoregulation of CBF .
Vasoconstriction or vasodilatation of cerebral vessels occurs in
response to changes in MAP, PaO2, PaCO2 and blood viscosity.
prevention of secondary brain injury involves manipulation of these
variables.
An increase in PaCO2 causes vasodilatation and an increase in CBF,
which may increase ICP; a decrease in PaCO2 causes vasoconstriction
leading to decreased CBF and ICP.
Thus inappropriate hyperventilation may cause ischaemia. A fall in
PaO2 causes vasodilatation with a consequent rise in ICP.
14. Initial assessment
multiple injuries.
The history of the mechanism of injury.
other injuries.
Initial management should be guided
by protocols suggested by Advanced Trauma Life
Support (ATLS).
Injury to the cervical spine should be assumed from
the start of assessment.
Brain injury may be worsened by airway or
circulatory compromise; use the ‘ABCDE’ approach to
identify and treat life-threatening injuries early.
15. Once the patient has a secure airway, is adequately
oxygenated and has a stable cardiovascular system,
to transfer to a neurosurgical unit.
mechanism of injury, any other injuries and the
results of a brief neurological assessment.
The surgeon will want to know the history, the
Glasgow Coma Score (GCS) at the scene, on arrival
at your hospital and the current GCS, the pupillary
size and reaction,(‘lateralising’ signs).
16.
17.
18. The Glasgow Coma Scale
Eye Opening
• Spontaneously 4
• To speech 3
• To pain 2
• None 1
Verbal response
• Orientated 5
• Confused 4
• Inappropriate 3
• Incomprehensible 2
• None 1
Motor response
• Obeys commands (for movement) 6
• Purposeful movement to painful stimuli (‘localises’) 5
• Flexion movement to painful stimuli (‘localises’)
• Abnormal (spastic) flexion, decorticate posture 3
• Extensor (rigid) response, decerebrate posture 2
• None 1
19.
20.
21. Management
The main aims
initial assessment and resuscitation, deciding whether ventilatory support is
necessary and establishing a diagnosis (with a CT head scan where available.)
Early contact with specialist neurosurgical units is vital; they will often advise on
specific therapies.
Early transfer, when indicated, is also important. The Association of Anaesthetists
of Great Britain and Ireland suggest a maximum time of 4 hours between injury
and surgery.
Throughout this process management should be equal to that in an ICU, directed
at maintaining the MAP and CPP and preventing rises in ICP.
Airway & cervical spine.
The main concern is whether the patient is able to protect their airway and
therefore whether intubation is necessary.
Indications for intubation & ventilation include:
• GCS ≤ 8
• Risk of raised ICP due to agitation (i.e. sedation required)
• Inability to control/protect the airway or loss of protective laryngeal reflexes.
Hypoxia.
Hypercarbia PaCO2>6.5,Hpocarbia PaCO2<3.0.
Significant facial injury & bleeding(swelling may make Intubation very difficult
if delayed).
22. Seizures.
Major injuries elsewhere,especially chest injuries.
Evidences of shock state(Tachycardia,low BP,Acidosis etc).
A restless patient who required transfer to CT.
Any patient requiring interhospital transfer.
• A fall of 2 or more points in the motor component of the GCS
• Bleeding into mouth/airway
• Bilateral fractured mandible
This is not an exhaustive list and clinical judgement is important.
If there is doubt it is safest to intubate and consider early
extubation rather than delay intubation and risk secondary brain
injury from hypoxia.
Rapid sequence intubation is almost always required. Maintain
cervical spine immobilisation during intubation, unless the
cervical spine has been cleared by meeting clinical and
radiological criteria.
23. Some hypnosis , analgesia & relaxants is required
to obtund the rise in ICP that is inevitably caused by
laryngoscopy.
Propofol, etomidate, benzodiazepines and
barbiturates all reduce ICP and are preferentially
used.
Ketamine produces a rise in ICP, but may be the
only induction agent available in certain countries.
Opioids and depolarising neuromuscular drugs do
not increase ICP and the fasciculation caused by
suxamethonium only causes a transient rise in ICP.
Nitrous oxide may also cause a rise in ICP by
increasing cerebral blood flow.
24. all patients with head injury should have plain X-rays
of the cervical spine and some may require a CT scan.
Breathing
Hypoxaemia is associated with a significant increase in
mortality. A drop in PaO2 below 8kPa (about
60mmHg) causes an increase in CBF and ICP.
Targets for gas exchange should be a PaO2 greater
than 13kPa (100mmHg) and a PaCO2 in the low-
normal range - usually 4.5-5.0 kPa (35-39mmHg).
Prolonged hyperventilation is not recommended
since cerebral vasoconstriction and ischaemia may
result, however short bursts of hyperventilation (a
few minutes) may help to control episodes of high ICP.
25. Circulation
The loss of the autoregulation of CBF can result in a reduction
in oxygen delivery.
