STUDY ON FACTORS INVOLVING EARLY NEUROLOGICAL DETERIORATION IN PATIENTS WITH ACUTE ISCHEMIC STROKE
WITH EMPHASIS ON BLOOD UREA NITROGEN/CREATININE RATIO AS PREDICTORS OF EARLY NEUROLOGICAL
DETERIORATION.
DISSERTATION SUBMITTED TO THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY, CHENNAI In partial fulfilment of the requirements for the degree of
M.D. BRANCH – I (GENERAL MEDICINE) Registration No.: 201711368
DEPARTMENT OF GENERAL MEDICINE TIRUNELVELI MEDICAL COLLEGE HOSPITAL
TIRUNELVELI – 627011 MAY-2020
BONAFIDE CERTIFICATE
This is to certify that the dissertation entitled “STUDY ON FACTORS INVOLVING EARLY NEUROLOGICAL DETERIORATION IN PATIENTS WITH ACUTE ISCHEMIC STROKE WITH EMPHASIS ON BLOOD UREA NITROGEN/CREATININE RATIO AS PREDICTORS OF EARLY NEUROLOGICAL DETERIORATION.”submitted byDr. J.SIVA RAM KUMAR , to the Tamilnadu Dr. M.G.R Medical University, Chennai, in partial fulfillment of the requirement for the award of M.D. Degree Branch – I (General Medicine) is a bonafide research work carried out by her under direct supervision & guidance.
Professor & Head of the Department, Department of General Medicine
Tirunelveli Medical College, Tirunelveli.
Unit Chief,
Department of General Medicine Tirunelveli Medical College,
Tirunelveli.
CERTIFICATE BY THE DEAN
I hereby certify that this dissertation entitled “STUDY ON FACTORS INVOLVING EARLY NEUROLOGICAL DETERIORATION IN PATIENTS WITH ACUTE ISCHEMIC STROKE WITH EMPHASIS ON BLOOD UREA NITROGEN/CREATININE RATIO AS PREDICTORS OF EARLY NEUROLOGICAL DETERIORATION.” is a record of work done by Dr. J SIVA RAM KUMAR , in the Department of General Medicine, Tirunelveli Medical College, Tirunelveli, during her postgraduate degree course period from 2017- 2020. This work has not formed the basis for previous award of any degree.
Date :
Place : TIRUNELVELI The DEAN
Tirunelveli Medical College, Tirunelveli - 627011.
DECLARATION
I solemnly declare that the dissertation entitled “STUDY ON FACTORS INVOLVING EARLY NEUROLOGICAL DETERIORATION IN PATIENTS WITH ACUTE ISCHEMIC STROKE WITH EMPHASIS ON BLOOD UREA NITROGEN/CREATININE RATIO AS PREDICTORS OF EARLY NEUROLOGICAL DETERIORATION.” is done by me at Tirunelveli Medical College Hospital, Tirunelveli Under the guidance and supervision ofProf.Dr.A.SENTHAMARAI M.D, the dissertation is submitted to The TamilnaduDr. M.G.R. Medical University towards the partial fulfilment of requirements for the award of M.D. Degree (Branch I) in General Medicine.
Place: Tirunelveli
Date: Dr.J.SIVA RAM KUMAR
Registration No.: 201711368 Postgraduate Student, M.D General Medicine, Department of General Medicine,
Tirunelveli Medical College Tirunelveli.
CERTIFICATE – II
This is to certify that this dissertation work entitled “STUDY ON FACTORS INVOLVING EARLY NEUROLOGICAL DETERIORATION IN PATIENTS WITH ACUTE ISCHEMIC STROKE WITH EMPHASIS ON BLOOD UREA NITROGEN/CREATININE RATIO AS PREDICTORS OF EARLY NEUROLOGICAL DETERIORATION”of the candidate Dr.J.SIVA RAM KUMAR with registration Number 201711368 for the award of M.D.Degreein the branch of GENERAL MEDICINE (I). I personally verified the urkund.com website for the purpose of plagiarism check.
I found that the uploaded thesis file contains from introduction to conclusion page and result shows5 percentageof plagiarism in the dissertation.
Guide & Supervisor sign with Seal.
ACKNOWLEDGEMENT
I wish to express my heartfelt gratitude to our Dean Prof.Dr. S. M. .Kannan M.S., MCh., Tirunelveli Medical College for allowing me to do the
study in this institution.
I would like to express my humble thanks to our professor & Head of the Department Prof .Dr .M.Ravichandran M.D., Department of General Medicine.
I express my sincere thanks to my renowned teacher and my guide , Prof.Dr.A.SENTHAMARAI M.DProfessor, Department of General Medicine, Tirunelveli Medical College for his guidance, valuable suggestions and constant encouragement throughout the study.
I express my sincere thanks to my EX professorsDr.S.Arumugapandian
@ Mohan,M.D., for their constant support, encouragement and suggestions which helped me greatly to expedite this dissertation .
I am greatly obliged to Dr.Marchwin Kingston,M,D, Dr.Madhavan.
M.D., DR. Shavana M.D., DR. Pattu Swarnalatha .M.D., Dr.Sheik Mohammed Raja.M.D., Dr.Annie Antony .M.D., Dr.Thanalakhsmi. .M.D., Dr.Narayanan .M.D Assistant Professors, Dept. of General Medicine for their valuable suggestions in preparing this dissertation.
CONTENT
S.NO TITLE PAGE.NO
1. INTRODUCTION 1
2. AIM AND OBJECTIVES OF THE STUDY 8
3. REVIEW OF LITERATURE 9
4. MATERIALS AND METHODS 48
5. RESULTS 50
6. DISCUSSION 75
8. CONCLUSION 77
9. LIMITATIONS OF THE STUDY 78
10. BIBILIOGRAPHY 11. MASTER CHART
12. PROFORMA
LIST OF TABLES
S.NO TITLE PAGE
NO
1 NIHSS SCORE FORMAT 3
2 MODIFIED RANKIN SCALE 46
3 AGE CATEGORY OF PATIENTS 51
4 SEX DISTRIBUTION 54
5 GLASCOW COMA VS END WITH CHI SQUARE
TEST 56
6 NIHSS AT TIME OF ADMISSION VS END WITH
CHISQUARE TEST 58
7 RANDOM BLOOD SUGAR VS END WITH CHI
SQUARETEST 60
8 DM VS END ,WITH CHISQUARE TEST 62
9 HBA1C VS END WITH CHI square test 63
10 BLOOD PRESSURE VS END WITH ITS CHI
SQUARE TEST 66
11 BUN/CREATININE RATIO VS END WITH ITS
CHISQUARE TEST 68
12 URINE SPECIFIC GRAVITY VS END 70
13 CT TERRITORRY VS END 72
14 CT EDEMA VS END 74
ABBREVIATIONS END-Early neurological deficit
GCS-glascow coma scale DM-Diabetes mellitus CT-Computed tomography RBS-Random blood sugar
NIHSS-National institute of health stroke scale BUN-Blood urea nitrogen
ATP-Adenosine tri phosphate OSA-Obstructive sleep apnea
INTRODUCTION
Stroke ,with its high mortality and morbidity rate,is a major health issue in India.Only few cases present to the emergency department with in window period of 4.5hours,also very few cases come to medical attention with in 24 hours ,especially in India.Patient presenting with early needs attention so that the neurological deficit does not worsens as hours go by. Early neurological deterioration[5] is defined as worsening of neurological status as shown by increase of three or more points in the NIHSS score or death not due to other cause, with in the first three days. NIHSS Score is a tool which health Care providers can quantify the deficit /disability caused by stroke. NIHSS score has 11 components, each having a score of 0 to 4.Maximum score is 42 for any patient, higher the score more severe is the stroke. This tool can be used to monitor and follow up to assess progressing worsening of deficits. Hence can be used to detect Early Neurological deficit in acute stroke patients.
