Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Cerebrovascular Accidents

13,133 views

Published on

  • Discover How Thousands of Men and Women Worldwide Have Already Used The Reverse Diabetes Today™ System To Lower Blood Sugar To Normal And Safely Reverse Their Type 2 Diabetes Without Drugs or Insulin. ●●● https://bit.ly/2swQ6OO
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Boost your brainpower with brain pill! find out more... ★★★ https://bit.ly/2GEWG9T
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Holistic clear skin Secrets, Eliminate blemishes in weeks acne cure e-book reveals all ♣♣♣ http://ishbv.com/buk028959/pdf
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

Cerebrovascular Accidents

  1. 1. Learning objectives 0 Anatomical language 0 The main bones of the skull 0 External and internal (sagittal) view of the brain 0 The forebrain, midbrain and hindbrain 0 The Circle of Willis
  2. 2. Anatomical language for the brain Before we go any further however, let’s go through the basics… Anatomy of the brain comes with its own weird and wonderful language. Understanding the anatomy of the brain becomes a lot easier as soon as you understand the language that comes with it.
  3. 3. Anatomical language for the brainrostra means beak/nose, so Rostral means closer to the nose Cauda means tail (ie cauda equina), so Caudal means closer to the spine
  4. 4. Anatomical Language for the brain0 The brain is folded into Gyri and sulci 0 Gyri (singular gyrus) are the raised bumps of the folds 0 Sulci (singular sulcus) are the grooves between the folds 0 The longitudinal fissure (aka the median fissure) splits the two halves of the cerebrum
  5. 5. Anatomical language for the brain 0 Grey Matter is matter composed of unmyelinated neuron bodies, neurons and glial cells 0 White matter is matter composed of myelinated axons and glial cells and is the lipid content of the myelin sheaths that makes this area appear white
  6. 6. Anatomical language for the brain There are 3 layers covering the brain: 0 The dura mater is the outermost layer. As its name might suggest its very durable and coats the whole of the brain and spinal cord in one continuous sheath 0 The arachnoid mater is the middle layer. All cerebral veins, arteries and cranial nerves lie beneath this layer in an area known as the subarachnoid space 0 The pia mater is a vascular membrane that intimately covers all gyri and sulci of the brain
  7. 7. The Skull A quick revision of the main bones of the skull
  8. 8. A brief overview of the brain External Structures Cerebrum Cerebellum brainstem Pons Medulla
  9. 9. A Brief Overview of the Brain Internal Structures Sagittal section of the brain
  10. 10. Functional areas of the brain The brain is grouped into 3 areas based loosely on embryological formation: 0 The Forebrain – cerebrum and the diencephalon 0 The Midbrain –tegmentum and tectum 0 The Hindbrain – cerebellum, medulla oblongata and pons
  11. 11. The forebrain The cerebrum 0 Also known as the telencephalon 0 Thought to be the seat of humanity as its so well developed in humans 0 Composed of two hemispheres (left and right) divided by the median fissure 0 Commissures (tracts of axons crossing the midline) connect these two hemispheres, the largest of which is the corpus callosum 0 Covered in a 2-4mm thick layer of grey matter - the cerebral cortex
  12. 12. Lobes of the Cerebrum 0 The lobes of the cerebrum are described in terms of the skull bones they lie behind
  13. 13. The cerebrum Functions of the cerebral cortex include: 0 Sensory perception 0 Memory 0 Planning/execution of voluntary movement 0 Language 0 Consciousness 0 Self Awareness 0 Cognitive functions
  14. 14. The cerebrum Brodmann’s map divides the cerebral cortex into 52 different functional areas that are either motor, sensory or associational.
