19. Akyuz M, Ucar T, Acikbas C, Kazan S, Yilmaz M, Tuncer R.

Effect of early bilateral

decompressive craniectomy on outcome for severe traumatic brain injury. Turk
Neurosurg. 2010;20(3):382-389. PMID: 20669113.
20. Wen L, Wang H, Wang F, et al. A prospective study of early versus late craniectomy
after traumatic brain injury. Brain Inj. 2011;25(13-14):1318-1324. PMID: 21902550.
21. TRAUMATIC BRAIN INJURY
Lu LQ, Jiang JY, Yu MK, et al. Standard large trauma craniotomy for severe traumatic
brain injury. Chin J Traumatol. Oct 2003;6(5):302-304. PMID: 14514369.
22. Olivecrona M, Rodling-Wahlstrom M, Naredi S, Koskinen LO. Effective ICP reduction
by decompressive craniectomy in patients with severe traumatic brain injury treated by an
ICP-targeted therapy. J Neurotrauma. Jun 2007;24(6):927-935. PMID: 17600510.
23. Soustiel JF, Sviri GE, Mahamid E, Shik V, Abeshaus S, Zaaroor M. Cerebral blood flow
and metabolism following decompressive craniectomy for control of increased
intracranial pressure. Neurosurg. 2010;67(1):65-72. PMID: 20559092.

cka

SURESH BISHOKARMA, MS
MCH RESIDENT, NEUROSURGERY
NINAS

23-Mar-18
35
 Definition

“A history of a blow to the head or the presence of a scalp wound or those

with evidence of altered consciousness after a relevant injury”

Definition by Jennett and MacMillan

 INTRODUCTION

Trauma is the single largest killer of youth

Deaths preventable by prompt decisive action in Golden Hour.
 BURDEN

* In USA, nearly 50,000cases of death was reported each year as a result of

traumatic brain injury,
* 45% of them were the result of road traffic accidents, and the rest where the
result of falls (26%), assaults (17%), sports injuries (13%), and domestic and
industrial injuries.
 CAUSATION

HEAD INJURY

SPORTS
13%
FALL
26%
ASSAULT
17%

RTA
44%
* Males are twice more likely to be injured than females, and most of the
victims are underthe age of 30.
 Primary brain injury

* Primary brain injury is the damage sustained as a direct result of the impact
on the skull and intracranial contents occurring at the moment of impact.
* Primary brain injury results from either contact or inertial forces to the head
that exceed the brain’s ability to sustain the insult.
* Contact forces commonly result in skull fractures, brain contusions, and/or
hemorrhages.
* Inertial forces are generally a consequence of acceleration and deceleration
and may result in focal or diffuse brain injuries.
* Because primary injuries are essentially irreversible, the focus of TBI
pathophysiology research has largely been on secondary brain injury.
 SECONDARY BRAIN INJURY

* Secondary injury is the delayed brain insult that occurs in the minutes,
hours, and days after the primary injury which triggered a sequence of
events that lead to cerebral edema, cerebral ischemia.

* Complex interplay of biochemical mediators that have the potential to

extend the injury beyond the primary insult.
* Mediators implicated in secondary brain injury include oxygen free radicals,
excitatory amines (most notably glutamate and aspartate), various cytokines,
and other inflammatory substances.
 SECONDARY

1. Cerebral ischemia
2. Cerebral herniation
3. Electrolyte disbalance
4. Hydrocephalus
5. SIADH
* These are the main causes of secondary brain injury, which can be divided
into intra and extracranial causes.
 Intracranial Secondary Injury
1. Neurotoxic cascades
Ischemia or reperfusion injury.
Excitatory amino acids,
platelet activating factor and
oxygen free radicals
Disruption of the blood–brain barrier, edema and neural death

2.Calcium channel disturbance:

Excitatory amino acids (EAAs), N-methyl-D-aspartate (NMDA) glutamate receptors of
calcium channels in the surroundings cells influx of calcium ions
Dizocilpine (MK-801): Antagonists to NMDA glutamate: Prevents brain injury in animals.
Nimodipine have also been shown to have some brain protective effects.
3. Oxygen free radical production
Metabolic failure, Ischemia and vascular damage, Platelet – activating
factor, Nitric oxide

Vascular damage vascular permeability and vasogenic oedema.

