"PROGNOSTIC INDICATORS FOR BETTER OUTCOME IN

MODERATE TO SEVERE TRAUMATIC BRAIN INJURY"

Dissertation submitted to

The Tamil Nadu M.G.R. Medical University

Chennai – 600032, April - 2015

In partial fulfillment of the

Regulations of the award of degree of

M.Ch. Neuro Surgery

Department of Neuro Surgery

Coimbatore Medical College Hospital

Coimbatore – 641 018

 

CERTIFICATE

This is to certify that this dissertation titled "PROGNOSTIC

INDICATORS FOR BETTER OUTCOME IN MODERATE TO SEVERE

TRAUMATIC BRAIN INJURY" submitted to the Tamil Nadu Dr. M.G.R.

Medical University, Chennai in partial fulfillment of the requirement for the award

of M.Ch. Degree Branch – III (Neuro Surgery) is a bonafide work done by

Dr.INDUNESH.K, post graduate student in Neuro Surgery under my direct

supervision and guidance during the period of june 2013 to August 2014.

Professor & Head of Department

Department of Neuro Surgery

Dr.A.Edwin Joe, MD, BL

Dean,

Coimbatore Medical College Hospital, Coimbatore.

DECLARATION

I solemnly declare that the dissertation titled "PROGNOSTIC

INDICATORS FOR BETTER OUTCOME IN MODERATE TO SEVERE

TRAUMATIC BRAIN INJURY" was done by me at Coimbatore Medical

College Hospital, Coimbatore – 641 018, during the period of my post graduate

study for M.Ch . Degree Branch – III (Neuro Surgery) from 2012 to 2015.

This dissertation is submitted to the Tamil Nadu Dr. M. G. R. Medical

University towards the partial fulfillment of the University regulations for the

award of M.Ch. Degree in Neuro Surgery (Branch –III).

Dr. INDUNESH.K

Post Graduate Student

M.Ch. Neuro Surgery

Coimbatore Medical College Hospital

 

 

ACKNOWLEDGEMENT

It would have not been possible to write this thesis without the help and support of the

kind people around me, to only some of whom it is possible to give particular mention here.

I would like to express my deepest gratitude to my guide Prof.Dr.R.Raju, Head of

Department, Department of NeuroSurgery, for his excellent guidance, patience, unflinching

support through thick and thin and his unwavering faith in me.

I would take this opportunity to thank Prof.Dr.G.Murugesan, Associate Professor,

Department of NeuroSurgery for his guidance and moral support all through.

My sincere thanks to Professors, Dr.R.Venkatesh, Associate Professor,

Department of NeuroSurgery and, Dr.S.Balamurugan, Assistant Professor, Department of

NeuroSurgery, for their their constant guidance, sincere advice and support, that has always

brought out the best in me.

I want to place on record my gratitude to the Dean of my college, Dr. A.Edwin joe,

MD,BL, for permitting me to conduct my study in this institution.

I express my thanks to all my friends and colleagues who have helped in the preparation

of this dissertation.

I would be failing in my duty if I dont thank all my patients who consented to be a part of this

study. My heartfelt thanks reaches out to them.

CONTENTS

S.NO TITLE PAGE

1 INTRODUCTION 1

2 AIMS AND OBJECTIVES 3

3 REVIEW OF LITERATURE 6

4 MATERIALS AND METHODS 34

5 RESULTS 41

6 DISCUSSION 55

7 CONCLUSION 80

8 BIBLIOGRAPHY 81

9 ANNEXURE

i. Proforma

ii. Master Chart

iii. Abbreviations

iv. Consent Form

INTRODUCTION

BACKGROUND:

Traumatic brain injury (TBI) is emerging as a major health burden and socio-economic problem affecting all countries and societies of the world.

Classification based on clinical severity, supplemented by structural and functional neuro- imaging have significantly advanced our knowledge and understanding of the mechanism involved in head injury, creating opportunities for effective intervention and treatment.

TBI is a major cause for concern around the world because of the many fold increase in vehicle accidents, violence and falls inspite of safety education programmes , effective law enforcement, improved techonology to protect people from automobile accidents, better helmets and seat belts.

There is an increase in morbidity and mortality associated with such accidents and the vulnerable groups are the most productive members of the society and children.

Trauma to the brain can be as a result of primary injury or secondary injury.

A cascade of events follow these injuries ranging from alteration in cerebral blood flow to alteration in pressure within the skull.

These cause effects that can result in physical, cognitive, behavioral, social changes, permenant disability and death.

India has the most pathetic record as far as traffic accidents are concerned. It has the highest incidence of head injuries due to road traffic accidents per 1000 vehicles in the world. Most of the reported incidences are from the cities.

Most of the reports may not be indicative of the true incidence as reporting from rural areas are lacking and most of the reports are based on medico-legal reports.

The high incidence may be due to the:

1) Geography of the area

2) Climate

3) Social activity of the people

4) Basic design of the roads , basic traffic construction and management

5) Poor sense of traffic safety awareness

6) lack of enforcement

7) increased urbanization and increased vehicular load

AIM AND OBJECTIVE OF THIS STUDY

To study the strength of the prognostic indicators chosen on the outcome in cases of TBI.

Prognostic models are necessary to predict clinical outcome in cases of traumatic injury of brain.they commonly use two or more criteria of patient data to predict outcome.

Inclusion criteria: 1) TBI patients more than 5 years of age admitted in the above mentioned

wards.

2) GCS ≤ 13.

Exclusion criteria:

1) patients on prolonged treatment for TBI at other hospitals

2) unknown patients

3) pregnant women

4) patients with bleeding disorders and hypertensive bleeds

5) patients brought dead

6) patients with third nerve damage caused by direct orbital trauma resulting in

a dilated and/or a fixed pupil

The study period is from june 2013 to August 2014.

Prospectively collected, individual, patient data was used.

Five possible predictors which had strong prognostic value were selected and a core prognostic group data base was arrived at.

Strongest predictor of outcome were demography, GCS, Pupillary reactivity, CT charecteristics and comorbid conditions.

A sample size of 200 patients was taken as the study group.

The five prognostic parameters, ie demography, GCS, pupillary reactivity, CT charecteristics and comorbid conditions of this group was analysed in detail.

At the end of the study the prognostic indicators were categorized based upon their impact on outcome as most important , less important and least important.

The 6 month outcome probability score was defined using the GOS score.

IMPORTANCE OF THIS STUDY:

1) They help in decision making about the treatment modality best suited for

the patient.

2) They are useful for randomized controlled trials in research studies to

compare outcome among different sets of people.

LIMITATIONS OF THIS STUDY:

1) The predictions do not in any way foresee better outcomes.

2) The effect of sedation or paralysis can affect the motor score.

3) They can only complement clinical judgement but not replace it.

REVIEW OF LITERATURE

DEFINITION:

TRAUMATIC BRAIN INJURY

Any damage to the brain from external forces in the form of rapid acceleration or deceleration impact, penetrating injuries or blast injuries that can result in temporary or permenant impairment of brain function with or without detectable structural damage.

The most comman cause of head injury is road accidents followed by falls.Birth trauma is the commonest cause in neonates.

Biomechanics of head injury

An understanding of the biomechanics of head injury is necessary to

a) Prevent accidents from occurring

b) To reduce the impact of injuries

c) Minimize the risk of subsequent complications

Types of mechanical forces

Mechanical forces that can cause head injuries can be classified as

a) Static b) dynamic

Static loading:

It is uncommon

The input force is applied relatively slowly ( over 200 ms )

There is slow crushing of the skull

They can cause multiple comminuted fractures

Examples are : injuries from slow moving vehicles , earthquakes

Dynamic loading

More common

Input force is applied over a very short period of time ( less than 50 ms )

Subclassified as

a) Impact loading b) impulsive loading

Impact loading

More common type

Combination of contact and inertial forces

A sudden impact causes head to accelerate resulting in inertial forces

Impulsive loading

Here the head is put into motion or motion of moving head is suddenly stopped

Traumatic brain injury is classified usually on the basis of:

1) Severity

2) Mechanism

3) Anatomical feature of the injury

4) Pathological features

SEVERITY:

It is classified into mild, moderate and severe.

The most commonly used system is the GLASGOW COMA SCALE (GCS)

POINTS BEST EYE OPENING

BEST VERBAL RESPONSE

BEST MOTOR RESPONSE

6 Obeys commands 5 Oriented Localizes to pain 4 spontaneous Confused Withdraws to pain 3 To speech Inappropriate Flexion(decortricate) 2 To pain incomprehensible Extension(decerebrate) 1 none None None

This scale is recommended for age ≥ 4 years

In children, a childrens coma scale is used. It differs from GCS in best verbal response and motor response.

POINTS BEST VERBAL MOTOR

6

5 Smiles, oriented to sound, follows objects, interacts Obeys commands

crying Interaction

4 consolable Inappropriate Localizes to pain

3 Inconsistently consolable Moaning Flexion to pain

2 inconsolable Restless Extension to pain

1 none None none

Severity of traumatic brain injury is graded as:

GCS POST TRAUMATIC AMNESIA

LOSS OF CONSCIOUSNESS

MILD 13 - 15 < 1 day 0 – 30 minutes

MODERATE 9 – 12 > 1 to < 7 days > 30 minutes to < 24 hours

SEVERE 3 - 8 > 7 days > 24 hours

MECHANISM:

It can be divided into

Closed (non penetrating) head injury – here the brain is not exposed Open(penetrating) head injury – here the duramater is breached.

In general "Traumatic Brain Injury" is used to refer to non penetrating injury to the brain.

PATHOLOGICAL FEATURES:

Pathologically it could be

Extra axial – ie when it is outside the brain but within the skull

Intra axial – ie when it is within the brain tissue (eg : orbito-frontal hematomas, temporal hematomas etc)

Focal – when it is confined to a specific area

Diffuse – when it is distributed in a general manner (eg: DAI, diffuse edema, concussion)

Extra axial lesions include – SDH , EDH , SAH , intraventricular hemorrhage.

Epidural hematoma:

Bleeding into the area between the inner table of skull and duramater, commonly due to disruption of the middle meningeal artery as it exits its bony groove at the pterion.

Usually they have brief period of loss of consciousness followed by lucid interval for several hours.

Later on ipsilateral pupillary dilatation, obtundation, contralateral hemiparesis.

Delayed epidural hematoma:

It is an epidural hematoma not found on initial CT Scan but found on subsequent CT Scans. It constitutes around 10% of all epidural hematomas.

Posterior fossa epidural hematoma:

Common in first two decades of life. It constitutes 5% of all epidural hematomas. There is a high incidence of tears of dural sinuses.

Subdural hematoma:

Here the bleeding occurs between the duramater and arachnoid mater. There is underlying brain injury.Symptoms may be due to compression of the underlying brain with midline shift along with injury to the brain parenchyma and cerebral edema. Lucid interval is usually not present.

They occur commonly due to laceration of surface or bridging vessels during violent head motion at the time of acceleration or deceleration.

Interhemispheric subdural hematoma:

Subdural hematoma between the two hemispheres along the falx, possibly associated with child abuse by violent shaking. In adults trauma and ruptured aneurysm may be the causes.

Delayed acute subdural hematoma:

Subdural hematoma that is not present in initial CT Scan but shows up on subsequent CT Scans. Incidence is around 0.5%.

Infantile acute Subdural hematoma:

It is acute Subdural hematoma due to minor trauma in an infant without loss of consciousness or cerebral contusion. The possible cause being rupture of the bridging veins.

Chronic Subdural hematoma:

Commonly occurs in elderly population. Usually greater than 60 years. Usually associated with trivial head trauma. Other causes could be coagulopathies, alcohol abuse, seizures, CSF shunts.

The fluid here is classically dark motor oil coloured fluid.It is called subdural hygroma when the subdural fluid is clear (CSF).

This is due to an inflammatory response to the blood within the subdural space.

Fibroblasts invade the clot and form a neo membrane on the cortical and dural surface.later neo-capillaries ingrowth occur.

Enzymatic fibrinolysis and liquefaction of clot occurs.

Fibrin degradation products get reincorporated into the clot and inhibit hemostasis.

Subarachnoid hemorrhage:

It is bleeding into the area between the arachnoid membrane and piamater.

It could be spontaneous or traumatic. Ruptured intra cranial aneurysm accounts for a majority of cases of spontaneous subarachnoid hemorrhage.

