1. CEREBROVASCULAR ACCIDENT (CVA)
DR JYOTI KHARE
FCCCM, Part II,
PSRI Hospital, New Delhi

2. Cerebrovascular Accident (CVA)
CVA is a disease of blood vessels involving the vital organ –BRAIN which manifest as STROKE. The blood supply to this organ is interrupted . It produces considerable morbidity and mortality.

3. The biology of stroke is such that each moment of ischemia and tissue injury increases the degree of irreversible tissue damage.

4. CVA
Ischaemic
Thrombosis
Embolus
Carotid/ VB
Cardiac
Aortic arch
Haemorrhagic
Epidural
Intracerebral
SAH
Subdural

5. RISK FACTORS OF STROKE Increasing Age Hypertension
Ischemic Heart Disease
Atrial fibrillation
Smoking
Diabetes Mellitus
Obesity
Use of Oral contraceptives
Raised Cholestrol or Heamtocrit

6. Differential Diagnosis of Stroke
Craniocerebral/ cervical trauma
Meningitis/ encephalitis
Intracranial mass
Tumor
Subdural hematoma
Seizure with persistent neurological signs
Migrane with persistent neurological signs
Metabolic
Hyperglycemia
Hypoglycemia
Post-cardiac arrest ischemia
Drug/ narcotic overdose

7. CEREBRAL INFARCTION
It is also k/o as Ischemic stroke resulting from inadequate perfusion of cerebral tissue due to occlusion of cerebral blood vessels with inadequate collateral circulation.
About 85% of stroke are ischemic stroke.
Third leading cause of death.

8. ETIOLOGY OF ISCHEMIC STROKE
Cardioembolic – ischemic /valvular heart disease, atrial fibrillation.
Atherothrombotic –occlusion of a large intra/extra cranial portion of the carotid/ vertebrobasilar system.
Lacunar – small blood vessel occlusion.
Watershed territory –from systemic hypotension with border4 zone infarction.
TIA

9. DIAGNOSIS History –sudden onset it is cardioembolic.
takes several hours it is atherothrombotic, headache, loss of consciousness.
Examination- complete neurological and look for cognitive ,memory ,contralateral numbness, weakness, deviation of mouth, aphasia, dysphasia, hemiparesis, hemiparesthesia, hemiplegia, visual loss, conjugate gaze paresis, gait disturbance , Glasgow coma scale.

10. Investigations-
Lab- CBC,LFT,RFT,PT/INR,CRP, RBS, Lipid profile ,Thyroid profile .In younger age group get protein-c,s , leiden factor V, antithrombin III, anticardiolipin antibodies, lupus anticoagulant antibodies, homocysteine levels also.

11. Radiological – Echocardiography, ECG.
Plain CT scan of head is a must to rule out ICH /SAH.
DPW-MRI with MRA for those who are within 3 hrs of onset and suitable for thrombolysis.
Echocardiography, ECG.

12. Glasgow Coma Scale BEHAVIOUR RESPONSE SCORE Eye opening response
Spontaneously 4
To speech 3
To pain 2
No response 1
Best Verbal response
Oriented to time, place and person 5
Confused
Inappropriate words
Incomprehensible sounds
Best Motor response
Obeys commands 6
Moves to localized pain
Flexion withdrawal from pain
Abnormal Flexion (decorticate)
Abnormal extension (decerebrate)
Total score:
Best response 15
Comatose client
8 or less
Totally unresponsive

13. The NIHSS is a 15-item impairment scale, intended to evaluate 1
The NIHSS is a 15-item impairment scale, intended to evaluate 1.neurologic outcome and degree of recovery for patients with stroke.
2. The scale assesses level of consciousness, extraocular movements, visual fields, facial muscle function, extremity strength, sensory function,coordination (ataxia), language (aphasia), speech (dysarthria), and hemi-inattention (neglect).
3.The NIHSS was designed to assess differences in interventions in clinical trials, although its use is increasing inpatient care as an initial assessment tool and in planning postacute care disposition.

14. The National Institutes of Health Stroke Scale (NIHSS) was developed to help physicians objectively rate severity of ischemic strokes.
Increasing scores indicate a more severe stroke and has been shown to correlate with the size of the infarction on both CT and MRI evaluation.
NIHSS scores when assessed within the first 48 hours following a stroke have been shown to correlate with clinical outcomes at the 3-month and 1-year mark.
(>22) is associated with increased risk of hemorrhagic conversion.