Experimental evidences suggest that antagonists to platelet – activating factor

and leucocytes antibody treatment may also limit secondary brain injury.
4. Hematoma

Compress the brain and cause local ischemia

Shift of midline structures and possible fatal brainstem damage
Blood in the subarachnoid space can cause vasospasm and further cerebral
ischemia.
 Extracranial Secondary causes

1. Respiratory failure
Any hypoxia will aggravate cerebral ischemia and increases cerebral
blood flow and cerebral blood volume.
2. Blood Loss
3. Infection
4. Epileptic seizures
Intracranial haematoma and depressed skull fracture.
Cerebral hypoxia.
PATHOPHYSIOLOGY
OF
SECONDARY INSULT
 CLASSIFICATION OF TBI

CLASS GCS LOC PTA

13-15 <1 hour <1hour
Mild

9-12 <24 hours <24 hours

Moderate

≤8 >24 hours >24 hours

Severe
SPECTRUM OF HEAD INJURY

Concussion Contusion EDH

SDH ICH SAH

SKULL BONE
DAI IVH
FRACTURE
 SKULL FRACTURES

1. Linear skull fracture

2. Diastatic fracture
3. Growing fracture
4. Ping-pong fracture
5. Skull Base fracture
6. Depressed fracture : 6% of TBI.
7. Compound communited fractures.
8. Crushed fracture
 Post traumatic seizure
* Post-traumatic seizures are classified as
* Early: <7 days of injury,
* Late: >7 days after the injury

* Posttraumatic seizures (PTSs) have been found to occur in up to 42% of patients up

to 36 months after incurring a head injury.
* The rates vary for early PTSs, defined as occurring within 7 days of injury (4% to
25%), and late seizures, occurring after 7 days (9% to 42%).
* The classic study by Jennett found post-traumatic epilepsy to occur in about 5% of
all patients admitted to the hospital with closed head injury and and in 15% of those
with severe head injuries.
* Sixty per cent of epileptic fits occur in the first 24 hours and about 10 per cent lead
to status epilepticus.
CONDITIONS WITH INCREASED RISK OF POST
TRAUMATIC SEIZURES

RISK FACTOR OF PTS:

1. Early seizures occurring within the

first week
2. An intracranial hematoma
3. Depressed skull fracture.

ASSOCIATION

1. GCS scores less than 10

2. Penetrating head wound, or
3. Seizure within the first 24 hours.
4. History of significant alcohol abuse.
 Antiepileptic prophylaxis

Prophylaxis with Phenytoin decreases the incidence of early posttraumatic

seizures from 14.2% to 3.6% when compared with placebo, this treatment has
not been shown to decrease the risk of late posttraumatic seizures and
epilepsy.

Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for
the prevention of post-traumatic seizures. NEJM.1990;323(8):497–502
 General physical condition
(oriented towards neuro assessment)
Visual inspection of cranium:
a) evidence of basal skull fracture (p.884):
● raccoon’s eyes: periorbital ecchym oses
● Battle’s sign: postauricular ecchymoses (around mastoid air sinuses)
● CSF rhinorrhea/otorrhea (p.387)
● hemotympanum or laceration of external auditory canal
b) check for facial fractures
● LeFort fractures: palpate for instability of facial bones, including zygomatic arch
● orbital rim fracture:
c) periorbital edema, proptosis
Cranio-cervical auscultation
a) auscultate over carotid arteries: bruit may be associated with indicate carotid dissection
b) auscultateoverglobeofeye:bruitmayindicatetraumaticcarotid-cavernousfistulaCCF;see
Carotid-cavernous fistula
Physical signs of trauma to spine: bruising, deformity
evidence of seizure: single, multiple, or continuing (status epilepticus)
 Neurologic exam
* Cranial nerve exam
* a) optic nerve function
If conscious: serial quantitation of vision in each eye is important. A Rosenbaumnear vision
card is ideal, otherwise use any printed material.
If patient cannot see this, check if they can count fingers. Failing this, check for hand motion
vision and lastly light perception.
Children may develop transient cortical blindness lasting 1–2 days, usually after a blow to
the back of the head
if unconscious: check for afferent pupillary defect, best demonstrated with swinging
flashlight test, indicates possible optic nerve injury
Funduscopic exam: check for papilledema, pre-retinal hemorrhages, retinal detachment, or
retinal abnormalities suggestive of anterior optic nerve injury. If a detailed exam is
required, pharmacologic dilatation with mydriatics may be employed, however,
this precludes pupillary exam for a variable period of time, and should be undertaken
* b) pupil: size in ambient light; reaction to light (direct &consensual)
* c) VII: check for peripheral VII palsy (p.884) (facial asymmetry of unilateral upper and lower
facial muscles)
* d) VI: abducens palsy (p.567) following trauma may occur as a result of ↑ ICP or with clival
fractures.
* Level of consciousness/mental status
* A) glasgow coma scale for quantitating level of consciousness in poorly responsive patient
* B) check orientation in patient able to communicate
* Motor exam (assesses motor tracts from motor cortex through spinal cord)
* A) if patient is cooperative: check motor strength in all 4 extremities
* B) if uncooperative: check for appropriate movement of all 4 extremities to noxious
stimulus
* (differentiate voluntary movement from posturing or stereotypical spinal cord reflex). This
also assesses sensation in an unresponsive patient
* C) if any doubt about integrity of spinal cord: also check “resting” tone of anal sphincter
on rectal exam, evaluate voluntary sphincter contraction if patient can cooperate, check
anal wink with pinprick, and assess bulbocavernosus reflex.

Neurologic exam
* Sensory exam
* a) cooperative patient:
Check pinprick on trunk and in all 4 extremities, touch on major dermatomes
(C4,C6,C7, C8, T4, T6, T10, L2, L4, L5, S1, sacrococcygeal)
Check posterior column function: joint position sense of LEs
* b) uncooperative patient: check for central response to noxious stimulus (e.g. grimace,
vocalization, as opposed to flexion-withdrawal which could be a spinal cord mediated
reflex)
* 5. reflexes
* a) muscle stretch (“deep tendon”) reflexes if patient is not thrashing: e.g. preserved reflex
indicates that a flaccid limb is due to CNSinjury and not nerve root injury (and vice versa)
* b) check plantar reflex for upgoing toes (Babinski sign)
* c) in suspected spinal cord injury: the anal wink and bulbocavernosus reflex are checked
on the rectal exam (see above)

Neurologic exam
INDICATION OF HEAD CT SCAN

SIGN
guideline 110:
Early
management
of patients
with a head
injury.
2009
 1. a change in level of consciousness (including difficult y in awakening)
2. abnorm al behavior
3. increased headache
Indications for initial brain CT 4.
5.
slurred speech
weakness or loss of feeling in an arm or leg
6. persistent vom iting
7. enlargem ent of one or both pupils (the black round part in the m iddle
when a bright light is shined on it
Presence of any moderate or high risk criteria which include:
8. seizures (convulsions or fits)
9. significant increase in swelling at injury site
* GCS≤14 Do not take sedatives or pain m edication stronger than acetam inophen (p
hours. Do not take aspirin or other anti-inflam matory m edications because
* Unresponsiveness, and theoretical increased risk of bleeding

* Focal deficit,
* Amnesia for injury, Findings
Table 54.7 Findings withwith moderate
m oderate risk
risk of ICIof ICI

* Altered mental status

1. history of change or loss of consciousness on or after injury
2. progressive H/A
3. EtOH or drug intoxication
(including those that are 4. posttraum atic seizure
5. unreliable or inadequate history
significantly inebriated), 6. age < 2 yr (unless trivial injury)
deteriorating neuro status, 7. vom iting
8. posttraum atic am nesia
* Signs of basal or calvarial 9.
10.
signs of basilar skull fracture
multiple traum a
skull fracture 11. serious facial injury
12. possible skull penetration or depressed fracture
832 Head Traum a 13. suspected child abuse
14. significant subgaleal swelling 21

Table 54.8 Findings with high risk of ICIFindings with high risk of ICI

●
b) in -h ospital obser vation to rule-out n eurologic deterioration
depressed level of consciousness not clearly due to EtOH, drugs, m etabolic abnormalities, postictal, etc.
● focal neurological findings in Table 54.5 (in cluding cases w h ere CT scan is n ot don e).
● decreasing level of consciousness
● penetrating skull injury or depressed fracture
 Associated injury

* 56–60% of patients with GCS score ≤8 have 1 or more other organ system
injured.
 IMAGING THE CERVICAL SPINE

* A head injury may, infrequently, be accompanied by a cervical injury.