  15. 15. The forebrain The diencephalon Composed of the hypothalamus, thalamus, epithalamus and subthalamus The hypothalamus: 0 thermoregulation and triggering sleep 0 part of the limbic system (generates goal directed behaviours - eating, drinking etc.) 0 Controls many endocrine functions via connections to the pituitary gland
  16. 16. The forebrain The diencephalon The Epithalamus: 0 Regulates circadian rhythm 0 Contains the pineal gland The Thalamus has multiple functions: 0 Emotion (limbic system) 0 Memory (frontal cortex) 0 Sensory and motor 0 Pain and visual attention 0 Sleep/wakefulness and arousal The Subthalamus is involved in movement
  17. 17. The Midbrain The mesencephalon 2 parts: 0 Tegmentum - receives cranial nerves III – V and contains substantia nigra 0 Tectum – receives cranial nerves II and VIII; mediates visual/auditory reflexes
  18. 18. The hindbrain The Cerebellum Makes up ¼ brain mass and ½ the brain’s total neurons Cortex is composed of grey matter folded into folia separated by transverse fissures White matter is called arbor vitae “tree of life” Concerned with high level functions: 0 timing and execution of a voluntary movement 0 Learning new motor skills 0 Cognition
  19. 19. The hindbrain Pons and Medulla Oblongata The centres for life support functions of the brain 0 Pons consists mainly of nerve fibres connecting the cerebellar hemispheres, forebrain, midbrain and spinal cord 0 Medulla consists of 2 pyramids separated by a median fissure 0 Descending fibres cross from left to right in the medulla, known as the decussation of the pyramids
  20. 20. The Circle of Willis 0 Circle of Willis is meant to be the brain’s insurance mechanism against arterial blockages which could cause CVAs 0 If one artery is blocked other arteries in the circle can compensate to continue supplying the affected area with blood 0 In reality the circle of Willis is often too small to be effective and isn’t really able to cope with large scale CVAs
  21. 21. The Circle of Willis 0 The Internal Carotid arteries and the vertebral arteries form the main blood supply 0 They meet in the middle via the two posterior communicating arteries and the basilar artery The basilar and vertebral arteries supply the brainstem Internal Carotid arteries Vertebral arteries Posterior communicating artery Basilar artery
  22. 22. Internal Carotid arteries Vertebral arteries Posterior communicating artery Basilar artery The Circle of Willis The Internal carotids branch form the anterior cerebral arteries. these supply: 0 the medial surface of the frontal and parietal lobes 0 1 inch of brain either side of the median fissure 0 Occlusion can damage motor nuclei cranial nerves V, VII and XII affecting movement of jaw, lips and tongue respectively The Anterior communicating artery links the 2 anterior cerbral arteries Anterior cerebral arteriesAnterior communicating artery
  23. 23. Internal Carotid arteries Vertebral arteries Posterior communicating artery Basilar artery The Circle of Willis 0 Middle cerebral arteries supply lateral parts of cerebral hemispheres except occipital and inferior temporal lobe 0 Anterior choroidal arteries supply thalamus and hypothalamus and various important forebrain groups Anterior cerebral arteryAnterior communicating artery Middle cerebral artery Anterior choroidal artery
  24. 24. Internal Carotid arteries Vertebral arteries Posterior communicating artery Basilar artery The Circle of Willis Posterior cerebral arteries supply: 0 Occipital lobe 0 Inferior temporal lobe 0 Midbrain Superior and inferior cerebellar arteries supply: 0 Pons 0 Medulla 0 Cerebellum Pontine arteries supply medial parts of pons and medulla Anterior cerebral arteryAnterior communicating artery Middle cerebral artery Posterior cerebral artery Superior cerebellar artery Inferior cerebellar artery Pontine arteries
  25. 25. Summary The brain has a 3 layer covering which allows it to be suspended in CSF The brain is divided anatomically into many different areas. It is composed of three functional parts: 0 The Forebrain – higher functions and endocrine regulation 0 The Midbrain – cranial nerves and substantia nigra 0 The Hindbrain – coordination, movement and life support functions The circle of Willis ensures a high arterial blood supply with the possibility of compensatory blood supply in a CVA
  26. 26. Thank you for your time 0 Any questions?