15. National Institutes of Health Stroke Scale
Score
Stroke Severity
1-4
Minor Stroke
5-15
Moderate Stroke
16-20
Moderate to Severe Stroke
21-42
Severe Stroke

16. Patients with a total score of 4 or less generally have favorable clinical outcomes and have a high likelihood of functional independence regardless of treatment.
Points to Keep in Mind
Many guidelines and protocols warn that administering tPA in patients with a high NIHSS score

19. MANAGEMENT Secure Airway ,Breathing and Circulation
If patient comes with 3 hrs of onset and CTscan head rules out bleed then THROMBOLYSIS with Tissue Plasminogen Activator is recommended (dose 0.9 mg/kg of which 10% is given as bolus and rest as infusion over 30 mts.)
Antiplatelets – Aspirin, clopidogrel.
Anticoagulant – LMWH caution while using in large infarct as may turn into haemorrhagic infarct.

21. Endovascular therapy
Cerebral protection- free radical scavengers, magnesium, glutamate antagonist.
Decompressive Craniotomy
Nursing care , nutrition,Physiotherapy, speech therapy.

22. COMPLICATIONS CEREBRAL OEDEMA HAEMORRHAGE IN INFARCTED AREA
SECONDARY HYDROCEPHALUS
PRESSURE SORES
CONTRACTURES

23. CEREBRAL HAEMORRHAGE
Intracerebral haemorrhage (ICH) is a type of stroke caused by bleeding within the brain tissue itself – a very life-threatening situation. A stroke occurs when the brain is deprived of oxygen due to an interruption of its blood supply.

24. Introduction Intracranial Haemorrhage Intracerebral Haemorrhage
Brain parenchyma
IVH
Meningeal space haemorrhage
EDH
SDH
SAH

25. Intracerebral haemorrhage accounts for 8-13% of all strokes and results from a wide spectrum of disorders. Intracerebral haemorrhage is more likely to result in death or major disability than ischemic stroke or subarachnoid haemorrhage.
Intracerebral haemorrhage and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.

26. Etiology Hypertensive ICH Non-hypertensive ICH Essential Eclampsia
Vascular malformation: AVM, Aneurysm, Cavernous hemangioma
Bleeding disorders/ anticoagulant
Amyloid angiopathy
Trauma
Tumor
Drug abuse: amphetamine, cocaine, PPA

27. Basal ganglia (40-50%),
Lobar regions (20-50%),
Thalamus (10-15%),
Pons (5-12%),
Cerebellum (5-10%),
Other brainstem sites (1-5%).

28. Clinical Presentation
Alteration in level of consciousness (approximately 50%)
Nausea and vomiting (approximately 40-50%)
Headache (approximately 40%)
Seizures (approximately 6-7%)
Focal neurological deficits

29. Focal deficit evolve over 20-30 minutes
Diminishing level of consciousness
Signs of raised ICP

30. Putamen C/L hemiparesis Arm & legs gradually weaken Slurred speech
Eye deviate away from side of hemiparesis
large – brain stem compression

31. Thalamic haemorrhage C/L hemiparesis Prominent sensory deficit
Dominant thalamus – aphasia
Non dominant – constructional apraxia
Ocular disturbance – extension into upper midbrain

32. Ocular disturbances Deviation of eyes downward & inward
Unequal pupils with absence of light reactions
Ipsilateral horner’s syndrome
Paralysis of vertical gaze, nystagmus

33. Pontine haemorrhage Deep coma with quadriplegia over few minutes
Pin point pupil reacting to light
Impaired reflex horizontal eye movements
Hyperpnoea, hyperhydrosis, hypertension are common

34. Cerebellar haemorrhage
Occipital headache
Repeated vomiting
Ataxia
Dizziness and vertigo may be prominent

35. Paresis of conjugate lateral gaze to the side of haemorrhage
Ipsilateral 6th nerve palsy
Dysphagia, dysarthria

36. DIAGNOSIS History Physical examination
CT scan shows site and size of haematoma.
MRI and MRA shows underlying vascular malformation
LP contraindicated as risk transtentorial herniation
Coagulation profile

38. TREATMENT Airway, Breathing protection
Control of BP with prevention of expansion of haemorrhage (keep BP 160/110 mmHg, Beta blockers agent of choice; vasodilators to be avoided as they increase cerebral oedema and elevateICP ).
Prevention of cerebral oedema and maintance of CPP between mmHg

39. TREATMENT OF ELEVATED ICP
Head of bed elevated to 30 degree
IV Mannitol g/kg 8 or 12 hrly.
Hyperventilation to keep Pco mmHg
Hypertonic saline to keep S Na to155 meq/l
Steroids only in CNS infections
Hypothermia –goal of32-34 dehrere.