* Clear the cervical spine.
* A systematic review of patients with blunt polytrauma and reduced levels of
consciousness (GCS<15) showed an incidence of cervical spinal injury of
between 5.2% and 13.9%. (Thomas M 2002)
* The sensitivity of plain radiography is between 39% and 61%
One in 25 polytrauma patients missed by plain radiography.
* CT is more effective in detecting cervical spine injury in high risk patients,
with a specificity of 98% for CT (95% confidence interval) compared to
52% for X-ray (95% CI)

Thomas M, Teece S. Towards evidence based emergency medicine: best BETs from Manchester Royal Infirmary. Computed tomography and the exclusion of
upper cervical spine injury in trauma patients with altered mental state. Emerg Med j 2002;19(6):551-2.
 Skull Xray in Head injury

* Detecting an unsuspected depressed skull fracture

* Pineal shift, Pneumocephalus, air fuid level in sinus, Skull fracture.
* Metallic objects in penetrating injury.
 EDH

* EDHs are found in up to 4% of TBI patients65,66 and 9% of patients who present in

a coma
* Because of the thinness and fragility of the temporal squamous bone compared to
the rest of the skull, 70-80% of EDHs are seen in the temporal. 5-8% in posterior
fossa.

* Vessels involved MMA, Dural venous sinus, bridging veins.

Classic clinical presentation

* Lucid interval
* Hutchinsons's pupil
* Kornohan's phenomenon
 Mass effect and herniation

* Midline shift
* Uncut of temporal lobe herniation
* Ipsilateral third nerve compression
* Brainstem (tonsils) herniation.
 EDH: ALGORITHM

MONITOR: Hourly examination of the pupils and level of consciousness and a follow up CT scan in 4- 6 hours from the injury or a
sooner scan done if any neurological deterioration is detected.
Another CT scan isobtained the following day.
 POSTERIOR FOSSA EDH

* Because of the confined space of the posterior fossa and its proximity to the
brain stem, any lesion there exhibits a unique concern and mandates a close
observation.
* The majority of lesions seen in the posterior fossa after a head injury are
EDHs, it constitutes 1.2-12.9% of all EDHs.
* A neurological deterioration or a mass effect demonstrated in the CT scan as
obliteration or distortion of the 4th ventricle, effacement of the basal cistern,
or obstructive hydrocephalus indicates a surgical intervention.
 SDH

* SDHs are generally divided into three main entities;

ACUTE, SUBACUTE, AND CHRONIC.

* The incidence of ASDH was found to be 12-29% in patients admitted with

severe TBI.
* Cortical vessels, most commonly cerebral veins.
* ASDHs are commonly found more and less, in the temporal and frontal
areas, respectively.
* Altered level of consciousness, dysphasia, hemiparesis, hemiplegia or signs
of increased intracranial pressure.
 INDICATIONS OF SURGICAL
EVACUATION
Standard fronto-temporal parietal trauma craniotomy.

■ ASDH with a thickness > 10 mm, regardless of GCS

■ ASDH with a midline shift > 5 mm, regardless of GCS
■ GCS < 8 and ICP > 20mmHg, regardless of thickness or midline shift
■ GCS < 8 and asymmetric or fixed and dilated pupil
■ GCS < 8 and decrease of 2 or more points on GCS since hospital admission
* Monitor ICP with GCS <9.
* Even a very thin layer of ASDH with a significant midline shift might be a
candidate for surgical intervention. This is because the variability in the
thickness of ASDH compared to the degree of the midline shift predicts the
outcome.

* Mortality rates ranges from40-60%

 Intracerebral hemorrhage
* Anterior and inferior frontal lobes as well as the anterior temporal lobes.
* CT appearance : initially small “salt and pepper” lesions
Later coalesce to form hematomas.
Delayed traumatic intracerebral hematoma: ~7.4% of TBI.

