25

26

27

A- Cerebral infarction:
There are 4 types of ischemic injury to the brain:
1.
Cerebral autolysis
2.
Cerebral infarction
3.
Selective ischemic necrosis of highly vulnerable neurons
4.
Demyelination of the central hemispheric white matter
The pathologic causes of cerebral infarction include:
I.
Arterial disease
II.
Cardio-embolic causes
III.
Hematological disorders
IV.
Miscellaneous conditions
I.
Arterial disease:
1.
Atherothromboembolism
2.
I.C. small vessel disease
3.
Trauma
4.
Dissection
5.
Fibromuscular dysplasia
6.
Congenital arterial anomalies
7.
Moyamoya syndrome
8.
Embolism from arterial aneurysm
9.
Inflammatory vascular diseases
10.
Benswanger’s disease
11.
Irradiation
12.
Infection
II.
Cardioembolic causes:
1.
Paradoxical embolism from venous system:

Atrial septal defect (ASD)

Ventricular septal defect (VSD)

Patent foramen ovale (PFO)

Pulmonary AV fistula
2.
Left atrial embolism:

Atrial fibrillation (AF)

Sino-atrial (SA) disease

Myxoma

Interatrial septal aneurysm
3.
Mitral valve disease:

Rheumatic stenosis or regurgitation

Infective endocarditis

Non-bacterial thrombotic endocarditis

Prosthetic valve

Mitral annulus calcification

Mitral leaflet prolapse

Libmann-Sachs endocarditis

Papillary fibroelastoma
4.
Left ventricular mural thrombus:

Acute MI
28


Left ventricular aneurysm

Cardiomyopathy

Myxoma

Blunt chest injury
5.
Aortic valve:

Rheumatic stenosis or regurgitation

Infective endocarditis

Non-bacterial thrombotic endocarditis

Prosthetic valve

Calcification &/or sclerosis

Syphilis
6.
Congenital cardiac disorders (with right to left shunt)
7.
Cardiac surgery, catheterization & angioplasty
III.
Hematological disorders:

Polycythemia

Essential thrombocythemia

Leukemia

Sickle cell disease/trait

Iron deficiency anemia

Paroxysmal nocturnal hemoglobinuria

Thrombocytopenic purpura

DIC

Hypercoagulability states
IV.
Miscellaneous conditions:

Pregnancy/puerperium

Oral contraceptives & other female sex hormones

Drug abuse

Cancer

Migraine

Inflammatory bowel disease

Homocysteinemia

Mitochondrial cytopathy

Hypercalcemia

Hypoglycemia

Fibrocartilagenous embolism

Snake bite

Fat embolism

Nephrotic syndrome
B- Intracerebral hemorrhage & Subarachnoid hemorrhage:
Hemorrhagic strokes represent 20 – 30 % of acute strokes
Risk factors for ICH:

HTN

AVM

Anticoagulants

Thrombolytic agents

Tumors

Blood dyscrasias
29


Cerebral amyloid angiopathy
Spontaneous SAH:

IC aneurysm

AVMs

Other causes of ICH
Primary ICH:

50 % in striate area

10 % in thalamus

8 % in cerebellum

12 % in pons

20 % in other areas in the hemisphere
C- Cerebral edema:
Cerebral edema & ↑ ICP →

Neurologic deterioration &

Death by transtentorial herniation
Cerebral edema & herniation represent the immediate cause of death in:

33% of all ischemic strokes &

75 % of all hemorrhagic strokes
Stroke is a “Brain Attack” resulting from occlusion or bursting of one of the blood vessels supplying the brain
Types of stroke

Ischemic Stroke

Cerebral thrombosis.

Cerebral embolism.

Hypoxia due to small artery disease in HTN.

Hemorrhagic Stroke
1.
Intracerebral hemorrhage (I.C.H.)

Hypertensive hemorrhage

Hemorrhage 2 ry to anticoagulants, bleeding diatheses or trauma

Amyloid angiopathy in the elderly
2.
Subarachnoid hemorrhage (S.A.H.)

Ruptured I.C. aneurysm

Ruptured I.C. AVMs

Other rare causes
30

ISCHEMIC STROKE
What are the warning signs of stroke?

Sudden paresis, paralysis, or numbness of face, arm & leg on one side of the body.

Aphasia or dysphasia.

Dimness or loss of vision in one eye.

Sudden severe headaches with no apparent cause.

Unexplained dizziness, unsteadiness or sudden falls.

TIAs.
What are the “Risk Factors” for Stroke?
A.
Non-modifiable (Risk markers):
1.
Increasing age.
2.
Male gender.
3.
African – American Race.
4.
A prior stroke.
5.
A positive family history for stroke or IHD.
B.
Modifiable Risk factors by medical treatment:
6.
Diabetes mellitus (DM)
7.
Hypertension (HTN)
8.
Heart disease.
9.
TIAs.
10.
Asymptomatic carotid bruit
11.
High RBC count (Polycythemia).
C.
Modifiable Risk factors by changing lifestyle:
12.
Cigarette smoking.
13.
Hyperlipidemia
14.
Physical inactivity & obesity.
15.
Stressful lifestyle.
16.
Alcoholism.
17.
IV drug abuse & cocaine use.
One third of all strokes occur in 10% of the population who have “a set of 5 risk factors”:
1.
Hypertension (HTN).
2.
Hypercholesterolemia.
3.
Diabetes mellitus (DM).
4.
Cigarette smoking.
5.
Left ventricular hypertrophy (LVH)
31

Factors that can increase the probability of stroke
Risk Factors
Risk markers (nonmodifiable) o
Age o Gender o Hereditary o Race-ethnicity
Risk factors (modifiable) o Hypertension (HTN) o Cardiac disease:
- Atrial fibrillation (AF)
- Mitral stenosis
- Recent myocardial infarction (MI)
- Intracardiac thrombus
- Left ventricular hypertrophy (LVH)
- Cardiomyopathy
- Endocarditis o Diabetes mellitus o
Hypercholesteremia o Asyptomatic carotid stenosis o Smoking o Heavy alcohol consumption o Transient ischemic attacks (TIAs) o Hematologic disorders:
- Elevated hematocrit
- Sickle cell anemia
- Hypercoagulability o Physical inactivity o Obesity
Potential risk factors for late stroke recurrence
Modification
Antihypertensives, diet, Antiplatelets
Anticoagulants, antiarrhythmics
Valve comissurotomy
Thrombolytic therapy
Control HTN
Antibiotics
Glucose control
Lipid – lowering medication, diet
Antiplatelets, endarterectomy
Cessation
Abstinence
Antiplatelets, endarterectomy, anticoagulants
Venesection
Anticoagulants
Exercise
Weight reduction
Probable o Age o Hypertension o
Heart disease