There are various factors that play a role in early neurological deterioration like presence of diabetes mellitus, extent of territory involved in NCCT, presence of edema around infarct, serum osmolality, NIHSS score at time of admission ,GCS at time of admission, hyperglycemia ,blood pressure[25,26].Patient of stroke mostly have some extent of depressed consciousness, dependant on others for daily activities, hence patient are unable to say adequately hydrated. In this study, role of dehydration in causing early deterioration of deficits is given
importance and it can be assessed by BUN/Creatinine ratio ,urine specific gravity etc. This particular aspect may have a play role in deciding the initial resuscitation of stroke patients. Also in this study the factors already mentioned are also put to test and their significance is reassessed in this limited study. The findings in thisstudy may help doctors in identifying the stroke patients who are at high risk of early worsening of neurological stability.
NIHSS SCORE
It is the quantitative way of measuring the severity of the stroke. Also helps in understanding the possible outcome of stroke in a patient. In NISS more severe the score more severe is the patient affected by the stroke. This scale has totally 11 parameters to be looked for. Each parameter can have a score of 0 to 4 range,0 being less severe and 4 being the most severe. This score helps in monitoring the progression of the disability, hence this scoring scale is being used in our study in monitoring the deterioration of stroke patients to detect Early neurological deterioration
NIHSS STROKE SCALE[2,22]
Category Score Description Date/Time
Initials Date/Time
Initials Date/Time
Initials Date/Time Initials 1a. Level of
consciousness: 0 = Alert;
1 = Not alert, but arousable by minor stimulation to obey, answer, or respond 2 = Not alert, requires repeated stimulation to attend, or is obtunded and requires strong or painful stimulation to make movements (not stereotyped)
3 = Responds only with reflex motor or autonomic effects or
is totally
unresponsive, flaccid, or areflexic
1b. Level of consciousness questions:
0 = Answers both questions correctly 1 = Answers one question correctly 2 = Answers neither question correctly 1c. Level of
consciousness commands:
0 = Performs both tasks correctly
1 = Performs one task correctly
2 = Performs neither task correctly
2. Best gaze: 0 = Normal
1 = Partial gaze palsy;
gaze is abnormal in one or both eyes, but
forced deviation or total gaze paresis is not present.
2 = Forced deviation, or total gaze paresis not overcome is by the oculocephalic maneuver
3. Visual: 0 = No visual loss
1 = Partial
hemianopia
2 = Complete hemianopia
3 = Bilateral hemianopia (blind including cortical blindness)
4. Facial
palsy: 0 = Normal
symmetrical movements
1 = Minor paralysis (flattened nasolabial fold, asymmetry on smiling)
2 = Partial paralysis (total or near-total paralysis of lower face)
3 = Complete paralysis of one or both sides (absence of facial movement in the upper and lower face)
5. Motor arm: 0 = No drift;
1 = Drift;
2 = Some effort against gravity;
3 = No effort against
Left
Right
gravity;
4 = No
movement
UN =
Amputation or joint fusion 5a. Left Arm 5b. Right Arm 6. Motor leg: 0 = No drift;
leg holds 30°
position for full 5 seconds 1 = Drift; leg falls by the end of the 5- second period but does not hit bed
2 = Some effort against gravity; leg falls to bed by 5 seconds, but
has some
effort against gravity
3 = No effort against
gravity, leg falls to bed immediately
4 = No
movement
UN =
Amputation, joint fusion 6a. Left Leg 6b. Right Leg
Left
Right
7. Limb
ataxia: 0 = Absent
1 = Present in one limb
2 = Present in two limbs
UN = Amputation or joint fusion
8. Sensory: 0 = Normal; no sensory loss.
1 = Mild to moderate sensory loss; patient feels pinprick is less sharp or is dull on the affected side or there is a loss of superficial pain with pinprick but patient is aware he/she is being touched
2 = Severe to total sensory loss; patient is not aware of being touched in the face, arm, and leg
9. Best
language: 0 = No aphasia;
1 = Mild to moderate aphasia;
2 = Severe aphasia; a 3 = Mute;
10. Dysarthria 0 = Normal
1 = Mild to moderate;
patient slurs at least some words and, at worst, can be understood with some difficulty
2 = Severe; patient’s speech is so slurred as to be unintelligible in the absence of or out of proportion to any dysphasia, or is mute/anarthric
UN = Intubated or
other physical barrier 11. Extinction
andinattention (formerly neglect):
0 = No abnormality 1 = Visual, tactile, auditory, spatial, or personal inattention or extinction to bilateral simultaneous stimulation in one of
the sensory
modalities
2 = Profound hemi- inattention or hemi- inattention to more than one modality;
does not recognize own hand or orients to only one side of space
AIMS AND OBJECTIVES
1. To investigate about the factors involved in early neurological deterioration in acute ischemic stroke
2. Special emphasis on role of blood urea nitrogen/creatinine ratio as predictors of early deterioration of neurological status in acute ischemic stroke
REVIEW OF LITERATURE
The term “STROKE” is defined as acute neurological deficit (focal generally or Global rarely) ,when there is occlusion or rupture of blood vessels supplying the brain causing decreased brain parenchymal perfusion.
EPIDEMIOLOGY
Most of the stroke are ischemic in nature. Based on regional studies in India, prevalence rate of stroke in india is found to be 40-470/100000.This wide variation is due to small sample size of these regional datas. Roughly 3% of adult population are affected annually in United states. There is no clear data to know about the proportion of ischemic and hemorrhagic stroke in India, but majority study shows ischemic stroke as the predominant stroke category. The prevalence of stroke is rising consistently compared to the western world. Das et al found the prevalence rate of stroke based on kolkatta stroke registry is 472/100000[3].This study is one of the largest survey done in india .Based on the kolkatta study ,the case fatality rate 41.08% is significantly higher that western world(men 38.18% and women 43.24%).In US fatality rate is from 10- 15%.This data indicates that incidence,prevalence and mortality of stroke are higher in India than developed countries
PATHOPHYSIOLOGY
The pathophysiology of ischemic stroke can be best understood by knowing events taking place in “ischemic core”. This region shows diminished blood flow which causes diminished metabolism of oxygen and glucose. Sequence of
events occurs including breakdown of cellular integrity, ionic imbalance, neurotransmitter mediated excitiotoxicity, overload of certain ions like calcium, mitochondrial dysfunction and apoptosis. There is total bioenergetic failure, ion homeostasis disruption, lipolysis resulting ultimately in cell death within minutes and hours. Ischemic penumbra is region of brain tissue that is functionally impaired but structurally intact. Resting membrane potential is maintained in this penumbra, action potential is restored once when collateral flow improves.
