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L39&40 - Pathology of Stroke and Trauma
Cerebrovascular disease
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L39&40 - Pathology of Stroke and Trauma
Cerebrovascular disease
- Classify the different types of cerebrovascular disease
- List the risk factors for the development of cerebrovascular disease
- Explain the pathogenesis and pathophysiology of cerebrovascular disease
- Outline the clinical presentations of cerebrovascular disease
- List, in brief, the morphological features of cerebrovascular disease
Intracranial haemorrhage
- Classify the different types of intracranial haemorrhage
- Explain the pathogenesis and pathophysiology of the different types of intracranial haemorrhage
- Outline the risk factors, typical clinical presentations and sequelae of the different types of intracranial haemorrhage
CNS Trauma
- Outline the main types and pathological features of traumatic parenchymal injuries to
the central nervous system
- Outline the main types and pathological features of vertebral artery injury*
Cerebrovascular Disease
- A pathological abnormality of blood flow leading to brain injury (neurological dysfunction
- Non-specific in the same way that cardiovascular disease is non-specific
Aetiologies Incldue;
- Ischaemia
- Haemorrhage
- Infarct
- Others - vascualitis, embolic disease, atherosclerosis, vascular
tumour, vascular malformation, hypertension, trauma,
Divisions of Cerebrovascular Disease
Ischaemia
Focal Cerebral Ischaemia (Stroke)
- Focal infarction due to hypoxia
- Comlication - focal loss of neuroglial tissue
- Retinal + Spinal Involvement - occlusive (retinal) hypoperfusion/trauma (spinal)
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Pathophysiology
- Ischaemia => cellular Hypoxia
- Depletion of ATP
- Cellular functions cease
3. Inability to maintain membrane potential and Ion gradients
- Incapable of Depolarisation
- Tendency toward seixure
- Reversal of ischaemia at this point =. TIA
- Unregulated influx - Ca, Na => H2O => cellular oedema (hyperosmolar cytoplasm)
- Cell Death
- Release of Glu
- Activates excitatory neurons => increased Ca influx => amplified problem
- Degeneration of BBB => Vasogenic Oedema
- Inflammation (non-specific/neutrophlic) => exacerbated Oedema
- Microcirculatory compromise
- Increased ICP
- Global oedema
- Herniation - more common wiht hemispheric and post. circulation stroke
Haemorrhagic Stroke - extravascular RBCs + haemolysis => neurotoxic => amplified cell damage-
Clinical Presentation
- Variable - Symptoms vary depend on region of the brain effected by hypoxia
- Constellation - combination of many signs + symptoms
- DDx - hypoglycaemia, malignant hypertension, meningitis/encephalitis, migraine, tumours, vasospasm, drugs, brain tumour
Motor
- Hemiparesis, monparesis, quadriparesis
- Dysarthria, facial droop
- Ataxia (spinal, cerebellar, cortical)*
Higher Function
- Aphasia - speach impairment?
- Decrease in level of consciousness
- Personality change, emotional lability - prefrontal cortex etc.
– Hemiattention/inattention
Sensory
- Visual Field Deficits - depends where the stroke has occured
- occlusive stroke => retinal impact
- Diplopia
- Vertigo
Principles of Management
- Urgent Hospitalisation - See within 3-4 hours (sooner the better) + A.B.C.
- Resolve Occlusion - Thrombolyse/ Recannalise
- Anticoagulants + Thrombolysis (alteplase>rt-PA) - Occlusive Strokes only
- Thrombolysis within 60 minutes - tPA as bolus within 4.5 hrs from onset
- Aspirin/Clopidogrel - first dose (300mg) + long term (100mg/day)
- Endovascular Thrombectomy - remove clot manually
- Blood Pressure and Glycaemic management
- BP - lowered to <185/110 if eligible for thrombolysis
- In ineligible pts, BP > 220/120 should be cautiously reduced (<10-20%)
- Glycaemic -
- Specialised Stroke Unit - 6% increase in survival
- Surgery if Haematoma
- Single most important recommendation
- Ongoing Rehabilitation (+ongoing aspirin use)
- lifestyle modifications - addressing risk factors
- Pharmacotherapy - addressing risk factors
Assessment
Principles -
- Rapid transport - paramedics decide which hospital to transport pt to
- RACE Stroke Scale - to assess if pt needs thrombolysis (only certain hospitals have this capacity)
- Imaging -
- CT (without contrast)
- MRI - after first 24 hrs
- Echocardiogram
- Angiogram
- Exclusion of ddx
- Masqueraders of stroke - migraine, seizure
- ROSIER - stroke scale for recognising stroke in emergency department
- Investigations
- ECG
- FBC + Coags, ESR, CRP, BSL
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Surgery Hemicraniectomy (less common these days)
- Remove piece of skull to alleviate ICP and allowing brain to swell
- Freeze piece for 6 weeks
- return skull on to brain
Global Cerebral Ischaemia (Hypoxic Encephalopathy)
- Duration -Transient, Mod, Severe
- Severe - oedematous brain (widened gyri, narrowed sulci)
- Poor demarcation of W/GM
- Pseudolaminar Necrosis
- Survival - liquefactive necrosis, autolysis and homogenisation of WM
- No reactive change (e.g. oxidative repurfusion injury)
Aetiology
- Global Hypoperfusion - hypovolaemic shock, reduced SBP (<50mmHg)
- Hypoxaemia - various types of anaemia, hypoventilation, poisoning etc.