AF

Congenital heart disease

CHF

IHD o
Diabetes o Hyperglycemia o Prior TIA or stroke
Possible o Race or ethnicity o Heavy alcohol use o
Lipoprotein (a) o
Anticardiolipin antibodies o Plasma antithrombin III o Low albumin-globulin ratio o Risk factor combinations
32

Stroke risk factors under continued epidemiologic investigation
Lifestyle factors

Physical inactivity

Obesity

Diet

Stress

Socioeconomic factors

Illicit
Cardiac disease

Spontaneous echo contrast

Patent foramen ovale

Atrial septal aneurysm

Mitral valve prolapse

Valve strands
Hematological parameters

Hematocrit

Anticardiolipin antibodies

Homocysteine

Lipoprotein fractions (e.g. Lipoprotein-a)

Fibrinogen
Subclinical diseases

Aortic atheroma

Intimal – medial thickness

Infarct – like lesions on MRI
What is a TIA?

TIAs are short-lived attacks of cerebral ischemia, each one lasts for few minutes to few hrs (max. 24 hrs).

They are commonly produced by emboli arising from atheromatous plaques in the extracranial portions of carotid or vertebral arteries, or in the aortic arch or subclavian artery; or from clots formed in the heart; or caused by a fall in arterial perfusion pressure.
Types of TIAs

Carotid TIAs

Ipsilateral amaurosis fugax.

Ipsilateral vascular headache.

Contralateral weakness & numbness

Dysphasia, apraxia & or confusion in Lt-sided lesions.

Vertebrobasilar TIAs

Dizziness, vertigo, tinnitus, nausea, vomiting.

Occipital headache.

Ataxia (unsteadiness).

Diplopia

Dysarthria & dysphagia.

Unilateral or bilateral numbness or weakness.

Homonymous field defect or cortical blindness.

Syncope, confusion, or coma, or temporal lobe seizures.
33

TIAs, RIND, Stroke-in evolution, & Completed Stroke

TIAs:
TIAs are episodes of neurologic dysfunction due to brain ischemia which resolve in < 24 hrs.

RIND: (Reversible Ischemic Neurological Deficit)
RIND is a neurologic deficit due to brain ischemia resolving completely within 3 wks.

Stroke – in – evolution:
An evolving or progressing infarction in which new signs & symptoms develop during the preceding 24 hrs.

Completed Stroke:
An established infarction: is one in which the neurologic deficit becomes static & there have been no new events within the preceding 24 hrs.
Middle cerebral artery syndromes
Arterial Territories
Prefrontal artery
Precentral artery
Lower posterior parietal / temporal arteries
Central sulcus artery
Upper posterior parietal / angular gyrus artery
Anterior parietal Artery
Clinical syndromes
Frontal syndrome LH: transcortical motor aphasia RH: motor hemineglect
Hemiparesis with proximal predominance
Premotor syndrome of Luria
LH: Minor variant of Broca’s aphasia, agraphia
Faciobrachial hemiparesis predominating distally, distal monoparesis of upper limb
Cheiro-oral sensory loss
LH: cortical dysarthria
BH: faciolinguopharyngeal masticatory diplegia (Foix-Chavany-Marie syndrome)
Pseudothalamic hemisensory lossLH: conduction aphasia, ideomotor apraxia, phonogic agraphia / alexia
RH: postrolandic motor hemineglect
Lateral hemianopia or lower-quadrant anopia
Cortical sensation dysfunction
LH: Wernicke’s aphasia, lexical alexia with agraphia, apraxia, Gertsmann’s syndrome
Leftward eye-tracking impairment
RH: Hemineglect & other visuospatial disturbances, asomatognosia, constructive apraxia, optic ataxia
BH: Balint’s syndrome, altitudinal neglect
Lateral hemianopia or upper-quadrant anopia
LH: Wernicke’s aphasia, asynbolia for pain
RH: Acute confusional state, spatial hemineglect, spatial delirium
BH: Pure word deafness, cortical deafness, rejection behavior
34

Common patterns of neurological deficits in patients with acute ischemic stroke
Left (dominant) hemisphere
Aphasia, right hemiparesis, right-sided sensory loss, right conjugate gaze, dysarthria, difficulty in reading, writing, calculating
Right (non-dominant) hemisphere
Neglect of the left visual space, left visual field defect, left hemiparesis, left-side sensory loss, poor left conjugate gaze, extinction of left-sided stimuli, dysarthria, spatial disorientation
Brain stem/cerebellum/posterior hemisphere
Motor or sensory loss in all four limbs, crossed signs, limb or gait ataxia, dysconjugate gaze, nystagmus, amnesia, bilateral visual field defects.
Small subcortical hemisphere or brain stem (pure motor stroke)
Weakness of face & limbs on one side of the body without abnormalities of higher brain function, sensation, or vision
Small subcortical hemisphere or brain stem (pure sensitive stroke)
Decreases sensation of face & limbs on one side of the body without abnormalities of higher brain function.
Clinical stroke subtypes classification (Bamford et al)
Clinical syndromes
Lacunar infarcts (LACI)
Total anterior circulation infarcts
(TACI)
Partial anterior circulation infarcts
(PACI)
Posterior circulation infarcts (POCI)
Symptoms & signs o
Pure motor stroke o
Pure sensory stroke o Sensory-motor stroke o Ataxic hemiparesis (faciobrachial
&brachiocrural involvement were included) o Combination of new higher cerebral o dysfunction (dysphasia, dyscalculia, o visuospatial disorders) o Homonymous visual field defects o
Ipsilateral motor &/or sensory deficit of at least two areas of the face, arm, or leg o Only two of the three components of the
TACI syndrome (higher cerebral dysfunction alone, or with motor/sensory deficit more restricted than those classified as LACI ) o Ipsilateral cranial nerve palsy with contralateral motor &/or sensory deficit o
Bilateral motor &/or sensory deficit o Disorder of conjugate eye movement o Cerebellar dysfunction without ipsilateral long-tract deficit o
Isolated homonymous visual field defect
35