Intra ventricular hemorrhage:

Here there is bleeding into the ventricular system of the brain.it may be as a result of extension of intra parenchymal hemorrhage.

In adults it could be due to spontaneous or due to rupture of an A-V malformation commonly.

In new borns it would be an extension of sub ependymal hemorrhage.

Sometimes there could be a pure intra ventricular hemorrhage due to rupture of an aneurysm, A-V malformation, intra ventricular tumor.

Causes of brain damage

Focal brain injury

These could be in the form of contusions and lacerations on the brain surface and secondary events like intracranial hematoma and raised intra cranial pressure.

Contusions:

Bruises present on the surface of the brain with intact duramater mostly due to blunt contact.Recent contusions are haemorrhagic and occur due to rupture of pial vessels.

Fracture contusions:

Are related to the site of fracture and are seen most commonly over the frontal regions.

Herniation contusions:

Seen in areas where medial edge of the temporal lobe comes in contact with free edge of the tentorium, or when the cerebellar tonsils comes in contact with the foramen magnum.

Gliding contusions:

Seen due to anteroposterior gliding of the brain over the duramater and falx cerebri, commonly near the superior sagittal sinus.

Coup contusions:

Seen at the site of impact without an underlying fracture.

Contre coup contusions:

Seen on the brain at a site away from the site of impact. Usually it is diagonally opposite from the area of impact.

Diffuse brain injury

Here the patients are unconscious at the time of impact. There is loss of cerebral function and residual sequelae.

Diffuse cerebral injury could be :

1) Diffuse vascular injury

2) Diffuse axonal injury

3) Diffuse ischaemic brain damage

4) Diffuse brain swelling

Diffuse vascular injury:

Here, following head injury multiple small haemorrhages occur due to mechanical stretching and shearing of small blood vessels with disruption of the vessel wall. As they are seen mostly near the brain stem they usually are incompatible with life.

Diffuse axonal injury:

This a diffuse form of white matter damage leading to vegetative state and post traumatic dementia. Usually they do not show any mass lesion. On imaging.there could be lesions in the corpus callosum , rostral brainstem , corona radiata , other long tract fibres. Diffuse axonal injury encompasses a spectrum of pathological changes from concussion to minor cerebral injury to severe brain impairment.

In the initial stage, the lesions are haemorrhagic which then become gliotic with progression of time and later scar formation.

Studies using immuno-histochemistry techniques showed the presence of beta amyloid precursor protein (β- APP) in patients surviving 3 hours or

more.Expression of β- APP is upregulated following injury and is an useful early marker.It is also associated with cerebral infarcts.

The direction in which head moves following impact also plays a major role in the distribution of axonal damage.wide axonal damage occurs mostly during lateral motion of head, during rotational acceleration.Certain regions of the brain like the brainstem, corpus callosum, basal ganglia, internal capsule move in the opposite direction to the rest of the structures causing maximum shear and tensile strains.These are areas along the midline, where the white matter tracts diverge out, thus showing maximum degree of axonal injury.

Another important aspect of diffuse axonal injury is the diffuse microglial proliferation at places forming clusters.These clusters are cellular reactions at the sites of minute tissue tears.These cells secrete cytokines that further aggravate tissue damage by ca++ ion influx.

Most characteristic finding on electron microscope in DAI was the separation of the myelin sheath and detachment of the axolemma from myelin. There was swelling of the axons filled with cytoskeletal components and mitochondria and extrusion of the axonal contents through the tear.

Fat embolism was another well recognized but relatively rare cause of progressive neurological deterioration in a patient with an acute intracranial expanding lesion.

Histological grading of diffuse axonal injury

Grade I only histological evidence of white matter axonal

Damage without focal lesions in brainstem and

corpus callosum.

grade II widely distributed axonal injury along with focal

lesions in corpus callosum.

grade III diffuse axonal damage with focal lesions in corpus

callosum and cerebral peduncle.

Diffuse ischemic brain damage:

It is seen in fatal brain injuries.Basal ganglia and hippocampus are commonly affected. Trauma leads to hypotension causing reduced cerebral blood flow.This causes ischemic lesions in the cerebral arterial territories, especially in the anterior cerebral , middle cerebral and posterior cerebral artery territories. Histology reveals laminar necrosis.

Diffuse brain swelling:

Three types of brain swelling are seen after TBI.

1) Swelling adjacent to an ICH and contusion

2) Unilateral diffuse brain swelling

3) Bilateral diffuse brain swelling

The basic mechanism is that neurotransmitters, ionic imbalance and physical injury cause deranged vasotonicity or vasoparalysis.

There is break down of the blood brain barrier causing localized vasogenic oedema.

Supra tentorial-expanding lesions with raised ICP after certain period of time cause downward displacement of brainstem , parahippocampal gyrus and uncus along with pressure necrosis.

For an infra tentorial –expanding lesion, there is an upward herniation of the vermis.

Raised ICP could also cause transfalcine supracallosal herniation of the cingulated gyrus with infarction due to involvement of the pericallosal arteries, kernohan’s notch due to compression of contralateral cerebral peduncle, infarction of the territories of anterior cerebral arteries, tectal herniation causing compression of the quadrigeminal plate at the level of superior colliculus, central herniation with downward shift of entire brainstem into foramen magnum, and tonsillar herniation with prolapse of cerebral tonsils into the foramen magnum.

In old age following trauma, the atropic brain may not manifest features of brainstem herniation inspite of raised intra cranial pressure due to the availability of enough intracranial space for expansion.

PATHOPHYSIOLOGY OF HEAD INJURY

Mechanical injury,seizures ,ischemia and a wid range of pathological insults induce C-fos,C-jun and junB which are immediate early genes (IEGs) which function as transcription factors that mediate long term adoptive response of neurons to acute stimuli.

C-fos,C-jun and junB were found to be increased in the cortex and hippocampus following manipulation in rats.

Inducible heat shock protein have been found upto 12 hours following trauma on the ipsilateral cortex of impact site indicating a stress response.

Following TBI there is a change in the cytoskeletal and electrical properties of cell membrane.

This is translated into an acute genomic response.

This manifests as pathological damage and behavioural deficits.

Most of the data on genomic study is from animal models.

Data on human beings is still in the early stages.

Ischemic brain damage is frequently superimposed on primary brain damage and can be widespread or perilesional.

Impaired cerebral perfusion, impaired oxygenation, excito-toxic injury and focal micro-vascular occlusion can contribute.

Secondary brain damage which occurs over hours or days is determined by the type of injury and the intensity of systemic insults.

They could be due to release of neurotransmitters, generation of free radical, calcium mediated cell damage, gene activation, mitochondrial dysfunction and inflammatory response.

Sequence of events in the pathophysiology of head injury

Traumatic brain injury

Acute perturbation

Mechanoporation in neurons lasting from minutes to 3- 4 hours

Transient separation of cell memberane lipid layer from protein components

influx of k+ inside and Na+ , Ca++ , Cl � to outside

Closure of defect by Ca++ activated lysolecithin patching and membrane fusion

Mild injury : returns to normal after few seconds to few minutes

Severe injury : Ca++ severe cell toxicity

Inflammation and cytokines

Following focal brain injury, polymorphonuclear leucocytes temporarily accumulate at the site of damaged tissue.

These cell enter the CSF and peripheral blood and cause a leucocytosis.

Macrophages replace polymorphs to start the repair process and scavenge necrotic debris.

They secrete cytokines like TNFα, IL-1β AND IL-6 that initiate an excito-toxic neurodegenaritive process.

Hence CNS derived cytokines may play a role in the pathophysiology of TBI.

They however may also play a protective role by astrocyte proliferation,inhibition of Ca++ currents,induction of growth factors and promote macrophage migration to injury site.

Role of Apolipoprotein E in head injury

It is a important component involved in lipid transport in the central nervous system.

Following head injury, there is an increase in the expression of Apo-E by astrocytes and LDL receptors.

People who die from head injury have deposits of amyloid beta –protien in the cerebral cortex this being present predominantly in patients with the Apo-E allele.

Patients with Apo-E allele have twice the chance of adverse outcome after 6 months.

CLINICAL ASSESSMENT OF HEAD INJURED PATIENT

To anticipate forthcoming sequelae and for successful management of head injury patients a comprehensive neurological examination is the single most efficient factor in diagnostic evaluation.

The first and foremost is to assess respiration and ensure clear airway and oxygenation .

All accumulated secretions,vomitus and blood should be sucked out.

Cervical injuries should be ruled out.

Vital parameters should be stabilized.

After stabilizing respiratory and vascular status a complete history should be obtained regarding time and mode of injury ,course of events following injury, duration and timing of loss of consciousness, drug intake , co-morbid conditions ,associated seizures etc.

A general physical examination should be done.

The state of consciousness is the single most important neurological examination and is recorded as per the GCS scale.

Pupillary size ,eye movements and optic nerve function should be assessed.

Motor examination ,reflex examination and sensory examination should be done.

An important part of examination in TBI is determination of brain death.

It is the irreversible cessation of all functions of the brainstem.

This may be due to primary brain stem damage or secondary brain stem damage from increased intra cranial pressure with compromised vascular supply.

This is important because it gives us an better understanding of the prognosis of the patient enabling decision making regarding elective stopping of mechanical ventilation.

This avoids the excessively long and tragic waiting period for the family and also the enormous cost of intensive care .

It also enables decision making regarding legal organ donation as each brain dead patient is a potential organ donor.

DIAGNOSTIC INVESTIGATION IN TBI

CT scan is the preferred diagnostic modality to detect structural damage and detect developing or developed intra cranial hemorrhage.

Currently, CT scan is advocated in all TBI patients with GCS of 14 or less and for patients with GCS 15, with presence of risk factors.

As the pathology in TBI is a dynamic process, follow up CT scan is advised if there is clinical deterioration or if lesions were seen on initial CT scan.

Studies have proven that in patients with diffuse lesions, new lesions could occur in roughly 16% of the cases.

MRI studies are not useful in the acute or early phase as they do not provide any additional information for decision making , they are more time consuming and are logistically complex.

In the subacute phase MRI is more informative than CT scan as it offers more information regarding white matter lesions seen in patients with DAI.

GUIDELINES FOR MANAGEMENT IN TBI

The BRITISH TRAUMA FOUNDATION and the AMERICAN ASSOCIATION OF NEUROLOGICAL SURGEONS came out with guidelines for the management of moderate and severe traumatic brain injury which was based on scientifically proven protocols.

These included prehospital emergency care, admission care, intensive care management and monitoring.

Prehospital emergency care

Its main goal is to prevent hypotension and hypoxia as these systemic insults cause secondary brain damage, identify patients who are at a risk for neurological deterioration and identify associated injuries.

Hypotension and hypoxia are associated with poor outcome.

Paramedics adequately trained in intubation and prevention of hypotension by early fluid resuscitation with crystalloids and colloids have been linked with better outcome.

Primary survey along with cervical spine care is to be undertaken.

It is important to transfer and treat all patients with head injury in a setting where round the clock neurosurgical facility and acess to specialized neuro criticalcare is available.

Admission care

Its main aim is stabilisation of patient and diagnostic assessment with priority for rapid detection and treatment of operable lesions.

Intensive care management

Its main aim is to limit and prevent progressive brain damage and provide the optimal condition for brain recovery by reducing brain edema and raised intra cranial pressure.

Optimum nutrition, glycemic control, oxygenation, perfusion, temperature and homoeostasis are maintained.

The brain is protected from silent seizures by anti-seizure prophylaxis.

Eventhough routine anti-seizure prophylaxis is debatable, for cases of depressed skull fracture, penetrating brain injury and post traumatic amnesia greater than 24 hours, routine prophylaxis is recommended.

Intracranial pressure monitoring helps in early detection of mass lesion and limits indiscriminate use of medicines that could be potentially harmful in TBI

Also theraputic CSF drainage can be achieved.

Rapid infusion of mannitol creates an osmotic gradient , thereby mobilising water across an intact blood brain barrier which in turn improves cerebral blood flow.

It should be administered rapidly because a rebound phenomenon could occur.

Its is associated with electrolyte imbalance, cardiac failure, bleeding disorders and thrombophlebitis on prolonged use.

Decompressive craniectomy

it is important as

1) It increases the buffering capacity of the brain.