Maintenance of the MAP and CPP is essential; resuscitation
and treatment of life-threatening circulatory instability should
take precedence over neurosurgical interventions.
This may require surgery for haemorrhage control.
Use fluids, and where necessary vasopressors, to achieve a
MAP greater than 80- 90mmHg.
This figure is recommended as a guide until ICP monitoring is
established, and assumes that the ICP is 20mmHg and
therefore ensures a CPP of at least 60-70mmHg (since CPP =
MAP – ICP).
Once ICP monitoring is established then treatment is targeted
at maintaining CPP 60-70mmHg. Aiming for higher CPP
targets has been associated with adverse cardiorespiratory
outcomes.
26. Ideally the MAP is measured using an arterial line and
a central venous catheter may be useful for
monitoring and the administration of vasopressors.
A urinary catheter allows monitoring of urine output
and fluid balance and is necessary if mannitol or other
diuretics are used.
28. Indications for referral to Neurosurgical centre.
CT Scan indicated not available locally.
CT Scan findings intracranial haemorrhage/midline shift.
CT Scan findings suggest diffuse axonal injury.
CT Scan findings suggest raised ICP / Hydrocephalous.
GCS <15 for >24 Hrs.
GCS deteriorate 2points or more.
GCS < 9.Basal Skull fracture or compound skull fracture.
29. Transfer to Neurosurgical Unit
Full resuscitation and stabilisation of the patient and
all injuries must be completed prior to transfer.
A doctor with appropriate training and experience .
Ideally monitoring for transfer should include ECG,
invasive blood pressure, pulse oximetry, urinary
catheter/output and capnography.
Pupillary size and reaction to light should also be
monitored. It is useful to check an arterial blood gas
prior to departure and to correlate the PaCO2 to the
end-tidal value.
Full monitors & ICP,CPP Care.
30. What the neurosurgical centre needs to know at time of referral
Patient’s age and past medical history (if known)
History of injury
● Time of Injury
● Cause and mechanism (height of fall, approximate impact velocity)
Neurological state
● Talked or not after injury
● Consciousness level on arrival at A&E dept
● Trends in consciousness level after arrival (sequential GCS)
● Pupil and limb responses
Cardiorespiratory state
● Blood pressure and pulse rate
● Arterial blood gases, respiratory rate and pattern
Injuries
● Skull fracture
● Extracranial injuries
Imaging findings
● Haematoma, swelling, other
Management
● Airway protection, ventilatory status
● Circulatory status and fluid therapy (Mannitol)
● Treatment of associated injuries (? emergency surgery)
● Monitoring
● Drug doses and times of administration
33. Monitoring intracranial pressure
Some clinical signs are suggestive of raised ICP. These
include:
• Headache
• Dizziness
• Loss of consciousness
• Confusion
• Hypertension and bradycardia (Cushing’s reflex)
• Nausea
• Vomiting
• Focal weakness or paresthesis
• Other focal neurological signs
• Change or asymmetry pupils
34. Measurement of ICP
ICP can be measured in the following ways
Method Benefits Disadvantages
Intraventricular catheter
(‘EVD’ or external
ventricular drain)
• Gold Standard method
• Allows CSF drainage
to lower ICP
• Calibration possible
• Most invasive method
• High infection rate
• May be difficult to
insert
• Simultaneous CSF
drainage and ICP
monitoring not possible.
Extradural probe • Low infection rate (no
penetration of dura)
• Easy to insert
• Limited accuracy
• Relatively delicate
Subarachnoid probe • Low infection rate
• No brain penetration
• Limited accuracy
• High failure rate
Transcranial Doppler Non invasive Limited precision
Lumbar CSF pressure • Extracranial procedure Inaccurate reflection of ICP• May
be dangerous when brain
oedema present.
Tympanic membrane
displacement
Non-invasive. Insufficient accuracy.
35. Management of raised ICP(NCCU)
(1)Improving venous drainage from the brain
• Elevation of the head of the bed to 30 deg.
• Good neck alignment – head in the neutral position.
• Ensuring ties holding the endotracheal tube in place do not
compress the neck veins. Alternatively tape the tube using
‘trouser-legs’.
• Where possible immobilise the patient’s cervical spine with
sandbags and tape rather than restrictive neck collars.
(2)Reducing cerebral oedema
• Use mannitol (an osmotic diuretic) 0.5-1g/kg (= 5-10ml/kg of
10% or 2.5-5ml/kg of 3or 5% NaCl). Some unit use small aliquots
of hypertonic saline as an alternative Use
frusemide (a loop diuretic) 0.5-1mg/kg
• Maintain serum Na+ in the range 140-145mmol/l
36. (3)Reduction of the cerebral metabolic rate for oxygen
• Close temperature regulation. Avoid hyperthermia, but do not actively induce
hypothermia.
• Use of sedation and anaesthetic drugs. Ensure that the patient is appropriately
sedated and has received adequate analgesia.