o o o
Characteristics of the Lausanne Registry (stroke subtypes etiologies)
(Bogousslavsky et al.)
Large-artery atherosclerosis o Atherosclerosis with stenosis: narrowing of ≥ 50 per cent of the lumen diameter or occlusion of the corresponding extracranial artery or large intracranial artery
(MCA,PCA, or BA), in absence of another etiology. o
Atherosclerosis without stenosis: plaques or < 50 per cent stenosis in the MCA, PCA, or
BA , in the absence of another etiology & in the patients with at least two of the following five risk factors (age ≥ 50 years, HTN, DM, cigarette smoking, or hypercholesterolemia).
Cardioembolism o
Intracardiac thrombus or tumor, rheumatic mitral stenosis, prosthetic aortic or mitral valves, endocarditis, AF, sick sinus syndrome, left ventricular aneurysm or akinesia after myocardial infarct, acute (>3months) MI, or global cardiac hypokinesia or diskinesia, in absence of another etiology.
Small artery disease o
Infarction in the territory of a deep perforating artery in a patient with Known hypertension, in the absence of another etiology.
Other etiologies o Other possible source must be identified: arterial dissection, fibromuscular dysplasia, saccular aneurysm, AVM, cerebral thrombosis on angiography, angiitis (multiple segmental arterial narrowing on angiography, pleocytosis in CSF), hematologic conditions (polycythemia, thrombocythemia, etc.), migraine (history of migraine, occurrence of stroke during an attack of migraine), or other.
Undetermined etiology o
None of the above causes of cerebral infarction could be determined.
The Modified Rankin Scale
Grade
0
1
2
3
4
5
Description
No symptoms at all
No significant disability despite symptoms: able to carry out all usual duties & activities
Slight disability: unable to carry out all previous activities but able to look after own affairs without assistance
Moderate disability: requiring some help, but able to walk without assistance
Moderately severe disability: unable to walk without assistance, & unable to attend to own bodily needs without assistance
Severe disability: bedridden, incontinent, & requiring constant nursing care & attention
36

Barthel Index (Mahoney & Barthel)
Evaluation
1.
Feeding o Totally dependent o
Needs help o Independent
2.
Bathing o Cannot perform without assistance o Performs without assistance
3.
Grooming o Needs assistance o Washes face, combs hair, brushes teeth
4.
Dressing o Totally dependent o
Needs help but does at least half of task within
5.
Bowel
control reasonable period of time o Independent: ties shoes, fastens fasteners, applies braces o Frequent accidents o Occasional accidents or needs help with enema or
6.
7.
8.
transfers
9.
control
Toilet
transfer
10.
Bladder
Chair bed
Stair-
climbing
Ambulation
/mobility suppository o No accident, able to use enema or suppository if needed o Incontinent or needs indwelling catheter o Occasional accidents or needs help with device o No accidents, able to care for collecting device if used o No use of toilet, bedridden o
Needs help for balance, handling clothes, or toilet paper o Independent with toilet or bedpan o Completely bedridden, use of chair not possible o Able to sit but needs maximum assistance to transfer o Minimum assistance or supervision o
Independent, including locks of wheelchair & lifting footrests o Sits on wheelchair but cannot wheel self o Independent with wheelchair 50 yards only if unable to walk o
Ambulates with help for 50 yards o Independent for 50 yards, may use assistive devices, except for rolling walker o Cannot climb stairs o May use assistive devices o
Independent
Score total:
Investigations of a Stroke Patient:

CT/MRI/MRA scan of brain

L.P. & CSF examination if CT/MRI is not available & in suspected S.A.H.

Carotid Duplex scanning

Transcranial Doppler (TCD)

Digital Subtraction Angiography (DSA)

Conventional Cerebral Angiography

EEG
0
5
10
15
0
5
10
100
(max)
0
5
10
0
5
10
Score
0
5
10
0
5
0
5
0
5
10
0
5
10
0
5
10
15
37


Brain scan

PET & SPECT in TIAs & Stroke-in-evolution

Lab. Works:
CBC with Hct & platelet count; ESR, BUN, Serum Creatinine,
Uric acid; Lipogram; FBS & P PBS

ECG, Echocardiography & Holter monitoring

Chest x-ray & Skull x-ray
Stroke outcome is influenced by:

Stroke subtype

Pt comorbidities
Stroke outcomes include:

Mortality

Worsening

Recurrence

Functional disability

Decreased quality of life
Poorest survival:

Large volume strokes

Impaired level of consciousness

Major hemispheric or basilar syndromes
Predictors of late mortality:

Definite: age & cardiac disease

Potential: CHF & hyperglycemia
Hyperglycemia increase infarct size by:
 ↑ local tissue acidosis
 ↑ BBB permeability

Hemorrhagic transformation
Lowering elevated blood glucose is:

Beneficial in acute non-lacunar stroke

Detrimental in acute lacunar stroke
Lacunar stroke → 2 % 30 - day mortality
Cardioembolic stroke → 15 % 30 - day mortality
Stroke worsening is attributed to:

Stroke-in-evolution

Cerebral edema

Mass effect

Hemorrhagic transformation

Metabolic disturbances
Stroke reoccurrence occurs in:

1 – 4 % within the first 30 days

5 – 25 % at one year

20 – 40 % at 5 years

18 % cumulative risk at 3 years
Stroke severity, age, gender & educational level influence functional disability & quality of life
38

Heidelberg protocol on management of massive hemispheric & cerebellar infarcts with secondary neurological deterioration:
Emergency assessment reveals massive cerebellar or hemispheric stroke
Neurological deterioration & admission to ICU
Vascular evaluation with either TCD or angiography
Hemispheric stroke: Continuous ICP monitoring
Cerebellar stroke: Serial SSEPs & acoustic EPs
Repetitive CT examination if deemed necessary
Hemispheric stroke: CT reveals significant midline shift within 24 hrs
Cerebellar stroke: CT reveals significant hydrocephalus
Massive Rt hemisph. stroke
Abnormal acoustic EPs
Massive cerebellar stroke with hydrocephalus
Massive Lt hemisph. stroke
Massive cerebellar stroke & basilar occlusion
Abnormal EPs
Normal acoustic EPs
Abnormal Normal
acoustic EPs acoustic EPs
Craniectomy External ventricular drain Decision to limit therapy
Medical treatment of raised ICP
General supportive therapy, prudent anticoagulation
39