2) It allows outward herniation of the brain thereby preventing brainstem

compression and it also improves brain perfusion.

3) It reduces ICP by 15-85%, depending on the size of the bone removed.

4) Durotomy helps further in decreasing ICP.

Whether it should be done or not depends on the patients GCS score, pupillary examination, age, comorbid condition and CT scan finding.

EDH

Indications for Conservative management:

a. Clot thickness < 15mm

b. Volume < 30cm3

c. Mid line shift < 5mm

d. GCS > 8 without focal deficit

Patient requires serial CT scan and close neurological monitoring

Surgical management:

a. GCS < 9 with anisocoria

b. EDH volume > 30cm3

c. Midline shift > 5mm

In case of temporal EDH the threshold for surgery should be low as these patients are prone for sudden neurological deterioration.

SDH

Indications for Conservative management:

a. Volume < 10cm3

b. Mid line shift < 5mm

c. Patient requires serial CT scan and close neurological monitoring

Indications for surgical management:

a. SDH volume > 10Cm3

b. Midline shift > 5mm

c. SDH with volume < 10cm3 and midline shift < 5mm and drop in GCS by 2

or more points from the time of injury to time of admission and / or

asymmetrical pupils or fixed and dilated pupils and / or ICP more than 20

mm Hg

Traumatic parenchymal lesions

Indications for Conservative management:

a. Patients with CT lesions but no significant mass effect seen on CT scan

b. stable neurological status

c. Stable ICP

Indications for surgical management:

a. Patients with GCS 6-8 associated with frontal or temporal contusions greater

than 20cm3 in volume

b. Midline shift of 5mm or more and / or effacement of cisterns on CT scan

c. Patients having lesions > 50 cm3

Posterior fossa lesions

Indications for Conservative management:

a) Patients with lesion and no significant mass effect on CT scan and no signs

of neurological deterioration

b) Patients with lesion less than 3 cm in diameter

Indications for surgical management:

a) Patients with mass effect on CT scan and / or neurological deterioration (ie

distortion , dislocation or obliteration of 4th ventricle – compression or

effacement of basal cisterns – presence of hydrocephalus )

b) Patients with lesion equal to or more than 3 cm

MATERIALS AND METHODS

The study is a prospective interventional study to highlight the importance of the five selected prognostic indicators on the outcome of the disease and to grade them accordingly.

Design

The study is being conducted among inpatients in the Zero delay ward , Trauma ward , Neuro Surgical ward and post operative ward of Neuro Surgery department at Government Coimbatore Medical College Hospital and who presented within 24 hours of the injury.

Methodology

Around 200 TBI patients admitted and who fit into the moderate to severe injury criteria were analysed. The five criteria chosen were applied and the outcome recorded. The criteria were then graded according to their outcome, by the Glasgow Outcome Scale at 6 months.

This has 5 categories:

1) DEAD

2) VEGETATIVE STATE

3) SEVERE DISABILITY

4) MODERATE DISABILITY

5) GOOD RECOVERY

In order to simplify analysis this was further considered into :

1) Favourable (good or moderate recovery)

2) Unfavourable(severe disability,vegetative,dead)

Outcome after 6 months was selected as experience show that about 85% of cases recover within this time period, but further recovery can occur later.

Discrepencies in classification of favourable and unfavourable outcome can be minimized by increasing the period of study. Hence 6 months period was chosen.

The study was compared to the outcome obtained in the IMPACT study

The applicability of the prognostic model was influenced by various factors like level of care available locally,the socio-economic status etc.The CRASH study gives a better prediction ability for low and middle income status.

A simple score was used which is given below.

AGE:

VALUE SCORE

≤ 30 0

30-39 1

40-49 2

50-59 3

60-69 4

≥ 70 5

MOTOR SCORE:

LOCALISES / OBEYS 0

NORMAL FLEXION 2

ABNORMAL FLEXION 4

NONE / EXTENSION 6

PUPILLARY REACTION:

BOTH PUPILS REACTING 0 ONE PUPIL REACTING 2 NO PUPILS REACTING 4

CT CLASSIFICATION: (Marshall system of classification was used)

Diffuse injury I - no intra cranial pathology visualised on CT Scan

Diffuse injury II - cisterns present, with midline shift < 5 mm and

few lesion densities seen. No high or mixed density

lesion > 25 ml

diffuse injury III - cisterns compressed or absent with midline shift

0-5mm.

No high or mixed density lesion > 25 ml

diffuse injury IV - Midline shift > 5mm. No high or mixed density lesion

> 25 ml

Evacuvated mass lesion V - any surgically evacuvated mass lesion

Non evacuvated mass lesion VI - high or mixed density lesion > 25 ml not

surgically evacuvated

The Marshall’s classification had limitations like wide differentiation between diffuse injuries and mass lesions and lack of specification on the type of mass lesion.

MARSHALL CLASSIFICATION:

GRADE I -2

GRADE II 0

GRADE III / IV 2

GRADE V / VI 2

SAH YES 2

NO 0

EDH YES -2

NO 0

HYPOXIA :

YES /SUSPECTED 1

NO 0

HYPOTENSION :

YES / SUSPECTED 2 NO 0

Using this chart sum scores was calculated for core (ie age, motor score, pupillary reaction) and the extended model (ie core + CT charecteristics + hypotension + hypoxia)

The 6 month outcome probability score was defined as 1 / ( 1+e-LP ). Here LP is the linear predictor in logistic regression model.

Using the online prognostic calculator which is based on this formula, the predicted probability of mortality and unfavourable outcome for 6 months was arrived at.

The outcome of this study was compared and validated with the IMPACT study.

The characteristics feature of IMPACT and CRASH patients with GCS score less than or equal to12 could be fairly compared. The patients in CRASH trial were slightly older than those in IMPACT trial, with slightly higher motor scores on admission. 6-month mortality in IMPACT group was around 28% and in CRASH study it was 32% Unfavorable outcomes were seen in nearly half of the patients (48% in IMPACT, 47% in CRASH).

SCORE CHART FOR PREDICTING OUTCOME IN IMPACT STUDY

Admission Characteristics Core: Age (14 years – 99 years) Motor score Pupils Core + CT: Hypoxia Hypotension CT classification Traumatic SAH Epidural mass on CT

      14 ‐ 19 

       Y / N 

BASED ON MARSHALL’S SCORE 

        Y / N 

        Y / N 

       GCS 

 REACTING 

 UNEQUAL 

 NOT REACTING        Y / N 

RESUL

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Male -

Female

0

20

40

60

80

100

120

140

160

180

200

LTS:

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170 (85%

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MALE

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collected

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profile wa

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FEMALE

30

EX DISTRIB

the follow

as:

BUTION OF

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F CASES IN

ics was arri

N THIS STU

ived at.

DY

GENDE

R GRAPH

Mode

Road trafalls and

Road tra

Self fall

Assault

of injury

affic accidd assault

affic accid

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y:

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)

M

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173

23

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MODE O

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SELF FALL

ASSAULT

elf

Age wis

< 30 ye

30 – 39

40 – 49

50 – 59

60 – 69

≥ 70 ye

25% ofthe age cases w69. Only

0

20

40

60

80

100

120

140

160

180

200

se break u

ars - 5

years - 3

years - 4

years - 4

years - 2

ars - 1

f the cases group of 5

was in the ay 5.5% ca

AGE < 30 Y

50

up was:

50 (25%

2 (16%

42 (21%

45 (22.5%

20 (10%

11 (5.5%

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e age grou1% of casof 30 to 39the age gr

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Y ≥ 70 Y

11

IS STUDY 

. 22.5% oroup of 40 in the age

AG

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GE GRAPH

as in % of 60 to

GLASG

Age wis

AGE CATIN YE

< 30

30 - 3

40 - 4

50 - 5

60 - 6

≥ - 7

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h the total npercentage

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TCOME S

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number of e of death

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SCORE (G

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deaths waswas in the

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est in the 4years grou

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UNFAVOURAB

FAVOURABLE

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RECOVE

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e group the

BLE

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Age wise favourable and unfavourable outcome:

AGE CATEGORY

IN YEARS

UNFAVOURABLE

%

FAVOURABLE

%

< 30 13 26% 37 74%

30 - 39 12 38.71% 19 61.29%

40 - 49 23 56.10% 18 43.90%

50 - 59 28 59.57% 19 40.43%

60 - 69 11 55% 09 45%

≥ - 70 09 81.82% 02 18.18%

Severity of injury :

The total number of patients with moderate injury was 90 and the number of patients with severe injuy was 110.

Moderate injury (GCS 9 – 12 ) - 90 (45%)

Severe injury (GCS – 3 – 8) - 110 (55%)

AGE-WISE GCS SCORE:

AGE CATEGORY IN

YEARS

GCS 3

GCS 4

GCS 5

GCS 6

GCS 7 – 12

< 30 02 01 01 01 45

30 – 39 06 01 01 01 23

40 – 49 05 02 02 01 31

50 – 59 07 01 02 01 32

60 – 69 01 01 02 01 18

≥ - 70 04 00 00 01 06

In the GCS 3, GCS 4 and GCS 5 category the mortality in the study group was 100%.

In the GCS 6 category the mortality was 66.67%.

In the GCS 7 – 13 category the mortality was 27.10%.

PUPILL

Out of tsluggish

Pupilla

Norm

Slugg

No

Une

M

LARY RE

the 200 cash reaction t

ary reactioLight

mally reacti

ishly react

o reaction

equal pupil

Mortality ch

EACTIVIT

ses 103 casto light and

on to N

ing

ting

ls

hart in %

1.94

77

TY:

ses had nord 22 cases

No of cases

103

75

22

25

for pupill

7.33

10

rmal reactihad no rea

s %

51.5%

37.5%

11%

12.5%

lary react

00

28

ion of pupiaction to li

Mort

%

%

%

%

tion among

0

20

40

60

80

100

ils to light,ght.

tality scor

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58

22

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g the study

n

s

n

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, 75 cases h

re %

1.94

77.33

100

28%

y group:

normally react

sluggishly reac

no reaction

unequal pupils

had

%

4%

3%

%

%

ting

cting

s

The mortality in the group which had no reaction to light was 100%, wheras the mortality in the sluggishly reacting group and normally reacting group was 77.33% and 1.94%.

Unequal pupils was seen in 25 cases, out of which 19 underwent surgery and 6 cases were treated conservatively. There was 2 deaths (10.53%), in the operated group and 5 deaths (83.33%) in the conservatively treated group.

CT SC

Out of tcases (2(15.5%lesions

As per thad gradlesions

MARC

GGRGRGRGR

0

20

40

60

80

100

120

140

160

180

200

CAN DETE

the 200 cas24.5%), 35), 26 cases(21.5%)

the Marshade II lesion(6.5%) an

RSHALL’CLASS

GRADE I RADE II RADE III RADE IV RADE V

I

12

ECTED I

ses 16 case5 cases hads had hemo

all’s CT scns (35%),

nd 71 had g

’S TO

II III

70

3

MARSHAL

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can classifi34 had gra

grade V les

OTAL CAS

12 70 34 13 71

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ontusion (1

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71

N CLASSIFIC

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2 cases hadons (17%)%).

%

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CATION

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d grade I le), 13 had g

IMS

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N GRADES

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In a compatientscases of

US OF BA

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mparative ss with EDHf SDH the

0255075100125150175200

7

ASAL CIST

00 cases, 85% mortalwith hemoand one ha

US OF BAS

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TERNS:

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rate was 53

3

d obliteratises were asontusion (3e lesions (1

TERNS -

n patients wmortality r3.62%. hen

2

ion of the ssociated w37.5%) an12.5%).