MOLECULAR BASIS:
The knowledge of the molecular basis of stroke give us understanding about the most important aspect of the stroke therapy. Normal CBF is between 45-60 ml blood/100g/min. Neuronal injury is dependent on flow and time. At CBF below 18 ml/100g/min, tissue infarction is time dependent. CBF of 5ml/100g/min lasting about 30mins causes infarction, CBF of 10ml/100g/min needs to last more than 3 hrs to cause infarction. Irreversible damage occurs if CBF below 18ml/100g/min permanently. If CBF falls to zero within seconds
causes loss of consciousness after approximately 10 seconds, eeg activity cease after 30-40 secs, cellular damage is iniated after a few minutes and death occurs within 10 minutes. The glucose and oxygen deficit occurs after severe vascular occlusion is the origin of the mechanisms that leads to cell death and cerebral injury. Main source of ATP generation and it is irreplaceable. Reduced ATP activates glycolytic metabolism causing an accumulation of protons and lactate, leads to rapid intracellular acidification. Further deficiency of glucose &
oxygen, sets vicious cycle and consumes residual ATP stores. Results in Na+/k+ ATPase failure leading to excessive calcium influx causing profound loss of ionic gradient across membrane and uncontrolled depolarization.
Excessive release of neurtrasmitter in synapse specially glutamate leads to neuronal insult called excitotoxicity by activating the ionotropic glutamate receptors at a pathophysiological level . Excitotoxicity is defined as cell death occurs due to toxic actions of excitatory amino acid. Results in alteration of mitochondrial function. Also causes oxidative stress by releasing reactive oxygen species and reactive nitrogen species.
Role of mitochondria has been underestimated in pathophysiology of ischemic stroke. The signaling pathways of glutamate excitotoxicity are shown below in the picture. Excessive calcium influx causes mitochondrial injury leading to ROS generation, mitochondrial induced apoptosis of neuronal cells, mitophagy, DNA damage and eventually in to cellular death.
RISK FACTORS:
Risk factors of ischaemic stroke can be divided into modifiable and non-modifiable. Acquired causes are usually falls under modifiable factor, includes those resulting from lifestyle choices, environmental which can be modified by health care professionals, treatment and proper education about the risk factors. Non-modifiable risk factors encompass factors related to hereditary or natural processes and cannot be modified .
NON MODIFIABLE MODIFIABLE
AGE
SEX
RACE
HEREDITY
SMOKING
ALCOHOL
HYPERTENSION
DIABETES MELLITUS
DYLIPIDEMIA
CORONARY HEART DISEASE
OBESITY
HYPERCOAGULABLE DISORDERS
NON-MODIFIABLE RISK FACTORS:
AGE:
Increasing age is the single most risk factor for stroke. More commonly occurs in people aged >45yrs accounts for about 95% of cases. And two-third of case occurs in people aged over 65 yrs
SEX:
Men have approximately 19% higher risk of stroke than women particularly in old age and have high mortality rate. In atherosclerosis risk in communities study the relative risk for all ischaemic subtypes was higher in men than in women.
RACE AND HEREDITARY:
Blacks have more incidence and prevalence of stroke compared to whites.
Genetics also plays a role in the prevalence of stroke and coronary heart disease.
MODIFIABLE RISK FACTORS:
SMOKING:
Smoking is an independent risk factors of ischaemic stroke.
According to Framingham heart study, relative risk of stroke is dose dependent.
Heavy smokers >40/day was twice that of light smokers >10 /day. consistent for all smoking. The reduction in risk ratio was significant by 2 years of cessation and reached the level of non smoker at 5 years. Smoking leads to endogenous fibrinolysis and reduced blood flow in the brain which results in vasoconstriction.
ALCOHOL CONSUMPTION:
Alcohol consumption increases the risk of stroke. There is J shaped association between alcohol consumption and ischaemic stroke. In light and moderate drinkers (upto 1drink/day for women and 2 drinks /days) plays a protective effect . But the risk increases with further alcohol intake. Protective effects in moderate consumption probably due to increased levels of HDL- C,apolipoprotein A1,and adiponectin. Heavy alcohol consumption may elevate stroke risk by increasing risks of hypertension, atrial fibrillation, cardiomyopathy and diabetes mellitus.
HYPERTENSION:
Strongest modifiable risk factor for ischaemic stroke in middle and old age. All the organs are vulnerable to consequences of hypertension.
ccording to JNC 8,hypertension is defined as systolic blood pressure more or equal to 140mmHg or a diastolic blood pressure more or equal to 90mmHg.
The prevalence of hypertension is approximately 60-70% among patients with a recent ischaemic stroke. The reduction of blood pressure after first stroke or TIA reduces the risk of stroke in future.
DIABETES MELLITUS:
Potent risk factor for stroke and are accountable for more than 8% of first ischaemic stroke. The principle disorders in diabetes spectrum is pre- diabetes, type 1 DM, type 2 DM. Prevalence of pre- DM in patients with ischaemic stroke is approximately 28% while for overt DM the prevalence is 25-45% . India has the world’s largest population of diabetes patients over 62 million people being reported in 2011. Diabetes and stroke risk is gender dependent; more prevalent in women. Diabetics causes small vessel disease and show a high occurrence of lacunes in subcortical region. Major pathological changes observed in diabetic stroke patients are endothelial proliferation and hyalinosis of small intraparenchymal vessels. Also influences the development of large artery atherosclerosis. patients with diabetic mellitus have a higher mortality rate, more severe disability and slower recovery from stroke than non –diabetic.
DYSLIPIDEMIA:
Dyslipidemia are also a potent modifiable risk factor for development of stroke. Modification of the LDL cholesterol(LDL-C)is an important step in the secondary prevention of ischaemic stroke. Other than LDL-C, raised serum triglyceride level, HDL level and elevated lipoprotein (a)level also associated with development of ischaemic stroke. Statin use shows reduction in the LDL-C level which subsequently decreases the risk of stroke.
According to THE STROKE PREVENTION BY AGGRESSIVE REDUCTION AND CHOLESTEROL LEVELS(SPARCL) trial ,achieving LDL-C level of <70mg/dl was related to a 28% reduction in the risk of recurrent ischaemic stroke .
OBESITY:
Obesity also plays an important risk factor for ischaemic stroke. Risk of development of stroke increases in a near-linear fashion starting at a BMI of 20 kg/m2. Each 1 kg/m2 increase in BMI is associated with the 5 %increase in risk for ischaemic stroke. More pronounced risk for stroke is associated with central obesity and middle aged adults. Factors associated with central obesity is endothelial dysfunction, an early marker for atherosclerotic disease as well as to other hemorrheological disorders such as hyperviscosity, hyperfibrinogenemia, reduced red cell deformability, and erythrocyte aggreability.
OBSTRUCTIVE SLEEP APNEA:
OSA present In about 50-75% patient presents with ischaemic stroke or TIA. It is diagnosed on the basis of apnea hypopnea index(AHI) with a cut off value of 5 per hour. AHI >5 indicates the increasing severity of OSA .in a meta analysis,72% of patients with stroke or TIA were found to have an AHI >5 events per hour, 63% having AHI >10/hour, and 38%having an AHI > 20 events/hour. Patients with stroke and OSA have poor functional outcome, higher mortality rates and psychiatric comorbidities. Presence of OSA in stroke patients shows poor prognosis. OSA have high risk of developing hypertension
and stroke. Below is the mechanism by which
hypertension develops in OSA and how it affects the health.