• If the patient has a witnessed seizure loading with an anticonvulsant, usually
phenytoin 20mg/kg, should be considered.
• In cases of intractable raised ICP,(Barbiturate Coma) a thiopentone infusion can be
used to reduce
the cerebral metabolic rate to a basal level. This is identified on EEG monitoring
as ‘burst supression’.
(4)Reducing intracranial blood volume
• Consider whether the patient has suffered a new or worsening intracranial
haemorrhage. Are there any new or lateralising signs? Is a repeat CT scan
required?
• Hyperventilation can be used to reduce the PaCO2 as a temporary measure, but
cerebral ischaemia may result if this is prolonged.
• The final resort if ICP remains raised is to perform a decompressive
craniectomy.
37. (5)Reducing CSF volume
• In a neurosurgical centre, use of an external
ventricular drain (EVD) allows drainage of CSF to
relieve raised ICP
(6)Glycaemic Control.
Maintain serum glucose between 4-10mmol/l.
(7)Hypothermia.
32-34*C
38. (8)Treat Hyperthermia---Paracetamol & ice sponging.
(9)Steroid
The guidelines of the American Society of
Neurological Surgeons recommend not using Steroid.
(10)Surgery for non-life Threatening Injuries
Hypotension in the first 24-48hrs of head injury is
associated with a worse outcome.
Ideally the minimum should be done in the first 48-
72hrs to allow the patient to stabilise.If surgery is
necessary within this time frame then it should
proceed under ICP control with careful.
maintenance of CPP, oxygenation, PaCO2 and
avoidance of anaemia.(10 g%)
39. (11)Support care
Nutrition & Ulcer prophylaxis.
Feeding usually begins within 72 hrs. of injury in order
to achieve full nutritional support
Feeding protocol : 50 kcal/kg/day
Protein content : 15 % of total calories
Enteral route is better ,Parenteral route : expensive,
increased risk of infection & gut atrophy.
Immune enhancing, immune modulating diets
containing glutamine, arginine, omega 3 fatty acids
are beneficial.
40. (12)DVT Prophylysis
Use of graduated compression stockings or
intermittent pneumatic compression stockings have
been recommended in patients with severe TBI
Use of prophylactic LMWH has also been
recommended .However its use increases the risk of
intracranial bleed.
(13)Infection control.
eg –Ventilator Care Bundle.
- Antibiotics.
41. (13)Positioning
When positioning the unconscious patient, proper body
alignment should be maintained. Limbs must be
supported in a position of function.
When turning the patient, alignment should be
maintained and log rolling should be done.
The patient's position should be changed to a new
weight-bearing surface every two hours.
This decreases the likelihood of complications such as
decubitus ulcers, orthostatic pneumonia, and
thrombophlebitis.
Chest & limb physiotherapy, Care of nasal & oral cavity.
Care of all invasive lines. Care of catheters.Care of back,
bladder & bowel.
42. (14)Others
Clotting abnormalities:
DIC may occur due to release of brain tissue thromboplastin into
systemic circulation
Gastrointestinal problems-
Stress ulcer, hemorrhage may occur after 3 – 4 days.
:Endocrinologic problems
Post. Pituitary dysfunction – frequent
DIABETES INSIPIDUS may occur after craniofacial trauma & basal
skull fracture.C/F polyuria, hypernatremia, high serum
osmolarity, dilute urine.Frequently it is transient
T/T – water replacement- Exogenous vasopressin administration
SIADH: Hyponatremia,Urine osmolarity > Serum osmolarity
C/F Anorexia, nausea, vomiting, Irritability,
personality changes ( due to water intoxication )Usually seen 3 –
15 days after trauma.T/T – water restriction.
43. Systemic causes of secondary brain injury.
Hypotension, acidosis, hypoxia, hypoglycaemia,
hyperglycaemia, hyperthermia, coagulopathy, sepsis,
Anaemia.
Intracranial causes of secondary brain injury.
Intracranial hypertension, oedema, vasospasm, infection,
epilepsy.
INDICATIONS FOR SURGICAL MANAGEMENT
The following sequelae need urgent neurosurgical
Intervention:
1. Skull fractures depressed greater than skull thickness.
Compound fractures with torn dura need repair to reduce
infection risk.
44. 2. Intracranial mass lesions with > 5 mm midline shift or
basal cistern compression on CT scan (i.e. a sign of
imminent transtentorial herniation).
3. Most acute subdural and epidural haematomas need
evacuation within 2–4 hours of injury to achieve optimal
chance of recovery.
4. Intracerebral haematoma: The decision to operate is
guided by the patient’s clinical condition and ICP. Urgent
surgical management is required for large temporal lobe
lesions (due to risk of transtentorial herniation) and
posterior fossa collections (causing brainstem
compression).
5. Refractory intracranial hypertension may improve
with decompressive craniectomy.
6. Delayed hydrocephalus occurs in 6% of severe HIs,
usually 14 days post-injury.