MORTAL

with EDH rate was 3nce SDH h

1

basal cistewith SDH (nd 2 case w

LITY CHA

and SDH, 30.56% whad a poor

mortality

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ART

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7 cases iated

er of or 69

53.62

30.56

0 20 40 60 80 100

SDH

EDH

MORTALITY  % IN EDH AND SDH

MORTALITY IN EDH AND SDH

Lesion Total cases Death % EDH 36 11 30.56 % SDH 69 37 53.62 %

Comorbid conditions:

Hypotension and hypoxia were considered and they were amenable to therapeutic modification.Of the 200 cases, 20 cases (10%) had hypotension and out of these cases 19 died (95%).8 cases (4%) had hypotension and hypoxia and all 8 died (100%)

COMORBID CONDITION

TOTAL CASES % TOTAL DEATHS %

HYPOTENSION 20 10% 19 95%

HYPOTENSION + HYPOXIA

08 04% 08 100%

PREDIC

Using th

months

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36.77%

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The pre33.82%

HYPOT

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edicted pro

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bability of

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f unfavoura

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95

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redicted pro

able outcom

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60 70 80 90 1

OMORBN %

D UNFAVO

obability o

me – core

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me– core

00

ID COND

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OURABLE

of mortality

after 6 mo

months wa

+ CT after

DITIONS

OMORBID CON

OUTCOM

y – core aft

onths was

as 23.25%

r 6 months

S 

NDITIONS

E

fter 6

%.

was

0

10

20

30

40

50

60

70

80

90

100

Predicteprobabilmonth mcore mod

25

Predicteprobabilmonth mcore mod

2

25.02

pp of 6 mont

pp of 6 mont

ed lity of 6

mortality del

5.02%

ed lity of 6

mortality del

28%

36.77

PRED

th mortality co

th mortality co

Predicteprobabilmonth unfavououtcome

36

Predicteprobabilmonth unfavououtcome

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DICTED P

ore 

ore + CT 

ed lity of 6

urable e core mode

6.77%

IMPA

ed lity of 6

urable e core mode

32%

23.25

PROBAB

el

Predicteprobabimonth mcore + C

23

ACT STUD

el

Predicteprobabimonth mcore + C

26

33.82

LITY CHA

pp of 6 month

pp of 6 month

ed ility of 6 mortality CT model

3.25%

DY

ed ility of 6 mortality CT model

6.50%

ART

h unfavourable

hs unfavourab

Predicteprobabimonth unfavououtcomemodel

33

Predicteprobabimonth unfavououtcomemodel

3

e oucome core

le outcome co

ed ility of 6

urable e core + CT

3.82%

ed ility of 6

urable e core + CT

1.60%

e

ore +CT 

T

T

DISCUSSION

Prognostic models enable us to predict fairly accurately at the time of admission, as to what the outcome for a given injury might be. Scores like the GCS help us to to predict outcome only 24 hours following injury.

Clinically, they help doctors as well as patients in decision making about the modality of treatment. They are also help in research studies to compare outcomes in various patients groups and in randomized controlled trials.

When considering prognostic predictors, charecters that can be reliably and easily determined within the initial few hours are chosen. Subsequenty five important predictors were chosen which had an important bearing on patient outcome They were:

1) GLASGOW COMA SCALE

2) DEMOGRAPHICS

3) PUPILLARY SIZE AND REACTION

4) CT CHARECTERISTICS (MARSHALL CLASSIFICATION)

5) COMORBID CONDITIONS (HYPOTENSION , HYPOXIA)

GLASGOW COMA SCALE SCORE In 1974 TEASDALE and JENNETT developed the GCS scoring system. It was an objective measure of the level of consciousness and is used widely as a clinical measure of the severity of injury in patients with traumatic brain injuries. There is inter hospital and intra hospital variation in practice with regard to the assigning of initial GCS score. Prediction of outcome was not reliable if all the three important components of GCS are not assessed. Another factor was regarding best location for application of painful stimuli for assessing motor response, ie nail bed pressure, supraorbital pressure, sternal pressure etc. Inspite of all these the predictive value of GCS in the score range of 3-5 was roughly 77% and in the range of 6-8 was around 26% as per the prospective study by Narayanan. Many investigators have analysed the predictive value of the initial GCS score using different logistic regression methods. Kaufman described the accuracy of outcome predictions for patients of severe TBI and categorized them as dead,vegetative, severely disabled, or capable of independent survival. These were predicted based on the best initial GCS scores that was obtained within 24 hours following injury. Very bad or very good outcomes had the best predictions. The two most important consideration for the use of initial GCS score for prognosis are

1) How reliable the initial measurement is.

2) lack of precision for prediction of a good outcome for lower GCS.

In this study the mortality outcome among patients with GCS score of 3, 4 and 5 was 100%. In the GCS 6 category, the mortality outcome was 66.67%. In the GCS 7 – 13 category, the mortality outcome was 27.10%.

This showed that patients with GCS 7 and above had a better outcome compared to to patients with lower GCS. This was because most of the patients with low GCS were in the older age group who had other associated comorbid conditions and such patients are at a higher risk for decline in cognitive function. Hence they had poor outcome.

AGE As age increases the probability of poor outcome also increases. This is not only due to the degenerative process of the brain due to aging, but also the type of injury that was more specific to each age group and general decline in health as one ages. In a TCDB (traumatic coma data bank) prospective study series, injuries due to motor-vehicle accidents accounted for 55% of patients between the ages 15–25, whereas injury due to falls accounted for only about 5% cases. However, in the age group above 55, 45% cases were due to falls and only about 15% were due to motor-vehicle accidents. Older patients had poorer outcomes when compared to younger patients, irrespective of the type of injury. In this study, there were a notable increase in the percentage of poor outcomes in those patients who had prior systemic disease in ages above 56, but this correlation was not seen in younger age groups. Also there was increasing intracranial hematomas in the older groups. This reduced the chance of survival among the older age group. Age itself was found to be an independent predictor as the brain had a decreased capacity for repair as it ages. Most studies have shown that younger individuals fare better than adults. There are contradictions in literature as to the defining the age point where prognosis worsens significantly. Some studies predict good outcomes below the age range of 40-50 years. A prospective study on age and outcome revealed that, patients older than 60 had a significantly worse outcome. After six months following severe head injury, 92% of the cases were dead, vegetative, or severely disabled. Age therefore is a strong independent predictor having significant influence over both morbidity and mortality.Inspite of some contradictions, most studies predict children having better outcomes than adults with severe brain injury. There is a significant increase in poor outcome above the age of 60. In this study patients below 30 years of age had a 26% unfavourable outcome as compared to 74% favourable outcome.

In the 30 -39 years age group the unfavourable outcome was 38.71% and the favourable outcome was 61.29%. In the 40 -49 years age group the unfavourable outcome was 56.10% and the favourable outcome was 43.90%. In the 50 -59 years age group the unfavourable outcome was 59.57% and the favourable outcome was 40.43%. In the 60 -69 years age group the unfavourable outcome was 55% and the favourable outcome was 45%. In the ≥70 years age group the unfavourable outcome was 81.82% and the favourable outcome was 18.18%. Patients above the age of 70 had a 82% mortality rate. The higher percentage of unfavourable outcome (59.57), in the 50 – 59 years age group as compared to the 60 – 69 years age group (55%) was probably because most of the patients in the 50 – 59 years group had multiple lesions on CT scan associated with effacement of basal cisterns.

PUPILLARY DIAMETER AND REACTION The light reflex pathway is mediated by the third cranial nerve which is located near to the brainstem areas which controls consciousness, and near the medial temporal lobe. Injury to the third nerve nucleus in the midbrain or to the third nerve efferent by compression of the temporal lobe can produces dilated pupils. An increase in intracranial pressure can cause uncal herniation causing compression of the third cranial nerve, which causes a reduction in parasympathetic tone to the constrictor fibers of the pupils. Significant compression or damage causes an unresponsive (fixed) pupil to light stimulus. This pupillary light reflex and the pupillary size is used as a clinical guide to assess trans-tentorial herniation and it therefore serves as a prognostic indicator. It is an indirect evidence of dysfunction of pathways subserving consciousness and, thus, an significant clinical parameter to judge outcome in traumatic coma. The third nerve can be damaged by direct orbital trauma causing a dilated and/or a fixed pupil and which is not related to ICH. We should therefore exclude direct oculomotor trauma before using pupillary size or reactivity as a prognostic criteria. Unilaterally Dilated and fixed pupil generally signifies herniation. Bilaterally dilated and fixed pupils indicates irreversible brainstem damage, and are associated with poor outcome. The timing of surgical evacuvation of significant hematomas and underlying pathology also influence the outcomes of bilateral nonreactive pupils . In comatosed patients with EDH with bilateral fixed pupils, the mortality was around 56% , as compared to 88% in patients with SDH. In a class 1study, it was shown that a delay by more than three hours in evacuating a traumatic ICH with bilateral fixed pupils, increased the chance of a poor outcome from 40% to 63%. Hence pupil reactivity to light can serve as an important prognostic indicator of outcome. 1.Pupillary light reflex for both eyes and duration of dilatation and fixation should be documented and used as a prognostic parameter. 2. the measure for a dilated pupil is, pupillary size greater than 4 mm.

3. A fixed pupil is one which does not constrict in response to bright light. 4.We should distinguish between right or left when there is asymmetry of pupils. 5. correct hypotension and hypoxia before assessing pupils. 6. Exclude direct trauma to the orbits. 7. pupillary examination should be carried out following evacuvation of a mass lesion, as it is an indirect indicator of tentorial herniation. In this study, 103 cases(51.5%), had normally reacting pupils, while 75 cases (37.5%), had sluggishly reacting pupils. 22 cases (11%), had no pupillary reaction to light (fixed) and 25 cases (12.5%), had unequal pupils. The mortality rate in the normally reacting group was 1.94%, whereas the mortality in the sluggishly reacting group was 77.33%. In patients who had no reaction to light (fixed), the mortality rate was 100% and in the patients with unequal pupils it was 12.5% . Patients with unequal pupils who underwent surgery had a mortality rate of 10.53% compared to 83.33% in patients who did not have surgery. Hence normally reacting pupils did not carry much prognostic significance, while sluggishly reacting pupils had a greater than 50% mortality. Fixed pupils has important prognostic significance, as they imply irreversible brainstem damage and is associated with 100% mortality.

CT SCAN FEATURES Many patients are brought to the hospital paralyzed , intubated and on ventilator support. Accurate estimation of the GCS score in the initial few hours after trauma are therefore often difficult. An EUROPEAN BRAIN INJURY CONSORTIUM suvey indicated that full GCS score could be testable in only 56% of patients at the time of admission . Hence prognostic features that depend on technical investigations like CT scans are therefore required. CT scan is ordered routinely in all patients with moderate and severe TBI as it provides vital information which have direct implications regarding operative intervention or for intracranial pressure (ICP) monitoring, and also important information regarding prognosis. CT characteristics that were found to be particularly important in terms of prognosis were: a. the status of basal cisterns b.traumatic sub arachnoid hemorrhage c. Presence of midline shift and degree of shift d. Presence and type of intracranial pathology e. Presence of mass lesion intracranially or its absence The incidence of CT scan abnormalities reported in patients with severe TBI varies between 68% - 94%. Studies have show that CT scan abnormalities have a PPV (POSITIVE PREDICTIVE VALUE) of 77%-78% with regard to unfavorable outcome in patients with GCS score less than 8. The predictive value of abnormalities present on initial CT examination is therefore limited. The negative predictive value- ie, the the relation between absence of abnormalities and favorable outcome , is of much more significance. In roughly one-third of the patients with an initial normal CT scan, new lesions may occur on follow up CT scan examination. Around 75% of these patients, could have raised ICP. The outcome in patients with such new lesions was less favorable compared to cases in whom CT scan remained normal (65% - 76%).

Patients with effacement of basal cisterns had unfavourable outcomes. Patients with SDH and SAH had better outcomes than the previous group. Comparatively favourable outcomes were seen in patients with EDH even with comparatively lesser GCS score. Patients with progression of lesions on follow up CT scanning had a poor outcomes. CT Classification of Head Injury and its importance Conventional CT differentiates between focal (EDH , SDH , ICH as well as contusions) and diffuse head injuries. Diffuse injuries are charecterised by the absence of mass lesions, although sometimes small contusions without underlying mass effect may occur. Patients with diffuse injuries had an intermediate outcome as compared to patients with EDH or SDH. Acute SDH along with a low GCS scores has a higher mortality rate compared to diffuse injuries with higher GCS scores which had low mortality and a higher incidence of good recovery. There is confusion in practice between the category of patients diagnosed with diffuse lesions and those with diffuse axonal injury (DAI). DAI is mainly characterized by wide-spread axonal shearing and / or shearing of smaller blood vessels. Radiologic criteria for DAI are tiny hemorrhagic lesions in the corpus collosum,at the cortico-medullary junction, in the midbrain, and in the brain stem, sometimes along with some intraventricular bleeding. diffuse brain swelling can sometimes get superimposed on DAI. Significantly better outcomes were seen in EDH without associated brain edema, simple contusion of the brain, generalized swelling, and when lesions were absent. Status of Basal Cisterns Absence or compression of the basal cisterns on CT scan is indicative of raised intracranial pressure (ICP). Third ventricle obliteration and the presence of small ventricles, is considered as an indication of diffuse brain edema, in the absence of midline shift.