* Patients who are awake and alert but demonstrate cerebral contusions can be
managed without surgery in the vast majority of cases.
* Comatose and have a significant midline shift usually need surgery.

ICH Contusion
Intracerebral hemorrhage: differ from contusions by the degree of blood content.
 Evolution of contusion

* Cerebral contusions have a 51% incidence of evolution in the first hours

after injury.
* Evolution is associated with clinical deterioration
* If a CT scan is obtained, the absence of pericontusional edema may be a
useful marker to predict that the contusion will not evolve.
* Intracerebral pressure monitors or proceed to surgical intervention.

Beaumont, A. and Gennarelli, T., CT prediction of contusion evolution of closed head injury: The
role of pericontusional edema. Acta Neurochir. Suppl., 96, 30, 2006.
 INDICATION OF SURGERY

Progressive neurological deterioration referable to the lesion

■ Signs of mass effect on CT scan.
■ Refractory intracranial hypertension.
■ GCS of 6-8 with frontal or temporal contusion > 20 ml in volume
with midlineshift > 5mm and/or cistern compression on CT scan.
■ Any lesion > 50 ml in volume.
■ Any hematoma more than 20 ml in the posterior fossa.
NEURO TRAUMA PROTOCALS
KEY PARAMETER TO MAINTAIN

PaCO2. : 4.5-5kPa
PaO2: >11kPa
MAP : 80-90mmHg
ICP : <20mmHg
CPP: >60mmHg
Na : 140meq/L
K: 4 meq/L
 HIERARCHY OF ICP MANAGEMENT
Initial
Head elevation
Optimise ventilation
Maintain perfusion
(MAP : 80-90mmhg;
ICP <20mmhg; CPP: >60mmHg)
Optimise electrolyte balance
Sedation
Seizure control
Prevent pyrexia
Intermediate
Mannitol 20% 100ml bolus/ frusemide
Ventilation therapy
Heavy sedation
CSF drainage via evd
Final
Induction of barbiturate coma
Hypothermia
Decompressive hemicraniectomy
 ICP
Indications
1. Severe diffuse head injury with flexion to pain or worse
2. Postoperatively, in all intraduralmass
3. EDH with postoperative dilated pupil
4. ICH of borderline size managed conservatively
5. Polytrauma patient requiring prolong ventilation
6. Following major intracranial surgery
 ICP-targeted therapy. J Neurotrauma. Jun 2007;24(6):927-935. PMID: 1760051
23. Soustiel JF, Sviri GE, Mahamid E, Shik V, Abeshaus S, Zaaroor M. Cerebral bl
and metabolism following decompressive craniectomy for control of increased
intracranial pressure. Neurosurg. 2010;67(1):65-72. PMID: 20559092.

UPDATE TREATMENT GUIDELINE

BRAIN TRAUMA FOUNDATION
4TH Edition; 2016

35

2. Prophylactic Hypothermia
LEVEL OF RECOMMENDATION*
INTRODUCTION
The Level of Recommendation is determined by the assessment of the quality of the body of evidence, rather than the class of the included studies.
Hypothermia is well recognized to preserve cells and tissue in the face
challenge. Evidence supports the administration of hypothermia as standa
23-Mar-18 TBI UPDATE
neuroprotection Dr. Suresh 1,2 Th
after cardiac arrest from acute coronary syndromes.
 DECOMPRESSIVE CRANIECTOMY

* Bifrontal DC is not recommended to improve outcomes as measured by the

GOS-E score at 6 mo post-injury in severe TBI patients with diffuse injury
(without mass lesions), and with ICP elevation to values >20 mm Hg for
more than 15 min within a 1-h period that are refractory to first-tier
therapies.
* However, this procedure has been demonstrated to reduce ICP and to
minimize days in the ICU.
* A large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm
diameter) is recommended over a small frontotemporoparietal DC for
reduced mortality and improved neurologic outcomes in patients with
severe TBI.
* RESCUEicp Trial: Awaiting updated BTF recommendation.

BTF: Class IIA

 HYPOTHERMIA

* Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia

is not recommended to improve outcomes in patients with diffuse injury.

BTF: Class IIB

* A Cochrane Database review in 2009: No benefit.