CORONARY HEART DISEASE:
Stroke caused by coronary heart disease is primarily due to embolism of thrombotic material forming on the atrial and ventricular wall or the left heart valves. Cardioembolism is responsible for approximately 20% of all ischaemic strokes. The most significant causes are,
Atrial fibrillation
Mural thrombus
Ischaemic cardiomyopathy
Rheumatic heart disease
Myocardial infarction
Prosthetic valves
Formed thrombi gets detached and embolize into the arterial circulation. the thrombus may fragment and lyse quickly, producing transient ischaemic attacks.
Similarly may last longer and produces stroke. Sudden maximum neurological deficit tends to occur with embolic strokes. Most common artery involved in embolic strokes are, intracranial carotid artery, the middle cerebral artery, the posterior cerebral artery or their branches. least common in anterior cerebral artery.
ATRIAL FIBRILLATION:
Atrial fibrillation accounts for about ~5% risk for the development of stroke.
The pathophysiology of stroke, is thrombus formation in the fibrillating atrium or atrial appendage, with subsequent embolization.
MYOCARDIAL INFARCTION:
Transmural MI involving anteroapical ventricular wall is considered as source of emboli for the development of stroke. Prophylactic anticoagulation following myocardial infarction shows reduction in the risk.
RHEUMATIC HEART DISEASE:
Rheumatic heart disease plays a risk for the development of stroke only when there is prominent mitral stenosis or atrial fibrillation.
BACTERIAL ENDOCARDITIS:
Septic emboli from bacterial endocarditis can be the risk for the development of stroke. Multifocal symptoms and signs in a patient with stroke makes bacterial endocarditis more likely.
HYPERCOAGULABLE DISORDER:
Increased risk of venous thrombi There by accounts for the risk of embolic stroke. Conditions involved are,
SLE with libman –sacks endocarditis
Homocysteinemia
Venous sinus thrombosis
Sickle cell anaemia
OTHER LEAST COMMON RISK FACTORS :
Fibromuscular dysplasia
Temporal arteritis
Necrotizing (or granulomatous ) arteritis
Primary central nervous system vasculitis
Moya moya disease
Drugs- cocaine, phenylpropanolamine, methamphetamine.
FIBROMUSCULAR DYSPLASIA
Often bilateral carotid involvement, coexisting vertebral artery disease, and, less commonly, disease in the external carotid, middle cerebral, anterior cerebral,
basilar, and anterior communicating arteries . Also associated with intracranial aneurysms
Image below shows the "string-of-beads" feature in multi-focal fibromuscular dysplasia. The sign is caused by areas of relative stenoses alternating with small aneurysms.
TEMPORAL ARTERITIS
Intracranial artery involvement is very rare. Infact vertebrobasilar system most commonly affected.
MOYA MOYA DISEASE
Chronic progressive cerebrovascular disease that causes occlusion of all arteries
around circle of willis, with development of multiple collaterals. Important cause of childhood stroke and young adult stroke
Diagnostic criteria for moya moya disease
JAPANESE RESEARCH COMMITTEE CRITERIA
Occlusion at the distal portion of the internal carotid artery and at the initial portion of the anterior and middle cerebral arteries on magnetic resonance angiography (MRA)
Abnormal vascular networks in the basal ganglia on MRA
Angiographic findings are present bilaterally;
EXCLUSION DIAGNOSIS FOR MOYA MOYA
A history of cranial irradiation
Arteriosclerosis
Meningitis
Brain neoplasm
Down syndrome
Head trauma
Neurofibromatosis
Autoimmune disease
Angiogram below extensive perforator colaterals giving the 'puff of smoke'characteristic of moya moya disease, and involving both anterior and posterior circulation.
CLINICAL FEATURES OF STROKES:
Symptoms of stroke depends upon affected brain region and arteries involved.
Most important feature of stroke is sudden onset. Except for rare circumstances, identification of stroke is relatively easy. Sudden onset of neurological deficit, peaking within a few minutes. 90% of strokes are supratentorial.
Common signs of supratentorial stroke, include contralateral hemiplegia with hemianopia accompanied with aphasia in left hemispheric infarction, hemispatial neglect in right hemispheric infarction. Small artery or lacunar
strokes present as pure motor hemiplegia, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis and dysarthria-clumsy hand syndrome.
Additional spectrum of symptoms seen in posterior circulation or strokes, these includes diplopia, bulbar palsy, dysphagia, incoordination, and sometimes reduced level of consciousness
Clinical features of stroke according to involved arterial territory:
INTERNAL CAROTID ARTERY:
Combined anterior cerebral artery syndrome and middle cerebral artery syndrome
Ipsilateral monocular visual loss
Ipsilesional altitudinal field cuts ANTERIOR CEREBRAL ARTERY :
Contralateral leg weakness
Transcortical motor aphasia (left ACA)
Ipsilesional or contralesional ideomotar apraxia
Motor neglect (right ACA) MIDDLE CEREBRAL ARTERY:
Contralateral face and arm weakness upper limb> lower limb
Aphasia(left MCA)
Ipsilateral gaze preference
Left hemispatial neglect(right MCA) POSTERIOR CEREBELLAR ARTERY:
Contralateral homonymous hemianopia
Alexia without agraphia(left PCA)
Weber syndrome
SUPERIOR CEREBELLAR ARTERY:
Ipsilesional limb and gait ataxia
ANTERIOR INFERIOR CEREBELLAR ARTERY:
Vertigo and ipsilesional deafness
POSTERIOR INFERIOR CEREBELLAR ARTERY:
Ipsilesional limb and gait ataxia
Wallenberg syndrome BASILAR ARTERY:
Impaired lateral gaze
Horizontal diplopia and dysconjugate gaze
Dysarthria
Locked in syndrome
CLASSIFICATION OF ISCHAEMIC STROKE:
A stroke classification facilitates acute therapy, secondary prevention, prognosis and research in stroke. Most widely used classification system at present for ischaemic stroke is TOAST classification (Trial of org 10172in acute stroke treatment). In this classification, Ischaemic strokes are classified basis of clinical features and investigations such as brain imaging (CT/MRI),proper evaluation for cardiac sources of stroke, vascular imaging, and laboratory assessments for prothrombotic conditions. These includes five broad categories,
Large artery atherosclerosis
Cardioembolism
Small artery occlusion (lacune)
Stroke of other determined aetiology
Stroke of undetermined aetiology
EVALUATION OF ISCHAEMIC STROKE:
CLINICAL APPROACH:
First step in the management of stroke establish the diagnosis.