Some authors take into account the condition of the third ventricle along with that of the basal cisterns to evaluate prognostic importance. Therefore the main CT findings suggestive of raised ICP, are the status of the basal cisterns and the third ventricles. Prognostic Value Studies have shown a 97% positive predictive value for unfavorable outcome in complete basal cisterns obliteration. However, due to overlap in prognostic information, the basal cisterns status was not selected as prognostic parameter when CT features were combined with clinical features like best motor response, pupil reactivity and age. Conclusions

1) There is a threefold associated risk of raised ICP when the basal cisterns are

compressed or absent.

2) Basal cisterns status has a strong relationship to outcome.

3) Effaced basal cisterns are associated with a threefold increase in mortality.

4) There is a strong association between pupil reactivity and status of the

basal cisterns .

5) There is some association of the status of the basal cisterns with GCS score.

Traumatic Subarachnoid Hemorrhage It is the presence of blood in the subarachnoid space. It could be over the convexity or in the basal cisterns. Studies have shown that the presence of traumatic SAH on CT scaning does not have high reliability. A few investigations have been performed regarding the localizing value of blood in the subarachnoid space. Most investigators use the grading system proposed by Fisher et al. Location of traumatic SAH in the Sylvian fissure is suggestive of local contusions.

Associations of traumatic SAH with Other Lesions Patients with traumatic SAH have a higher incidence of acute SDH, intraventricular hemorrhage, contusions and signs of raised ICP. Prognostic value of traumatic SAH Studies show a PPV of 72%, for unfavorable outcome in patients having traumatic SAH in the suprasellar cisterns or ambient cisterns as seen on CT scan.

The presence of traumatic SAH, especially in the peri-mesencephalic region is associated with poor outcome. The predictive value of traumatic SAH was shown to add to the predictive value of other CT scan parameters. Based on the predictive value of CT parameters alone, traumatic SAH was rated second to obliteration of the basal cisterns. The outcome in patients with traumatic SAH was significantly poor compared to that of patients whose initial CT scan did not show SAH.

Unfavorable outcomes were seen in 60% of patients with traumatic SAH compared to 30% in patients without sub arachnoid hemorrhage.

Conclusions

1) Traumatic SAH occurs frequently in severe head injury (ranges from 26%-

53%).

2) It is most frequently located over the convexity region.

3) Mortality is doubled in the presence of traumatic SAH.

4) The extent of traumatic SAH is related to outcome.

5) A PPV for unfavourable outcome is seen in around 70% of cases having

presence of blood in basal cisterns.

6) Traumatic SAH is an important independent prognostic factor.

Midline shift It is the absolute distance (in mm) of the displacement of the midline structures of the brain with respect to the midline. It is defined at the level of the foramen of monro. It is calculated using the equation: MIDLINE SHIFT = BPD _ SP 2 Where BPD is biparietal diameter and SP is septum pellucidium on the side of the shift. Association of midline shift with Other Prognostic varients Studies have shown the prognostic value of midline shift to be more important in patients with single contusions or ICH, than for those with multiple lesions and extraaxial or SDH. The presence of midline shift correlates better with the GCS score and type of pathology, rather than when taken alone. Prognostic significance of Midline Shift Studies have shown that the degree of midline shift rates third after GCS score and highest mean ICP in patients with secondary deterioration to coma . Poor outcomes were described with a midline shift greater than 10 mm. The limited prognostic value of midline shift less than 10 mm could be partly explained by the presence of DAI and bilateral hemorrhagic lesions in a majority of these patients. The risk of death corresponded to the degree of midline shift. To Conclude

1) Midline shift is inversely related to prognosis.

2) A PPV of 78% to poor outcome, is seen in the presence of shift more than 5

mm in patients over the age of 45.

3) Presence of midline shift is indicative of raised ICP.

4) The prognostic value of midline shift appears less important than other CT

parameters, because the degree of shift is also influenced by the presence of

bilateral abnormalities and the location of intracerebral lesions.

5) The presence and degree of midline shift seen on CT scan at the time of

admission can be significantly altered following the surgical evacuation of

mass lesions.

Degrees of shift are: 1) none

2) < 5 mm

3) 5-10 mm

4) > 15 mm

Intracranial Lesions They are differentiated into extracerebral and intracerebral lesions. Extracerebral lesions - consist of epidural and subdural hematomas (in the acute phase following head injury). It is important to determine the type of lesions,the number of lesions, their location, sizes, and mass effect as it can be used to quantify the severity of primary damage and also for management.

Parenchymal lesions Intraparenchymal lesions are poorly defined lesions. They may be differentiated into high-density, mixed-density, and low-density lesions. High-density lesions may be small, and located in the basal ganglia, brain stem or in the sub cortical white matter forming part of the so-called “diffuse axonal injury”. There may be lesions, of variable density, and size and causing mass effect. The demarcation between hemorrhagic contusion and intracerebral hematoma is not clear. Reliability of Scoring No studies concerning the reliability of scoring of intracranial lesions were obtained.

Association of intracranial lesions with Other Lesions and/or Prognostic Variables In patients with acute SDH, intracerebral lesions are common. Patients with intracerebral lesions were older. studies have shown that patients aged 20 or younger had a 20% incidence of associated intracerebral lesions and patients over the age of 60 had a 80% association with such lesions. Such patients had more falls as mechanism of injury, had a lower GCS score at the time of treatment, and had more extracranial injuries. Hemorrhagic contusions are seen more frequently in the elderly, where falls are the commonest cause of head injury. Intraparenchymal hemorrhage is more frequent in patients who use alcohol. Predictive Value A higher percentage of favorable outcome is seen in patients with EDH and severe head injury, and a lower percentage of favorable outcome in patients with acute SDH in comparison to patients with diffuse lesions. Studies shows a PPV of 77% for unfavorable outcome in severely head-injured patients with mass lesions which were evacuated, and a PPV of 89% when mass lesions were not evacuated.

Studies shows a PPV of 67% to unfavorable outcome in the presence of a combination of high-density intracerebral and extracerebral lesions. Hematoma volume in EDH, SDH as well as in intraparenchymal lesions correlates well with outcome. Studies have shown poor outcomes in 20% of patients with epidural clots less than 150 cc versus 58% in patients with clot volume greater than 150 cc. In patients with an acute SDH volume of less than 100 cc, the mortality rate was in the order of 51% and those with hematoma over 100 cc had a mortality of 79%. Studies have also described a direct relationship between the number of intracerebral lesions and outcome. In patients with a single hematoma, 58% have a favorable outcome, compared to 20% when patients had two clots, while no patients with three or more hematomas had a favorable outcome. Conclusions

1) Intracerebral and extracerebral lesions frequently occur in comatose patients

associated with head injury.

2) Presence of mass lesions has a 78% PPV for unfavorable outcome .

3) In patients over 45 years of age, presence of mass lesion carries a PPV of

79% for poor outcome.

4) Mortality is higher in acute SDH than in EDH.

5) Outcome is more favorable in patients with EDH and severe head injury, and

it is less favorable in patients with acute subdural hematoma when compared

to patients with diffuse injuries.

6) Volume of hematoma correlates to outcome.

7) Intraparenchymal lesions are poorly defined.

In this study out of the 200 cases chosen 68 underwent decompressive craniectomy.(34%). Out of these the number of mortality was 29 (42.64%). Most of the mortality was in the lower GCS score group.Patients with EDH had a better outcome postoperatively when compared to patients with SDH. Patients with multiple lesions and effaced basal cisterns, had poor outcome following surgery. COMORBID CONDITIONS – HYPOTENSION AND HYPOXIA Secondary brain injury is defined as insults to the brain following trauma arising from extracranial sources and intracranial hypertension. They are commonly seen due to hypotension, hypoxia, ischemia, low hemoglobin, infective causes etc. There is a evidence to prove that they occur frequently and have influence on outcome. The best studied and most severe of these is hypotension. As hypotension can be treated medically, a thorough knowledge of its effect helps in predicting outcome immediately and recovery later on. Definition: Hypotension is recording of a single systolic blood pressure below 90 mm Hg. The presence of more than one episodes of hypotension from time of injury to time of resuscitation had a significant increase in morbidity and mortality. Hypotension by itself is an independent predictor for outcome other than predictors like age, trauma to multiple extracranial organs etc. The effect of systemic trauma on outcome in head injury is mainly influenced by hypotension. Hypotension is the only major predictor among the five, which can be managed by medical means.

A Class II study of hypoxia along with hypotension proved that both had a negative influence on prognosis, with hypotension having a significant effect on determining outcome. A single episode of hypotension reduced the percentage of favorable outcome. The presence of secondary damage to the brain has correlation to the subsequent appearance of other factors strongly linked with prognosis and increases the chance for subsequent development of ICH. A TCBD survey showed early onset hypotension in 14% of cases and late onset hypotension in 32% of case. late hypotension as the only insult was present in 24%. The percentage of vegetative state or death was 17% in patients not having any hypotensive episodes, 47% in those cases with early onset hypotension, 66% in cases of late onset hypotension, and 77% for the two combined. Here early as well as late onset hypotension were important , independent predictors for outcome in head injury patients. Out of the total cases 20 cases presented with hypotension (4%) and the mortality rate was 95%. In the group which had both hypotension and hypoxia the mortality rate was 100%. So hypotension is an important independent predictor with very high prognostic significance along wiyh hypoxia. This is the only prognostic indicator that can be altered by medical management in the early stages of traumatic brain injury.

OUTCOME OF THIS STUDY:

1) All the chosen predictors had a strong correlation to the 6 month Glasgow

outcome scale (GOS)

2) An increase in age was associated with twice the risk for poor outcome

compared to younger age group.

3) The lower the GCS at the time of admission , the worse was the outcome.

With GCS above 7, there was a significant reduction in the mortality with improvement in outcome.

4) Pupillary size and reactivity had a direct bearing on the outcome with

unreactive pupils having worst prognosis.

5) Patients with pupillary inequality at the time of admission , who were

operated upon earlier, had better outcome even with low GCS.

6) Comorbid conditions especially hypotension and hypoxia was associated

with poor outcomes.

7) CT features with features of mass effect and increased intra cranial pressure

had a corresponding rise in risk and poor outcome.Effacement of the basal

cisterns and significant midline shift also contributed significantly to poor

prognosis.

8) Patients with EDH had a comparatively good outcome even with low GCS

compared to other CT feature

CONCLUSION:

These prognostic indicators gave a reasonable discrimination among patients

for good and poor outcome 6 months after traumatic brain injury.

Patients who presented with GCS 5 and below had 100% mortality.

Patients with dilated pupils and hypotension along with hypoxia also had a

mortality rate of 100%.

Patients with unequal pupils who underwent early surgery had a significant

improvement in outcome compared to those who didn’t undergo surgery.

Patients above the age of 70 had 82% unfavourable outcome.

Patients with multiple lesions along with mass effect and midline shift at the

time of admission also had a poor prognosis.

Based on these prognostic variables, probable outcome could be arrived at,

thereby enabling us to take suitable decisions regarding the use of

appropriate medical or surgical management techniques in order to achieve

a better outcome in these group of patients.