40. Seizures control
Surgical intervention- Ventriculostomy for Hydrocephalus
Decompressive hemicraniectomy
Correction of coagulation profile – transfusing FFP ,Vitamin K,Factor VII, Platelets.
Foue vessel angiography to evaluate vascular malformations.
Nursing care, prevention of bed sores,nutritional balance ,physiotherapy.

41. SUBARACHNOID HAEMORRHAGE
Subarachnoid haemorrhage is bleeding in the area between the brain and the thin tissues that cover the brain. This area is called the subarachnoid space.

42. CAUSES
Bleeding from a tangle of blood vessels called an arteriovenous malformation (AVM) – Most common
Bleeding disorder
Bleeding from a cerebral aneurysm
Head injury
Unknown cause (idiopathic)
Use of blood thinners

43. RISK
Aneurysm 
Fibromuscular dysplasia (FMD) and other connective tissue disorders
High blood pressure
History of polycystic kidney disease
Smoking
A strong family history of aneurysms may also increase your risk.

44. SYMPTOMS and SIGNS Headache (48%) – worst headache ever
Dizziness (10%)
Orbital pain (7%)
Diplopia (4%)
Visual loss (4%)
Signs present before SAH include the following:
Sensory or motor disturbance (6%)
Seizures (4%)
Ptosis (3%)
Bruits (3%)
Dysphasia (2%)

45. Physical Examination reveals
Neck stiffness
Altered sensorium
Focal signs- hemiparesis, oculomotor palsy, visual loss, paraparesis.

46. DIAGNOSIS Non contrast CT scan Lumbar puncture if CT nondiagnotic
Four vessel angiography for vascular malformation
Routine investigation including coagulation profile.

48. GRADING and STAGING The WFNS scale is as follows:
Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent
Grade 2 - GCS of 13-14, motor deficit absent
Grade 3 - GCS of 13-14, motor deficit present
Grade 4 - GCS of 7-12, motor deficit absent or present
Grade 5 - GCS of 3-6, motor deficit absent or present

49. The Hunt and Hess grading system is as follows:
Grade 0 - Unruptured aneurysm
Grade I - Asymptomatic or mild headache and slight nuchal rigidity
Grade Ia - Fixed neurological deficit without acute meningeal/brain reaction
Grade II - Cranial nerve palsy, moderate to severe headache, nuchal rigidity
Grade III - Mild focal deficit, lethargy, or confusion
Grade IV - Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Grade V - Deep coma, decerebrate rigidity, moribund appearance

50. The Fisher scale (CT scan appearance) is as follows:
Group 1 - No blood detected
Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm
Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness
Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present

51. MANAGEMENT Airway,breathing, circulation.
Bed rest with head end elevated, control of BP ( maintain systolic <160 mmHgwith Beta blocker which also reduced cardiac arrhythmias ).
Hydrocephalous may develop within 24 hrs may require ventticular drainage.
Anticonvulsant –phenytoin, levetiracetam.
Steroids to limit inflammation , edema.
hyponatrmia due to hypothalamic dysfunction causing cerebal salt wasting syndrome treated with isotonic saline.

52. SURGICAL Craniotomy with clip occlusion of aneurysm.
Endovascular repair- coil embolisation.
Surgical clipping is definitive but higher percentage develop epilepsy post repair.

53. COMPLICATIONS
Cerebral vasospasm- peak between 4th -12th day., leading to cerbral ischemia .
Diagnosed by angiography or by Transcranial dopppler
Treated with Calcium channel blockers- Nimodepine 60 mg every 4hrly ( if hypotension 30 mg every 2nd hrly )for 21 days.
HMG-Co reductase inhibitors- Simavastatin 80 mg daily.

54. Hyper Dynamic Threapy (triple H therapy )-
Hypertension increases cerebral blood flow.
Hypervolumia causes Hemodilution and decreases viscosity and improves cerebral microcirculation.
Risk- MI,CHF,Dysrhythmias ,Heamorrhagic infarct,Rebleeding,Hyponatremia,Heamotho0rax.

55. Transluminal balloon angioplasty
Transluminal balloon angioplasty is recommended for treatment of vasospasm after failure of conventional therapy. 

56. EPIDURAL HAEMATOMA
Epidural hematoma (ie, accumulation of blood in the potential space between dura and bone) may be intracranial (EDH) or spinal (SEDH)
occurs in approximately 2% of patients with head injuries and 5-15% of patients with fatal head injuries. Intracranial epidural hematoma is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. 