All sudden onset neurological deficits are not strokes, stroke mimics condition which look like stroke. The etiology of stroke mimics variable and includes psycogenic, seizure ,migraine with aura, hypoglycaemia, wernicke’s encephalopathy, drug toxicity and others. 20% of all stroke presentations are stroke mimics. History taking and clinical examination is precious tool in neurology.90% stroke diagnosis can be achieved by proper history taking and physical examination. Following questions extracts the diagnostic points from
history,
Temporal course of the neurological deficit
Accompanying symptoms such as headache and vomiting
Presence of significant risk factors and family history
TEMPORAL COURSE OF THE NEUROLOGICAL DEFICIT:
Course of the illness gives clues for the probable mechanism of stroke. If the patient has rapid reversible deficit, it is likely to be a transient ischaemic attacks. Embolic strokes has maximum deficit at onset whereas thrombotic stroke may have stuttering course.
ACCOMPANYING SYMPTOMS:
Accompanying symptoms greatly influences the accuracy of probabilities.
Presence of seizure may complicate early course of embolic strokeor intracranial hemorrhage. Vomiting indicates posteriorly located hemorrhage, infarct or raised intracranial pressure. Loss of consciousness at onset indicates large hemorrhage, large volume infarct or involvement of brainstem.
PRESENCE OF SIGNIFICANT RISK FACTORS AND FAMILY HISTORY:
Presence of certain diseases and consumption of medicines helps in diagnostic possibilities and gives as better understanding of stroke mechanism. For example, if the patient is known case of hypertension, diabetes mellitus,
coronary artery disease the probabilities will be thrombotic stroke. While, if the patient is only hypertensive ,the probabilities are lacunar stroke, or hemorrhagic stroke. If the patient is had atrial fibrillation then the probabilities will be cardioembolic stroke.
CLINICAL EXAMINATION:
Clinical examination provides more information for the diagnosis of stroke. Starts with the observation of the level of consciousness, deviation of gaze ,position of limbs, any abnormal movements, and respiratory pattern.
Initial examination should be prompt ,it should not delay the administration of thrombotic therapy in eligible stroke patient. ABCs (airway, breathing and circulation) should be checked routinely. If level of consciousness is reduced, elective intubation is required. Should quickly assess the orientation, languagehemianopia, cranial nerves,motor sensory function and if possible check co-ordination also. Presence of cortical signs like aphasia and hemianopia suggest a stroke due to large artery occlusion. National institutes of health stroke scale(NIHSS) should be used for assessment of neurological deficit. Blood pressure monitoring should be done carefully and treated according to the guidelines particularly for those who eligible for intravenous rtPA (iv rtPA) therapy and whose BP is above 185/110mmHg.
OTHER SYSTEMIC AND PERIPHERAL EXAMINATION:
CARDIAC EXAMINATION:
Cardiac examination is essential in stroke patients to rule out potential source of stroke. Cardiac silhouette enlargement, presence of murmur, and rhythm irregularity favors cardiac source of embolism. auscultation has reported sensitivity of 70% and specificity of 98% for detection of valvular heart disease.
PERIPHERAL EXAMINATION:
Peripheral examination like examination of blood vessels provides important information about the aetiology and mechanism of stroke. Radial pulse should be palpated simultaneously bilaterally for rhythm irregularity.
ipsilateral subclavian stenosis may reduce radial pulse. Femoral artery should be auscultated in inguinal area for lack of pulsation or presence of bruit. Femoral bruit can be manifestation of the focal narrowing as well as systemic disease.
carotid artery should be palpated in the neck gently followed by auscultation . without examination of fundus, examination of stroke is incomplete. Eyes are considered as the gate to brain. Apart from detecting papilledema, examination of retinal vessels provides clue about condition of the intracranial vasculature.
Embolic particles can be visualized in the retinal vessels commonly as bright yellow orange cholesterol crystals or longer white grey platelet fibrin emboli.
MANAGEMENT OF ACUTE ISCHAEMIC STROKE:
After clinical diagnosis of stroke ,imaging study should be done as soon as possible. Selection of treatment is based on the imaging reports.
Thrombolytic and intervention in ischaemic stroke is a highly time sensitive.
Therefore imaging should be interpreted within 45 mins, so that patient can be thrombolysed in time.
IMAGING TECHNIQUES IN THE ACUTE PHASE:
Imaging studies in acute condition are aimed to rule out stroke mimics and stroke. Non-contrast CT(NCCT) scan has low sensitivity (39%) and high specificity (100%) for detection of acute ischaemic changes. Alberta strokeprogram early CT score (ASPECTS), a 10-point scoring system of the middle cerebral artery (MCA) territory, is an objective tool to measure the extent of early ischaemic changes. An aspect score <& has been shown to predict poor functional outcome and hemorrhage after thrombolysis. MR diffusion weighted imaging(DWI) is more sensitive (99%) for detecting ischaemic changes. However, DWI is the modality of choice to assess ischaemic lesions in the posterior fossa, and if diagnosis of stroke is uncertain.
CT SHOWING INFARCT WITH EDEMA AND MIDLINE SHIFT
RECOMMENDATIONS IN ACUTE PHASE:
NCCT is the investigation of choice for ischaemic stroke in acute setting, should be performed before starting therapy.
Non invasive intracranial vascular study is strongly recommended if endovascular therapy is planned, but should not delay intravenous r-tPA if indicated.
At present the benefits of CT perfusion or diffusion weighted imaging, for selecting patients for endovascular therapy are being validated, but not well established.
EMERGENCY MANAGEMENT IN ACUTE ISCHAEMIC STROKE:
Biochemistry test including platelet counts, INR, troponin and ECG, should be obtained during initial emergency evaluation. There is no need to wait for the result to start rtPA administration unless there is some contraindication.
Estimation of blooc glucose level before rtPA therapy is mandatory
Hypoglycaemia (blood glucose <60)should be treated till achievement of normoglycemic state. In hyperglycaemics blood sugar should be maintained between 140-180mg/dl.
Cardiac monitoring atleats for 24 hrs to screen for atrial fibrillation and other serious cardiac arrhythmias
Oxygen saturation should be maintained >94%. Airway support and ventilator assistance should be provided for the patient with decreased consciousness or with bulbar dysfunction.
BP should be maintained at or below 180/105 mmHg during anf after rtPA or other acute reperfusion therapy at least for 24 hours. If patient have high BP ,their BP should have lowered carefully to level of 185/105 mmHg. Drug of choice is nicardipine and labetalol. And hydralazine, enalapril, sodium nitroprusside can be considered in appropriate situations.
In patients with elevated blood pressure who do not receive thrombolysis, blood pressure should not be lowered for first 24 hrs unless systolic BP IS>220 mmHG and diastolic BP >120 mmHg.
Temperature should be monitored every 4 hours for atleast first 48 hours.
Hyperthermia >38 c should be treated with antipyretics and causes for fever should be identified and treated. Hypothermia <34 c should be avoided as well, it may complicate the situation by inducing coagulopathies, electrolyte imbalance, infection and cardiac arrhythmias.
INTRAVENOUS THROMBOLYSIS:
Eligibilty criteria for thrombolytic therapy in acute ischaemic stroke guidelines by American heart association and American stroke association.
INCLUSION CRITERIA:
Diagnosis of acute ischaemic stroke.