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PROFORMA NAME: D.O.A: AGE: D.O.D: SEX: IP/OP NO: EDUCATION: OCCUPATION: ADDRESS: CHIEF COMPLAINTS: MODE OF INJURY HOPI: H/O OF LOSS OF CONSCIOUSNESS / SEIZURES / ENT BLEED / VOMITING PAST HISTORY: FAMILY HISTORY: PERSONAL HISTORY:

GENERAL PHYSICAL EXAMINATION: PULSE__________/min RESPIRATORY RATE: / MIN BP_____/______mm/hg PALLOR: ICTERUS: PEDAL EDEMA: GCS SCORE:

E V M

PUPILS EXAMINATION: SYSTEMIC EXAMINATION: RS: CVS: PA: LOCAL EXAMINATION: DIAGNOSIS:

INVESTIGATIONS: BLOOD ROUTINE: SERUM ELECTROLYTES: URINE ROUTINE: ECG / X-RAY CHEST: CT SCAN: MANAGEMENT: SURGERY PERFORMED: POSTOPERATIVE PROGRESS:

MORTALITY:

 

 

 

 

 

 

MASTER CHART SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

1  RAMASAMY  M  50  02/06/13  32359  RTA  E1 V1 M2  R5 / L5 NR  HYPO   SAH/FRONT HG CONT/B STEM  HG/E F CISTERN  DEAD 

2  ANAND KUMAR  M  30  02/06/13  32519  RTA  E1 V1 M1  R5 / L5 NR  HYPO  L‐ FTP SDH/L‐TEMP HG CONT/SAH  DEAD 

3  BAKIYAM  F  44  02/06/13  32365  RTA  E3 V3 M5  R3 / L3 RL    L‐FTP SDH  (DECOMPRESSED)  GOOD 

4  SHANKAR  M  26  03/06/13 33023 RTA E1 V1 M5 R4 / L2 SR R‐FTP SDH (DECOMPRESSED) MODERATE

5  VIVEK  M  23  03/06/13 33037 RTA E3 V2 M5 R3 / L3 RL R‐FRONT EDH (EVACUVATED) GOOD

6  GANESH  M  45  30/06/13 38863 RTA E2 V2 M5 R3 / L3 SR R‐FTP SDH (DECOMPRESSED) DEAD

7  SUBRAMANI  M  50  06/07/13  39944  SELF FALL E3 V2 M5  R3 / L3 RL    L‐PARIETAL EDH (EVACUVATED)  GOOD 

8  KITTATHAL  F  31  11/07/13  41429  RTA  E3 V4 M5  R4 / L2 SR    R‐FRONT ICH/SAH  (DECOMPRESSED)  GOOD 

9  SENTHIL  M  36  12/07/13  41628  SELF FALL E3 V3 M5  R3 / L3 RL    L‐PARIETAL EDH (EVACUVATED)  GOOD 

10  GNANASEKHARAN  M  56  13/07/13  41888  RTA  E2 V1 M5  R3 / L3 SR    R‐FTP SDH / E F CISTERN (DECOMPRESSED)  DEAD 

11  MURUGAN PILLAI  M   47  14/07/13  42053  RTA  E4 V3 M5  R3 / L3 RL    R‐FTP SDH/L‐TEMP HG CONT  GOOD 

12  SATHISH  M  25  18/07/13 43059 RTA E3 V3 M5 R3 / L3 RL L‐FRONT HG CONT GOOD

13  KUPPUSAMY  M  48  18/07/13 43139 RTA E1 V1 M5 R3 / L3 RL B/L FRONT HG CONT MODERATE

14  KARUPUSAMY  M  30  18/07/13 43142 RTA E1 V1 M1 R5 / L5 NR HYPO / HYPOX  SAH DEAD

15  MOORTHY  M  18  18/07/13  43319  RTA  E3 V2 M5  R4 / L2 SR    R‐PARIETAL EDH  (EVACUVATED)  GOOD 

16  THENMOZHI  F  29  21/07/13  44056  RTA  E3 V3 M5  R3 / L3 RL    SAH/DIFFUSE CEREBRAL EDEMA  GOOD 

17  MURUGAN  M  38  22/07/13  44098  RTA  E4 V3 M5  R3 / L3 RL    R‐FTP SDH/SAH/B/L ‐FRONT HG CONT   GOOD 

18  BALAMANI  F  57  23/07/13  44107  RTA  E3 V3 M5  R3 / L3 RL    R‐FTP SDH/SAH  GOOD 

19  GOPALAKRISHNAN  M  29  24/07/13  44170  RTA  E1 V1 M5  R4 / L2 SR  HYPO  DAI  MODERATE

20  PALANISAMY  M  56  24/07/13 44306 RTA E1 V1 M5 R3 / L3 RL R‐FTP SDH (DECOMPRESSED) MODERATE

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / FRONT‐frontal / 

TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX – hypoxia/ E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

21  NATARAJAN  M  85  27/07/13  44974  SELF FALL E2 V2 M5  R5 / L2 SR    R‐FTP SDH/ TEMP HG CONT (DECOMPRESSED)  DEAD 

22  SAKTHIVEL  M  29  28/07/13 45137 RTA E1 V1 M2 R5 /L5 NR HYPO  L‐ PARIETAL EDH (EVACUVATED) DEAD

23  SELVARAJ  M  42  28/07/13  45169  RTA  E1 V1 M5  R3 / L3 SR    L‐FTP SDH (DECOMPRESSED)  DEAD 

24  SUBRAMANYAM  M  60  28/07/13 45202 RTA E3 V3 M5 R3 / L3 SR DAI DEAD

25  PRABAKARAN  M  42  29/07/13  45379  RTA   E1 V1 M1  R5 / L5 NR  HYPO  B/L‐SDH/SAH  DEAD 

26  RAJESH    M  27  31/07/13 45897 SELF FALL E2 V2 M5 R4 / L2 RL R‐TEMP EDH (EVACUVATED) MODERATE

27  PATTUSAMY  M   40  04/08/13  46715  RTA  E3 V3 M5  R3 / L3 RL    R‐FTP SDH  GOOD 

28  PRAKASH  M  32  04/08/13 46716 RTA E2 V2 M5 R3 / L3 RL SAH GOOD

29  PONNAMBALAM  M  45  05/08/13  46832  RTA  E1 V1 M5  R3 / L3 SR    B/L‐FTP SDH/B/L FRONT HG CONT  DEAD 

30  KANAGARAJ  M  45  05/08/13 46903 RTA E1 V1 M1 R5 / L5 NR HYPO / HYPOX  L‐FTP SDH DEAD

31  SUBRAMANI  M  48  05/08/13  46919  RTA  E1 V1 M1  R2 / L4 NR  HYPO  L‐FTP SDH  DEAD 

32  YUVARAJ  M  46  05/08/13 46993 RTA E1 V1 M4 R4 / L2 SR L‐FTP SDH/SAH DEAD

33  GEORGE  M  60  06/08/13  47079  RTA  E3 V1 M5  R3 / L3 SR    L‐TEMP HG CONT/SAH  DEAD 

34  SARAVANAN  M  40  07/08/13 47415 RTA E2 V1 M5 R3 / L3 SR R‐TEMP EDH (EVACUVATED) DEAD

35  POOCHAMMAL  F  69  07/08/13  47439  RTA  E2 V2 M5  R3 / L3 RL    SAH  MODERATE

36  RAMASAMY  M  80  07/08/13 47562 SELF FALL E1 V1 M5 R3 / L3 SR R‐FTP SDH DEAD

37  KARUPUSAMY  M  42  10/08/13  47909  RTA  E3 V3 M5  R3 / L3 RL    B/L FRONT HG CONT  MODERATE

38  DURAISAMY  M  65  10/08/13 47974 SELF FALL E1 V1 M5 R3 / L3 RL R‐THALAMIC ICH VEGETATIVE

39  JAYAKUMAR  M  35  10/08/13  47987  RTA  E1 V1 M5  R3 / L3 SR    L‐PARIETAL EDH (EVACUVATED)  DEAD 

40  PONNAN  M  70  11/08/13 48111 SELF FALL E1 V1 M1 R5 / L5 SR HYPO / HYPOX  B/L FTP SDH DEAD

 

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral Hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX ‐ hypoxia/ E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

41  LAKSHMI  F  29  11/08/13  48130  RTA  E1 V1 M5  R3 / L3 RL     DAI  GOOD 

42  SHIVAKUMAR  M  38  14/08/13  48710  RTA  E1 V1 M3  R3 / L3 NR  HYPO / HYPOX  R‐FTP SDH (DECOMPRESSED)  DEAD 

43  MURUGAIYAN  M  70  14/08/13  48802  SELF FALL E1 V1 M4  R4 / L2 SR    R‐FTP SDH (DECOMPRESSED)  VEGETATIVE

44  MUNIRAJ  M  19  15/08/13 48935 RTA E1 V1 M5 R2 / L5 RL L‐FRONTO‐PARIETAL EDH (EVACUVATED) MODERATE

45  KALLIAPPAN  M  40  16/08/13 49398 RTA E1 V1 M3 R3 / L3 SR R‐PARIETO‐ OCCIPITAL EDH (EVACUVATED) DEAD

46  SHIVA  M  50  16/08/13 49405 RTA E1 V1 M4 R3 / L3 SR L‐FTP SDH VEGETATIVE

47  DHARMARAJ  M  40  17/08/13 49712 RTA E1 V1 M5 R2 / L4 SR L‐FTP SDH DEAD

48  YESURAJ  M  42  20/08/13 50012 RTA E3 V4 M5 R3 / L3 RL L‐FRONT HG CONT/SAH GOOD

49  LAKSHMI  F  55  20/08/13  50273  RTA  E2 V2 M5  R3 / L3 RL    R‐TEMP HG CONT/SAH  MODERATE

50  MURUGAN  M  55  22/08/13  50827  RTA  E3 V4 M5  R3 / L3 SR    B/L FRONT EDH  DEAD 

51  KRISHNAVENI  F  51  23/08/13  50989  RTA  E1 V1 M5  R3 / L3 SR    DAI  DEAD 

52  BASKAR  M  54  25/08/13  51367  RTA  E1 V1 M1  R3 / L3 NR  HYPO / HYPOX  R‐TP HG CONT / E F CISTERN  DEAD 

53  SATHISH KUMAR  M  29  25/08/13  51409  RTA  E1 V1 M1  R5 / L5 NR  HYPO  R‐FTP SDH  DEAD 

54  NATCHI  M  60  25/08/13  51421  SELF FALL E1 V1 M5  R3 / L3 RL    SAH  SEVERE 

55  RAMAN  M  47  27/08/13  51985  RTA  E2 V1 M5  R3 / L3 SR    R‐TEMPORO‐PARIETAL EDH (EVACUVATED)  DEAD 

56  AYAPPAN  M  70  28/08/13  52205  SELF FALL E1 V1 M1  R5 / L5 NR    R‐FRONT HG CONT/SAH  DEAD 

57  MYILSAMY  M  30  29/08/13  52341  SELF FALL E2 V1 M5  R3 / L3 RL    L‐PARIETO‐OCCIPITAL EDH (EVACUVATED)  MODERATE

58  MURUGAN  M  38  02/09/13 52925 RTA E3 V3 M6 R3 / L3 RL R‐TEMPORO‐PARIETAL EDH (EVACUVATED) GOOD

59  ZAHEER HUSSAIN  M  30  06/09/13 53914 SELF FALL E2 V1 M5 R3 / L3 RL L‐FTP SDH (DECOMPRESSED) MODERATE

60  SANTHOSH  M  28  08/09/13 54254 RTA  E2 V2 M5 R3 / L3 RL R‐TEMP EDH GOOD

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX ‐ hypoxia/ E F CISTERN – Effaced cistern /GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