Heidelberg protocol on recanalization strategies for acute stroke:
Emergency assessment of stroke pts includes vascular & cerebral imaging
Emergency management of stroke pts includes BP & Resp function control
Moderate to severe
Brainstem
Moderate to severe
Hemispheric
Moderate to severe
Hemispheric/
Moderate to severe
Hemispheric
Moderate to severe
Hemispheric syndrome
Basilar occlusion without CT hypodensity syndrome
IC occlusion without CT hypodensity
Brainstem syndrome
IC occlusion with CT hypodensity syndrome
No IC occlusion with/without
CT hypodensity syndrome
Extracranial occlusion without CT hypodensity
Prophylaxis of raised ICP, anticoagulation
Hypervolemic hemodilution Hypervolemic hemodilution
Local intraarterial thrombolysis
IV thrombolysis
Neuronal protection
Emergency endarterectomy
General principals & special interventions of ICU therapy
Secondary prophylaxis & rehabilitation
Strategies for Reducing the Burden of Stroke:
I.
Primary Prevention:

Lifestyle Changes o Smoking cessation. o Abstaining alcohol intake. o Improving diet. o
Increasing exercise.

Risk Factor Modification o Control HTN, DM, Hyperlipidemia, …… etc.
II.
Acute Treatment

To reduce morbidity & mortality.
III.
Rehabilitation

To reduce disability & dependence
IV.
Secondary Prevention

To reduce stroke recurrence.
Essential elements for acute stroke care
The following must be available 24 hours per day regardless of the type of services:

Neurologist

CT scanner

Neuroradiologist

Continuous monitoring

Laboratory

Angiography services / Doppler ultrasonography

Neurosurgeon
40

Stroke Prevention
I.
Primary Prevention of Stroke
A.
Control Risk Factors




Control HTN.
Control DM.
Control hyperlipidemia e.g. low-fat diet.
Cessation of cigarette smoking.







Abstaining alcohol.
Reducing body weight in obesity
Regular physical exercise.
Relaxation therapy.
Avoiding oral contraceptives in high-risk women.
Treating heart disease e.g. AF, MI.
Treating TIAs: Antiplatelets/Anticoagulant therapy; carotid
II.
endarterectomy.
B.
Aspirin (100-325 mg/d) → 18% risk reduction of nonfatal MI, nonfatal stroke, & C.V. death.
Secondary Prevention of Stroke
A.
Control Risk Factors
B.
Antiplatelet Therapy

Aspirin (ASA).

Aspirin (ASA) + Dipyridamole (Persantin).

Ticlopidine (Ticlid).

Clopedogrel (Plavix).
C.
Anticoagulant therapy: for high-risk pts e.g. AF

Low-dose heparin, 5000 U, s.c. bid.

Warfarin (Marevan).
D.
Pts with recurrent TIAs, Stroke, MI

Add dipyridamole to aspirin.
 
dose of aspirin.
E.
Pts with Carotid Stenosis ≥70

Carotid Endarterectomy (CE).
Antihypertensive Treatment in Acute Ischemic Stroke (Heidelberg regimen) o Systolic BP < 220 mmHg o Diastolic BP < 120 mmHg o Diastolic BP > 120 mmHg o
Systolic BP slightly increased over repeated measures o Systolic BP > 220 mmHg & /or o
Diastolic BP 110-120 mmHg

 a) b)
Do not treat
Do not treat
Nitroglycerin 5 mg iv or 10 mg po
Sodium nitroprusside (Nipride a) Nifedipine (Adalat ) 10 mg sl b) Clonidine (Catopres) 0.075 mg sc c) Urapidil 12.5 mg iv
Main issues in a basic protocol for acute stroke management & nursing care

Support of vital functions

Stroke subtype identification

Etiologic diagnosis
41


Prevention of worsening

Prevention of complications

Guidelines for thrombolysis

Early rehabilitation

Treatment of risk factors

Secondary prevention with lifestyle changes, drugs, & surgery
Common reasons for clinical deterioration &/or confusion in acute stroke patients

Pulmonary embolism

Pneumonia

Urinary tract infection (UTI)

Urinary retention

Hyponatremia

Cardiac arrhythmias

Heart failure (HF)

Myocardial infarction (MI)

Poor tissue oxygenation

Gastrointestinal bleeds

Hypotension due to dehydration & hypovolemia

Drugs, alone or in combinations
Risk factors for hemorrhagic transformation

Large cerebral infarction

Impaired consciousness

Hypertension

Excessive anticoagulation

Marked enhancement on CT scan

Midline shift on CT scan
Two major approaches:
1.
Thrombolytic therapy (Recanalization)
2.
Neuroprotective therapy
Thrombolytic Therapy for Acute Ischemic Stroke

Thrombolytic Therapy → Recanalization

Therapeutic Time Window:

3 hrs: Approved.

6 hrs: Doubtful.
 “Too soon is unnecessary, too late is useless”.
Inclusion Criteria:

Acute ischemic stroke with clearly definable time of onset.

Pt presenting within 3-6 hrs from onset of symptoms.

A base-line brain CT scan excluding ICH.
 Patient’s age between 25-75 yrs.
Exclusion Criteria:

Pts with history of stroke or serious head trauma within the preceding 3 months.

Pts who had undergone major surgery within 14 days.

Pts who had a history of ICH.

Pts who had a systolic BP > 185 mmHg.
42


Pts who had a diastolic BP > 110 mmHg.

Pts who had rapidly improving or minor symptoms.

Pts who had symptoms suggestive of SAH.

Ps who had G.I. hemorrhage or U.T. hemorrhage within the previous 21 days.

Pts who had arterial puncture at a non-compressible site within the previous7 day

Pts who had a seizure at the onset of stroke.

Pts who were taking anticoagulants within 48 hrs preceding the onset of stroke & had elevated PTT.

Pts with PT > 15 seconds.

Pts with platelet counts < 100.000/cubic mm.

Pts with glucose concentrations < 50 mg/dl, or > 400 mg/dl.
Tissue Plasminogen Activator (rt-PA) (Actilyse)

Dose: 0.9 mg per kg of body wt (max. 90 mg)

10% of this dose is given as a bolus

Followed by i.v. infusion of the remaining 90% over a period of 60 min.

No anticoagulants or antiplatelet agents be given for 24 hrs after treatment.