  27. 27. Pathophysiology of a Cerebrovascular Accident By Tim Sale and Nicola Tribley
  28. 28. Aims: • Define a stroke • Distinguish between types • Explain what goes wrong
  29. 29. A stroke is an acute neurological deficit, lasting longer than 24 hours. A Transient Ischaemic Attack (TIA) is an acute neurological deficit lasting less than 24 hours. Definitions:
  30. 30. 3rd most common cause of death in developed world More common in men 25% of patients die More likely to occur in the morning More common in Black Africans The Facts…
  31. 31. Types of C.V.A... Ischaemic stroke/ Infarction – 80-90% Small vessel Large vessel stenosis Cardio-embolic Haemorrhagic – 10-20% TIA – Transient Ischaemic Attack
  32. 32. Large Vessel Disease  Also called Large vessel stenosis  Rupture of a local plaque  Most common type
  33. 33. Cardio-embolic Stroke  Common embolic source  Atrial fibrillation  Valvular changes
  34. 34. Small Vessel Disease/ Lacunar Infarct0 25% of strokes 0 Infarcts in the deep (perforating) arteries, from branches of the middle cerebral artery 0 Very localised, lesions (<5mm) are in the deep brain – lots of important structures! 0 (37% putamen, 16% pons, 14% thalamus and 10% caudate) 0 Microatheroma (main cause) and Lipohyalinosis (thickening of arteriolar wall and reduction in lumen diameter)
  35. 35. Haemorrhagic • Intraparenchymal- 8-13% of strokes • Resulting haematoma can damage surrounding brain tissue due to increase in pressure • Hypertension damage to vessel walls (most common) • Anuerysm/ arteriovenous malformation rupture • Altered hemostasis (coagulation disorders)
  36. 36. Cellular Changes ↓blood flow =↓O₂ Na˖/K˖ pump fails (Na˖ accumulates in cell) H₂O enters cell causing it to swell Swelling causes ↑intracranial pressure Further ↓bloodflow
  37. 37. Also… 0 High Na˖ causes cells to continually depolarise =EXCITOTOXICITY 0 ↑Ca2˖ enters cell leading to necrosis and Inflammation (via cytokine release) Cells with CBF <10ml/100g tissue/min will die within minutes of a stroke - the ‘core’ Cells with CBF <25ml/100g tissue/min can remain viable for several hours - the ‘penumbra’
  38. 38. Anterior Cerebral Artery
  39. 39. Middle Cerebral Artery
  40. 40. Posterior Cerebral Artery
  41. 41. Features Anatomy Prognosis Total Anterior Circulation Infarct (15%) TACI 1. High cerebral dysfunction 2. Hemanopia 3. Ipsilateral motor/sensory deficit Middle Cerebral Artery occluded High mortality Poor outcome Partial Anterior Circulation Infarct (35%) PACI 2/3 of TACI features Middle cerebral artery/ Anterior Cerebral artery branch occluded Fair High chance of recovery Lacunar Circulation Infarct (25%) LaCI Motor/ sensory/ataxic hemipareisis Occlusion of small, deep perforating artery Often good recovery Posterior Circulation Infarct (25%) PoCI 1.Cranial nerve palsy 2.Contralateral motor/sensory deficit/cerebral deficit/hemanopia Brain stem/ cerebellum/ occipital lobe Good recovery High reoccurrence Categorizing strokes
  42. 42. Possible causes and differential diagnosis of cerebro-vascular accidents  Zeenat Umerji
  43. 43. What is stroke? A sudden attack of weakness due to an interruption to the flow of blood to the brain. Usually affects one side of the body.  Either:  Ischeamic (50% cerebral hemisphere, 25% brainstem, 25% lacunar)  heamorrhagic  from prolonged reduction of BP  Varies in severity from a passing weakness/tingling in a limb (TIA) to profound paralysis, coma or death
  44. 44. Causes  Chief causes:  Thrombosis  Atherothromboembolism  Heart emboli  CNS bleed (BP increased, trauma, aneurism rupture)
  45. 45. Causes  Rare causes:  Vasculitis  Venus sinus thrombosis  Young patients:  Thrombophilia  Vasculitis subarachnoid haemorrhage  Venus-sinus thrombosis  Carotid artery dissection
  46. 46. Presentations  Cerebral hemisphere infarcts: initially flaccid then spastic contra-lateral hemiplegia, contra-lateral sensory loss, hemianopia, dysphasia  Brainstem infarction: quadriplegia (paralysis affecting all four limbs), disturbances of gaze & vision, locked-in syndrome  Lacunar infarcts: poor motor/sensory signs, ataxia, intact cognition/consciousness