 HYPEROSMOLAR THERAPY

* Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg

body weight.
* Effective not only in decreasing the ICP but also in improving the CBF.

* Avoided arterial hypotension (systolic blood pressure <90 mm Hg) and

osmolality >320mOsm/L: Renal failure and acidosis.

* Restrict mannitol use prior to ICP monitoring to patients with signs of

transtentorial herniation or progressive neurologic deterioration not
attributable to extracranial causes.

Recommendations from the third Edition not supported by evidence meeting current standards.
 FRUSEMIDE

* A dose of 0.3 to 0.5 mg/kg of furosemide given intravenously is reasonable.

* When using diuretics the blood pressure must be monitored closely to

prevent hypotension.

* This drug is not commonly used in TBI management at present.

Not mentioned in BTF 4th ed 2016

 CSF DRAINAGE

* An EVD system zeroed at the midbrain with continuous drainage of CSF

may be considered to lower ICP burden more effectively than intermittent
use.
* Use of CSF drainage to lower ICP in patients with an initial GCS <6 during
the first 12 h after injury may be considered.

BTF: Class III

 ICP MONITORING

ICP should be monitored in all salvageable patients with severe TBI (GCS 3-
8) and an abnormal CT scan, defined as a scan showing contusions, edema,
herniation, hematomas, or compressed basal cisterns.
BTF 2007: Class II

ICP monitoring is indicated in patients with severe TBI and two or more of the
following features: (1) age >40 years, (2) unilateral or bilateral motor
posturing, or (3) SBP <90 mm Hg.
BTF 2007: Class III
 ICP TREATMENT THRESHOLD

* ICP treatment should be initiated at an upper threshold of 20 mm Hg.

BTF 2007: Class II

* ICP treatment should be initiated at an upper threshold of 22 mm Hg.

BTF 2016: Class II

* A combination of ICP values and clinical and brain CT findings should be used
in the decision making for duration and type of ICP-lowering therapy.

BTF 2007: Class III

 VENTILATION THERAPY

* Prolonged prophylactic hyperventilation with PaCO2 of <25 mm Hg is not

recommended.
* Hyperventilation is recommended as a temporizing measure for the
reduction of elevated ICP.
* Hyperventilation should be avoided during the first 24 h after injury when
CBF often is reduced critically.
* Disproportionate reduction in CBF as compared with cerebral blood volume
when PaCO2 is reduced. (Fortune JB 1995)
* Jugular venous oxygen saturation, arteriojugular venous oxygen content
differences, and cerebral blood flow monitoring may help to identify
cerebral ischemia if hyperventilation resulting in PaCO2 values <30 mm Hg
is necessary.

BTF: Class IIB

 CEREBRAL PERFUSION PRESSURE

* Aggressive attempts to maintain CPP >70 mm Hg with fluids and pressors

should be avoided owing to associated risk of ARDS.

BTF 2007: Class II

* CPP <50 mm Hg should be avoided.

CPP optimal target value lies between 50 and 70 mm Hg. Patients with
intact cerebral autoregulation tolerate higher CPP values.
Ancillary monitoring of cerebral parameters such as cerebral blood flow,
cerebral oxygenation, or cerebral metabolism facilitates CPP management.

BTF 2007: Class III

 ANAESTHETICS, ANALGESIC AND
SEDATIVES
* Administration of barbiturates to induce burst suppression measured by EEG
as prophylaxis against the development of intracranial hypertension is not
recommended.
* High-dose barbiturate administration is recommended to control elevated
ICP refractory to maximum standard medical and surgical treatment.
Hemodynamic stability is essential before and during barbiturate therapy.
* Prophylactic use of barbiturates for burst suppression EEG is not
recommended.
* Although propofol is recommended for the control of ICP, it is not
recommended for improvement in mortality or 6-month outcomes.
* Caution is required as high-dose propofol can produce significant morbidity

BTF: Class IIB

 STEROIDS

* The use of steroids is not recommended for improving outcome or reducing ICP.
* In patients with severe TBI, high- dose methylprednisolone was associated with
increased mortality and is contraindicated.

BTF: Class I

Corticosteroid Randomization after Significant Head Injury; BMC:2001

 ANTIFIBRINOLYTICS

Ongoing international, multicenter, randomized, double-blind, placebo-

controlled trial to quantify the effects of the early administration of TXA on
death and disability in patients with traumatic brain injury.