BP should be maintained within pre-specified values.
Guidelines for Thrombolytic Therapy for Acute Stroke
[Adapted from the American Heart Association Guidelines]
I.
Intravenous r-TPA (0.9 mg/kg, maximum 90 mg) with 10% of the dose given as a bolus followed by an infusion lasting 60 minutes is recommended treatment within 3 hours of onset of ischemic stroke.
II.
Thrombolytic therapy is not recommended unless the diagnosis is established clinically & CT of the brain has excluded ICH.
III.
Thrombolytic therapy cannot be recommended for persons excluded from the NINDS
Study for one of the following reasons:
1.
Current use of oral coagulants or PT> 15 seconds (International Normalized
Ratio [INR] > 1.7);
2.
Use of heparin in the previous 48 hours & a prolonged PTT.
3.
A platelet count less than 100 000/mm3;
4.
Another stroke or a serious head injury in the previous 3 months;
5.
Major surgery within the preceding 14 days;
6.
Pretreatment systolic blood BP> 185 mm Hg or diastolic BP>110 mm Hg;
7.
Rapidly improving neurological signs;
8.
Isolated, mild neurological deficits, such as ataxia alone, sensory loss alone, dysarthria alone, or minimal weakness;
9.
Prior intracranial hemorrhage;
10.
Blood glucose less then 50 mg/dl, or more than 400 mg/dl
11.
Seizure at the onset of stroke;
12.
Gastrointestinal or urinary bleeding within the preceding 21days; or
13.
Recent myocardial
IV.
Thrombolytic therapy should not be given unless the emergent ancillary care & the facilities to handle bleeding complications are readily available.
V.
Caution is advised before giving r-TPA to persons with severe stroke (NIH Stroke
Scale Score greater than 22).
VI.
Because the use of thrombolytic drugs carries the real risk of major bleeding, whenever possible the risks of potential benefits of r-TPA should be discussed with the patient & his or her family before treatment is initiated.
43

BP Management after tPA for Ischemic Stroke
1.
If diastolic BP is > 140 mm Hg, start an infusion of sodium nitroprusside (Nipride)
(0.5-10 mcg/kg/min).
2.
If systolic BP is > 230 mm Hg &/or diastolic BP is 121-140 mmHg, start labetalol
(Trandate) 10 mg I.V. over 1-2 minutes. The dose may be repeated &/or doubled every 10 minutes up to150 mg total. Continue BP measuring q 15 minutes. If labetalol cannot be used or is ineffective, nitroprusside (Nipride) or nifedipine
(Adalat) may be used.
3.
If systolic BP is > 180-230 mm Hg &/or diastolic BP is > 110-120 mm Hg on two readings 5-10 minutes apart, give labetalol (Trandate) 10 mg I.V. over 1-2 minutes.
The dose may be repeated or doubled every 10-20 minutes, up to 150 mg total. If labetalol is contraindicated (e.g. CHF), use nifedipine (Adalat) , 10 mg PO or SL
Neuroprotective Therapy

Neuroprotection aims at preventing or limiting the brain tissue damage that occurs in areas of reduced CBF (e.g. the penumbra region surrounding an infarct)

Hypothermia has a CNS neuroprotective effect:

Transient mild to moderate hypothermia (30 – 35 o C) → ↓ infarct size during
 temporary but not permanent focal ischemia

CNS hypothermia can be achieved by:



Blankets containing ice
IV iced saline
IV drugs e.g. barbiturate coma









Classes of neuroprotective agents:
 Calcium channel antagonists:
 Voltage sensitive (e.g. Nimodepine )
 Sodium channel antagonists (e.g. Phenytoin )
 N – methyl – D – aspartate ( NMDA ) antagonists


Competitive (e.g. Dextromethorphan
Non – competitive (e.g.
)
Cerestat, Memantine )
 Glutamate & glycine antagonists



Presynaptic release inhibitors
Postsynaptic antagonists
Synaptic modulators
AMPA antagonists
GABA antagonists
Calpane antagonists
Endothelium antagonists
Adenosine enhancers
Polypeptide growth factors
Antiadhesion molecules
Apoptosis inhibitors
Antioxidants (e.g. Tirilazad )
Examples of Currently Available Neuroprotectants:

Phenytoin (Epanutin)

Nimodipine (Nimotop)

Naloxone (Narcan)

Piracetam (Nootropil)

Lubeluzole (Prosynap)
44

Candidates for Short-term Prophylactic Neuroprotection
Cardiac surgery
Neurological procedures o Coronary artery bypass grafts o
Cardiac valve replacement o Heart transplant o Left ventricular assist devices o Aortic dissection repair o
Carotid endarterectomy o Aneurysmectomy o Arteriovenous malformation resection o Endovascular therapy o
Cerebral angioplasty
Neuroprotective agents
Class Mechanism
Calcium channel inhibitors o
Voltage sensitive Ca channel antagonist o Noncompetitive NMDA antagonists o
Competitive NMDA
Medications
Nimodepine
Cerestat
Selfotel
Calcium channel modulators
Presynaptic glutamate inhibition
Other ion channels antagonists o Glycine site antagonists o Polyamine site antagonists o Adenosine transport inhibitors o Presynaptic voltage sensitive o Sodium channel antagonists o Unclear mechanism o AMPA receptor antagonists o GABA receptor agonists o
Plasma membrane abuse-
ACEA-1021
ZD9379
Eliprodil
Propentofylline
BW619C89
Fosphenytoin
Lubeluzole
NBQX
Chlomethizoale
Monogangliosides
Agents directed against delayed effects of ischemia dependent antagonism o Lipid peroxidase inhibitor o Anti-adhesion molecules
Tirilizad
CD11b/18 o
Synthesis of phosphatidylcholine o Trophic agents
NMDA = N – methyl – D – aspartate bFGF = basic fibroblast growth factor
ICAM-I (Enlimolab)
Citicoline bFGF
GABA = gamma amino butyric acid
AMPA = α-amino-3-hydroxy-5-methyl-4-isoxozole propionate receptor antagonists
Candidates for Long-term Prophylactic Neuroprotection

Multiple stroke risk factors

Atrial fibrillation (AF)

Asymptomatic carotid stenosis

Subclinical diseases:
-
Intimal-media carotid plaque
-
Elevated ankle-brachial blood pressure ratio
45

-
High-intensity transient signal by transcranial Doppler
-
Silent stroke

Transient ischemic attack (TIA)

Minor stroke
Prophylactic Measures in Acute Stroke

Immobilization causes several problems in stroke pts, e.g. DVT , pressure ulcers, & infection.

All stroke pts are at risk of DVT & should receive prophylactic treatment.

DVT may cause pulmonary embolism, which may be fatal.