  47. 47. Differential diagnosis  CNS tumour  Subdural haemorrhage  Seizure (Todd's palsy)  Hypoglycaemia  Hyperglycemia  Drug overdose (if comatose)  Meningitis  Migraine
  48. 48. Differential diagnosis  CNS tumour  Subdural haemorrhage  Seizure (Todd's palsy)  Hypoglycaemia  Hyperglycemia  Drug overdose (if comatose)  Meningitis  Migraine Altered consciousness Hemiparesis Signs of trauma
  49. 49. Differential diagnosis  CNS tumour  Subdural haemorrhage  Seizure (Todd's palsy)  Hypoglycaemia  Hyperglycemia  Drug overdose (if comatose)  Meningitis  Migraine Altered consciousness Hemiparesis (Todd's paralysis) History of seizures Seizure medication
  50. 50. Differential diagnosis  CNS tumour  Subdural haemorrhage  Seizure (Todd's palsy)  Hypoglycaemia  Hyperglycemia  Drug overdose (if comatose)  Meningitis  Migraine When glucose is ≤50 or ≥300 Altered consciousness Hemiparesis (Todd's paralysis)
  51. 51. Differential diagnosis  CNS tumour  Subdural haemorrhage  Seizure (Todd's palsy)  Hypoglycaemia  Hyperglycemia  Drug overdose (if comatose)  Meningitis  Migraine
  52. 52. Questions? Thank you for listening :)
  53. 53. Investigations for Cerebrovascular Accident (CVA) / Stroke By Rosie Vincent 9th Nov 2012
  54. 54. How would you know someone is having a stroke? • FAST (Face, Arms, Speech, Time)
  55. 55. What are the Signs and Symptoms? • All strokes tend to be sudden onset, occasionally with further progression over a few hours. Focal signs relate to distribution of the affected artery, but collateral supplies cloud the issue. You can not reliably differentiate between ischemic and haemorrhagic strokes but some pointers are: • Ischemic (A): Carotid bruit, AF, past TIA, IHD • Haemorrhagic (B): Menigism, severe headache, and coma within hours.
  56. 56. Other Symptoms • Difficulty swallowing • Excessive drooling • Choking • Difficulty walking • Change in vision (double vision/loss of vision) • Eyes fail to move in unison • Difficulty with balance • Clumsiness • Loss of coordination • Symptoms typically occur on one side of the body • Less common symptoms of a stroke may include: • Altered smell sense, Headache, Dizziness, Excessive sleepiness, Excessive salivation, Drooping eyelid, Trismus (can’t open mouth), Vertigo, Urinary incontinence, Memory loss, Confusion, Delusions, Coma, Impotence, Generalised weakness, Fatigue
  57. 57. Investigation/Examination • Needs to be prompt! • Confirm the clinical diagnosis (exclude other causes e.g. Tumour) • Distinguish between haemorrhage and ischemic infarction • Look for underlying causes for the stoke, therefore we can reduce risk factors and prevent further strokes • Identify where the stroke has occurred, what has been damaged and how it is affecting the patient- So we can start to plan treatment/management and rehabilitation.
  58. 58. Awareness and consciousness – Glasgow coma scale/AVPU
  59. 59. Cranial Nerve Exam • Cranial nerves 1 and 2 originate from the cerebrum, whereas 3-12 originate from the brain stem. Therefore strokes in these areas may affect the function of these nerves. • You know what each one does so think about what symptoms you might get e.g. • 1 (Olfactory)= altered smell • 2(Optic)= loss of vision (total/ partial), Pupil Un- reactive to light • 9(Glossopharyngeal)=?
  60. 60. Neurological Exams • Motor and Sensory examination • If the area of the brain affected contains one of the three prominent Central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include: • hemiplegia and muscle weakness of the face • numbness • reduction in sensory or vibratory sensation • In most cases the symptoms are usually on just 1 side of the body, with the defect in the brain on the opposite side (depends on which part of the brain is affected) • BE CAREFUL - The symptoms do not always mean there is a stroke- as these pathways also travel in the spinal cord and lesions there can produce the same symptoms.
