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:
Frequency Percentage
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):
Frequency Percentage
< 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:
Frequency Percentage
<= 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
Frequency Percentage
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
Frequency Percentage
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.
23.3% had lethal outcome with MRS 4.
21.7% had lethal outcome with MRS 3.
3.3% had lethal outcome with MRS 2.
20% had lethal outcome with MRS 1.
46
GOS at discharge
Outcome MRS 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
Outcome MRS at discharge
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%
Total Count 28 19 13 60
% 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%
Total Count 28 19 13 60
% 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.
Among patients with blood pressure with Mean Arterial Pressure
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
Among patients with blood pressure with Mean Arterial Pressure
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
Among patients with blood pressure with Mean Arterial Pressure
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 .
BIBLIOGRAPHY
1. Qureshi Al, Tuhrim ST, Broderick JP, Batjer HH, Hondo H
Hanley DF. Spontaneous intracerebral hemorrhage. N Engl J Med
2001;344:1450-60.
2. Zhang LF, Yang J, Hong Z, Yuan GG, Zhou BF, Zhao LC, et al.
For the collaborative group of China multicentre study of
cardiovascular epidemiology. Proportion of different types of
subtypes of stroke in China. Stroke 2003;34:2091-6.
3. Fogelholm R, Nuutila M, Vuorela AL. Primary intracerebral
hemorrhage in the Jyvaskyla region, Central Finland, 1985-89:
Incidence, case fatality rate, and functional outcome. J Neurol
Neurosurg Psychiatry 1992;55:546-52.
4. Waga S, Miyazaki M, Okada M, Tochio H, Matsushima S,
Tanaka Y. Hypertensive putaminal hemorrhage: Analysis of 182
patients. Surg Neurol 1986;26:159-66.
5. Calandre L, Arnal C, Ortega JF, Bermejo F, Felgeroso B, del
Ser T, et al. Risk factors for spontaneous cerebral hematomas:
Case-control study. Stroke 1986;17:1126-8.
6. Gorelick PB. The status of alcohol as a risk factor for stroke.
Stroke 1989;20:1607-10.
7. Fogelholm R, Eskola K, Kiminkinen T, Kunnamo
I. Anticoagulant treatment as a risk factor for primary
intracerebral hemorrhage. J Neurol Neurosurg Psychiatry
1992;55:1121-4.
8. Antiplatelet Trialists’ Collaboration. Collaborative overview of
randomised trials of antiplatelet therapy, I: Prevention of death,
myocardial infarction, and stroke by prolonged antiplatelet
therapy in various categories of patients. BMJ 1994;308:81-106.
9. De Jaegere PP, Arnold AA, Balk AH, Simoons ML. Intracranial
hemorrhage in association with thrombolytic therapy: Incidence
and clinical predictive factors. J Am Coll Cardiol 1992;19:
289-94.
10. Fogelholm R, Murros K. Cigarette smoking and risk of primary
intracerebral haemorrhage: A population-based case-control
study. Acta Neurol Scand 1993;87:367-70.
11. MacKay J, Mensah GA. Global Burden of Stroke. In: MacKay J,
Mensah GA. The Atlas of Heart Disease and Stroke. Geneva:
World Health Organization; 2004; p. 50-51.
12. Robert G. Hart, Bradley S. Boop, David C. Anderson. Oral
Anticoagulants and Intracranial Hemorrhage. Stroke. 1995; 26:
1471-7.
13. Schievink WI. Intracranial aneurysms. N Engl J Med. 1997;
336:28-40.
14. Gebel JM, Broderick JP. Intracerebral hemorrhage. Neurol Clin.
2000; 18: 419-38.
15. Viswanathan A, Greenberg SM. Cerebral amyloid angiopathy in
the elderly. Ann Neurol. 2011; 70:871.
16. Lovelock CE, Molyneux AJ, Rothwell PM, Oxford Vascular
Study. Change in incidence and aetiology of intracerebral
haemorrhage in Oxfordshire, UK, between 1981 and 2006: a
population-based study. Lancet Neurol. 2007; 6: 487.