61  SANTHOSH KUMAR  M  14  09/09/13  54125  RTA  E2 V2 M5  R3 / L3 RL    R‐TEMPERO‐PARIETAL EDH (EVACUVATED)  GOOD 

62  VIJAYA KUMAR  M  17  10/09/13 54577 RTA E1 V1 M5 R3 / L3 RL L‐TEMPORO‐PARIETAL EDH (EVACUVATED) MODERATE

63  MANI  M  28  12/09/13 55205 SELF FALL E3 V2 M5 R2 / L4 RL L‐TEMPORO‐PARIETAL EDH (EVACUVATED) GOOD

64  MURUGESHAN  M  50  13/09/13  55225  RTA  E2 V2 M5  R3 / L3 SR    R‐FRONT HG CONT / E F CISTERN (DECOMP)  DEAD 

65  SHEIK SALIM  M  20  13/09/13  55438  RTA  E3 V4 M5  R3 / L3 RL    SAH  GOOD 

66  PANEERSELVAM  M  54  15/09/13  55441  RTA   E1 V1 M1  R5 / L5 NR  HYPO  SAH  DEAD 

67  GOWRI SHANKAR  M  50  15/09/13 55825 RTA E1 V1 M5 R5 / L3 SR R‐PARIETAL EDH (EVACUVATED) MODERATE

68  JEYACHANDRAN  M  40  15/09/13 55846 RTA E2 V2 M5 R3 / L3 RL L‐FRONT HG CONT GOOD

69  KUMARESHAN  M   25  15/09/13  55874  RTA  E2 V3 M5  R3 / L3 RL    DAI  MODERATE

70  PANDIYAN  M  40  15/09/13  55882  RTA  E2 V2 M5  R3 / L3 RL    B/L TEMP HG CONT (DECOMPRESSED)  GOOD 

71  ANAND  M  20  16/09/13  56105  RTA  E1 V1 M5  R3 / L5 SR    L‐FRONTO‐PARIETAL EDH (EVACUVATED)  MODERATE

72  IBRAHIM  M  65  17/09/13 56245 RTA E2 V2 M5 R3 / L3 RL R‐FRONT HG CONT MODERATE

73  AMSAVENI  F  30  18/09/13 56511 ASSAULT E3 V2 M5 R3 / L3 RL L‐FRONTO‐TEMP EDH (EVACUVATED) GOOD

74  PALANI  M  33  20/09/13  57076  RTA  E1 V1 M1  R5 / L5 NR  HYPO  SAH  DEAD 

75  SHIVA  M  30  21/09/13  57365  RTA  E2 V1 M5  R3 / L3 RL    L‐FTP SDH  GOOD 

76  RAMATHAL   F  52  22/09/13  57475  RTA  E2 V2 M5  R3 / L3 RL    R‐FTP SDH  MODERATE

77  KARUPUSAMY  M  29  22/09/13 57506 RTA E1 V1 M5 R3 / L3 RL L‐FTP SDH SEVERE

78  KRISHNASAMY  M  50  24/09/13  57967  RTA  E1 V1 M5  R3 / L3 SR    SAH / E F CISTERN  DEAD 

79  SHIVA  M  28  26/09/13  58529  RTA  E1 V1 M5  R3 / L3 SR    SAH  SEVERE 

80  KRISHNASAMY  M  50  28/09/13  58851  RTA  E3 V2 M5  R3 / L3 RL    B/L TEMP HG CONT/SAH  GOOD 

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX – hypoxia / E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

81  SARAVANAN  M  31  28/09/13  58939  RTA  E1 V1 M1  R5 / L5 NR   HYPO / HYPOX  SAH  DEAD 

82  KUMAR RAJ  M  35  02/10/13 59121 RTA E1 V1 M1 R4 / L2 SR R‐FTP SDH (DECOMPRESSED) DEAD

83  JAYAPRAKASH  M  17  02/10/13 59174 RTA E1 V1 M5 R3 / L3 RL R‐FRONTAL EDH (EVACUVATED) SEVERE

84  PREMA  F  48  02/10/13 59892 RTA E2 V1 M5 R3 / L3 SR L‐FTP SDH DEAD

85  VENKETESH  M  45  04/10/13 60287 RTA  E2 V2 M5 R3 / L3 RL SAH MODERATE

86  SHANKARA NARAYANAN  M  45  05/10/13  60519  RTA  E3 V3 M5  R3 / L3 RL    L‐TEMP HG CONT (DECOMPRESSED)  GOOD 

87  RANGAMMAL  F  55  05/10/13  60473  RTA  E2 V2 M5  R3 / L3 RL    L‐FTP SDH/L‐FRONT HG CONT  GOOD 

88  BASKER  M  30  05/10/13  60566  RTA  E2 V2 M5  R3 / L3 RL    R‐FRONT HG CONT  GOOD 

89  SELVAM  M  42  05/10/13  60594  RTA  E1 V1 M5  R3 / L3 SR    R‐FTP SDH  DEAD 

90  RANGASAMY  M   25  05/10/13  60607  RTA  E2 V1 M5  R3 / L3 RL    R‐FTP SDH/L‐FRONT TEMP HG CONT  MODERATE

91  SURESH  M  30  08/10/13 61115 RTA E3 V2 M5 R3 / L3 RL R‐PARIETAL HG CONT GOOD

92  ARUCHAMY  M  40  09/10/13 61259 RTA  E2 V2 M5 R3 / L3 SR R‐FTP SDH (DECOMPRESSED) DEAD

93  MANIKANDAN  M  37  09/10/13 61448 RTA E2 V2 M4 R5 / L3 RL R‐FTP SDH (DECOMPRESSED) MODERATE

94  RANGASAMY  M  37  10/10/13  61601  RTA  E3 V4 M5  R3 / L3 RL    SAH  GOOD 

95  SANTHOSH KUMAR  M  24  10/10/13  61628  RTA  E2 V2 M5  R3 / L3 RL    L‐FTP SDH/L‐OCCIPITAL EDH  GOOD 

96  JOTHI MANI  F  55  11/10/13  61807  RTA  E2 V1 M5  R3 / L3 SR    R‐FRONTO TEMPORAL EDH (EVACUVATED)  DEAD 

97  JOSEPH MENDIS  M  60  11/10/13  61864  RTA  E1 V1 M5  R3 / L3 SR    SAH/R‐FRONT HG CONT  MODERATE

98  MURUGAN  M  25  11/10/13  61893  RTA  E1 V1 M4  R3 / L3 RL    SAH  DEAD 

99  PALANISAMY  M  65  12/10/13 61930 RTA E1 V1 M4 R3 / L3 SR R‐FRONT HG CONT/SAH (DECOMPRESSED) DEAD

100  SUBBULAKSHMI  F  56  12/10/13 61981 SELF FALL E2 V1 M5 R5 / L3 SR R‐FTP SDH/ EF CISTERN (DECOMPRESSED) SEVERE

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX – hypoxia / E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

101  KARUPUSAMY  M  45  12/10/13  62023  RTA  E1 V1 M5  R3 / L5 RL    L‐FTP SDH  (DECOMPRESSED)  SEVERE 

102  ARAVINDHAN  M  19  14/10/13  62230  RTA  E1 V1 M5  R3 / L3 RL    L‐FRONTAL EDH (EVACUVATED)  GOOD 

103  PALANISAMY  M  65  15/10/13 61930 RTA E1 V1 M5 R3 / L3 SR R‐FRONTAL CONTUSION (DECOMPRESSED) DEAD

104  KAILASHAM  M  50  16/10/13 62136 RTA E1 V1 M5 R3 / L3 SR R‐TEMP‐  CONT/ E F CISTERN (DECOMPRESSED)  DEAD

105  RAMESH  M  40  16/10/13  62702  RTA E1 V1 M5  R4 / L2 RL    R‐TEMPORAL EDH (EVACUVATED)  MODERATE

106  NALLAN  M  50  17/10/13  63060  RTA  E1 V1 M3  R3 / L3 SR  HYPO  DAI  DEAD 

107  ANTHONY  M  65  17/10/13  63121  RTA  E2 V1 M5  R3 / L3 RL    L‐TEMP PARIETAL SDH/SAH  MODERATE

108  SETHUPATHY  M  25  18/10/13 63293 RTA E3 V4 M5 R3 / L3 RL DAI GOOD

109  SURENDERA MOHAN  M   65  20/10/13 63630 RTA E3 V2 M5 R3 / L3 RL SAH GOOD

110  CHELLAMUTHU  M  50  20/10/13  63674  RTA  E2 V2 M5  R3 / L3 RL    DAI  GOOD 

111  UMASELVI  F  53  21/10/13  63866  RTA  E1 V1 M5  R3 / L3 SR    L‐TEMP HG CONT  DEAD 

112  LAKSHMI  F  67  21/10/13  63879  RTA  E1 V1 M3  R3 / L3 SR    R‐OCCIPITAL SDH  DEAD 

113  RAJESHWARI  F  45  22/10/13  63962  RTA  E1 V1 M5  R3 / L3 SR    R & L TEMP HG CONT  DEAD 

114  SOKKALINGAM  M  70  22/10/13 64005 RTA E4 V1 M5 R4 / L2 SR R‐FTP SDH (DECOMPRESSED) DEAD

115  ARUMUGAM  M  65  23/10/13 64351 RTA E1 V1 M2 R3 / L3 SR R‐FRONT TEMP HG CONT/SAH DEAD

116  SRINIVASAN  M  39  23/10/13 64411 RTA E1 V1 M1 R5 / L5 NR HYPO  SAH DEAD

117  MANI  M  80  23/10/13  64412  SELF FALL E2 V2 M4  R3 / L3 SR    R‐FTP SDH/IVH  DEAD 

118  RADHA  F  30  25/10/13  64756  RTA  E3 V2 M5  R3 / L3 SR    R‐FTP SDH  GOOD 

119  ARUMUGAM  M  55  25/10/13  64784  RTA  E1 V1 M5  R3 / L3 SR    SAH / E F CISTERN  SEVERE 

120  ARUSAMY  M  25  26/10/13  64905  RTA  E3 V2 M5  R3 / L3 RL    DAI  GOOD 

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX – hypoxia / E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

121  MADDHAPPAN  M  81  26/10/13  64908  SELF FALL E1 V1 M1  R5 / L5 NR  HYPO  R‐FTP SDH/SAH  DEAD 

122  KANDASAMY  M  45  26/10/13 64943 RTA E3 V2 M5 R3 / L3 RL R‐PARIETAL SDH GOOD

123  SELVI  F  45  27/10/13 65154 RTA E1 V1 M5 R4 / L2 SR R‐TEMP OCCIPITAL SDH/SAH DEAD

124  VENKATAPATHY  M  73  28/10/13 65224 SELF FALL E1 V1 M1 R3 / L3 SR R‐FTP SDH DEAD

125  KANNIYAMMAL  F  50  28/10/13  65234  SELF FALL  E2 V2 M5  R3 / L3 RL    SAH  GOOD 

126  SUNDARI  F  68  29/10/13  65514  SELF FALL  E1 V1 M5  R3 / L3 SR    SAH  DEAD 

127  KOTHANDARAMAN  M  50  29/10/13  65639  RTA  E4 V1 M5  R2 / L4 SR    L‐TEMP HG CONT  DEAD 

128  GOPAL  M  25  30/10/13  65889  ASSAULT  E1 V1 M5  R3 / L3 SR    L‐FTP SDH / E F CISTERN (DECOMPRESSED)  DEAD 

129  SIVAPANDI  M   25  31/10/13  65862  RTA  E2 V3 M5  R3 / L3 RL    R‐TEMP HG CONT/SAH  GOOD 

130  SARDAR  M  55  31/10/13  65991  RTA  E3 V1 M5  R3 / L3 RL    R‐TEMP HG CONT  SEVERE 

131  KALIMUTHU  M  33  31/10/13 66021 RTA E2 V3 M5 R3 / L3 RL R‐PARIETAL SDH GOOD

132  GOPALAKRISNAN  M  55  01/11/13 66013 RTA E3 V3 M5 R3 / L3 RL R‐TEMP EDH (EVACUVATED) GOOD

133  GUNASEKHAR  M  55  01/11/13 66181 RTA  E2 V2 M5 R3 / L3 SR DAI DEAD

134  DINESH  M  22  01/11/13  66215  RTA  E2 V2 M5  R3 / L3 RL    SAH  GOOD 

135  RAVI  M  35  02/11/13  66276  SELF FALL E1 V1 M5  R3 / L3 RL    R‐FTP SDH (DECOMPRESSED)  SEVERE 

136  VADIVEL  M  23  02/11/13  66337  RTA  E2 V2 M5  R3 / L3 RL    L‐TEMP EDH  GOOD 

137  RANGASAMY  M  45  02/11/13  66363  RTA  E2 V2 M5  R3 / L3 RL    DAI  GOOD 

138  NAGENDRA PRASAD  M  19  02/11/13  66391  RTA  E1 V1 M5  R3 / L3 SR    SAH  SEVERE 

139  CHINNADURAI  M  35  03/11/13 66520 RTA E2 V3 M5 R3 / L3 RL R‐FRONT HG CONT GOOD

140  MANJUNATHAN  M  40  03/11/13 66605 RTA  E2 V2 M5 R3 / L3 RL DAI GOOD

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX – hypoxia/ E F CISTERN – Effaced cistern /GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