Pneumatic stockings & / or s.c. heparin should be used.

Heparin dose is adjusted to prolong the PTT to 1.2-1.5 times control values

Another option is the use of coumadin to prolong the PT to 1.2-1.5 control values.

Frequent turning (every 2 hrs) & early identification & treatment of pressure ulcers is essential

C.V.L
., urinary catheters, & endotracheal tubes are prone to cause infection & should be discontinued as soon as possible.

Frequent turning , suctioning , & chest percussion prevent atelectasis & mobilize pulmonary secretions.

Swallowing disorders

the risk of aspiration pneumonia.

NGT feeding is used in pts who are unable to tolerate oral nutrition.

Percutaneous gastrostomy & tracheostomy may be needed for pts with severe swallowing or aspiration difficulties.

Stress ulcer prophylaxis is needed in stroke pts.

Cimetidine (Tagamet) or sucralfate (Ulcar) may be used for this purpose.
Treatment & therapy to improve stroke outcome
Specific Therapies

Increase cellular resistance to ischemia

Minimize neurotoxic effects of dying neurons

Reduce edema or inflammation

Improve flow in ischemia penumbra (by collaterals or reperfusion)

Enhance neuronal repair

Prevent early recurrence (e.g. recurrent embolus)
Nonspecific Treatments

Improvement in wakefulness (may reduce aspiration pneumonia)

Prevention of secondary complications (e.g. venous thrombosis)

Prevention of depression after stroke (occurs in approximately 40%)

Management of sequelae (e.g. physical & occupational therapy)
Major therapies for acutely increased intracranial pressure

Hyperventilation

Osmotic diuretics e.g. Mannitol 20%

Intravenous barbiturates

Ventriculostomy
Factors that contribute to increased intracranial pressure

Hypertension
46


Hypoxia

Seizures

Fever

Head positioning

Increased intrathoracic pressure
Comparing ordinary stroke care on general medical wards with structured stroke care on neurologic wards

Patients treated by structured management on neurologic wards were able to leave hospital on an average 16 days earlier (shorter hospital stay)

Of each 100 patients treated by structured management on neurologic wards, 13 more were able to return home at hospital discharge.

Of each 100 patients treated by structured management on neurologic wards, 17 more were totally independent in their daily life at 1 – year follow up.
Estimated outcomes after ischemic stroke
Worsening
Mortality
30 – day
1 – year
5 – year
Stroke recurrence
30 – day
1 – year
5 – year
Functional disability
Quality of life
24% stroke evolution during hospitalization
8 – 20%
15 – 25%
40 – 60%
3 –10%
5 – 14%
25 – 40%
24 – 53% of stroke survivors with complete or partial dependence
27% decrement in the mean Quality of Well
Being Score at 6 months
34% at 52 months post-stroke Dementia
Therapeutic Protocol of Ischemic Stroke
1.
Care of the comatose (or bedridden) patient
2.
Control risk factors
3.
Anticoagulants in:

Stenotic lesions (+ surgery)

TIAs, RIND, Stroke - in - evolution

Completed stroke with a minor deficit

Embolic lesions e.g. in AF, MI

If embolic source is unknown use:
-
Warfarin (Marevan) for several months, then Antiplatelets (e.g.
Asprin )
-
Avoid anticoagulants in infective endocarditis & in massive infarcts
47

Heparin

IV bolus: 5000 - 10000 units

IV infusion: 1000 - 1500 units / hr
-
Check PTT initially & daily
-
Adjust the dose to keep PTT at 1½ - 2 times that of control
-
Antidote: Protamine i.v.
Marevan (Warfarin)

5 mg tid on first day

5 mg bid on 2 nd day

5 mg o.d. on 3 rd day & afterwards
-
Check PT initially & daily for 1 wk, then every 2-3 wks
-
Adjust the dose to keep PT at 1½-2 times that of control
-
Antidote: Vitamin K i.v. 50 mg + fresh frozen plasma
4.
Antiplatelet Agents:

Aspirin (ASA) 150 –325 mg daily & /

Or: Persantin (Dipyridamole) 75 mg tid

Or: Ticlid (Ticlopidine) 250 mg bid

Or: Plavix (Clopidogrel) 75 mg o.d.
5.
Surgery:

Carotid endarterectomy (Stenosis > 70%)

Posterior fossa decompression in massive cerebellar infarction & brainstem compression

Symptomatic extracranial vertebral artery disease, subclavian steal, & aortic arch disease

Temporal artery to MCA anastomosis is not superior to medical treatment
6.
Anti-edema agents
7.
Anticonvulsants for seizures
8.
Vasodilators reduce perfusion to ischemic areas (Intracerebral steal). Must be activated in acute stroke
9.
Thrombolytic Therapy (rt – PA)

Therapeutic time window : 3 – 6 hrs

Inclusion & Exclusion Criteria

Dose: 0.9 mg/kg wt., Max. 90 mg i.v. o
10% as an i.v bolus, o 90% as ifusion over 60 min.
10.
Neuroprotectants :

Epanutin (Phenytoin)

Nootropil (Piracetam)

Narcan (Naloxone)

Nimotop (Nimodipine)
11.
Other medications:

Trental (Pentoxifylline), 400 mg bid – tid

Duxil (Almitrin+Raubasine) , bid

Dilution therapy : Low-molecular weight dextran
12.
Physical Therapy & Rehabilitation

Occupational Therapy

Speech Therapy
48

HEMORRHAGIC STROKE
INTRACEREBRAL HEMORRHAGE
Establishing the diagnosis of Intracerebral Hemorrhage
Causes & Risk factors for Intracerebral hemorrhage
Primary

Hypertension (50%)
Secondary

AVMs & Aneurysms (5%)

Cerebral amyloid angiopathy (12%)

Cerebral neoplasm (8%)

Anticoagulants (10 %)

Thrombolytic therapy

Vasculitis

Trauma

Sympathomimetic drug abuse

Alcohol abuse
Clinical Assessment

Abrupt onset

The stroke evolves gradually over minutes or hrs without the stepwise progression
seen in thrombotic strokes

Putaminal hemorrhage: resembles M.C.A. occlusion

Thalamic hemorrhage: → contralateral hemiplegia + hemianesthesia + restricted upward gaze, downward deviation, skew deviation, or even conjugate deviation away from the side of lesion (wrong-going eyes)

Pontine hemorrhage: → coma + pinpoint pupils that react to light + bilateral decerebrate posturing + impaired caloric response

Cerebellar hemorrhage → sudden dizziness & vomiting + marked truncal ataxia with inability to stand or walk + ipsilateral pontine compression → paresis of lateral conjugate gaze toward the lesion, ipsilateral facial paresis & corneal areflexia ± coma & death from brainstem compression if untreated. Surgical evacuation is lifesaving.
Investigations:
 L.P → bloody CSF (Threat of herniation in cerebellar hemorrhage.)