3. Hypoperfusive Stroke (cause other than Occlusion, haemorrhage)
- Reduced Cardiac output
- Reduced systolic Blood Pressure - <50mmHg
- Global > Focal/multifocal - hypoperfusive stroke is less likely to cause focal/multifocal stroke
Pseudolaminar necrosis and white matter homogenisation, widened gyri etc.
Other Vasculopathies
Reversible Cerebral Vasoconstriction
- Increasing vasoconstriction, which reduced cerebral blood floow
- Clinical Presentation - 3 to 4 weeks of headaches
Aetiology
- Drugs - SSRI, Triptans, cold and flu
- Pregnancy - during and post-partum
- Accelerated hypertension
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Venous Sinus Thrombosis
- Clinical Presentation - headache +/- vomiting (since ICP=raised), papilloedemam focal neurological deficit, AMS
- Treat with anticoagulation
Aetiology
- Thrombophillic Conditions - OCP, Pregnancy
- Neoplasia
- Infection
- Trauma
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Epidemiology of Stroke and CVD
Prevalence and Incidence
- 475 000 Aust. have had stroke - 3.4% of Aust.
- 56 000 Strokes p.a.
- Incidence Increases with Age
- M~F - men more common below 85, women more common above
Burden of Disease
- 40% of Total Disability in Aust. - 65% of survivors will have associated disabilities
- 3rd Cause for premature Death - 10 000 p.a.
Preventable
- Reducing Incidence - improved 1ry, 2ry, 3ry prevention technique
- Yet 80% can still be prevented
Risk Factors for Stroke + CVD
- Overlap With Coronary Art. Disease
- RF for HT - SMOKING, alcohol abuse diabetes, obesity
- RF for athersclerosis - hyperlipidaemia, HT, Diabetes, smoking, obesity
- RF for Thrombophillia thrombosis/thrombembolism - pregnancy, OCP,
- Atrial Fibrillation - 11% of deaths
- Haemophillia
- Anything which damages Cerebral BVs
- Congenital predispositions to Aneurysm - Erhlers-Danlos, Marfan's Polycystic KD etc.
- Vasculitis
- CAA (Amyloid angiopathy), AVM's (arteriovenous malformations)
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Intracranial Haemorrhage
Officially in Trauma - Canadian CT Brain criteria
In Practice (especially ward)
CT Brain for any fall (even low energy) where;
- There are features of AMS or focal neurological deficit to suggest possible intra-cranial pathology
- Anti-coagulated patient where the historian seems unreliable and the fall was unwitnessed
- Anti-coagulated patient where the fall was witnessed or the patient specifically mentions head trauma
In many low energy falls, the most likely type of intracranial bleed will be a subdural, which is a classically a slow bleed. Here, performing a CT immediately may not capture the bleed, since these take time to form a haematoma. In patients without AMS, it may be possible to observe the on the ward and image if they develop AMS
Subdural Haemorrhage
- Aetiology - can be associated with trauma (usually minimal - old people)
- Complication - occlusive stroke (compression of brain parenchyma
- Pathology
- Image
- Banana Shaped - no dural attachments to compartmentalise haemorrhage
- Clinical Presentation
- Slow progression of symptoms
- May present with a seizure or LOC days-weeks post head trauma
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Sub-arachnoid Haemorrhage
- Aetiology - usually non-traumatic causes (berry aneurysm, Vert.Art. dissection) can be associated with trauma as well
- Complication - intraventricular Bleeding, haemorrhagic stroke (sometimes - haematomal compression of parenchyma, invasion of parenchyma)
- Clinical Features - thunderclap headache, high mortality, MENINGISM, does not usually lead to ICP
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Intracerebreal Haemorrhage (haemorrhagic stroke)
- Aetiology -
- 1ry - Usually spontaenous Hypertensive bleeds
- 2ry - can be associated with trauma, arteriovenous malformations/vascular tumours, cerebral amyloid angiopathy, vasculitis, malignancy
- Complication - intraventricular Bleeding, haemorrhagic stroke (always, ICH=HS)
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Extradural Haemorrhage
- Aetiology - can be associated with trauma
- Complication - occlusive stroke (compression of brain parenchyma
- Pathology
- Arterial Bleed - commonly resulting from trauma to middle meningeal artery
- IMAGING - non-contrast CT brain
- Biconvex Lemon shaped, peels dura from underlying bone. Haematoma compartmentalised by dural attachments to skull.