141  SHANMUGASUNDARAM  M  45  04/11/13 66584 RTA E2 V1 M5 R3 / L3 SR   SAH DEAD

142  RANGANATHAN  M  26  04/11/13  66893  RTA  E3 V3 M5  R3 / L3 RL    R‐TEMP PARIETAL EDH (EVACUVATED)  GOOD 

143  GANESH  M  27  05/11/13  67059  RTA  E1 V1 M1  R5 / L5 NR  HYPO /HYPOX  R‐TEMP HG CONT  DEAD 

144  DHANRAJ  M  35  05/11/13 67131 RTA E3 V2 M5 R3 / L3 RL R‐FRONT HG CONT GOOD

145  MUTHUSAMY  M  40  05/11/13  67135  RTA  E1 V1 M1  R3 / L3 SR  HYPO  L‐FTP SDH  DEAD 

146  PAPPAN  M  55  05/11/13 67154 RTA E2 V2 M5 R3 / L3 RL SAH GOOD

147  LAKSHMI  F  60  06/11/13  67323  RTA  E2 V2 M5  R3 / L3 RL    B/L PARIETAL SDH  GOOD 

148  BALASUBRAMANI  M  15  06/11/13  67344  RTA  E2 V2 M5  R3 / L3 RL    R‐PARIETAL HG CONT/SAH  GOOD 

149  SAKTHIVEL  M   27  06/11/13 67347 RTA E1 V1 M5 R3 / L3 SR DAI DEAD

150  HUSSAIN IBRAHIM  M  60  07/11/13  67875  RTA  E1 V1 M1  R3 / L3 SR  HYPO  R‐FTP SDH/SAH  DEAD 

151  RAGHAVAN  M  55  07/11/13 67885 RTA E1 V1 M1 R3 / L3 SR HYPO  R‐FTP SDH/SAH DEAD

152  MYILATHAL  F  50  09/11/13  68039  RTA  E2 V1 M5  R3 / L3 RL    L‐FTP SDH  GOOD 

153  KARTIKEYAN  M  32  10/11/13  68213  RTA  E2 V2 M4  R3 / L3 RL    SAH  MODERATE

154  CHINNASAMY  M  55  11/11/13 68331 RTA E1 V1 M5 R3 / L3 RL L‐FRONT PARIETAL HG CONT DEAD

155  SHANMUGAM  M  60  11/11/13  68392  SELF FALL E1 V1 M3  R5 / L5 NR    TEMP ICH (EVACUVATED)  DEAD 

156  MALAIAPPAN  M  75  11/11/13 68478 SELF FALL E2 V2 M5 R3 / L3 RL R‐ FRONT HG CONT GOOD

157  DHARMARAJ  M  37  12/11/13  68831  RTA  E1 V1 M5  R3 / L3 SR    IVH  DEAD 

158  MOHAN  M  49  12/11/13  68875  ASSAULT  E1 V1 M1  R3 / L3 SR    R‐FTP SDH/R‐TEMP HG CONT (DECOMPRESSED)  DEAD 

159  SHANKAR  M  20  13/11/13 69002 RTA E1 V1 M3 R3 / L3 SR HYPO  L‐TEMP PARIETAL EDH/SAH (EVACUVATED)) DEAD

160  SHANMUGANATHAN  M  42  13/11/13  69075  RTA  E1 V2 M5  R3 / L3 RL    SAH  MODERATE

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX ‐ hypoxia/ E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

161  NALLASAMY  M  60  13/11/13  69081  RTA  E3 V4 M5  R3 / L3 RL     L‐POLAR EDH  GOOD 

162  SHIVASUBRAMANI  M  26  13/11/13 69104 RTA E3 V3 M5 R3 / L3 RL R‐TEMP EDH/L‐TEMP HG CONT GOOD

163  MANIKANDAN  M  20  14/11/13 69320 RTA E2 V2 M5 R3 / L3 SR L‐PARIETAL EDH/SAH GOOD

164  SAMUVEL  M  60  15/11/13  69405  RTA  E3 V2 M5  R3 / L3 SR    R‐FRONT HG CONT/SAH  DEAD 

165  MUTHAMMAL  F  72  15/11/13  69446  SELF FALL E3 V2 M5  R3 / L3 RL    R‐PARIETAL SAH  GOOD 

166  RANGASAMY  M  55  17/11/13 69904 RTA E1 V1 M1 R5 / L5 NR HYPO  DAI DEAD

167  PRABHU  M  39  19/11/13 70106 RTA E1 V1  M4 R3 / L3 SR R‐FTP SDH (DECOMPRESSED) DEAD

168  SARASAL  F   60  21/11/13  70804  RTA  E2 V2 M5  R3 / L3 RL    L‐FRONT TEMP HG CONT  GOOD 

169  SURESH  M  50  23/11/13  71197  RTA  E2 V1 M5  R3 / L3 RL    L‐FTP SDH (DECOMPRESSED)  MODERATE

170  SIVARAMAN  M  45  23/11/13 71202 RTA E1 V1 M2 R3 / L3 SR L‐FTP SDH (DECOMPRESSED) DEAD

171  VINCENT  M  29  24/11/13 71500 ASSAULT E3 V2 M5 R3 / L3 RL R‐FRONTAL EDH (EVACUVATED) GOOD

172  SARAN  M  16  25/11/13  71724  RTA  E2 V2 M5  R3 / L3 RL    SAH  GOOD 

173  MANIKANDAN  M  23  25/11/13  71784  RTA  E2 V2 M5  R3 / L3 RL    DAI  GOOD 

174  LAKSHMANAN  M  25  26/11/13 72059 RTA  E2 V2 M5 R3 / L3 RL L‐FRONT TEMP HG CONT/SAH GOOD

175  VISALAKTCHI  F  45  28/11/13 72440 RTA E3 V4 M5 R3 / L3 RL R‐FTP SDH/SAH GOOD

176  SENTHIL KUMAR  M  42  28/11/13  72510  RTA  E1 V1 M5  R3 / L3 RL    R‐FTP SDH/R‐FRONT HG CONT  MODERATE

177  ALIMA BEGUM  F  31  29/11/13  72722  RTA  E1 V1 M2  R3 / L3 SR  HYPO  L‐FTP SDH  DEAD 

178  HYDER ALI  M  52  29/11/13  72755  RTA  E2 V2 M5  R3 / L3 RL    SAH  MODERATE

179  MANOJ KUMAR  M  27  02/12/13 73187 RTA E1 V1 M5 R3 / L3 SR L‐FRONT HG CONT (DECOMPRESSED) DEAD

180  JOEL  M  23  04/12/13  73721  RTA  E2 V4 M5  R3 / L3 RL    SAH  MODERATE

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / 

FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage/HYPO‐ hypotension /HYPOX ‐ hypoxia/ E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

SNO  NAME  SEX  AGE  D.O.AD I.P.NO M.O.INJ G.C.S PUPILS CO.MORBID  CT  FINDINGS OUTCOME

181  PALANISAMY  M  53  04/12/13 73795 RTA E1 V1 M1 R5 / L5 NR   HYPO / HYPOX  L‐FTP SDH DEAD

182  THANNASIAPPAN  M  55  06/12/13  74244  RTA  E3 V3 M5  R3 / L3 RL    R‐TEMPORO PARIETAL EDH (EVACUVATED)  GOOD 

183  ARUCHAMI  M  37  06/12/13 74248 RTA E1 V1 M5 R3 / L3 SR R‐FTP SDH (OPERATED) DEAD

184  RAGHUPATHY  M  22  06/12/13  74317  RTA  E1 V1 M5  R3 / L3 SR    L‐PARIETAL EDH (EVACUVATED)  DEAD 

185  ELANGO  M  33  06/12/13  74540  RTA  E1 V1 M5  R3 / L3 RL    L‐FTP SDH (DECOMPRESSED)  MODERATE

186  MANJULA  F  48  08/12/13 74690 RTA E3 V1 M5 R2 / L4 RL L‐TEMP HG CONT/SAH (DECOMPRESSED) GOOD

187  MAYANGATTHAL  F  55  10/12/13  75113  RTA  E2 V2 M5  R3 / L3 SR    B/L HG CONT (DECOMPRESSED)  DEAD 

188  PALANIAMMAL  F  53  11/12/13 75408 RTA E1 V1 M1 R5 / L5 NR SAH DEAD

189  MADHAN  M  53  13/12/13  75779  RTA  E2 V2 M5  R3 / L3 RL    R‐FTP SDH  MODERATE

190  HASSAN  M  50  13/12/13 75941 RTA  E1 V1 M1 R5 / L5 NR HYPO  SAH DEAD

191  SAKTHIVEL  M  29  14/12/13  76057  RTA  E1 V1 M5  R5 / L3 RL    R‐TEMP EDH (EVACUVATED)  MODERATE

192  DINESH KUMAR  M  28  14/12/13 76063 RTA E2 V3 M5 R3 / L3 RL SAH GOOD

193  PANJARATHINAM  M  47  16/12/13  76398  RTA  E1 V1 M3  R3 / L3 SR    L‐FTP SDH  DEAD 

194  SUBRAMANI  M  50  16/12/13  76427  RTA  E2 V2 M5  R3 / L5 RL    L‐FTP SDH (DECOMPRESSED)  GOOD 

195  MURUGESHAN  M  23  17/12/13 76449 RTA E2 V2 M5 R5 / L3 RL R‐FTP SDH (DECOMPRESSED) GOOD

196  RAJAGOPALAN  M  55  19/12/13  77165  RTA  E2 V2 M5  R5 / L3 RL    R‐FTP SDH (DECOMPRESSED)  MODERATE

197  KUPPUMUTHU  M  50  21/12/13 77562 RTA E1 V1 M3 R3 / L3 SR R‐FTP SDH (DECOMPRESSED) DEAD

198  BASAVARAJ  M  44  22/12/13  77663  RTA  E1 V1 M2  R3 / L3 SR    R‐TEMP EDH (EVACUVATED)  DEAD 

199  NANDHA KUMAR  M  22  22/12/13 77742 RTA E2 V2 M5 R3 / L3 RL DAI MODERATE

200  SHANMUGAM  M  42  25/12/13  78381  RTA  E1 V1 M2  R3 / L3 SR  HYPO  L‐TEMP EDH (EVACUVATED)  DEAD 

ABBREVIATION   :  SDH‐sub dural hematoma / EDH‐epi dural hematoma / SAH‐sub arachnoid hemorrhage / HG CONT‐hemorrhagic contusion/ TP‐temporo‐parietal / FRONT‐frontal / TEMP‐temporal / DAI‐diffuse axonal injury / B/L‐bilateral / B STEM‐brain stem / RTA‐road traffic accident / RL‐reacting to light / SR‐sluggishly reacting to light / NR‐not reacting to light / R‐right / L‐left / HG‐hemorrhage / HT‐hypertension / DM‐diabetes mellitus / ICH‐intracerebral hemorrhage / IVH‐intra ventricular hemorrhage /HYPO‐ hypotension /HYPOX ‐ hypoxia/ E F CISTERN – Effaced cistern/GOOD‐ good recovery/MODERATE‐ moderate disability/SEVERE‐ severe disability/ VEG‐ vegetative state/DEAD‐ dead 

ABBREVIATIONS

TBI – Traumatic brain injury

GCS – Glasgow coma scale

CT – computerized tomography

GOS – Glasgow outcome score

DAI – Diffuse axonal injury

IMPACT- International mission on prognosis and analysis of clinical trials in TBI

CRASH – Corticosteroid randomization after significant head injury

PPV – Positive predictive value

CSF- Cerebrospinal fluid

ICP – Intra cranial pressure

TNFα – Tumor necrosis factor - aipha

IL-1β - Interleukin - 1 beta

IL-6 – Interleukin – 6

SDH – Subdural hematoma

EDH – Extradural hematoma

SAH – Sub arachnoid hemorrhage

 

 

 

 

 

CONSENT FORM

It has been explained to me in my mother tongue and I completely understand

my condition and I have been explained in detail regarding this study -

"PROGNOSTIC INDICATORS FOR BETTER OUTCOME IN

MODERATE TO SEVERE TRAUMATIC BRAIN INJURY" I hereby give

my consent to participate in the above mentioned study.

Date:

Place:

Signature/ thumb print of the patient

with name:

 

 

 

 

 

 

 

 

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Jiwapy; gl;l gapYk; khztd; mth;fs; nkw;bfhs;Sk; "PROGNOSTIC 

INDICATORS FOR BETTER OUTCOME IN MODERATE TO SEVERE TRAUMATIC BRAIN 

INJURY" Fwpj;j Ma;tpy; bra;Kiw kw;Wk; midj;J tptu';fisa[k; nfl;Lf;

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