57. Epidural Hematoma Source of Bleed : Clinical Features:
Temperoparietal locus (most likely) – Middle meningeal artery
Frontal locus – anterior ethmoidal artery
Occipital locus – transverse or sigmoid sinuses
Vertex locus – superior sagittal sinus
Clinical Features:
LOC>>>Lucid Interval>>unconciousness
s/s of raised ICP
Focal neurological deficit
s/s of cerebral herniation

58. Spinal epidural hematoma typically causes severe localized back pain with delayed radicular radiation that may mimic disk herniation. Associated symptoms may include the following:Weakness
Numbness
Urinary incontinence
Fecal incontinence

59. EPIDURAL HAEMATOMA
Biconvex shape

61. Subdural Hematoma (SDH)
Blood collects between dura and arachnoid
Tom cortical bridging veins
10-20% of all cranial trauma cases
Demographics:
Elderly (60-80y) with brain atrophy.
Large intracranial subarachnoid spaces
“Shaken baby syndrome”

62. Classification Scheme
Acute SDH (upto 7 days)
Sub acute SDH (7-21 days)
Chronic SDH (more than 21 days)

63. Extradural Hematoma Subdural Hematoma Biconvex or lenticular
Temporal or temporoparietal
Middle meningeal artery
0.5% of all head injured pts
“Lucid” interval classically
Outcome related to status prior to surgery
Diffuse and concave
Entire surface of brain
Tearing of bridging veins
30% of severe head injuries
Underlying brain damage more severe
Prognosis is worse than extradural

64. Epidural and Subdural Hematomas
Epidural Hematoma
Subdural Hematoma

67. Risk Factors
Extreme age
Anticogulants
Long term alcohol abuse

68. Diagnosis
It is important that a patient receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan will usually detect significant subdural hematomas.

69. TREATMENT
The 2 treatment options for these patients are (1) immediate surgical intervention and (2) initial, conservative, close clinical observation with possible delayed evacuation

70. Management Supportive Measures:
Endotracheal intubation for patients with decreased level of consciousness and poor airway protection.
Cautiously lower blood pressure to a MAP less than 130 mm Hg, but avoid excessive hypotension.
Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.
Maintain euvolemia, using normotonic rather than hypotonic fluids, to maintain brain perfusion without exacerbating brain edema.
Avoid hyperthermia.
Facilitate transfer to the operating room or ICU.

71. Management Contd… Decrease cerebral edema:
Modest passive hyperventilation to reduce PaCO2
Mannitol, gm/Kg slow iv push
Furosemide 5-20 mg iv
Elevate head degrees, avoid any neck vein compression.
Sedate and paralyze if necessary with morphine and vecuronium (struggling, coughing etc will elevate intracranial pressure)

72. Management Contd… Surgical Evacuation of hematoma:
No surgical intervention if collection < 10 ml
Indication of surgical decompression:
The GCS score decreases by 2 or more points between the time of injury and hospital evaluation
The patient presents with fixed and dilated pupils
The intracranial pressure (ICP) exceeds 20 mm Hg
Exception:
In subdural hematoma with GCS = 15- hematoma > 10 mm, or > 5 mm midline shift --- requires surgical decompression
SAH: when a cerebral aneurysm is identified on angiography, clipping and coiling is done to prevent re-bleed

73. Management Contd… Surgical Decompression contd… Types: Burr-hole
Craniotomy- bone flap is temporarily removed from the skull to access the brain
Craniectomy – in which the skull flap is not immediately replaced, allowing the brain to swell, thus reducing intracranial pressure
Cranioplasty – surgical repair of a defect or deformity of a skull

74. Management Contd… Medical Therapy:
Antihypertensives – reduce blood pressure to prevent exacerbation of intracerebral hemorrhage in hypertensive encephalopathy. Eg. Nicardipine, labetolol: CCB help relieve vasospasm in SAH and decreases further damage
Diuretics – Mannitol, CAI
Anticonvulsants – reduce frequency of seizures and prophylaxis of seizures eg: Fosphenytoin
Antipyretics – to Rx fever and pain relief eg: Acetaminophene
Antidote –
Vitk/FFP for warfarin overdose;
protamine for heparin overdose
Antacids – prophylaxis for Cushing’s gastric ulcer eg: Famotidin
Glucorticoids may help reduce the head and neck ache caused by the irritative effect of the subarachnoid blood.

75. Rehabilitation Ambulatory and Home Care Nutrition
Bowel and bladder management
Spasticity
Dysphagia
Seizure disorders
Family participation and education

76. THANK YOU