A STUDY OF CLINICAL AND RADIOLOGICAL PROFILE IN …repository-tnmgrmu.ac.in/4970/1/200100216bharani.pdf · dissertation on “A Study of clinical and radiological profile in patients

A Dissertation on

A STUDY OF CLINICAL AND RADIOLOGICAL

PROFILE IN PATIENTS WITH

INTRA CEREBRAL HAEMORRHAGE

Submitted to

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

CHENNAI – 600032

In partial fulfilment of the Regulations

for the Award of the Degree of

M.D. BRANCH - I

GENERAL MEDICINE

DEPARTMENT OF GENERAL MEDICINE

STANLEY MEDICAL COLLEGE

CHENNAI – 600 001

APRIL 2016

CERTIFICATE BY THE INSTITUTION

This is to certify that Dr. BHARANI.P , Post - Graduate Student

(May 2013 TO April 2016) in the Department of General Medicine

STANLEY MEDICAL COLLEGE, Chennai- 600 001, has done this

dissertation on “A Study of clinical and radiological profile in patients

with Intra cerebral haemorrhage”, under my guidance and supervision

in partial fulfillment of the regulations laid down by the Tamilnadu Dr. M.

G. R. Medical University, Chennai, for M.D. (General Medicine), Degree

examination to be held in April 2016.

Dr.R.JAYANTHI, M.D.

Professor and HOD

Department of Medicine,

Govt. Stanley Medical College

& Hospital,

Dr . ISAAC CHRISTIAN

MOSES, M.D,FICP,FACP

Dean

Govt. Stanley Medical

College & Hospital,

Chennai – 600001

CERTIFICATE BY THE GUIDE

This is to certify that DR. BHARANI.P , Post - Graduate

Student (MAY 2013 TO APRIL 2016) in the Department of General

Medicine STANLEY MEDICAL COLLEGE, Chennai- 600 001, has done

this dissertation on “A Study of clinical and radiological profile in

patients with Intra cerebral haemorrhage” under my guidance and

supervision in partial fulfillment of the regulations laid down by the

Tamilnadu Dr.M.G.R. Medical University, Chennai, for M.D. (General

Medicine), Degree Examination to be held in April 2016.

DR.P. SOUNDARA RAJAN, M.D.

Professor,

Department of Medicine,

Govt. Stanley Medical College & Hospital,

Chennai – 600001.

DECLARATION

I, DR. BHARANI.P, declare that I carried out this work on “A

Study of clinical and radiological profile in patients with Intra

cerebral haemorrhage” in patients in the department of Medicine,

Government Stanley Hospital. I also declare that this bonafide work or a

part of this work was not submitted by me or any other for any award,

degree, or diploma to any other university, board either in India or abroad.

This is submitted to The Tamilnadu DR.M.G.R. Medical

University, Chennai in partial fulfilment of the rules and regulation for the

M. D. Degree examination in General Medicine.

DR. BHARANI.P

ACKNOWLEDGEMENT

At the outset I thank our Dean DR.ISAAC CHRISTIAN MOSES,

M.D.,FICP,FACP. for permitting me to carry out this study in our

hospital.

I express my profound thanks to my esteemed Professor and

Teacher DR. R. JAYANTHI, M.D., Professor and HOD of Medicine,

Stanley Medical College Hospital, for encouraging and extending

invaluable guidance to perform and complete this dissertation.

I immensely thank my unit chief DR.P. SOUNDARA RAJAN,

M.D., Professor Of Medicine for his constant encouragement and

guidance throughout the study.

I wish to thank Dr. S . GEETHA, M.D , DR. T. B. UMADEVI,

M.D, DR. G. SATHYA, MD, DM. , Assistant Professors of my unit

Department of Medicine, Stanley Medical College Hospital for their

valuable suggestions, encouragement and advice.

I sincerely thank the members of Institutional Ethical Committee,

Stanley Medical College for approving my dissertation topic.

I thank all my colleagues, House Surgeons, and Staff nurses and

other para medical workers for their support.

I also sincerely thank all those patients who participated in this

study, for their co-operation.

CONTENTS

S.NO. TITLE Page.No.

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 2

3. AIMS AND OBJECTIVES 26

4. MATERIALS AND METHODS 27

5. RESULTS 36

6. DISCUSSION 48

7. CONCLUSION 77

ANNEXURES

1. BIBLIOGRAPHY

2. PROFORMA

3. CONSENT FORM

4. ETHICAL COMMITTEE

APPROVAL LETTER

5. MASTER CHART

6. ABBREVIATIONS

ABBREVIATIONS

sICH : Spontaneous intra cerebral hemorrhage

GCS : Glasgow Coma Scale

NIHSS : National Institutes of Health Stroke Scale

GOS : Glasgow Outcome Scale

MRS : Modified Rankin scale

ICP : Intracranial pressure

CPP : Cerebral perfusion pressure

MAP

: Mean arterial pressure

IVH : Intra ventricular haemorrhage

CBF : Cerebral Blood flow

INTRODUCTION

Among all the strokes the intra cerebral haemorrhage comprises

of about 8-13%. Hypertension accounts for majority about 50 % of

cases. Spontaneous intra cerebral hemorrhage (sICH) is a type of stroke

usually caused by a vessel rupture followed by spontaneous leakage of

blood in the brain parenchyma. The intra cerebral haemorrhage carries a

significant mortality even after better care. Hence factors causing

significant decline in neurological status as well affecting the Glasgow

outcome score need to be analysed in detail..

2

REVIEW OF LITERATURE

Intra cerebral haemorrrhage makes about 10% of all strokes and

carries a 50% case fatality rate.14.

RISK FACTORS 15

Modifiable

These are

Hypertension,

1. Anti- coagulant use,

2. Thrombolytic therapy,

3. Alcoholism,

4. Drug abuse (particularly cocaine).

Hypertension being the most common cause constituting about 60%

of cases. About 66% of patients with intra cerebral bleed do have

associated hypertension. Hypertensive bleed occurs form rupture of

small aneurysms 16,17

Anticoagulation use causes about up to tenfold increase in the risk for

intra cerebral bleed. 18.Most intracranial aneurysms do not rupture

3

during the entire life period and go unnoticed. But some do rupture and

cause subarachnoid hemorrhage, constituting about 5-15% of

hemorrhages.19 Hypertension and smoking do produce structural defects

by inducing endovascular changes. 19,20 The tunica media layer is often

involved, resulting in focal areas of weakness in the vessel wall. This

causes aneurysmal ballooning especially at bifurcations. 19

Hypertensive intracerebral haemorrhages are common. In fact

hypertension is the most common cause of intracerebral haemorrhages.

They can be conveniently divided according to their typical locations

which include, in order of frequency: basal ganglia haemorrhage

(especially the putamen),thalamic haemorrhage,pontine haemorrhage,

cerebellar haemorrhage

Long standing poorly controlled hypertension leads to a variety of

pathological changes in the vessels. These are microaneurysms of

perforating arteries (Charcot-Bouchard aneurysms) small (0.3-0.9 mm)

diameter occur on small (0.1-0.3 mm) diameter arteries in the

distribution, which matches incidence of hypertensive haemorrhages

about 80% lenticulostriate, 10% pons, 10% cerebellum. These may

thrombose, leak (see cerebral microhaemorrhages) or rupture.

4

Cerebral aneurysms typically occur at branch points of larger

vessels but can occur at the origin of small perforators which may not be

seen on imaging. Approximately 15-30% of these patients have multiple

aneurysms. As the aneurysm grows it may become irregular in outline,

and may have mural thrombus. Typically rupture occurs from the dome

The aneurysms in brain vasculature vary in size, shape and

location.

Size: Small aneurysms are less than 5 mm (1/4 inch), Medium

aneurysms are 6–15 mm (1/4 to 3/4 inch), Large aneurysms are 16–25

mm (3/4 to 1 1/4 inch), Giant aneurysms are larger than 25 mm (1 1/4

inch).

Shape: Aneurysms can be: Saccular (sac-like) with a well-defined neck,

Saccular with a wide neck, Fusiform (spindle shaped) without a distinct

neck.

Location : Anterior circulation: ~90% - Anterior Cerebral A/Anterior

Communicating A complex: 30-40%, supraclinoid portion of Internal

Carotid A &Internal Carotid A / Posterior Communicating A junction:

~30%,Middle Cerebral A (M1/M2 junction) bi/trifurcation: 20-30%.

Posterior circulation: ~10% - basilar tip, Superior Cerebral A,Posterior

Inferior Cerebellar A )

5

Arteriovenous malformation (AVM) consists of a tangle of blood

vessels in the brain or on its surface which by passes normal brain

tissue and directly diverts blood from the arteries to the veins. They can

occur anywhere on the brain or its covering meninges. They can bleed

which can occur in any region

6

Non modifiable

These are 14,15,17,21increasing age,

1. Negroid ethnicity,

2. Cerebral amyloid angiopathy ,

3. Coagulopathies,

4. Vasculitis,

5. Arteriovenous malformations (AVMs), and

6. Intracranial neoplasms.

7. Lower cholesterol , LDL cholesterol and Lower triglycerides

Intracranial bleed due to cerebral amyloid angiopathy is caused

by mutations in the amyloid precursor protein or cystatin C protein .