17. Ariesen MJ, Claus SP, Rinkel GJ, et al. Risk factors for
intracerebral hemorrhage in the general population: a systematic
review. Stroke. 2003; 34:2060.
18. Robert G. Hart, Bradley S. Boop, David C. Anderson. Oral
Anticoagulants and Intracranial Hemorrhage. Stroke. 1995; 26:
1471-7.
19. Schievink WI. Intracranial aneurysms. N Engl J Med.
1997;336:28-40.
20. Jonathan L. Brisman, Joon K. Song, David W. Newell. Cerebral
aneurysms. N Engl J Med. 2006;355:928-39.
21. Garcia JH, Ho KL. Pathology of hypertensive arteriopathy.
Neurosurg Clin N Am 1992; 3:497.
22. Hamaguchi T, Yamada M. Genetic factors for cerebral amyloid
angiopathy. Brain Nerve. 2008 Nov; 60(11):1275-83.
23. Beslow LA, Licht DJ, Smith SE, et al. Predictors of outcome in
childhood intracerebral hemorrhage: a prospective consecutive
cohort study. Stroke 2010; 41: 313.
24. Brott T, Broderick J, Kothari R, et al. Early hemorrhage growth in
patients with intracerebral hemorrhage. Stroke. 1997;28:1-5.
25. Kazui S, Naritomi H, Yamamoto H, et al. Enlargement of
spontaneous intracerebral hemorrhage: incidence and time course.
Stroke. 1996;27:1783-7.
26. Kazui S, Minematsu K, Yamamoto H, et al.
27. Predisposing factors to enlargement of spontaneous intracerebral
hematoma. Stroke. 1997;28:2370-5.
22. Becker KJ, Baxter AB, Bybee HM, et al. Extravasation of
radiographic contrast is an independent predictor of death in
primary intracerebral hemorrhage. Stroke. 1999; 30:2025-32.
28. Ohwaki K, Yano E, Nagashima H, et al. Blood pressure
management in acute intracerebral hemorrhage: relationship
between elevated blood pressure and hematoma enlargement.
Stroke. 2004; 35:1364-7.
29. Toyoda K, Okada Y, Minematsu K, et al. Antiplatelet therapy
contributes to acute deterioration of intracerebral hemorrhage.
Neurology. 2005; 65: 1000-04.
30. Yasaka M, Minematsu K, Naritomi H, et al. Predisposing factors
for enlargement of intracerebral hemorrhage in patients treated
with warfarin. Thromb Haemost. 2003; 89: 278-83.
31. Flibotte JJ, Hagan N, O’Donnell J, et al. Warfarin, hematoma
expansion, and outcome of intracerebral hemorrhage. Neurology.
2004; 63: 1059-64.
32. Elliott J, Smith M. The acute management of intracerebral
hemorrhage: a clinical review. Anesth Analg. 2010; 110(5):
1419-27.
33. Rincon F, Mayer SA. Clinical review: Critical care management
of spontaneous intracerebral hemorrhage. Critical Care. 2008;
12: 237.
34. Broderick J, Connolly S, Feldmann E., et al. Guidelines for the
management of spontaneous intracerebral hemorrhage in adults:
2007 update: a guideline from the American Heart Association/
American Stroke Association Stroke Council, High Blood
Pressure Research Council, and the Quality of Care and
Outcomes in Research Interdisciplinary Working group. Stroke.
2007; 38: 2001-23.
35. Tiebosch, I.A.C.W.. Effects of anti-inflammatory treatments on
stroke outcome in animal models. Geneeskunde Proefschriften,
2012.
36. Wada, R., Aviv, RI., Fox, AJ., et al. CT Angiography “Spot Sign”
Predicts Hematoma Expansion in Acute Intracerebral
Hemorrhage. Stroke. 2007; 38(4):1257-62.
37. Sahni R, Weinberger J. Management of intracerebral hemorrhage.
Vasc Health Risk Manag. 2007 October; 3(5): 701-9.