Clinical Randomisation of an Antifibrinolytic in Significant Head Injury

PHASE III
 NUTRITION

* Feeding patients to attain basal caloric replacement at least by the fifth day
and at most by the seventh day post-injury is recommended to decrease
mortality.
BTF: Class IIA

* Transgastric jejunal feeding is recommended to reduce the incidence of

ventilator-associated pneumonia.

BTF: Class IIB

 INFECTION PROPHYLAXIS

* Early tracheostomy is recommended to reduce mechanical ventilation days

when the overall benefit is thought to outweigh the complications associated
with such a procedure.
* However, there is no evidence that early tracheostomy reduces mortality or
the rate of nosocomial pneumonia. BTF: Class IIB

* The use of PI oral care is not recommended to reduce ventilator-associated

pneumonia and may cause an increased risk of acute respiratory distress
syndrome.
BTF: Class IIA
 ANTI SEIZURE PROPHYLAXIS

* A double-blind study of 404 patients with severe head injury

* Phenytoin or placebo beginning within 24 hours of injury and continuing
for 1 year
* phenytoin reduced the incidence of seizures in the first week after injury
but not thereafter.
* In patients who have had a seizure, anticonvulsants are continued for at
least a year.
Temkin NR et al.; NEJM:1990

* Phenytoin and valproate are indicated to prevent early onset seizure but not
indicated to prevent late onset seizure activity.
BTF: Class IIA

* Levetiracetam: equally effective as Phenytoin , with its relatively low side

effect profile.
Bullock MR; J Neurotrauma 2007
 RESCUE ICP TRIAL
Hutchinson PJ et al. 2016

* Randomized comparative study who undergo decompressive craniectomy or

receive ongoing medical care (Barbiturate) following severe head injury
with ICP >25.
* 52 centres in 20 countries
* 408 randomised; data available for 389 patients at 6 months and 373 patients
at 12 months.
* From 2004 through 2014, we randomly assigned 408 patients, 10 to 65 years
of age, with traumatic brain injury and refractory elevated intracranial
pressure (>25 mm Hg).
* The primary outcome was the rating on the Extended Glasgow Outcome
Scale (GOS-E) (an 8-point scale, ranging from death to “upper good
recovery” [no injury-related problems]) at 6 months. Primary outcome at 6
months.
PRIMARY OUTCOME

Total: 389 Patients

Surgical(201) Vs Medical (188)
Death : 26.9% vs 48.9.0%
Vegetative state : 8.5% vs 2.1%

RESCUE ICP TRIAL

SECONDARY OUTCOMES

Total: 373 Patients

Surgical(194) Vs Medical (179)
Death : 30.4% vs 52.0%
Vegetative state : 06.2% vs 1.7%

RESCUE ICP TRIAL

 CRITIQUES
* Slow recruitment over 10 years with 50% of centres only recruiting 3 or
fewer patients.
* Therapeutic hypothermia may have a deleterious effect on neurological
outcome after TBI based on Eurotherm3235.
The study was commenced before Eurotherm3235 was published. Whilst
therefore not a criticism of the study design, this may have affected overall
GOS-E
* Clinical teams who cared for the patients were aware of trial-group
assignments.
* A large proportion of patients in the medical group underwent
decompressive craniectomy (37%); this situation may have diluted the
observed treatment effect.
* Long term outcomes of survivors with severe disability would be useful.
This follow up data may be planned for future?

RESCUE ICP TRIAL

 DECRA TRIAL
“Decompressive Craniectomy in Diffuse Traumatic Brain Injury”
* The multicenter, randomized, controlled trial to test the efficacy of
bifrontotemporoparietal decompressive craniectomy in adults under the age of 60
years with traumatic brain injury in whom first-tier intensive care and neurosurgical
therapies had not maintained intracranial pressure below accepted targets
* DURATION: 2002 – 2010
* AREA: 15 tertiary care hospitals in Australia, New Zealand, and Saudi Arabia were
recruited.
* POPULATION: Of 3478 patients who were assessed for trial eligibility, 155 were
enrolled, 73 to undergo early decompressive craniectomy and 82 to receive standard
care.
* Functional outcome at 6 months after injury
* At 6 months, 70% in the craniectomy group had an unfavourable outcome versus
51% in the standard care group
* Decompressive craniectomy dereaase CIP but was associated with more unfavorable
outcomes and that by adopting standard medical therapy rather than surgical
decompression