No evidence of hemorrhage on non-contrast CT scan brain
Onset of deficit within 4.5 hrs of beginning treatment
Measure neurological deficit (national institute of health stroke scale 4-25
Neurological deficit of low NIHSS score but significant functional disability:
Aphasias
Hemineglect
Hemianopia EXCLUSION CRITERIA:
Significant head trauma or prior stroke in previous 3 month
Symptoms suggest subarachnoid hemorrhage
Arterial puncture at noncompressible site in previous 7 days
History of previous intracranial hemorrhage
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Recent intracranial or intraspinal surgery
Elevated BP (systolic >185 mmHg or diastolic >110mmHg)
Active internal bleeding and acute bleeding diathesis
Platelet count <100000/mm3
Heparin received within 48hrs,resulting in abnormally elevated aPTT
Greater than the upper limit of normal (<35 seconds)
Blood glucose concentration <50mg/dl or more than 300mg/dl
NCCT demonstrates multilobar infarction.
RELATIVE EXCLUSION CRITERIA:
Only minor or rapidly improving stroke symptoms
Pregnancy
Seizure at onset with postictal residual neurological impairment
Major surgery or serious trauma within previous 2 weeks
Gastrointestinal or urinary tract hemorrhage within previous 3 weeks
Acute myocardial infarction(within previous 3 months).
The simplified protocol for infusion of the rtPA is ,
Infuse rtPA at 0.9 mg/kg (maximum dose of 90mg) over 60mins with 10% of the dose given as bolus over 1 minute
Admit the patient to an intensive care unit or a stroke unit for monitoring
Neurological assessments should be done every 15 minutes during the infusion every 30 minutes for next 6 hours and then hourly till 24 hours after infusion.
Severe headache, acute hypertension ,nausea or vomiting, are the indicationsto stop the infusion and need for urgent NCCT.
BP measurement should be done every 15 minutes for the initial 2 hours and then every 30 minutes for the next 6 hours, then hourly until 24 hours after infusion goal is to maintain B below 180/105mmHg
Anticoagulants/antiplatelet can be started after 24 hours but only after obtaining a NCCT.
Delay placement of nasogastric tubes, bladder cathers or intra-arterial pressure catheters.
ENDOVASCULAR THERAPY IN ACUTE STROKE:
American heart association/American stroke association in 2015 has given updated recommendations for endovascular management in acute ischaemic stroke. Endovascular therapy with stent retrievers is recommended over intra- arterial fibrinolysis as first-line therapy. The summary for recommendations are,
1. Prestroke modified ranking score (mRS) score 0-1
2. Acute ischaemic stroke receiving iv rtPA within 4.5 hours of onset, according to guidelines form professional medical societies
3. Causative occlusion of the internal carotid artery(ICA) or proximal middle cerebral artery(M1)
4. Age > or equal to 18 years 5. NIHSS score of > or equal to 6 6. Aspects of > or equal to 6
Patient eligilble for iv rtPA should receive iv rtPA even if intra-arterial treatment is being considered.
MANAGEMENT OF RAISED INTRACRANIAL PRESSURE(ICP):
Raised intracranial pressure can be managed with mannitol 0.25 to 0.5 g/kg IV.
Administered over 20mins lowers ICP and can be infused every 6 hours upto maximum dose of 2 g/kg. In patients with clinical transtentorial herniation caused by carious supratentorial lesions including ischaemic and to be associated with a rapid decrease in intra cranial pressure. These interventions should be considered temporizing,extending the window for efinitive treatments.
Decompressive craniectomy:
Patients with MCA infarction, meeting all of the criteria below should be considered for decompressive hemicraniectomy and operated within 48 hours,
Age 60 years or below
Decrease in the level of consciousness (decreased score 1 or more on item 1 a of NIHSS , or GCS score between 6 and 13)
Infarction of at least 50% of the MCA territory on CT scan, with or without infarction in ipsilateral ACA and PCA territory or infarct volume
>145cm3 on DWI.
Patients with large cerebellar infarct causing compression of brainstem and altered consciousness should be surgically managed with suboccipital craniectomy.
Symptomatic hydrocephalus should be treated surgically with ventriculostomy
RIGHT SIDE IMAGE DECOMPRESSIVE CRANIECTOMY DONE AFTER ISCHEMIC STROKE
OTHER SUPPORTIVE MEASURES:
Subcutaneous heparin for the prophylaxis of the DVT
Swallowing screening should be done before starting oral feeding.
Nasogastric tube feeding if dysphagia persists
Early mobilization should be advised for less severly affected patients.
SECONDARY PREVENTION:
Secondary prevention should be offered to all patients with transient ischeamic attacks or ischaemic stroke to reduce the risk of recurrence. Every patient should be evaluated for modifiable risk factors within a week of the stroke onset.
MANAGEMENT OF RISK FACTORS:
Lifestyle modification:
It includes salt restriction(<2.4g/day), weight loss, consumption of a diet rich fruits, vegetables, and low-fat dairy products, cessation of smoking (both active and passive smoking),limited alcohol consumption(upto 2 drinks per day for men and 1 drink per hour for non pregnant women) and regular physical activity for at least 40 minutes,(3-4 sessions per week of moderate to vigorous intensity aerobic physical exercise).
Hypertension:
All patients with TIA or IS should be treated for HTN if systolic BP is
>140mmHg and diastolic BP is >90 mmHg. Target BP is <140 systolic and <90 mmHg diastolic. For lacunar strokes target systolic BP <130 mmHg is reasonable.
Hyperlipidaemia:
The treatment goals should be total cholesterol of <200 mg%, and LDL cholesterol of <100mg% (<70 mg% for high risk individuals). Statin therapy should be offered to the patient irrespective of presence or absence of atherosclerotic cardiovascular disease.
TREATMENT OF THE LARGE ARTERY DISEASE:
Extracranial carotid artery:
More than 50% stenosis of carotid artery is considered hemodynamically significant. Along with optimum medical therapy and strict control of risk factors ,carotid endarterectomy (CEA)and carotid artery stentingCAS) are procedures of choice for symptomatic extracranial carotid artery stenosis.the recommendations are as follows:
Ipsilateral symptomatic stenosis of 70-99% CEA indicated within 6months
Ipsilateral symptomatic stenosis of 50-69%, CEA is recommended depending on patient-specific factors
Neither CEA nor CAS is recommended for the patients with <50%
stenosis.
If young patient, carotid artery stenting is preferred Extracranial vertebral artery disease:
Antithrombotic therapy, lipid lowering agents and lifestyle modification
Vertebral artery Stenting or open surgical procedures, including certebral endarterectomy and vertebral artery transposition considered if symptomatic even after optimum medical therapy.
Intracranial artery disease:
For the symptomatic intracranial stenosis of 50-99%,intensive medical therapy including aspirin 325mg/day, systolic BP <140mmHg and intensive lipid lowering therapy should be instituted.
For recent stroke or TIA (within 30days)with stenosis of 70-99%, clopidogrel 75mg/day should be added to aspirin for 90 days.
Intracranial stenting or intracranial –extracranial bypass is not recommended for any degree of stenosis.