- Clinical Presentation symptoms - Fast Progression
- skull fracture,
- Lucid interval - brief loss of consciousness following inciting event, return of consciousness (lucid). Sleep/LoC
- Symptoms of raised ICP (headache, neurological deficits - contralateral hemiparesis)
- Ipsilateral Pupil Dilation/Mydriasis - 90% of trauma to side of head
- Decerebrate Posturing - May assume decerebrate posture if severe
- Management
- ABCDE - IVH for MAP > 60, consider IV mannitol, remove devices that obstruct venous drainage (C-Spine collar, obstructive lung disease, position bed to assist drainage), hyperventilate to lower CO2 and prevent intra-cerebral vasodilatation
- N/S input + Anaes for Rapid Sequence intubation - burr-hole evacuation haematoma or decompression craniotomy
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CNS Trauma
Types of Injuries
- Abrasion - graze
- Incision - a sharp force injury, object moves across tissue (slicing with knife)
- Puncture - a sharp force injury, object penetrates tissue (stab, needle)
- Avulsion - separation of an antomical structure by pulling? (Finger torn off)
- LACERATION - a blunt force injury, with tearing tissue (punch, rotational)
- CONTUSION - a blunt force injury, without tearing but, causing compression of tissue (bruising)
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Epidemiology
- Trauma - Significant cause of traumatic deaths is linked with Head injury
- Commonest Associations - falls, motor accidents, interpersonal violence
Ischaemia (CVD), Haemorrhage (ICH), Trauma - Commonalities
Haemorrhage, of any kind, will likely cause Ischaemia.
- Ischaemia leads to Infarction (Cerebral Infarction = Stroke).
- Infarction leads to Necrosis
Terminology
Haemorrhage
- Abnormal loos of blood from the vasculature
- Irreversible - once lost blood is extravasated
- Haemolysis of Extravasated RBCS - neurotoxic, can directly lead to necrosis
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Hypoxaemia (reduced oxygenation of Blood)
- Reduced oxygenation of Hb
- High altitude
- Mixing of oxyg+deoxyge blood
- Pulmonary Abnormality - V/Q
- Reduced O2 Carriage Capacity
- Anaemia
- Poisoning (carbon monoxide etc.)
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Ischaemia (hypoperfusion)
- Deficient Blood Supply to the Tissue
- Reversible (potentially)
- Focal
- Multifocal
- Global Cerebral Ischamia => Global Cerebral Hypoxia
- i.e. reduced systolic pressure = <50mmHg
Hypoxia
- Failed Tissue oxygenation
Focal, Multifocal, Global
Infarction
- Cell and tissue death attributable to Ischamia
- Irreversible
Focal, Multifocal, Global
Necrosis
- Dysregulated Cell Death
- Physiological response to Infarction
Stroke
- Acute focal neurological (CNS+retina) dysfunction at one/more sites - attributable to cerebrovascular disease that has caused severe hypoxia of brain parenchyma
- Acute Focal Infarction - follows
- IRREVERSIBLE damage
ICD-11 - Formal Stroke definition;
- Acute Focal Neurological Dysfunction - >24hrs
- Due to an hypoxic event that causes/leads to acute focal infarction
- Neuroimaging Evidence of Acute Cerebral Infarction - mri, ct
TIA - transient Ischaemic Attack
- Transient episode of neurological dysfunction/deficit - <24hrs
- Transient hypoxia - restored with resolution of ischaemia, hypoxaemia, anaemia etc
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Precursor to Stroke
- Risk is highest in first 24-72 hours
- Prompt further investigation into cause for TIA
Must be Treated as though it were a stroke
- Only able to discern a TIA from a Stroke is if the symptoms subside spontaneously - risky gamble
Clinical Correlation
- HPC = visual loss in left eye - Pt with repeated bouts of transient loss of sight no complains of prolonged visual loss
- Sensory Loss - earlier bouts had resolved within 10 minutes (TIA), yet this bout has lasted for 2 hours (TIA/stroke)
- If sensory loss, ask for motor loss - inquire about weakness
- Symptoms of ICP? - irregular resp rate, reflex bradycardia, hypertension?
- CHx - assess for risk factors
- HyperT - smoking, diabetes, hyperlidaemia/obesity, chronic stress, risk of malignant hypertension
- Fragile blood vessels - age, smoking, CVD (diabetes, atherosclerosis)
- FHx - check for cerebrovascular disease
Stroke may be a likely risk
Hypertensive (ischaemic) Encaphalopathy
- Aetiology - severe hypertension - leading to hyaline arterioscleoris, hyperplastic arterioscleoris >200mmHg, diastolic >125mmHg
- Complications - global neurological dysfunction
- Brain diffusely swollen, oedematous (imbalance of Starling’s forces)
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Vertebral Artery Dissection
- Rotational movement (e.g. MVC, “king hit”)
- Direct neck trauma (i.e. cricket ball)
- Hyperextension/hyperflexion injury (deceleration)
- Iatrogenic (interventional radiology)
- “Minimal trauma”, egg chiropractic manipulation
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