This is inherited as a autosomal dominant pattern. 22 This more

commonly remains asymptomatic. but it is an important cause of

primary lobar intracerebral haemorrhage in the elderly.16

Coagulopathies have propensity to cause excessive bleeding which can

be due to inherited factor deficiencies or due to acquired liver disease.

Coagulopathies which are acquired can be due to anticoagulants

use, anti platelets and substances which have anticoagulant tendencies.

Sustained use of certain drugs can produce intra cerebral bleed. These

7

are amphetamines, Phencyclidine and Cocaine. The Vascular

malformations (AVMs), are common cause in children for intra cranial

bleed . 15,17,23.

PATHOGENESIS

This has three distinct stages or phases:

(1) haemorrhage which occurs initially,

(2) expansion of the haematoma, and

(3) edema surrounding the haematoma. 24

The haemorrhage which occurs initially is as a result of rupture of

cerebral arteries which are pathological as a result of the various risk

factors. The prognosis and the end result relies on the second and third

phase of the haemorrhage. The expansion of the haematoma, which

occurs some hours later after the onset of symptoms. This consists of

rise in intracranial pressure (ICP) which interferes with the integral

functioning of the brain tissue as well as the blood-brain barrier. In

addition, the resultant venous outflow obstruction initiates tissue

thromboplastin release. This results in coagulopathy locally24. The

expansion of the haematoma is associated with hyperglycemia,

hypertension and use of anti coagulation in about 33 % of the

8

cases.25,26,27,28,29-31 The haemorrhage volume at the time of presentation

and the rapidity of hematoma expansion subsequently are important

factors in prognostication . The volume of Hematoma more than 30 ml

is likely to cause more morbidity and mortality. 32.

Subsequent to the expansion of the haematoma, cerebral edema

develops around the bleed, as a result of inflammatory mediators and

the breakdown of the blood-brain barrier. The edema around the bleed

is an important cause for worsening of the neurological status The

edema starts developing over the next two days after the bleed. The

haemorrhage can extend into the cerebral ventricles a condition termed

intraventricular extension of hemorrhage in some patients. 33 The intra

ventricular extension of the bleed can be complicated by the

development of acute obstructive hydrocephalus which carries a more

poorer prognosis. 33,34 The intra cerebral bleed associated with the

surrounding edema can compress as well as disrupt the surrounding

brain parenchyma. This leads to dysfunction of the surrounding neurons.

The overall mass effect can cause elevation of intracranial pressure

which can lead to the displacement of adjacent brain tissue and may

result in herniation with consequences. 36.

9

10

11

CLINICAL MANIFESTATION

The usual manifestation is acute onset neurological deficit .This is

usually associated with headache of raised intra cranial tension type,

nausea, vomiting, decline in the sensorium and increase in blood

pressure 37 There is an abrupt onset of neurological manifestations

when compared to ischemic stroke. 34.

.

12

13

Most of the symptoms due to intra cerebral bleed is due to

increased in the Intracranial pressure within the skull. This is manifested

as Cushing’s triad which consists of increased blood pressure, decreased

heart rate and irregularity in respiration which are caused by the

Cushing’s reflex38 . Alteration in the autonomic function is commonly

seen with intra cranial bleed as well. This explains increased respiratory

rate, decreased heart rate, increased body temperature, increased blood

pressure and increased sugar levels. 32,34

Rarely the manifestations in intra cerebral bleed may pose a

difficulty in diagnosis due to myriad of clinical manifestations. 39 So, it

is always advisable to have a neuroimaging done at the earliest. This

would be crucial in identification as well as in the prognostications with

respect to the complication based on various parameters in the imaging.

The most common site is putamen followed by internal capsule.

The sentinel sign is contralateral hemiparesis. Over 30 minutes,facial

lag will be there, slurring of speech, gradual weakness of arms and legs,

deviation of eyes away from the side of hemisphere. Flaccid weakness

of limbs will be seen. There will be signs of upper brain stem

compression with larger size haemorrage. With worsening coma,

14

respiration becomes irregular ,dilated fixed pupil and decererate

rigidity.

Contralateral hemiplegia is seen with thalamic haemorrhage and

is also associated with prominent sensory symptoms. With dominant

side involvement, aphasia with preserved repetition, with non dominant

side involvement, constructional apraxia or mutism will be seen. With

extension of upper mid brain,homonymous visual field defect

,downward and inward gaze, anisocoria with absent light reflex, Horner

syndrome on the same side, loss of convergence, vertical gaze palsy

with retraction nystagmus. At a chronic stage, patient will develop

chronic pain syndrome (Dejerrine Roussy Syndrome).

With pontine haemorrhages,quadriplegia with deep coma will be

the presentation. Pin point pupils with decerebrate rigidity, horizontal

gaze palsy which can be evoked by turning the head (oculo cephalic

maneuver). The common features are severe hypertension, hyperpnea

and hyperhydrosis. With severe haemorrhages, death occurs within few

hours. But life compatible with smaller haemorrhages.

With cerebellar haemorrhages, symptoms develop over several

hours. Ataxic gait, repeated vomiting and occipital headache are the

15

common presenting symptoms. Often there will be horizontal gaze palsy

with deviation of eyes towards the side of lesion. Skew deviation,

involuntary closure of one eye, ocular bobbing, blepharospasm are the

other findings. Dysphagia and dysarthria also occur. With development

of brainstem compression and obstructive hydrocephalus, patient

becomes stuporous and comatose. External ventricular drainage relieves

hydrocephalus from fourth ventricle. But for survival, evacuation of

haematoma should be done.

With lobar haemorrhages, signs and symptoms develop over

minutes. The neurological deficits with frontal haemorrhages are arm

weakness, parietal haemorrhages with sensory deficits, temporal

haemorrhages with delirium and aphasia and occipital haemorrhages

with hemianopia. Compression of thalamus or midrain will present with

stupor or coma.

The associated complication of malignant hypertension in crisis

is encephalopathy. With nausea, vomiting, convulsions, confusion,

stupor, coma are the presenting features. There are retinal

haemorrhages, exudates and papilledema, cardiac and renal involvement

would be present.

16

Imaging :

The main purpose of imaging is to identify between infarct vs

bleed and to identify or to rule out etiologies which can cause similar

neurological manifestations. 40 CT scan plain and MRI brain are the

available initial imaging investigations 41 In case if MRI brain can be

done immediately then it is the imaging of choice. Or else in situations

where MRI Brain is not available immediately or the patient has any

contraindication for MR imaging , CT Brain plain which is readily

available in most of the centres can be done as early as possible. CT

scan has certain advantages in intra cerebral bleed that it easily

identifies acute bleed accurately with sensitivity 100%, even

immediately after the clinical manifestations with the added advantage

that it needs less time which would be of advantage in patients with

supportive care.. MR imaging has advantage that it can detect any

causative factor for the intra cerebral bleed like malformations,

tumours and other causes. 34 43

CT angiography can be useful in identifying the expansion of

hematoma in intra cerebral bleed patients. Wada et al. have shown than

there was contrast enhancement in 91% of patients who had expansion

of haematoma. 44,43 The presence of spot sign would help identification

17

of expansion of haematoma. Hence it can help in prediciting the

prognosis in intra cerebral bleed. This is highly specific about 85-

89%, the negative predictive value being 76-96% and a positive

likelihood ratio being 2.7-8.544-47.

Park et al. have shown that patients having expansion of

haematoma as evidenced by spot sign had a longer stay in the hospital

when compared with the patients without expansion of the haematoma

which was statistically significant (p < 0.001). Also the outcome at 90

days with lethality was also significantly different- 40.5% for spot sign

group vs.13.4% for those without spot sign and this had been

statistically significant ( p < 0.001). 43 So, the presence or absence of

spot sign can be used in predicting neurological worsening and poorer

outcome in cases of intra cerebral bleed.

PROGNOSIS :

The outcome with lethality occurs in the initial 24 hours or within

30 days in about 50 % of the cases. 44-48 The parameters that predicts a

poorer outcome are 36-44

1. Large volume of bleed- more than 30 mL,

18

2. Bleed in the posterior fossa where there is much less room when

mass effect occurs,

3. increasing age,

4. Blood pressure - mean arterial blood pressure more than130

mmHg at the onset of symptoms,

5. Higher NIH score

6. GCS score of less than 4 at the time of presentation

7. Association of intra ventricular extension

All these parameters are also the predictors of lethal outcome at

30 days. The expansion of haematoma is an important predictor

independent of other factors in producing poorer outcomes 49,50,51.

Alvarez-Sabín et al. 63 have shown that increase in the level of

matrix metalloproteinase at the onset would lead to expansion of

haematoma with surrounding edema and lethal or poorer outcome. 52

Maya et al 64 have shown increase in blood pressure especially

diastolic pressure, low GCS, Increase NIHSS score, volume of the bleed

19

in addition to the above mentioned factors for poor outcome. In their

study the outcome in males was better when compared to females.

Sunil et al 65 had also shown the same factors predicting poorer

outcomes. In addition they have shown that the parameter the

association of intra ventricular extension is associated with poorer

outcomes.

Arboix et al 66 had stated that the presence of diabetic status is an

important independent factor prognosticating mortality in patients with

intra cerebral bleed.

Eva etal 67 in their article have stated that inflammatory cascade

mechanisms initiated by intra cerebral bleed can cause brain damage

secondarily days after the acute bleed probably by altered immune

cells.