TREATMENT OF CARDIOEMBOLIC STROKE:
Conditions responsible for the cardiac source of embolism are as follows,
Atrial fibrillation(AF)
Acute MI and LV thrombus
Cardiomyopathy
Severe mitral valve disease
Prosthetic heart valve
For secondary prevention of cardioembolic stroke, use of vitamin k antagonists (warfarin and other coumarin derivatives) or newer agents eg. dagibatrin rivaroxaban, and apixaban are recommended. Indications for anticoagulation with vitamin k antagonist:
Ischemic stroke or TIA with paroxysmal or permanent AF
Rheumatic mitral valve disease with or without AF
Acute MI complicated by left ventricular mural thrombus
Mechanical mitral valve and a history of ischaemic stroke or TIA
Mechanical aortic valve and a history of ischaemic stroke or TIA
Bio prosthetic aortic or mitral valve disease STROKE SCALES[30,31,32]
Many stroke scales have been devised to quantify the severity and prognosis of the stroke patients .There are various tools in regards to assessing stroke patients which are useful in assessing the disability degree, severity in acute settings as well as in assessing the prognosis.
Various stroke scales are as follows
STROKE IMPAIRMENT SCALE
DISABILITY SCALE
QUALITY OF LIFE SCALE
HANDICAP SCALES
STROKE IMPAIRMENT SCALES
NIHSS
EUROPEAN STROKE SCALE
CANADIAN STROKE SCALE
SCANDINAVIAN STROKE SCALE NIHSS
National Institutes of Health Stroke Scale both reliable and valid, used both in clinical trials and part of clinical care. However it does not cover all impairments as a consequence of stroke especially stroke involving posterior circulation2
EUROPEAN STROKE SCALE
It was designed specifically to assess the severity of stroke. It has many similarities to NIHSS scale
CANADIAN STROKE SCALE
Simpler and easier way of assessing the impairments due to stroke, however it misses many impairment when quantifying the scores
SCANDINAVIAN STROKE SCALE
Parameters looked for are consciousness, gaze palsy, arm and leg weakness, dysphasia, orientation, facial palsy, and gait. The scale has good reliability.It is based on data recorded in the medical record and can be used for retrospective purpose .
HANDICAP SCALE
MODIFIED RANKIN SCALE
SCORE DESCRIPTION
0 No symptoms at all
1 1No significant disability despite symptoms; can carry out all usual duties and activities
2 light disability; unable to carry out all previous activities, but able to look after own affairs without assistance
3 Moderate disability,requiring some help ,but able to walk without assistance
4 Moderately severe disability,unable to walk without assistanceand unable to attend to own bodily needs without assistance
5 Severe disability,bedridden,incontinent,requires nursing care continuously
6 DEAD
DISABILITY SCALES
BARTHAL INDEX
FUNCTIONAL INDEPENDENCE MEASURE
INSTRUMENTAL ACTIVITIES OF DAILY LIVING BARTHAL INDEX[31,32]
Measures 10 aspects of physical independence and self care.Normal score is 100,lower the score severe is the disability
Correlates moderately well with infarct size
BI has significant limitations related to floor and ceiling effects, meaning that the BI is relatively insensitive to change in function at the extreme ends of the scale
FUNCTIONAL INDEPENDENCE MEASURE
This scale involves 13 parameters of motor function and 5 parameters of cognition
Helps in monitoring improvements in disability during rehabilitative therapy
INSTRUMENTAL ACTIVITIES OF DAILY LIVING
IADL scales bridges the gap between disability and Handicap
Intended to capture the patients ability to work independently working at home
MATERIALS AND METHODS
Study Design–Observational study
Place of study- Tertiary care centre (DEPARTMENT OF GENERAL MEDICINE )
STUDY PERIOD- 1 ½ YEARS INCLUSION CRITERIA-
All cases of acute ischemic stroke >18years of age with in 24hours of symptom onset
EXCLUSION CRITERIA
1. Haemorrhagic stroke 2. Transient ischemic attack 3. Renal failure
4. Decompensated liver disease 5. <18years of age
The following patients details will be collected from patients :age, sex,s ymptom and duration. Patients will undergo thorough general and systemic physical examination and following details will be collected :GCS,NIHSS scores.
Laboratory investigations including complete blood count with heamtocrit, blood urea nitrogen(calculated),serum creatinine, BUN/Creatinine ratio(calculated),serum electrolytes, blood glucose at admission, urine specific gravity, serumbilirubin, lipid profile, ECG, and radiological investigations like abdominal ultasonogram and NCCT /MRI SCAN of BRAIN to study about cerebral edema and extent of hypodensity.
Parameters like BUN(Calculated), creatinine, urine specific gravity will be tested at time of admission and then on first, second and third day .Rest of all parameters were assessed only once with in 24hours of admission. BUN Calculation=Urea/2.14
RESULTS
EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL
DETORIATION NO OF
PATIENTS PERCENTAGE
PRESENT 31 62%
ABSENT 19 38%
62%
38%
EARLY NEUROLOGICAL DETERIORATION
PRESENT ABSENT
AGE DISTRIBUTION
AGE IN YEARS NO OF PATIENTS PERCENTAGE
< 50 13 26%
51-60 21 42%
61-70 13 26%
> 70 3 6%
26%
42%
26%
6%
AGE DISTRIBUTION
< 50 51-60 61-70 > 70
AGE VS EARLY NEUROLOGICAL DETERIORATION
AGE IN YEARS EARLY NEUROLOGICAL DETERIORATION
PRESENT ABSENT
< 50 7 6
51-60 12 9
61-70 11 2
> 70 1 2
KRUSKAL WALLIS TEST P VALUE - 0.189
NON SIGNIFICANT
7 6
12
9 11
1 2 2
PRESENT ABSENT
EARLY NEUROLOGICAL DETORIATION
AGE VS END
< 50 51-60 61-70 > 70
MEAN AGE VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETERIORATION AGE IN YEARS
MEAN SD
PRESENT 58.35 9.35
ABSENT 54.16 8.55
UNPAIRED T TEST P VALUE - 0.119 NON SIGNIFICANT
58.35
54.16
PRESENT ABSENT
MEAN AGE VS END
SEX
SEX NO OF PATIENTS PERCENTAGE
MALE 28 56%
FEMALE 22 44%
56%
44%
SEX DISTRIBUTION
MALE FEMALE
SEX VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETORIATION SEX
MALE FEMALE
PRESENT 17 14
ABSENT 11 8
CHI SQUARE TEST P VALUE - 0.437 NON SIGNIFICANT
17
14 11
8
MALE FEMALE
SEX
SEX VS END
PRESENT ABSENT
GLASGOW COMA SCALE
GCS NO OF PATIENTS PERCENTAGE
LESS THAN 8 20 50%
MORE THAN 8 30 60%
40%
60%
GLASGOW COMA SCORE
LESS THAN 8 MORE THAN 8
GCS VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETERIORATION
GCS LESS THAN