  61. 61. Cerebral Cortex • If the cerebral cortex is involved the CNS pathways can again be affected, but also can produce the following symptoms: • Aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area) • Apraxia (altered voluntary movements) • Visual field defect • Memory deficits (involvement of temporal lobe) • Hemineglect (involvement of parietal lobe) • Disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe) • Anosognosia (persistent denial of the existence of a, usually stroke- related, deficit) • If the ''cerebellum'' is involved, the patient may have the following symptoms: • trouble walking • altered movement coordination • vertigo and or disequilibrium
  62. 62. Stroke Classification (Bamford/Oxford classification) • Total Anterior Circulation Infarct (TACI) • Combination of new higher cerebral dysfunction (eg,dysphasia); homonymous visual field defect; and ipsilateral motor and/or sensory deficit of at least two areas of face, arm and leg. • Partial Anterior Circulation Infarct (PACI) • Two of the three components of the TACI syndrome with higher cerebral dysfunction alone, or with a motor/sensory deficit more restricted than those classified as LACI • Posterior Circulation Infarct (POCI) • Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit;bilateral motor and/or sensory deficit; disorder of conjugate eye movement; cerebellar dysfunction without ipsilateral long tract deficits; or isolated homonymous visual field defect. • Lacunar Infarct (LACI) • Pure motor > 2/3 face, arm, leg Pure sensory > 2/3 face, arm, leg Pure sensorimotor > 2/3 face, arm, leg Ataxic hemiparesis, No higher dysphasia or visuospatial or hemianopia or vertebrobasilar problems
  63. 63. Investigations - Bloods • Baselines FBC, U+E Clotting and ESR • Random Glucose -Do they have hypoglycaemia or hyperglycaemia. Diabetes?? • Lipid Profile –Do they have hyperlipidaemia • Hyperhomocysteinaemia? • Hyperviscosity - Polycythaemia? • Infection- Vasculitis? • Prothrombotic States – Thrombophilla? (Blood clotting disorders) • Syphilis? • Thrombocytopenia? • Genetic Tests: Check for Fabry’s disease and CADASIL
  64. 64. CT- Computerised Tomography • CT has the advantage of being available 24 hours a day • Non-Contrast CT is the gold standard for haemorrhage, haemorrhage on MR images can be quite confusing. • On CT 60% of infarcts are seen within 3-6 hours and virtually all are seen in 24 hours. • The overall sensitivity of CT to diagnose stroke is 64% and the specificity is 85%. • It may be difficult to identify early cerebral infarction • Posterior fossa and brainstem regions may not be visible • May not detect small infarcts especially lacunar infarcts • Can not differentiate between old infarcts and old intracerebral haemorrhages
  65. 65. MRI- Magnetic Resonance Imaging • Not as easily available as takes longer to organise • Has a specific sequence (stroke sequence) called Diffusion-weighted imagine (DWI)- this becomes positive within minutes-hours of stroke onset as a white ‘light bulb’ which remains for 2-3 weeks • DWI can detect the haemorrhage as early as CT • Much better at visualising the posterior fossa • More sensitive to small infarcts (95%) • You can differentiate between old infarcts and haemorrhages (with MRI + gradient echo)
  66. 66. CT vs. MRI In summary MRI is a lot easier to diagnose due to DWI changes being so apparent, making the diagnosis relatively easy for the non-specialist... BUT CT can differentiate between infarction and haemorrhage instantly, and is faster to carry out, therefore it is usually the 1st line approach and is carried out ASAP after patients admission CT MRI
  67. 67. Investigation for Signs of Hypertension • Retinopathy- Ophthalmoscopy/Fundoscopy • Nephropathy- U+E’s (Urea:Creatinine) Renal ultrasound, Urinalysis • Big heart- CXR • Blood Pressure commonly high in early stroke but usually do not treat! It may harm the patient and even a 20% decrease may compromise brain perfusion as auto regulation is impaired
  68. 68. Investigation for Signs of Cardiac sources of Emboli • 24 tape ECG – Do they have AF? • CXR - Enlarged left atrium? • Echocardiogram (Transoesophageal is more sensitive than transthoracic) Looking for: • Mural thrombus due to AF or a hypokinetic segment of cardiac muscle post-MI • Valvular lesions which could be due to ineffective endocarditis or rheumatic heart disease • Patient foramen ovale (especially in younger patient)