Chang et al 68 have stated that for mediating brain damage after

stoke, caveolin-1 a structural protein of caveolae, is involved in the

signaling mechanisms, a possible target for therapeutic intervention in

future.

20

Management:

The patient should preferably be managed in an intensive care

unit set up. The vital signs should be continuously monitored and any

alteration to be addressed as per the directives in the literature. 34

Most of the intra cerebral bleed patients have difficulty in

maintaining their airway and hence elective intubation to be planned

and done especially if the Glasgow coma scale is less than 8. Serum

sugar levels are to be sampled periodically to identify increased or

decreased sugar levels ,the goal being to maintain euglycemic status. 58.

All these patients are prone to develop stress induced GI ulcers and

Hence should suitably managed with Proton pump inhibitors

Antacids and sucralfate. Thromboembolic prophylaxis can be done with

compression stocking. Fever must be controlled. The achievement of

near normal temperature is important because increase in temperature

can worsen the cascade of events taking place in border zone region.

If the bleed is associated with anti coagulation usage, then

normalization of coagulation parameters to be achieved with fresh

frozen plasma, pro thrombin concentrates along with vitamin K 58,60.

21

Huttner et al. have showed that pro thrombin concentrates were better

than fresh frozen plasma in reducing the expansion of haematoma.

The rise in the intracranial pressure can be treated with head

elevation by 40 degrees. This helps in aiding the juglar venous return .

The edema can be managed with 20 % mannitol as well as by 3 % saline

Barbiturate anesthesia can be used if mannitol fails to lower ICP

to an acceptable range. Barbiturate coma acts by reducing cerebral

metabolism, which results in a lowering of cerebral blood flow and thus

decreases ICP. The ICP lowering effect of hyperventilation to a PaCO2

of 25 to 30 mmHg is dramatic and rapid. However, the effect only lasts

for minutes to a few hours. Thus, we reserve hyperventilation until the

other therapies have been utilized . Neuromuscular blockade is

sometimes employed to reduce ICP in patients who are not responsive

to analgesia and sedation alone, as muscle activity can contribute to

increased ICP by raising intrathoracic pressure, thereby reducing

cerebral venous outflow . Drawbacks of neuromuscular blockade

include an increased risk of pneumonia and sepsis. In addition, the

ability to evaluate the neurologic status is lost once the patient is

paralyzed.

22

Patients who had seizures should be treated with lorazepam and

maintenance phenytoin for seizure control.8 There is no need for

initiating anti epileptics in patients who did not have seizure.

23

With non traumatic subrachnoid heamorrhage, apart from

evaluation to identify aneurysm and supportive care, nimodipine to be

used the anticipated complication vasospasm and anti epileptic drug to

be considered as seizure prophylaxis, as an episode of seizure may

produce more bleed.

Continuous watch of BP must be done , the goal being to ensure

required cerebral blood flow pressure greater than 70 mmHg.34,58 .

Aggressive anti hypertensive therapy to be cautiously done to prevent

24

hypotensive situation causing ischemia 61. The blood pressure

management depends upon each and every individual case. The

following strategies can be used

To consider BP reduction aggressively with intra venous BP

lowering agents if systolic pressure more than 200 and mean arterial

pressure more than 150 nm Hg

If associated with raised intra cranial pressure then to consider

intra venous BP lowering agents even if systolic pressure more than

180 and mean arterial pressure more than 130 nm Hg.

If not associated with raised intra cranial pressure then to

consider modest BP reduction with intra venous BP lowering agents

if systolic pressure more than 180 and mean arterial pressure more than

130 nm Hg with plan to have mean arterial blood pressure less around

110 mm Hg.

INTERACT-1 trial have shown that aggressive BP reduction has

the advantage of reduction in the volume and expansion of haematoma.

This was not associated with any significant increase in ischemic

events.

25

INTERACT 2 trial have studied the outcome with blood

pressure reduction and have shown that there was no statistically

significance in the lethal and disability outcome with recommended

blood pressure reduction.

The Intracerebral Hemorrhage Acutely Decreasing Arterial

Pressure Trial (ICH ADAPT) have observed that the proportionate

cerebral blood flow around the haematoma did not differ significantly

in patients of intra cerebral bleed managed with aggressive with systolic

less than 150 mm Hg or modest reduction with systolic less than 180

mm Hg with regard to blood pressure management.

Ravi menon et al 69 based on the observations in the study have

stated that cerebral ischemia did occur in about 33 % of patients with

acute intra cerebral bleed among whom 25 % also had radiological

evidence. They have stated probable aggressive reduction in blood

pressure in the setting of a diseased state of blood vessels in the patients.

Prabhakaran et al 70 have also stated the possibility of occurrence

of cerebral ischemia after intra cerebral hemorrhage, as a result of

aggressive blood pressure reduction and other factors.

26

AIM AND OBJECTIVES

Objectives:

1) Identification of causative factors, risk factors, neurological

presentation, Neuro imaging aspects and the final outcome of

adult patients with intracerebral bleed.

2) Analysis of these factors so as to and to plan for modifying the

diagnostic and management aspects.

27

MATERIALS AND METHODS

SETTING:

The study was done in patients admitted in the Department of

medicine of Government Stanley medical college Hospital, Chennai.

ETHICAL COMMITTEE APPROVAL: Obtained

DESIGN OF STUDY:

Single centre, Observational study

PERIOD OF STUDY:

March 2015- September 2015

SAMPLE SIZE:

60 patients

SELECTION OF STUDY SUBJECTS

INCLUSION CRITERIA:

Patients of intracerebral bleed admitted within 2 weeks of the

neurologic manifestations.

28

EXCLUSION:

1) Patients with traumatic intracerebral hemorrhage.

2) Patients with coagulation disorders.

3) Intra cerebral haemorrhage of more than 14 days duration.

4) Patients on thrombolytics, anti coagulants

5) Intracerebral haemorrhage not proven by CT or MRI,

haemorrhagic transformation.

METHODOLOGY

The above planned study was carried out in the wards of the

Department of Medicine , Government Stanley Hospital , Chennai.

Patients with spontaneous intracerebral haemorrhage confirmed

by CT were selected in this study. A total of 60 patients were included

as per the selection criteria. They were enrolled in this study after

obtained informed consent and from their close relatives in case of

altered sensorium patients.

Patients social, economic and demographic details have been

recorded in the proforma sheet. Also the preceding illness were

recorded.

29

Neurological assessment was done by taking the history including

the demographic, various risk factors, co morbid etiological diseases

and treatment history regarding use of any anti coagulation or

haematological disease.

The onset stroke severity was assessed by Glasgow coma scale

and neurological deficit on admission by NIH stroke Scale based on

detailed neurological evaluation.

The final outcome at discharge was evaluated by Glasgow

outcome score (GOS) as well as by the modified Rankin scale (MRS).

CT scan plain was done. The following aspects of intra cerebral

bleed were noted.

Its location whether supratentorial or infra tentorial and specific

location as well like capsuloganglionic region, cerebellum, brain stem,

lobe location and multiple lobe involvement.

Any presence of intraventricular extension.

Any Mass effect - midline shift displacement by 0.5mm or more

or effacement of basal cisterns or presence of hydrocephalus

30

The haematoma volume was calculated based on the formula

31

32

Glasgow Coma Scale/Score (GCS)

BEHAVIOUR RESPONSE SCORE

EYE OPENING

RESPONSSE

spontaneous 4

To speech 3

To pain 2

No repsone 1

BEST VERBAL

RESPONSE

Oriented to Time Place and Person 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No Response 1

BEST MOTOR RESPONSE Obeys commands 6

Moves to localized pain 5

Flexion withdrawl from pain 4

Abnormal Flexion ( decorticate) 3

Abnormal extension ( decerebrate) 2

No Response 1

TOTAL SCORE Best Response 15

Comatose patient 8 or less

Totally unresponsive 3

For patients who are on endo tracheal intubation - ET

33

NIH stoke scale:

34

Glasgow Outcome Scale (GOS)

The glasgow outcome scale is graded as shown in the box below

GLASGOW

OUTCOME SCALE

CONDITION OF THE PATIENT

GOS 1

DEAD

GOS 2

VEGETATIVE STATE

GOS 3 SEVERE DISABILITY

Able to follow /

unable to live independently

GOS 4 MODERATE DISABILITY

Able to live independently/

Unable to return to work or school

GOS 5 GOOD RECOVERY

Able to return to work or school

35

Modified Rankin scale (MRS)

Analysis:

Statistical analysis would be performed with Statistical package .

36

RESULTS

Age:

Age Group Frequency Percentage

Below 40 3 5.0

41-50 2 3.3

51-60 15 25.0

61-70 33 55.0

Above 70 7 11.7

Total 60 100.0

55 % of the patients were in the age group 61-70 followed by

25 % in the 51-60 age group.

Sex:

Frequency Percentage

Male 42 70.0

Female 18 30.0

Total 60 100.0

70 % were males and 30 % were females

37

Comorbid conditions:


Nil 12 20.0

DM 27 45.0

HT 7 11.7

HT and DM 8 13.3

HT and CAD 5 8.3

CAD 1 1.7

Total 60 100.0

33 % had systemic hypetension alone or with associated co

morbidities. 20 % did not have any co morbidities or identifiable

causative factor.