COOPER DJ et. Al. 2011

 CRITIQUES

* These conclusions are not really supported by closer examination of the basic
data.There were problems with randomization such that the patients in the
surgical arm appeared to have sustained a more severe primary TBI, the ICP
threshold of >20 mm Hg for >15 minutes.
* Minimal mean elevations in intracranial pressure leading up to randomization
(median for both groups during the 12 hours before randomization at the upper
limit of normal, 20 mm Hg).
* 27% of the patients randomized to surgery had bilateral nonreactive pupils,
compared to only 12% of the patients in the medical group.
* There was a high crossover rate from the standard care arm to the surgical
arm.(18%)
* The DECRA trial contains no data or valuable information to inform modern
management of TBI and thus should be ignored by practitioners evaluating
treatment options for severe TBI.

DECRA TRIAL: COOPER DJ et. Al. 2011

RECENT ADVANCES
 NOVEL ADJUNCTIVE THERAPIES

1. Brain Tissue Oxygenation Monitoring

2. Microdialysis
3. Chemotherapy
 Brain Tissue Oxygenation Monitoring

*A polarographic cerebral oxygen monitor (Licox system) can be placed to the brain
parenchyma itself to monitor brain tissue oxygenation levels.
* Several retrospective studies correlated poor outcome with low cerebral oxygenation (jugular
saturation) and low values for partial pressure of oxygen in brain tissue (Pbto2 (<10 mm Hg for
>2 hours).
* This finding opens up the possibility that therapeutic interventions to manipulate the Pbto2
value could potentially alter the traditionally poor outcome in traumatic brain injury, notably
the 36% mortality rate.

Strategy
1. Treat low Pbto2.
2. Increasing the CPP to 70 mm hg
3. Transfusion to keep a hematocrit level above
30
4. Optimization of cardiac output, and
5. Increasing the Fio2 by intervals of 20% on
the ventilator.
Licox system
 Microdialysis

* Blood-brain barrier tight junctions can be transiently opened artificially by

the intra-arterial injection of a bolus of an osmotic agent, such as mannitol,
that dehydrates the endothelial cells or high-frequency ultrasound.
* During this brief interval, which lasts for a few hours, certain
chemotherapeutic or other agents can be administered that would not
otherwise be able to cross the blood-brain barrier to reach the glia.
 Chemotherapy

* Blood-brain barrier tight junctions can be transiently opened artificially by

the intra-arterial injection of a bolus of an osmotic agent, such as mannitol,
that dehydrates the endothelial cells or high-frequency ultrasound.
* During this brief interval, which lasts for a few hours, certain
chemotherapeutic or other agents can be administered that would not
otherwise be able to cross the blood-brain barrier to reach the glia.
CHRONIC TRAUMATIC ENCEPHALOPATHY
“Pugilistic dementia”

Stage I: Stage II: Stage III: Stage IV:

Hot spots of tangled tau pop
up isolated areas of the
cortex
Multiple hot spots of Tau hot spots begin to Dense tau tangles
tangled tau appear in blend with one another. cover the brain
the cortical sulci and Tangles appear more corted and appear
tau begins to migrate diffusely and collect in in most regions,
the hippocampus and including spinal
amygdala. cord.
 Second impact syndrome (SIS)

A rare condition described primarily in athletes who sustain a second head

injury while still symptomatic from an earlier one.
Classically, the athlete walks o the field under their own power after the
second injury, only to deteriorate to coma within 1–5 minutes and then, due to
vascular engorgement, develops malignant cerebral edema that is refractory to
all treatment and progresses to herniation.
Mortality: 50–100%.
First described by Schneider in1973,and was later dubbed the “second impact
syndrome of catastrophic head injury” in 1984.
Although it is contended that SIS is rare (if it exists at all) and may be
overdiagnosed, its apparent predilection for teens and children still warrants
extra precaution following concussion.