38. Mayer, SA.; Chong, JY. Critical care management of increased
intracranial pressure. Journal of Intensive Care Medicine. 2002;17
(2):55-67.
39. Nor AM., Davis J., Sen B. et al. The recognition of stroke in the
emergency room (ROSIER) scale: development and validation of
a stroke recognition. Lancet Neruology. 2005;4: 727-34.
40. Yew, KS., Cheng, E. Acute stroke diagnosis. American Family
Physician, 2009; 80(1): 33-40.
41. Djulbegovic B, Loughran TP Jr, Hornung, CA et al. The quality
of medical evidence in hematology-oncology. Am J Med. 1999;
106(2): 198-205.
42. Yew, KS., Cheng, E. Acute stroke diagnosis. American Family
Physician, 2009; 80(1): 33-40.
43. Nentwich, LM., Veloz, W. Neuroimaging in acute stroke.
Emergency Medicine North America. 2012; 30: 659-80.
44. Wada, R., Aviv, RI., Fox, AJ., et al. CT Angiography “Spot Sign”
Predicts Hematoma Expansion in Acute Intracerebral
Hemorrhage. Stroke. 2007; 38(4):1257-62.
45. Delgado Almandoz, JE., Kelly HR., Schaefer, PW., et al. CT
angiography spot sign predicts in-hospital mortality in
patients with secondary intracerebral hemorrhage. Journal of
NeuroInterventional Surgery. 2012; 4(6): 442-7.
46. Brouwers, HB., Falcone, GJ., McNamara, KA., et al. CTA Spot
Sign Predicts Hematoma Expansion in Patients with Delayed
Presentation After Intracerebral Hemorrhage. Neurocritical Care.
2012; 17(3): 421-428.
47. Delgado Almandoz, JE., Yoo, A. J., Stone, M. J., et al. The Spot
Sign Score in Primary Intracerebral Hemorrhage Identifies
Patients at Highest Risk of In-Hospital Mortality and Poor
Outcome Among Survivors. Stroke. 2009; 41(1): 54-60.
48. Stone, CK., Humphries, RL. Current Diagnosis & Treatment
Emergency Medicine 7e. McGraw-Hill Companies. 2011
49. Kazui S, Naritomi H, Yamamoto H, et al. Enlargement of
spontaneous intracerebral hemorrhage: incidence and time course.
Stroke. 1996;27:1783-7.
50. Kazui S, Minematsu K, Yamamoto H, et al. Predisposing factors
to enlargement of spontaneous intracerebral hematoma. Stroke.
1997;28:2370-5.
51. Davis SM, Broderick J, Hennerici M, et al. Recombinant
Activated Factor VII Intracerebral Hemorrhage Trial
Investigators. Hematoma growth is a determinant of mortality and
poor outcome after intracerebral hemorrhage. Neurology. 2006;
66: 1175-81.
52. Alvarez-Sabin J, Delgado P, Abilleira S, et al. Temporal Profile
of Matrix Metalloproteinases and Their Inhibitors After
Spontaneous Intracerebral Hemorrhage: Relationship to Clinical
and Radiological Outcome. Stroke. 2004; 35: 1316-22.
53. Hemphill JC III, Bonovich DC, Besmertis L, et al. The ICH score:
a simple, reliable grading scale for intracerebral hemorrhage.
Stroke. 2001; 32(4): 891-7.
54. Rost NS, Smith EE, Chang Y, et al. Prediction of functional
outcome in patients with primary intracerebral hemorrhage: the
FUNC score. Stroke 2008; 39(8): 2304-9.
55. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines
for the management of spontaneous intracerebral hemorrhage: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. Sep 2010;
41(9): 2108-29.
56. Fogelholm R, Murros K, Rissanen A, et al. Long term survival
after primary intracerebral haemorrhage: a retrospective
population based study. J Neurol Neurosurg Psychiatry. 2005; 76:
1534-8.