Alcohol consumption < 48 hrs

Frequency Percent

Yes 7 11.7

No 53 88.3

Total 60 100.0

11.7 % had an alcoholic binge within 48 hours of the event.

38

Blood pressure ( Mean arterial pressure):


< 110 14 23.3

110-130 25 41.7

130-150 14 23.3

> 150 7 11.7

Total 60 100.0

41.7 % had MAP 110-130 mm Hg. 23 % had 130-150 mm Hg,

11.7 % had MAP >150 mm Hg

Clinical presentation:

Frequency Percent

Weakness,

hemiplegia 28 46.7

Sensory 3 5.0

Ataxia 4 6.7

LOC 17 28.3

Seizures 4 6.7

39

Isolated headache 4 6.7

Total 60 100.0

46.7 % presented with motor weakness in the form of hemiplegia.

5 % presented with sensory impairment. 6.7 % presented with ataxia.

28.3 % had alteration in sensorium with loss of consciousness.6.7 % had

seizures. 6.7% presented with isolated headache as the isolated

manifestation.

Admission GCS:

Frequency Percent

< 5 12 20.0

5-10 14 23.3

11-14 11 18.3

15 23 38.3

Total 60 100.0

38.3 % had admission GCS of 15 without any worsening during

hospital stay. 18.3 % had admsission GCS 11-14.23.3 % had

admsission GCS 5-10. 20 % had admsission GCS <5.

40

Admission NIHSS:


<= 5 24 40.0

6-15 17 28.3

16-25 5 8.3

> 25 14 23.3

Total 60 100.0

40 % had NIHSS < 5, 28.3% had NIHSS 6-15, 28.3 % had

NIHSS 16-25, 23 % had NIHSS >25.

ICH location

Location Frequency Percentage

Capsulo ganglionic 34 56.7

Lobar 12 20.0

Mixed 3 5.0

Brain stem 5 8.3

Cerebellum 4 6.7

Subarachnoid hemorrhage 2 3.3

Total 60 100.0

56.7 % was capsulo ganglionic and 20% was of lobar location.

41

ICH volume

Location

Subarachnoid hemorrh

Cerebellum

Brain stem

Mixed

Lobar

Capsulo ganglionic

%

<30 ml

30-60 ml

more than 60ml

42

Tentorial division


Supratentorial 51 85.0

Infratentorial 9 15.0

Total 60 100.0

85 % had supra tentorial, 15 % had infra tentorial bleed.

ICH volume

Volume in cub. mm Frequency Percentage

< 3 0 28 46.7

30-60 19 31.7

> 60 13 21.7

Total 60 100.0

46.7 % had ICH volume <30 % , 31.7 % had 30-60 cub.mm,

21.7% had > 60 cub.mm .

43

Associated IVH


Yes 14 23.3

No 46 76.7

Total 60 100.0

23.3% had associated intraventricular extension.

Alcohol consumption < 48 hrs * ICH volume :

ICH volume Total

< 30 30-60 > 60

Alcohol

consumption < 48

hrs

Yes Count

2 4 1 7

% within Alcohol

consumption < 48

hrs

28.6% 57.1% 14.3% 100.0%

% within ICH

volume 7.1% 21.1% 7.7% 11.7%

No Count 26 15 12 53

% within Alcohol

consumption < 48

hrs

49.1% 28.3% 22.6% 100.0%

% within ICH

volume 92.9% 78.9% 92.3% 88.3%

Total Count 28 19 13 60

% within Alcohol

consumption < 48

hrs

46.7% 31.7% 21.7% 100.0%

% within ICH

volume 100.0% 100.0% 100.0% 100.0%

44

As per the literature alcoholic binge consumption 24- 48 hours prior to

the bleed has been considered as an important risk factor for intrra

cerebral bleed. But the was no significant difference between the

alcohol binge group and the absence of binge group in this study.

GOS at discharge:

Frequency Percent

Valid 1 17 28.3

2 2 3.3

3 14 23.3

4 13 21.7

5 14 23.3

Total 60 100.0

28.3 % had lethal outcome with GOS 1.

3.3 % had GOS2. and 23.3 % had GOS 3 had poor outcome.

21.7% had GOS 4 and 23.3 % had GOS 5 had better outcome.

45

Outcome MRS at discharge

Outcome MRS Frequency Percent

1 12 20.0

2 2 3.3

3 13 21.7

4 14 23.3

5 2 3.3

6 17 28.3

Total 60 100.0

28.3% had lethal outcome with MRS 6.

3..3% had lethal outcome with MRS 5.




20% had lethal outcome with MRS 1.

46

GOS at discharge


%

GOS 1

GOS 2

GOS 3

GOS 4

GOS 5

%

MRS 1

MRS2

MRS 3

MRS 4

MRS 5

MRS 6

47

Descriptive Statistics

N Minimum Maximum Mean

Std.

Deviation

Age in years 60 35 84 62.78 9.067

SBP 60 100 240 175.47 32.799

DBP 60 60 140 102.43 13.876

MAP 60 73 173 126.78 19.055

GCS 60 3 15 10.45 4.848

Admsission

NIHSS 60 0 28 13.22 9.104

ICH volume 60 10 85 39.92 22.180

GOS at

discharge 60 1 5 3.08 1.533

Outcome MRS

at discharge 60 1 6 3.72 1.814

Valid N

(listwise) 60

48

DISCUSSION

Age:

Age in years GOS at discharge Total

1 2 3 4 5

Below 40 Count 3 0 0 0 0 3

% within

Age in years 100.0% .0% .0% .0% .0%

100.0

%

% within

GOS at

discharge

17.6% .0% .0% .0% .0% 5.0%

41-50 Count 1 0 0 1 0 2

% within

Age in years 50.0% .0% .0% 50.0% .0%

100.0

%

% within

GOS at

discharge

5.9% .0% .0% 7.7% .0% 3.3%

51-60 Count 7 0 2 2 4 15

% within

Age in years 46.7% .0% 13.3% 13.3% 26.7%

100.0

%

% within

GOS at

discharge 41.2% .0% 14.3% 15.4% 28.6% 25.0%

61-70 Count 4 2 9 9 9 33

% within

Age in years 12.1% 6.1% 27.3% 27.3% 27.3%

100.0

%

% within

GOS at

discharge

23.5% 100.0% 64.3% 69.2% 64.3% 55.0%

Above 70

Count 2 0 3 1 1 7

% within

Age in years 28.6% .0% 42.9% 14.3% 14.3%

100.0

%

% within

GOS at

discharge

11.8% .0% 21.4% 7.7% 7.1% 11.7%

Total Count 17 2 14 13 14 60

% within

Age in years 28.3% 3.3% 23.3% 21.7% 23.3%

100.0

%

% within

GOS at

discharge 100.0% 100.0%

100.0

%

100.0

%

100.0

%

100.0

%

49

Among patients with lethal outcome, 41.2 (50-60 ), 23.5

( 61-70 ),11.8% >70 yrs, 76.5% were in the above 60 yrs 24.5 % were

< 50 yrs.

This implies that more mortality is observed with increasing age.

This observation is consistent with the previous studies in the literature

like sunil et al and maya et al.

Sex:

GOS at discharge Total P

value

1 2 3 4 5

Sex Male Count 14 1 10 9 8 42

.603

% within

Sex 33.3% 2.4% 23.8% 21.4% 19.0% 100.0%

% within

GOS at

discharge 82.4% 50.0% 71.4% 69.2% 57.1% 70.0%

Female Count 3 1 4 4 6 18

% within

Sex 16.7% 5.6% 22.2% 22.2% 33.3% 100.0%

% within

GOS at

discharge 17.6% 50.0% 28.6% 30.8% 42.9% 30.0%

Total Count 17 2 14 13 14 60

% within

Sex 28.3% 3.3% 23.3% 21.7% 23.3% 100.0%

% within

GOS at

discharge 100.0% 100.0% 100.0% 100.0% 100.0% 100.0%

50

Among patients who had lethal outcome

GOS 1- about 33.3% were males 16.7% were females.

Among patients with poor outcome -

GOS 2 2.4% were males 5.6 % were females,

GOS 3- 23.8% were males and 22.2% were females .

Among patients with better outcome

GOS 4- 21.4% were males 22.2 % were females,

GOS 5- 19.0% were males and 33.3% were females .

The lethal and poorer outcome observed had been more in males

when compared to females in this study. Among better outcome group

females had better outcome than males. These were not statistically

significant the p value being 0.603

These observations were similar with the previous studies like

study by sunil et al who have observed that among patients who had

died 72% were males and 28% were females in their study. But maya et

al in their study had stated that male patients had better out-come than

female ones .