8
MORE THAN 8
PRESENT 17 14
ABSENT 3 16
CHI SQUARE TEST P VALUE - 0.006 NON SIGNIFICANT
17
14
3
16
LESS THAN 8 MORE THAN 8
GCS
GCS VS END
PRESENT ABSENT
NIHSS AT TIME OF ADMISSION
NIHSS NO OF PATIENTS PERCENTAGE
MORE THAN 12 27 54%
LESS THAN 12 23 46%
46% 54%
NIHSS
MORE THAN 12 LESS THAN 12
NIHSS VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETORIATION
NIHSS MORE THAN
12
LESS THAN 12
PRESENT 21 10
ABSENT 6 13
CHI SQUARE TEST P VALUE - 0.013 NON SIGNIFICANT
21
10 6
13
MORE THAN 12 LESS THAN 12
NIHSS
NIHSS
PRESENT ABSENT
RANDOM BLOOD SUGAR
RANDOM BLOOD SUGAR NO OF PATIENTS PERCENTAGE
MORE THAN 110 31 62%
LESS THAN 110 19 38%
62%
38%
RANDOM BLOOD SUGAR
MORE THAN 110 LESS THAN 110
RBS VS EARLY NEUROLOGICALDETERIORATION
EARLY NEUROLOGICAL DETERIORATION
RANDOM BLOOD SUGAR
MEAN SD
PRESENT 168.45 95.96
ABSENT 126.21 49.34
UNPAIRED T TEST P VALUE - 0.046 SIGNIFICANT
168.45
126.21
PRESENT ABSENT
RBS VS END
DIABETES MELLITUS
DIABETES MELLITUS NO OF PATIENTS PERCENTAGE
PRESENT 30 60%
ABSENT 20 40%
DM VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETERIORATION
DIABETES MELLITUS PRESENT ABSENT
PRESENT 23 8
ABSENT 7 12
CHI SQUARE TEST P VALUE - 0.009 SIGNIFICANT
23
7 8
12
PRESENT ABSENT
DIABETES MELLITUS
DM VS END
PRESENT ABSENT
HBA1C
HBA1C NO OF PATIENTS PERCENTAGE
LESS THAN 7.5 35 70%
7.5-9 9 18%
MORE THAN 9 6 12%
70%
18%
12%
HBA1C
LESS THAN 7.5 7.5-9 MORE THAN 9
HBA1C VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETERIORATION HBA1C
MEAN SD
PRESENT 7.63 1.63
ABSENT 6.36 0.98
UNPAIRED T TEST P VALUE - 0.004 NON SIGNIFICANT
PRESENT ABSENT
7.63
6.36
MEAN HBA1C VS END
BLOOD PRESSURE
BLOOD PRESSURE NO OF PATIENTS PERCENTAGE
> 130/80 MMHG 24 48%
< 130/80 MMHG 26 52%
48%
52%
BLOOD PRESSURE
> 130/80 MMHG < 130/80 MMHG
BLOOD PRESSURE VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL
DETERIORATION
BLOOD PRESSURE
> 130/80 MMHG
< 130/80 MMHG
PRESENT 18 13
ABSENT 6 13
CHI SQUARE TEST P VALUE - 0.001 SIGNIFICANT
18
13
6
13
> 130/80 MMHG < 130/80 MMHG BLOOD PRESSURE
BLOOD PRESSURE VS END
PRESENT ABSENT
BLOOD UREA NITROGEN / CREATININE RATIO
BUN/CREATININE RATIO NO OF PATIENTS PERCENTAGE
<15 29 58%
>15 21 42%
58%
42%
BUN/CREATININE RATIO
NORMAL HIGH
BLOOD UREA NITROGEN / CREATININE RATIO VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETERIORATION BUN/CREATININE RATIO
MEAN SD
PRESENT 22.41 5.66
ABSENT 16.28 4.83
UNPAIRED T TEST P VALUE - 0.001 SIGNIFICANT
22.41
16.28
PRESENT ABSENT
BUN/CREATININE RATIO
URINE SPECIFIC GRAVITY
URINE SPECIFIC GRAVITY >
1.010
NO OF PATIENTS
PERCENTAG E
YES 27 54%
NO 23 46%
54%
46%
URINE SPECIFIC GRAVITY > 1.010
YES NO
URINE SPECIFIC GRAVITY VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETORIATION
URINE SPECIFIC GRAVITY >
1.010
YES NO
PRESENT 24 7
ABSENT 3 16
CHI SQUARE TEST P VALUE - 0.001 SIGNIFICANT
24
7 3
16
YES NO
URINE SPECIFIC GRAVITY > 1.010
URINE SPECIFIC GRAVITY > 1.010
PRESENT ABSENT
CT TERRITORY
CT TERRITORY NO OF PATIENTS PERCENTAGE
MORE THAN 1/3RD 17 34%
LESS THAN 1/3RD 33 66%
34%
66%
CT TERRITORY
MORE THAN 1/3RD LESS THAN 1/3RD
CT TERRITORY VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETORIATION
CT TERRITORY MORE THAN
1/3RD
LESS THAN 1/3RD
PRESENT 14 17
ABSENT 3 16
CHI SQUARE TEST P VALUE - 0.104 NON SIGNIFICANT
14
17
3
16
MORE THAN 1/3RD LESS THAN 1/3RD
CT TERRITORY
CT TERRITORY VS END
PRESENT ABSENT
CT EDEMA
CT EDEMA NO OF PATIENTS PERCENTAGE
PRESENT 23 46%
ABSENT 27 54%
54% 46%
CT EDEMA
PRESENT ABSENT
CT EDEMA VS EARLY NEUROLOGICAL DETERIORATION
EARLY NEUROLOGICAL DETORIATION CT EDEMA
PRESENT ABSENT
PRESENT 20 3
ABSENT 10 17
CHI SQUARE TEST P VALUE - 0.006 SIGNIFICANT
20
10 3
17
PRESENT ABSENT
CT EDEMA
CT EDEMA VS END
PRESENT ABSENT
DISCUSSION
In our case series,a total of 50 patients participated in the study,of which 28 patients were male and 22 female. Early neurological deterioration was seen in 62% of patients.The mean age of the patients with END was 58.35years and without END is 54.16years . 60percent of subjects with END were male.No significant association was not seen between age ,sex and END .
In our case series association between GCS at time of admission, nihss score and END at tme of admission was tested and found to be no significant association between GCS,NIHSS score and END .Bhatia e al in their study found GCS score ,NIHSS score to be significant risk factor for END ,in contrast to our findings.Elevated blood sugar was found to be a significant risk factor with significant association with END.Average blood sugar in subjects with END was 168.45mg/dl.[17]Lactic acidosis ,reactive oxygen and other free radicals could explain the negative effect on the neurological state of the patient.Presence of comorbidity Diabetes Mellitus and hyperglycemia showed significant association with END,hence indicating it to be a risk factor for early neurological deterioration[17,18,19].However mean values of HbA1c showed no significant association with END .
BUN/creatinine ratio of more than 15 are considered to be high values and indicates volume depletion.In our case series,42percent subjects had high values of BUN/CREATININE RATIO.Our case series showed significant association between BUN/CREATININE RATIO >15 and END which supports the notion that relative dehydration could be a risk factor for early neurological deterioration as suggested in Bhatia et al study[27].Volume depletion could worsen the high viscosity ,and the collateral circulation[28] ,which could be the mechanism behind neurological deterioration in END patients.Hence adequate hydration plays a major role in early management of stroke patients.Though Urinary specific gravity also found to have direct significant association between END and USG>1.010,its not known how reliable this finding can be as the test was performed using dipstick method.
Stroke involving more than 33% of the territory was found to be risk factor for early neurological deterioration in ECASS study(European cooperative acute stroke study).However in our study there was no significant association found between extent of CT territory involved and END.But presence of CT edema in NCCT imaging showed significant association between END and Edema,which is in agreement with other stroke studies .