CT scan of brain confirms the diagnosis
Treatment:

Care of the comatose (or bedridden) pt.: as usual

Blood pressure control

Anti-edema agents: Steroids, Mannitol or Glycerol

Surgery: Evacuation of hematomas in accessible locations

Anti-convulsants for seizures

Correction of clotting abnormalities

Platelets for thrombocytopenia

Fresh-frozen plasma & vit. K for coumarin overdose

Protamine for heparin overdose
Current recommendations regarding surgical or nonsurgical treatment of
49

intracerebral hemorrhage (modified from Minematsu & Yamaguchi)
ICH location Clinical/CT features Treatment
Putamen Alert, small
Comatose, large cc)
(30-60 cc)
ICH (≤ 30 cc)
ICH (> 60
Drowsy, intermediate ICH
Non-surgical
Non-surgical
Consider evacuation
Caudate
Thalamus
Alert or drowsy, with intraventricular hemorrhage
& hydrocephalus
Drowsy or lethargic, with
Consider ventriculostomy
Consider evacuation
Lobar white matter
Cerebellum
Pons, midbrain, medulla blood in 3rd ventricle & hydrocephalus
Drowsy or lethargic, with intermediate ICH (20-60cc),
Progressive decline in level of consciousness
Non-comatose, with ICH ≥ 3 cm in diameter, & /or hydrocephalus, &/or effacement of quadrigeminal cistern
Consider evacuation
Non-surgical
Evacuation recommended, preceded by ventriculostomy if patient is actively deteriorating
50

SUBARACHNOID HEMORRHAGE (SAH)
Establishing the diagnosis of SAH
Clinical Assessment:
A.
Aneurysmal rupture:

Sudden onset of severe headache ± coma or confusion

Meningeal signs + low-grade fever

Funduscopy usually reveals subhyaloid hemorrhage

Focal neurologic deficits from blood spreading to brain, or later from vasospasm

Infarction from compromised blood flow or thrombosis

Hydrocephalus , early or late, & may require shunting

Clinical localization of the aneurysm:
-
Cavernous carotid artery aneurysms → Pain behind the eye + dysfunction of
2 nd to 6 th cranial nerves.
-
M.C.A. aneurysms → hemiplegia ± aphasia
-
Aneurysms at the junction of posterior communicating & int. carotid arteries
→ 3 rd n. palsy
-
Ant. Communicating artery aneurysms → abulia or paresis of lower limb
-
Basilar & vertebral artery aneurysms → lower cranial nerve palsies
B.
AVMs:
 Usually → seizures or hemorrhage ± ischemia around
 Usually → a combination of intracerebral & SAH

Chronic headache, sometimes migrainous, prior to hemorrhage

A bruit over the eyeball, carotid artery, or mastoid
 ± Telangiectasias, cavernous angiomas, & venous angiomas
C.
SAH with no demonstrable lesion may result from:

Rupture of cryptic AVMs, or

Spinal AVMs with a bruit heard over the spine
Hunt & Hess, & WFNS Grading System of Subarachnoid hemorrhage
Headache Nuchal rigidity
Hunt & Hess
Consciousness Deficit Grade GCS
WFNS
Major focal
+
++
*
*
*
+
++
*
*
*
Alert
Alert
Lethargy,
Confusion
Stupor
Deep coma
-
- or III, IV
+
++
Decerebrate
Rigidity
0
I
II
III
IV
V
15
13-14
13-14
7-12
3-6 deficit
Absent
Absent
Present
+ or –
+ or –
Grade 0: enraptured or intact aneurysm; GCS: Glasgow coma scale; WFNS: World
Federation on Neurosurgery.*There are no descriptions about these in the original article; but they are present more or less
51

Investigations
1.
CT scan of brain: usually shows the SAH, edema, parenchymal & ventricular hemorrhage, & hydrocephalus
2.
L.P. & CSF exam: if CT scan is not available or is nondiagnostic → bloody CSF
3.
Skull x-rays may show calcification in an AVM & in an aneurysm
4.
Cerebral Angiography : o Early in pts ē minor neurologic deficit o
Later in pts ē severe neurologic deficit
5.
If cerebral angiography is –ve: o Re-angiogram after a few weeks o Look for a spinal AVM:
A bruit over the spine
Spinal angiography
MRI of the spine
Therapeutic Protocol of SAH:

Surgery is the treatment of choice for suitable pts whose aneurysms are surgically accessible

AVMs may or may not be amenable to surgery
A.
Pre-operative measures:
1.
General precautions:

Control HTN by antihypertensive drugs

Sedation ē Phenobarbital or Diazepam

Prophylactic anticonvulsants to prevent seizures

Stool softeners to prevent straining

Darkened quite room

Volume expansion in hypovolemia (from hemorrhage)
2.
Antifibrinolytic agents:

Epsilon-aminocaproic acid ( Amicar ), 30 mg/day, mixed in 1 liter of 5 % dextrose & 0.45% normal saline & given IV over 24hrs. or 4g PO q3hrs.
Continued until the time of surgery or for 6 wks
3.
Antiedema agents : Dexamethasone, Mannitol, or Glycerol for

ICT
Management of vasospasm:

Vasospasm → drowsiness or focal neurologic signs starting 2-3 days after SAH & maximum at 7 days, due to release of vasoactive compounds e.g. serotonin, catecholamines, peptides & endothelin

Vasospasm is diagnosed by TCD

IV isoproterenol & nitroglycerin are useful

Volume expansion by 5% albumin IV (C/I in low cardiac output & CHF). Monitored
CVP (adjusted to 8-12 mm Hg). Hypervolemia may be combated ē phlebotomy & hemodilution to achieve a hematocrit of 30-35%

Dilatation of vasospastic segments of cerebral arteries using balloon angioplasty

Nimodipine ( Nimotop ), 30-60 mg PO q 4 hrs (avoid hypotension) may prevent vasospasm following SAH.
B.
Surgery:
1.
Contraindications: o
Coma o Severe neurologic deficits
52

2.
Timing: o Early aneurysm surgery in the first 24-48 hrs is now preferred (before vasospasm)
+ Irrigation of the S.A. space to remove blood
± Instillating tissue plasminogen activator to dissolve adherent clot after clipping
the aneurysm
Procedures:

Clipping the neck of the aneurysm is the most common procedure

Wrapping the aneurysm with muscle

Coating the aneurysm with plastic material

Occluding the internal carotid artery in the neck

Endovascular occlusion of the aneurysm with Guglielmi electro – detachable coils ( GDC )

Endovascular application of cellulose acetate polymer ( CAP )

Block resection or ligation of the major arteries is done for AVMs

Balloon occlusion of giant aneurysms of I.C. carotid artery.