51

AGE and GOS at discharge

SEX and GOS at discharge

Age in years

Above 7061-7051-6041-50Below 40

Co

un

t

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

Sex

FemaleMale

Co

un

t

16

14

12

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

52

GCS and GOS

GOS at discharge Total

1 2 3 4 5

GCS

grading < 5 Count 11 0 0 1 0 12

% within

GCS grading 91.7% .0% .0% 8.3% .0% 100.0%

% within

GOS at

discharge

64.7% .0% .0% 7.7% .0% 20.0%

5-10 Count 5 1 5 3 0 14

% within

GCS grading 35.7% 7.1% 35.7% 21.4% .0% 100.0%

% within

GOS at

discharge

29.4% 50.0% 35.7% 23.1% .0% 23.3%

11-14 Count 0 1 6 3 1 11

% within

GCS grading .0% 9.1% 54.5% 27.3% 9.1% 100.0%

% within

GOS at

discharge

.0% 50.0% 42.9% 23.1% 7.1% 18.3%

15 Count 1 0 3 6 13 23

% within

GCS grading 4.3% .0% 13.0% 26.1% 56.5% 100.0%

% within

GOS at

discharge

5.9% .0% 21.4% 46.2% 92.9% 38.3%

Total Count 17 2 14 13 14 60

% within

GCS grading 28.3% 3.3% 23.3% 21.7% 23.3% 100.0%

% within

GOS at

discharge

100.0% 100.0% 100.0% 100.0% 100.0% 100.0%

53

Among patients with lethal outcome of GOS 1- 64.7% had GCS

<5, 29.4 % had GCS 5-10 . only 6 % >GCS 10.

Among patients with lethal outcome of GOS 2 0% GCS <5, 50

% had GCS 5-10 , 50 % >GCS 10].

Among patients with lethal outcome of GOS 3 - 0 % GCS <5,

35.7 % had GCS 5-10 . 42.9% >GCS 10.

Among patients with lethal outcome of GOS 4 - - 7.7% had GCS

<5, 23.1 % had GCS 5-10 . 23.1% >GCS 10.

Among patients with lethal outcome of GOS 5--- 0% had GCS

<5, 0% had GCS 5-10 . 100% >GCS 10.

Patients had lethal outcome if GCS < 5, a poorer outcome for

GCS 5-10 and a better outcome if GCS>10.

54

GCS grading

1511-145-10< 5

Cou

nt

14

12

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

GCS and GOS at discharge

Admission NIHSS and GOS at discharge:

NIHSS grading

> 2516-256-15<= 5

Co

un

t

14

12

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

55

This implies that admission Glasgow Coma Scale directly

correlates directly with the outcome as per the Glasgow Outcome Scale

at discharge.

The correlation is statistically significant ( p – 0.000**).

Admission NIHSS and GOS:

Among patients with lethal outcome of GOS 1 -- 5.9% had NIHS

<5 , 11.8 %had NIHSS 5-15, 11.8 % had NIHSS -15-25 ,70.8% had

NIHSS >25.

Among patients with lethal outcome of GOS 2, -- 0% had NIHSs

<5, 100% had NIHSS 5-15, 0% had NIHSS-15-25, 0% had

NIHSS >25.

Among patients with lethal outcome of GOS 3 -- 35.7 %had

NIHSs < 5,57.1% had NIHSS 5-15, 7.1 % had NIHSS -15-25 , 0% had

NIHSS >25.

Among patients with lethal outcome of GOS 4--38.5-%had

NIHSs <5 ,30.8% had NIHSS 5-15, 15.4 % had NIHSS -15-25 ,15.4 %

had NIHSS >25.

56

Among patients with lethal outcome of GOS 5-- 92.9% had

NIHSs <5 ,28.3% had NIHSS 5-15, 8.3 % had NIHSS -15-25 ,0 % had

NIHSS >25.

Patients who presented with NIHSS >25 85.7% had died and

only 14.3 % had survived.

But among patients who presented with NIHSS < 5 – significant

proportion of about 92.9 % had a better outcome GOS 5.

This again emphasizes clearly that like Glasgow coma scale that

the outcome as measured by the Glasgow Outcome Scale has inverse

correlation with NIH Stroke Scale .

The correlation is statistically significant ( p – 0.000**).

Hence Glasgow coma scale and NIH stroke scale at the time of

admission are most helpful in prognosticating a patient with intra

cerebral bleed.

57

IVH and GOS:

Among patients with lethal outcome of GOS 1-- about 52.9%

had intraventricular extension and 47.1% did not have associated

intraventricular extension.

Among patients with lethal outcome of GOS 2 - 14.3% had

intraventricular extension 0% had no IVH, GOS 3- 21.4% had IVH

78.6% did not have associated intraventricular extension.

Among patients with lethal outcome of GOS 3--0% had

intraventricular extension 100% had did not have associated

intraventricular extension,

Among patients with lethal outcome of GOS 5 -- 0 % had IVH

and 100% did not have associated intraventricular extension

The presence of Intra ventricular extension is associated with a

poorer or a lethal outcome, whereas the absence of Intra ventricular

extension had better outcome GOS 5 at the time of discharge.

The correlation is statistically significant ( p – 0.000**)

58

IVH and GOS:

Tentorial division and GOS:

Associated IVH

NoYes

Co

un

t

16

14

12

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

GOS at discharge

54321

Co

un

t

14

12

10

8

6

4

2

0

Tentor ial division

Supratentorial

Infratentorial

59

Tentorial division and GOS:

Tentorial division Total

Supratentorial Infratentorial

GOS at

discharge 1 Count 13 4 17

% within

GOS at

discharge

76.5% 23.5% 100.0%

% within

Tentorial

division

25.5% 44.4% 28.3%

2 Count 2 0 2

% within

GOS at

discharge

100.0% .0% 100.0%

% within

Tentorial

division

3.9% .0% 3.3%

3 Count 13 1 14

% within

GOS at

discharge

92.9% 7.1% 100.0%

% within

Tentorial

division

25.5% 11.1% 23.3%

4 Count 12 1 13

% within

GOS at

discharge

92.3% 7.7% 100.0%

% within

Tentorial

division

23.5% 11.1% 21.7%

5 Count 11 3 14

% within

GOS at

discharge

78.6% 21.4% 100.0%

% within

Tentorial

division

21.6% 33.3% 23.3%

Total Count 51 9 60

% within

GOS at

discharge

85.0% 15.0% 100.0%

% within

Tentorial

division

100.0% 100.0% 100.0%

60

ICH volume and GOS:

Outcome MRS and ICH volume:

GOS at discharge

54321

Cou

nt

12

10

8

6

4

2

0

ICH volume

< 30

30-60

> 60


654321

Co

un

t

10

8

6

4

2

0

ICH volume

< 30

30-60

> 60

61

The lethal outcome GOS 1 was seen in 44.4 % of infra tentorial

and 25.5 % with supra tentorial locations .The better outcome GOS 5

was seen with 78.6 % of supra tentorial and 21.4 % of infra tentorial

regions.This implies that bleed in infra tentorial location has a

comparatively poorer outcome when compared to supra tentorial

location.

ICH volume and GOS:

GOS at

discharge

ICH volume Total

P value

< 30 30-60 > 60

1

Count 5 3 9 17 0.005**

% within GOS

at discharge 29.4% 17.6% 52.9% 100.0%

% within ICH

volume 17.9% 15.8% 69.2% 28.3%

2

Count 1 0 1 2

% within GOS

at discharge 50.0% .0% 50.0% 100.0%

% within ICH

volume 3.6% .0% 7.7% 3.3%

3

Count 8 5 1 14

% within GOS

at discharge 57.1% 35.7% 7.1% 100.0%

% within ICH

volume 28.6% 26.3% 7.7% 23.3%

62

GOS at

discharge

ICH volume Total

P value

< 30 30-60 > 60

4

Count 4 8 1 13

% within GOS

at discharge 30.8% 61.5% 7.7% 100.0%

% within ICH

volume 14.3% 42.1% 7.7% 21.7%

5

Count 10 3 1 14

0.000**

% within GOS

at discharge 71.4% 21.4% 7.1% 100.0%

% within ICH

volume 35.7% 15.8% 7.7% 23.3%


% within GOS

at discharge 46.7% 31.7% 21.7% 100.0%

% within ICH

volume 100.0% 100.0% 100.0% 100.0%

The volume the intra cerebral bleed less than 30 ml had a better

outcome with GOS 4 and 5.

Among the patients with the volume the intra cerebral bleed

between 30-60 ml-- 15.8% had lethal outcome, 28.3 % had poorer

outcome and 57.9 % had better outcome.

63

Among the patients with the volume the intra cerebral bleed

more than 60 ml-- 69.2 % had lethal outcome, 14.8 % had poorer

outcome and only 15.4 % had better outcome.

This implies that the volume of ICH has a direct correlation with

the outcome GOS at the time of discharge.

The correlation is statistically significant ( p – 0.005*).These

observations are consistent with previous studies in the literature.

Outcome MRS and ICH volume:

ICH volume Total P value

< 30 30-60 > 60

Outcome

MRS at

discharge

1 Count 8 3 1 12 .000

% within

Outcome

MRS at

discharge

66.7% 25.0% 8.3% 100.0%

% within

ICH volume 28.6% 15.8% 7.7% 20.0%

2 Count 2 0 0 2

% within

Outcome

MRS at

discharge

100.0% .0% .0% 100.0%

% within

ICH volume 7.1% .0% .0% 3.3%

3 Count 4 8 1 13

% within

Outcome

MRS at

discharge

30.8% 61.5% 7.7% 100.0%

% within

ICH volume 14.3% 42.1% 7.7% 21.7%

4 Count 8 5 1 14

% within

Outcome 57.1% 35.7% 7.1% 100.0%

64

MRS at

discharge

% within

ICH volume 28.6% 26.3% 7.7% 23.3%

5 Count 1 0 1 2

% within

Outcome

MRS at

discharge

50.0% .0% 50.0% 100.0%

% within

ICH volume 3.6% .0% 7.7% 3.3%

6 Count 5 3 9 17

% within

Outcome

MRS at

discharge

29.4% 17.6% 52.9% 100.0%

% within

ICH volume 17.9% 15.8% 69.2% 28.3%


% within

Outcome

MRS at

discharge

46.7% 31.7% 21.7% 100.0%

% within

ICH volume 100.0% 100.0% 100.0% 100.0%

Among the patients with the outcome MRS 6 - lethal outcome

was seen in 69.2% with the volume of bleed more than 60 ml, 15.8%

with 30-60 ml , 17.9% with less than 30 ml.