57. Leira R, Davalos A, Silva Y, et al. Stroke Project,
Cerebrovascular Diseases Group of the Spanish Neurological
Society. Early neurologic deterioration in intracerebral hemor-
rhage: predictors and associated factors. Neurology. 2004; 10(63):
461-7.
58. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines
for the management of spontaneous intracerebral hemorrhage: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. Sep 2010;
41(9): 2108-29.
59. Huttner HB, Schellinger PD, Hartmann M, et al. Hematoma
growth and outcome in treated neurocritical care patients with
intracerebral hemorrhage related to oral anticoagulant therapy:
comparison of acute treatment strategies using vitamin K, fresh
frozen plasma, and prothrombin complex concentrates. Stroke.
Jun 2006; 37(6): 1465-70.
60. Boulis NM, Bobek MP, Schmaier A, et al. Use of factor ix
complex in warfarin-related intracranial hemorrhage.
Neurosurgery. 1999; 45: 1113–18.
61. Martins SCO, deFreitas GR, Pontes-Neto OM et al. Guidelines
for acute ischemic stroke treatment – Part II: Stroke treatment.
Arq Neuropsiquiatr. 2012; 70(11): 885-93.
62. Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure
reduction in acute cerebral haemorrhage trial (INTERACT): a
randomised pilot trial. Lancet Neurol. 2008;7:391-9.
63. Anderson CS, Heeley E, Huang Y, et al. Rapid Blood-Pressure
Lowering in Patients with Acute Intracerebral Hemorrhage. New
England Journal of Medicine. 2013.
64. Clinical and neuroimaging studies in patients with acute
spontaneous intracerebral hemorrhage. Maya P. Danovska1,
Margarita L. Alexandrova2, Nachko I. Totsev3, Irena
I.Gencheva4, Plamen G. Stoev1 Journal of IMAB - Annual
Proceeding (Scientific Papers) 2014, vol. 20, issue 2.
65. Etiology and outcome determinants of intracerebral hemorrhage
in a south Indian population, A hospital-based study. Sunil K.
Narayan, P. Sivaprasad1, Sharma Sushma, Ratnakar K. Sahoo1,
Tarun Kumar Dutta1, Ann Indian Acad Neurol 2012;15:263-6.
66. Arboix A, Massons J, Garcia-Elores J, Oliveres M, Targa C.
Diabetes is an independent risk factor for in hospital mortality
from acute spontaneous intracerebral hemorrhage. Diabetes Care
2000;23:1527-32.
67. Neuroinflammation after intracerebral hemorrhage: Eva
Mracsko1 and Roland Veltkamp Neurosci., 20 November 2014
68. Caveolin-1 deletion reduces early brain injury after experimental
intracerebral hemorrhage: Chang CF1, Chen SF, Lee TS, Lee HF,
Chen SF, Shyue SK., Am J Pathol. 2011 Apr;178(4):1749-61.
doi: 10.1016/j.ajpath.2010.12.023.
69. PREDICTORS OF HIGHLY PREVALENT BRAIN ISCHEMIA
IN INTRACEREBRAL HEMORRHAGE: Ravi S. Menon, et al.
Ann Neurol. Author manuscript; available in PMC 2013 Feb 1.
70. Acute brain infarcts after spontaneous intracerebral hemorrhage: a
diffusion-weighted imaging study: Prabhakaran S1, Gupta R,
Ouyang B, John S, Temes RE, Mohammad Y, Lee VH, Bleck
TP.. Stroke. 2010 Jan;41(1):89-94. doi: 10.1161/ STROKEAHA.
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
S NO NAME age sexCo morbid conditions
Alcohol consumption
< 48 hrsSBP DBP MAP Presentation
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
S NO NAME age sexCo morbid conditions
Alcohol consumption
< 48 hrsSBP DBP MAP Presentation
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
S NO NAME age sex ICH location location specficSupra / infra
tentorialICH
volume IVH GOS at dicharge
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
S NO NAME age sex ICH location location specficSupra / infra
tentorialICH
volume IVH GOS at dicharge
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
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