Radiotherapy of AVMs using a proton beam, or using the gamma rays from a cobalt source

Shunt for hydrocephalus complicating SAH early late

Embolization of aneurysm in pts in whom surgery is contraindicated, using horse hair or fine coils
Initial management in Aneurysmal Subarachnoid Hemorrhage
Airway management o Intubate with mechanical ventilation for aspiration, neurogenic pulmonary edema, or motor score at withdrawal or worse o IMV mode (8-10 breaths/min) & PEEP of 5 (assist-control mode if patient is moribund or has possible progression to brain death) o Consider pressure-controlled ventilation for significant aspiration or early ARDS
Fluid management o 2-3 liters of 0.9 % NaCl o
3 % NaCl, 50 ml tid, in patients at risk for cerebral vasospasm o Fludrocotisone acetate (0.4 mg in 200 ml of glucose 5 % bid.) if hyponatremia is present
Blood pressure management o Accept MAP ≤ 125 mmHg ; if MAP > 125,
Esmolol bolus, 500 µg/kg in 1 min, or
Enalapril , 1-5 mg IV
Nutrition management o Enteric nutrition with continuous on day 3
Additional measures o Nimodipine , 60 mg qid. o Stool softener o Pneumatic compression devices o Acetaminophen with codeine or morphine, 1-2 mg, for pain management
ARDS, adult respiratory distress syndrome; IMV, intermittent mandatory ventilation; IV, intravenously; MAP, mean arterial pressure; PEEP, positive end-expiratory pressure
53

Guidelines for management of symptomatic cerebral vasospasm o Discontinue any antihypertensive or diuretic agent o Insert pulmonary catheter o Start volume replacement with albumin 5 % , 250 ml, or hypertonic saline & add dobutamine , 5-15 mg/kg/min, to attain cardiac index > 41/min/m2 & pulmonary artery wedge pressure of 12-14 mmHg o If no clinical improvement within 1-2h, transcranial Doppler ultrasonography (TCD) o TCD velocity > 120 m/s, consider phenylephrine , 10 mg/min, & increase mean arterial pressure to 20 mmHg above baseline. Consider discontinuation of nimodipine for 24 hours o No success, perform cerebral angiography o Focal cerebral vasospasm, consider angioplasty o
Diffuse cerebral vasospasm, consider intra-arterial papaverine
Substances considered to generate vasospasm
1.
Proteinaceous substances hemoglobin, angiotensin, thrombin, fibrin degradation product, bradykinin, vasopressin, endothelin
2.
Amine Serotonin, norepin, epinephrine, dopamine, acetylcholine, histamine, plasmin
3.
Eicosanoide Prostaglandine, thromboxane A2, leukotrine, lipideroxide
4.
Free radicals
5.
Ca 2+, K+
6.
Hypothalamic
Peri-operative management

Nimodipine administration for 10 days to 2 weeks

Triple H therapy (Hemodilution, Hypervolemia, Hypertension)

Endovascular angioplasty with intra-arterial papaverine administration

Barbiturate coma therapy if vasospasm remains intractable
Intra-operative management

Topical administration of papaverine to spastic vessels

Third ventriculostomy of the lamina terminalis

Opening of the Liliequist membrane

Closure of aneurysm (s) with Yasargil’s clip

Hemodynamic monitoring ( Peltier, micro-Doppler )

Closure of craniotomy without any drainage (no cisternal drainage, no decompressive craniotomy)
54

Comparison between surgical clipping & endovascular occlusion with Guglielmi electro-detachable coils
Surgical Invasiveness
Radiation doses
Surgical clipping
High
0
Endovascular occlusion with GDC
Low
1000 - 3000 rad.
Duration of procedure
Accessibility
2.5 - 3 h
Difficult to access in certain anatomical location
Almost possible
1-3 h
Relatively easy to access except remarkable atherosclerosis
Complete occlusion Sometimes not possible in wide-necked AN (neck size
> 4 mm)
5 - 10 % Thromboembolic complication Rare
Aneurysm re-growth Rare 10 - 50 %: - coil compaction
- coil migration
Suspicious Alleviating the mass effect Possible
Emerging trends in acute stroke treatment from surgical point of view
SAH

Aneurysm rupture
 Timing of surgery


Vasospasm prevention:
Triple H therapy, calcium antagonist, radical scavenger, intra-operative t – PA,
 endovascular angioplasty with papaverine
 Clipping or coiling

AVM bleeding
Surgery, embolization, radiosurgery
ICH

Amyloid angiopathy

Anticoagulant therapy

Cavernous angioma

Surgical removal compared with stereotaxic aspiration
Cerebral ischemia

Arterial dissection

Revascularization procedures: Thrombolysis, endovascular surgery, microsurgery

Surgical decompression: Strokectomy
55

Comparison of microsurgery, endovascular embolization & radiosurgery in treatment of cerebral AVM
Microsurgery Radiosurgery
Invasiveness
Accessibility
High
Sometimes difficult in deep seated
AVMs
Larger
Endovascular embolization
Low
Relatively easy
Smaller
Low
Easy
Smaller Effect on adjacent brain
Functional evaluation of the adjacent brain
Complete cure
Difficult
Usually possible
Possible
(Superselective
Amytal testing)
Rare (10 – 20 %)
Difficult
NPPB Rare
85 – 90 % in small AVMs
None Sometimes occurs
(especially in large, high flow AVMs)
Rare 2 – 5 % None Hemorrhagic complications
Ischemic complications
Radiation dose
Rare
0
2 – 10 %
1000 – 2000 rad
Rare
Rare
2000 – 3000 rad
(marginal dose)
2 – 10 % Adverse effect of radiation
Length of hospitallization
None
1 – 2 weeks
NPPb = normal perfusion pressure
3 – 7 days 2 – 3 days
56