Among the patients with the outcome of Severe disability MRS 5

- 3.6% with less than 30 ml, 0% with 30-60 ml , 7.7% with more than

60 ml.

65

Among the patients with the outcome of moderate disability

MRS 4 – 28.6% with less than 30 ml, 26.3% with 330-60 ml , 7.7%

with more than 60 ml.

Among the patients with the outcome of moderate disability

MRS 3- 57.1%with less than 30 ml, 35.7% with 30-60 ml , 7.1% with

more than 60 ml.

Among the patients with the outcome of slight disability MRS 2

–7.1 %with less than 30 ml, 15.8% with 30-60 ml , 17.9% with more

than 60 ml.

Among the patients with the outcome of NO disability MRS 1 –

28.6 with less than 30 ml, 15.8% with 30-60 ml , 7.7% with more than

60 ml.

This implies that that outcome Modified Rankin Score directly

correlates with volume of the intracerebral bleed. The correlation is

statistically significant ( p – 0.011*).

66

MAP and GOS:

Level of MAP

Total

< 110

110-

130

130-

150 > 150

GOS at

discharge

1 Count 2 4 6 5 17

% within GOS at

discharge 11.8% 23.5% 35.3% 29.4% 100.0%

% within Level of

MAP 14.3% 16.0% 42.9% 71.4% 28.3%

2 Count 0 0 2 0 2

% within GOS at

discharge .0% .0% 100.0% .0% 100.0%

% within Level of

MAP .0% .0% 14.3% .0% 3.3%

3 Count 3 7 2 2 14

% within GOS at

discharge 21.4% 50.0% 14.3% 14.3% 100.0%

% within Level of

MAP 21.4% 28.0% 14.3% 28.6% 23.3%

67

4 Count 5 4 4 0 13

% within GOS at

discharge 38.5% 30.8% 30.8% .0% 100.0%

% within Level of

MAP 35.7% 16.0% 28.6% .0% 21.7%

5 Count 4 10 0 0 14

% within GOS at

discharge 28.6% 71.4% .0% .0% 100.0%

% within Level of

MAP 28.6% 40.0% .0% .0% 23.3%

Total Count 14 25 14 7 60

% within GOS at

discharge 23.3% 41.7% 23.3% 11.7% 100.0%

% within Level of

MAP 100.0% 100.0% 100.0% 100.0% 100.0%

Among patients with blood pressure with Mean Arterial Pressure

more than 150 mm Hg 71.4% had died, only 28.6% had survived with

poor outcome GOS 3.


between 130-150 mm Hg- about 42.9 % had died, 28.6 % had survived

with a poorer outcome, 28.6 had survived with a better outcome.

68


between 110-130 mHg -- only 16 % had died, 28% had survived with

a poorer outcome, 56% 6 had survived with a better outcome.

(GOS 4 and 5 ).

MAP and GOS:

GOS at discharge

54321

Co

un

t

12

10

8

6

4

2

0

Level of MAP

< 110

110-130

130-150

> 150

69


between less than 110 mm Hg, only 14 % had died, 21 % had survived

with a poorer outcome and 64.3% had survived with a better outcome

(GOS 4 and 5). The correlation is statistically significant ( p – 0.001*).

ICH volume vs GOS at discharge and Tentorial location:

In supratentorial location group

And patients with Lethal outcome GOS -1

-- 15.4 %, with 30 ml , 23.1 % with volume between 30-60 ml

and 81.5% with volume greater than 60 ml.

And patients with better outcome GOS -5

-- 81.8 % with 30 ml , 18.2 %, with volume between 30-60 ml

and 0% with volume greater than 60 ml.

With infratentorial location,

And patients with Lethal outcome GOS -1

75 % with 30 ml , 0 % with volume between 30-60 ml and 25%

with volume greater than 60 ml.

70

Tentorial division Volume of ICH and GOS:

Tentorial

division GOS at discharge Total

1 2 3 4 5

Supratentorial ICH

volume

< 30 Count 2 1 7 4 9 23

% within ICH

volume 8.7% 4.3% 30.4% 17.4% 39.1% 100.0%

% within

GOS at

discharge

15.4% 50.0% 53.8% 33.3% 81.8% 45.1%

30-60 Count 3 0 5 7 2 17

% within ICH

volume 17.6% .0% 29.4% 41.2% 11.8% 100.0%

% within

GOS at

discharge

23.1% .0% 38.5% 58.3% 18.2% 33.3%

> 60 Count 8 1 1 1 0 11

% within ICH

volume 72.7% 9.1% 9.1% 9.1% .0% 100.0%

% within

GOS at

discharge

61.5% 50.0% 7.7% 8.3% .0% 21.6%

Total Count 13 2 13 12 11 51

% within ICH

volume 25.5% 3.9% 25.5% 23.5% 21.6% 100.0%

% within

GOS at

discharge

100.0% 100.0% 100.0% 100.0% 100.0% 100.0%

71

Infratentorial ICH

volume

< 30 Count 3 1 0 1 5

% within ICH

volume 60.0% 20.0% .0% 20.0% 100.0%

% within

GOS at

discharge

75.0% 100.0% .0% 33.3% 55.6%

30-60 Count 0 0 1 1 2

% within ICH

volume .0% .0% 50.0% 50.0% 100.0%

% within

GOS at

discharge

.0% .0% 100.0% 33.3% 22.2%

> 60 Count 1 0 0 1 2

% within ICH

volume 50.0% .0% .0% 50.0% 100.0%

% within

GOS at

discharge

25.0% .0% .0% 33.3% 22.2%

Total Count 4 1 1 3 9

% within ICH

volume 44.4% 11.1% 11.1% 33.3% 100.0%

% within

GOS at

discharge

100.0% 100.0% 100.0% 100.0% 100.0%

This implies that more volume of intra cerebral bleed was

associated with lethal and poor outcome with the bleed in supra

tentorial location. But with infra tentorial even small volume of the

bleed was associated with lethal outcome. The correlation is statistically

significant ( p – 0.001*).

72

Tentorial division=Supratentorial

ICH volume

> 6030-60< 30

Cou

nt

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

Tentorial division=Infratentorial

ICH volume

> 6030-60< 30

Coun

t

3.5

3.0

2.5

2.0

1.5

1.0

.5

GOS at discharge

1

3

4

5

73

ICH location and GOS and volume:

ICH location=Cap gang

ICH volume

< 30

Coun

t

3.2

3.0

2.8

2.6

2.4

2.2

2.0

1.8

GOS at discharge

1

3

5

ICH location=Lobar

ICH volume

> 6030-60< 30

Coun

t

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

ICH location=Brain stem

ICH volume

> 60< 30

Coun

t

3.5

3.0

2.5

2.0

1.5

1.0

.5

GOS at discharge

1

3

74

Among patients with intracerebral bleed with capsulo ganglionic

location with volume less than 30 ml- 28.6 % was associated with lethal

outcome.42.9% had better outcome GOS 5.

Among patients with intracerebral bleed with lobar location --

lethal outcome was seen in 72 % with volumes greater than 60 ml and a

poor outcome was seen in in 27.3 % with volume between 30-60 ml.

But a better outcome was observed in patients with lobar location

in 50.1 % with the volume of the bleed between 30-60 ml and 9.1 % of

the patients with volume of the bleed greater than 60 ml..

Among patients with intracerebral bleed with brain stem location-

even with the volume of bleed less than 30 ml, 75 % had a lethal

outcome, 25 % had a poorer outcome GOS 3 and none had a better

outcome.

This implies that a poor outcome was observed with whether the

volume of the intracerebral bleed was more or even less in the

brainstem location.

However patients with cerebellar bleed as well as subarachnoid

haemorrhage in the study had a better outcome. But the number of

patients in the study group was very less to infer any conclusions in

this observation.

The correlation was statistically significant ( p – 0.001*) for lobar

bleed, but for other locations the p value was not significant.

75

Co morbid conditions and GOS:

GOS at discharge Total

1 2 3 4 5

Co morbid

conditions Nil Count 3 0 2 2 5 12

% within Co

morbid

conditions

25.0% .0% 16.7% 16.7% 41.7% 100.0%

% within GOS at

discharge 17.6% .0% 14.3% 15.4% 35.7% 20.0%

DM Count 10 2 3 5 7 27

% within Co

morbid

conditions

37.0% 7.4% 11.1% 18.5% 25.9% 100.0%

% within GOS at

discharge 58.8% 100.0% 21.4% 38.5% 50.0% 45.0%

HT Count 1 0 4 2 0 7

% within Co

morbid

conditions

14.3% .0% 57.1% 28.6% .0% 100.0%

% within GOS at

discharge 5.9% .0% 28.6% 15.4% .0% 11.7%

HT and

DM Count 1 0 3 2 2 8

% within Co

morbid

conditions

12.5% .0% 37.5% 25.0% 25.0% 100.0%

% within GOS at

discharge 5.9% .0% 21.4% 15.4% 14.3% 13.3%

HT and

CAD Count 1 0 2 2 0 5

% within Co

morbid

conditions

20.0% .0% 40.0% 40.0% .0% 100.0%

% within GOS at

discharge 5.9% .0% 14.3% 15.4% .0% 8.3%

CAD Count 1 0 0 0 0 1

% within Co

morbid

conditions

100.0% .0% .0% .0% .0% 100.0%

% within GOS at

discharge 5.9% .0% .0% .0% .0% 1.7%

Total Count 17 2 14 13 14 60

% within Co

morbid

conditions

28.3% 3.3% 23.3% 21.7% 23.3% 100.0%

% within GOS at

discharge 100.0% 100.0% 100.0% 100.0% 100.0% 100.0%

76

Among the patients who had Lethal outcome GOS 1 about 58.8

% were diabetic patients, 17.7 % had isolated or hypertension

associated diseases, and in about 17.6% of patients the etiology was un

identifiable. The reason for this observation should have been

multifactorial .

The correlation was not statistically significant. But these

observations differed from the observations in the study by maya et al.

Co morbid conditions

CAD

HT and CAD

HT and DM

HT

DM

Nil

Cou

nt12

10

8

6

4

2

0

GOS at discharge

1

2

3

4

5

77

CONCLUSION

The lethal and poorer outcome is more with increased age.

The lethal and poorer outcome was more in males compared to

females

The lethal outcome is also influenced by the associated co morbid

conditions. Among patients with lethal outcome significant proportion

had associated diabetic status.

The Glasgow Outcome Score GOS score has inverse correlation

with NIHSS score and a direct correlation with Glasgow coma scale

GCS.

The presence of Intra ventricular extension has poorer or lethal

outcome, whereas absence of Intra ventricular extension had better

outcome.

The lethal outcome was more with infra tentorial and better

outcome was more with supra tentorial.

The volume of ICH is direct correlation with the outcome GOS at

discharge.

78

The outcome Modified Rankin Score had a direct correlation with

the volume of intracerebral bleed.

The more the Mean arterial pressure MAP, lethal and poorer was

the outcome. Lesser MAP was associated with a better the outcome.

More the volume of the bleed more the lethal and poor outcome

with supra tentorial location. But with infra tentorial even small volume

bleed had significant lethal outcome.

The capsule ganglionic and lobar location had better outcome

compared to the brainstem location .

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109.566257.

PROFOMA

Age

Sex

Seizures

SHT DM alcohol smoking CAD Coagulation disorders

antiplatelets /anticoagulants/thrombolytic use aneurysmal

Alcohol consumption within 48hrs

Neurologic Examination

BP: SBP DBP

1.Limb weakness- hemiparesis

2.Sensory deficit

3.Ataxia

4.Visual defects

5.Seizures

6. speech defedcts

7. others

Basseline GCS(day 0): E V M =

Baseline NIHSS (day0)=

INVESTIGATION

Routine

CT Brain

ICH Location:

Thalamus

Baasal ganglia and internal capsule

Lobar: Frontal Parietal Temporal

Occipital

Brain stem

Cerebellar

intraventricular haemorrhage

Outcome assessment:

GOS at dishcharge

MRS at discharge

S NO NAME age sexCo morbid conditions

Alcohol consumption

< 48 hrsSBP DBP MAP Presentation

Admission GCS

GCSAdmsission

NIHSSSugar level

1 sethuraman 67 M SHT 2 180 100 127 headache, vomiting f/b LOC E1, V1, M1 #### 26 98 mg%2 Murugesan 63 M SHT 2 180 110 133 Headache, Rt sided weakness E4, V5, M6 15 5 F-108, PP-1323 Shanmugam 66 M SHT/T2DM 2 150 100 117 Headache, Rt sided weakness E4, V3, M6 13 5 F-162, PP-2624 sampath 68 M T2DM 1 150 80 103 Headache,It sided weakness E3, V4, M5 13 12 RBS-262mg5 Thirunavukarasu 55 M SHT 2 160 100 120 severe headache E4, V5, M6 15 1 RBS-98mg6 Navaneetham 62 F SHT 2 220 110 147 headache, vomiting f/b LOC E2, V2,M3 7 22 RBS-132mg7 pugazhenthi 68 M T2DM 2 130 90 103 headache, vomiting E3, V2, M4 9 14 F-174, PP-2868 Murugan 62 M SHT/T2DM 2 150 100 117 Headache, dizziness & imbalance E4, V5, M6 15 3 F-94, PP-173

9 Fathima 64 F SHT/T2DM 2 170 100 123Headache f/b altered sensorium, focal seizure E4, V4, M6 14 6 RBS-154

10 Loganayagi 84 F SHT 2 180 120 140 Headache, altered sensorium, LOC E1, V1, M3 5 26 FBS-96, PP-13211 Chandran 72 M NO SHT/NO DM 2 130 90 103 Lt sided weakness E4, V5, M6 15 5 FBS-87, PP-12812 Raju 65 M SHT/CAD 2 150 90 110 Giddiness, fall, Lt hemiplegia E3, V4, M5 12 10 F-64, PP-12413 Gopal 69 M T2DM 2 140 100 113 Rt hemiplegia E4, V5, M6 15 3 F-226, PP-28914 Aravi 63 F SHT 2 150 100 117 Alterered sensation Rt half of the body E4, V5, M6 15 5 F-88, PP-11015 Jamal mohamad 35 M SHT 1 210 100 137 LOC E1, V1, M1 3 26 RBS-136

16 Shanmugam 56 M SHT 2 190 100 130Headache, Lt hemiplegia, alterered sensorium E2, V2,M3 7 22 FBS-96, PP-132

17 Srinivasan 58 M SHT 2 180 120 140 Vomiting, Rt hemiplegia E4, V5, M6 15 5 F-76, PP-10418 Boopalan 48 M SHT/CAD 2 180 110 133 Headache, Focal seizure,Rt hemiplegia E2, V2, M4 8 22 F-96, PP-11619 Jamal mohamad 64 M SHT 2 150 100 117 Abnormal behaviour, Rt hemiparesis E4, V4, M6 14 14 F-84, PP-13220 Pattu 58 F NO SHT/NO DM 2 130 90 103 Headache E4, V5, M6 15 5 F-68, PP-9821 Parthiban 60 M SHT 1 210 100 137 Headache, altered sensorium, LOC E1, V1, M1 3 26 RBS-16422 Amsha 56 F NO SHT/NO DM 2 150 90 110 Status epilepticus, LOC E1, V1, M1 3 26 F-104, PP-14623 Dhayalan 65 M SHT 2 140 90 107 Headache, vomiting, gait disturbance E4, V5, M6 15 26 F-98, PP-113

24 Subhulakshmi 66 F NO SHT/NO DM 2 210 140 163 Headache, vomiting, altered sensorium E2, V2, M4 8 10 RBS-14025 Kandan 65 M SHT 2 140 100 113 Headache, vomiting, Lt heiplegia E3, V3, M5 11 14 F-92, PP-116


Alcohol consumption


Admission GCS

GCSAdmsission

NIHSSSugar level

26 Rajan 74 M SHT/T2DM 2 170 110 130 Headache, Rt hemiplegia E4, V5, M6 15 5 F-289, PP-31627 Rajagopalan 59 M SHT/T2DM 2 190 100 130 Vomiting, Altered Sensorium E1, V1, M1 3 28 F-252, PP-31928 Dhanalakshmi 64 F SHT 2 150 100 117 Headache, Rt hemiplegia E4, V5, M6 15 3 F-94, PP-13229 Mohan 65 M NO SHT/NO DM 2 140 90 107 Rt hemiplegia, focal seizures E4, V5, M6 15 5 F-88, PP-106

30 Murugan 60 M SHT 2 190 100 130 Headache,vomiting f/b LOC E1, V1, M1 3 26 RBS-14431 Farose 54 M SHT 2 150 100 117 Headache, Rt hemiplegia E4, V5, M6 15 5 F-86, PP-11232 Ravi 65 M SHT/T2DM 2 180 110 133 Headache, Rt hemiplegia E2, V2, M4 8 22 F-240, PP-28033 Muniyammal 70 F NO SHT/NO DM 2 160 100 120 Headache E4, V5, M6 15 5 F-64, PP-98

34 Murali 60 M SHT 2 220 120 153 headache, vomiting f/b LOC E1, V1, M1 3 26 RBS-16235 Narayanan 67 M SHT 2 190 110 137 Headache, LOC E1, V1, M1 3 26 F-104, PP-14636 Lavanya 60 F T2DM 2 140 90 107 Headache, altered sensorium E2, V1, M2 5 14 F-224, PP-30837 Jayammal 67 F SHT/T2DM 2 140 90 107 Headache, dizziness & imbalance E4, V5, M6 15 5 F-112, PP-16838 Ramesh 36 M NO SHT/NO DM 1 240 130 167 Sudden LOC E1, V1, M1 3 26 RBS-13239 Ibrahim 72 M SHT 2 190 100 130 Rt hemiplegia E4, V4, M6 14 14 F-84, PP-11040 Ganesan 64 M SHT 2 240 120 160 Headache, Rt hemiplegia E4, V4, M4 12 10 RBS- 14241 Raman 66 M SHT 2 180 100 127 Headache, Rt hemisensonsory loss E4, V5, M6 15 5 F-98, PP-11342 Munusamy 68 M SHT/CAD 2 160 100 120 Giddiness, Rt hemiparesis E3, V3, M4 10 14 RBS-12343 Kamatchi 58 F SHT 2 210 120 150 Altered sensorium, Lt hemiplegia E3, V3, M3 9 14 RBS-9744 Solai 62 F NO SHT/NO DM 2 140 90 107 Lt hemiparesis E4, V5, M6 15 3 RBS-11645 Abdul Ahamed 48 M DM 2 150 90 110 Rt hemisensory loss E4, V5, M6 15 3 F-146,PP-17846 Purusothaman 63 M DM 1 178 96 123 Rt hemiparesis E4, V5, M6 15 0 F-223,PP-32147 Muthu 78 M CAD 1 100 60 73.3 LOC E1, V1, M3 5 24 RBS-8948 Joseph 55 M SHT/CAD 2 180 100 127 Lt hemiparesis E3, V5,M6 14 14 F-98, PP-11349 Chittu 66 F SHT 2 240 140 173 Lt hemiplegia E4, V4, M5 13 5 RBS-10250 Anandan 70 M SHT/DM 2 190 120 143 Giddiness, Rt hemiparesis E3, V3, M4 10 14 F-99,PP-16851 Nagammal 74 F NO SHT/NO DM 2 160 80 107 Altered sensorium E2, V1, M3 6 14 RBS-112


Alcohol consumption


Admission GCS

GCSAdmsission

NIHSSSugar level

52 Murugesh 68 M SHT 1 200 110 140 Lt hemiplegia, Focal seizure E3, V4, M5 12 14 F-98, PP-13253 Pugalendhi 54 M SHT 2 190 100 130 Headache, giddiness E4, V5, M6 15 5 F-108, PP-14654 Ponnammal 69 F SHT 2 180 100 127 Lt hemiparesis E4, V5, M6 15 5 RBS-16455 Govindaraj 57 M SHT/DM/CAD 2 210 110 143 LOC E1, V1, M1 3 26 RBS-34256 Sekar 38 M NO SHT/NO DM 2 240 120 160 LOC E1, V1, M1 3 26 RBS-14257 Selvam 78 M NO SHT/NO DM 2 160 90 113 imbalance gait E4, V5, M6 15 5 RBS-8658 Thangam 65 F SHT 2 220 100 140 Rt hemiplegia, altered sensorium E2, V2, M3 7 14 FBS-76, PP-11059 Velu 66 M SHT 2 240 120 160 Sudden LOC E1, V1, M1 3 26 RBS-15360 Kanniyammal 68 F T2DM 2 180 100 127 Lt hemiplegia E4, V5, M6 15 3 F-143, PP-280

S NO NAME age sex ICH location location specficSupra / infra

tentorialICH

volume IVH GOS at dicharge

Out come MRS

1 sethuraman 67 M capsuloganglionic Thalamus supra tentorial 80 NO 1 62 Murugesan 63 M capsuloganglionic Putamen supra tentorial 40 NO 4 33 Shanmugam 66 M capsuloganglionic Internal capsule supra tentorial 25 YES 3 44 sampath 68 M lobar Rt parieto occipital lobe supratentorial 40 NO 3 45 Thirunavukarasu 55 M subarachnoid hamorrhage subarachnoid hamorrhage supratentorial 20 NO 5 16 Navaneetham 62 F capsuloganglionic Basal ganglia and putamen supratentorial 65 yes 3 47 pugazhenthi 68 M capsuloganglionic Subthalamus and putamen supratentorial 45 NO 4 38 Murugan 62 M cerebellum cerebellum infratentorial 80 NO 5 1

9 Fathima 64 F capsuloganglionic Caudate supratentorial 75 NO 4 310 Loganayagi 84 F capsuloganglionic Thalamus supratentorial 70 1 611 Chandran 72 M capsuloganglionic Internal capsule supratentorial 25 NO 4 312 Raju 65 M capsuloganglionic Putamen supratentorial 30 NO 4 313 Gopal 69 M Capsuloganglionic region thalamus&putamen supratentorial 10 YES 3 414 Aravi 63 F Capsulo ganglionic Lt thalamic supratentorial 15 NO 5 115 Jamal mohamad 35 M Brainstem Pons infratentorial 20 NO 1 6

16 Shanmugam 56 M capsuloganglionic Putamen supratentorial 85 yes 1 617 Srinivasan 58 M capsuloganglionic Thalamus and Caudate supratentorial 55 NO 4 318 Boopalan 48 M capsuloganglionic Thalamus supratentorial 45 NO 4 319 Jamal mohamad 64 M capsuloganglionic putamen and caudate supratentorial 30 NO 5 120 Pattu 58 F capsuloganglionic Internal capsule supratentorial 30 NO 5 121 Parthiban 60 M capsuloganglionic Rt parieto occipital supratentorial 60 YES 1 622 Amsha 56 F capsuloganglionic Rt parietal supratentorial 40 NO 4 323 Dhayalan 65 M cerebellum cerebellum infratentorial 35 NO 4 3

24 Subhulakshmi 66 F LobarLt Fronto Parieto Temporal with midline shift supratentorial 80 YES 1 6

25 Kandan 65 M capsuloganglionic Thalamus supratentorial 55 NO 4 3


tentorialICH


Out come MRS

26 Rajan 74 M capsuloganglionic Basalganglia and caudate supratentorial 45 NO 3 427 Rajagopalan 59 M mixed Putamen supratentorial 75 YES 1 628 Dhanalakshmi 64 F capsuloganglionic caudate and putamen supratentorial 35 NO 4 329 Mohan 65 M Lobar Lt Frontal supratentorial 20 NO 5 1

30 Murugan 60 M mixedLt Fronto Parieto Temporal with midline shift supratentorial 65 YES 1 6

31 Farose 54 M capsuloganglionic Putamen supratentorial 30 NO 5 132 Ravi 65 M capsuloganglionic Caudate and basalganglia supratentorial 30 NO 4 333 Muniyammal 70 F Subarachnoid hemorrhage subarachnoid hamorrhage supratentorial 40 NO 5 1

34 Murali 60 M mixedRt Fronto Parieto Temporal with midline shift supratentorial 80 YES 1 6

35 Narayanan 67 M Brainstem Pons infratentorial 15 NO 1 636 Lavanya 60 F Brainstem Pons infratentorial 20 NO 3 437 Jayammal 67 F cerebellum cerebellum infratentorial 15 NO 5 238 Ramesh 36 M Lobar Rt Fronto Parietal with midline shift supratentorial 60 NO 1 639 Ibrahim 72 M Lobar Lt Parietal supratentorial 35 NO 3 440 Ganesan 64 M capsuloganglionic Putamen supratentorial 40 NO 3 441 Raman 66 M Capsulo ganglionic Lt thalamic supratentorial 10 NO 5 142 Munusamy 68 M capsuloganglionic Caudate supratentorial 20 NO 3 443 Kamatchi 58 F Capsuloganglionic Rt internal capsule supratentorial 10 YES 1 644 Solai 62 F Capsuloganglionic Rt internal capsule supratentorial 15 NO 5 145 Abdul Ahamed 48 M capsuloganglionic Lt thalamic bleed supratentorial 10 NO 1 646 Purusothaman 63 M Lobar Lt pareital supratentorial 25 NO 3 447 Muthu 78 M lobar Lt parietal supratentorial 40 YES 1 648 Joseph 55 M Capsuloganglionic Rt internal capsule supratentorial 10 NO 3 449 Chittu 66 F capsuloganglionic Thalamus supratentorial 30 NO 3 450 Anandan 70 M Lobar Lt parietal supratentorial 45 NO 3 451 Nagammal 74 F lobar Rt Frontal supratentorial 25 NO 3 4


tentorialICH


Out come MRS

52 Murugesh 68 M mixed Rt Fronto Parietal with midline shift supratentorial 65 YES 2 553 Pugalendhi 54 M capsuloganglionic Internal capsule supratentorial 30 NO 5 254 Ponnammal 69 F capsuloganglionic Subthalamus and putamen supratentorial 45 NO 5 155 Govindaraj 57 M Brainstem Pons infratentorial 10 NO 1 656 Sekar 38 M lobar Rt Fronto Parietal with midline shift supratentorial 65 YES 1 657 Selvam 78 M cerebellum cerebellum infratentorial 60 NO 5 158 Thangam 65 F lobar Lt parietal supratentorial 30 YES 2 559 Velu 66 M Brainstem Pons infratentorial 70 NO 1 660 Kanniyammal 68 F lobar Rt Parietal supratentorial 20 NO 4 3

Documents

A STUDY OF CLINICAL AND RADIOLOGICAL PROFILE IN …repository-tnmgrmu.ac.in/4970/1/200100216bharani.pdf · dissertation on “A Study of clinical and radiological profile in patients