  69. 69. Signs of Carotid Artery Stenosis • Carotid Doppler Ultrasound • CT/MRI Angiography
  70. 70. Assessing handicap, disability and independence in daily life • Two people with the same impairment (e.g. Paralysed arm) may have different disabilities (One can dress and the other cannot) • Treatments are usually aimed at reducing disability and improving quality of life, not curing disease. • Usually use Barthel’s Index of activities of daily living to establish the patient’s degree of independence from any help. You score the patient on the following aspects of daily living, and total the scores, gaining a value from 0- 20 (20 = completely able). • For example: Bowels 0 = incontinent (or needs to be given enema) 1 = occasional accident (once/week) 2 = continent • This is also carried out for: • Bladder • Grooming • Toilet use • Feeding • Transfer • Mobility • Dressing • Stairs
  71. 71. Summary After carrying out these investigations and examinations on a patient you should know: • If they had a stroke •What type of stroke it was •Where the stroke occurred •What caused the stroke •What the stroke’s effects have been on the patient Knowing this will now enable you to inform the patient what has happened to them, and together you will be able to decide on treatment/management that is best tailored to the patients needs.
  72. 72. The End Q&A
  73. 73. Cases CVA Ella Ward-Baker
  74. 74. Case 1 • 55 year old woman presents Tuesday morning feeling faint. • Notable left-sided hemiparesis and dysarthria. • Consequently unable to break her fall as she fell What other relevant information might we need?
  75. 75. Onset and duration • Came on within 5 minutes (walking from home to the bus stop) • Resolved after 10 minutes • Followed by another episode that came on within 5 minutes of arriving at hospital
  76. 76. Other necessary information Prior to episode Mrs X had been getting ready for work… • No chance of head trauma No history of bleeding disorders… Past medical history of Hypertrophic cardiomyopathy • Less likely to be haemorrhagic stroke
  77. 77. Other necessary information What does the medication reveal? • Bisoprolol 7mg/day – used to treat hypertension • Hypertension is a risk factor for both ischaemic and haemorrhagic stroke, exacerbated by patient’s hypertrophic cardiomyopathy Family history? Mother and father both died of MI
  78. 78. Investigations • CT scan • Labs: U&Es, FBC, Glucose • ECG • Carotid Doppler • Physical examination
  79. 79. • CT Scan: No sign of haemorrhage No sign of infarction – may not appear for 6-24 hours or up to one week (if at all) Investigations
  80. 80. Left hypertrophic cardiomyopathy… Don’t be misled into thinking this woman’s symptoms are because of a cardiac emergency, however this may be another factor leading to her stroke…
  81. 81. ECG • Left hypertrophic cardiomyopathy… • Patient also known to have paroxysmal AF… Emboli more likely to form due to impeded passage of blood through the heart From there, emboli may travel easily to brain, causing stroke
  82. 82. Other results • Bloods: Normal • Carotid Doppler – no sign of stenosis • Physical examination – no bruits, BP 148/78, slightly tachycardic, aforementioned neurological symptoms
  83. 83. Management • Alteplase Tissue Plasminogen activator Thrombolytic treatment • Warfarin Because of intermittent AF Inhibits factors… II VII IX X
  84. 84. Criteria for Atleplase: • Present within 3 hours of symptoms (as infarcted tissue more prone to bleeding) • CT rules out haemorrhage (would be bright white bleed on CT) • Thrombolysis must take place in specific stroke unit (reason why there is always a bed kept spare on the ward)
  85. 85. Non-Pharmacological interventions (MDT) • Physiotherapy – Important to encourage patient to use affected limbs/relearn use… - Even once partial use is regained, muscle wasting from inactivity may be a problem • Speech and Language Therapy (SALT) – helping to prevent psychological problems associated with inability to communicate
  86. 86. … • Occupational Therapist – help the patient by providing strategies and coping methods to deal with disability - Enables patient to begin/continue with daily tasks/ work/ self-care etc • Dietician – fair enough to tell a patient to ‘cut down on salt’, but that doesn’t generally help in itself… • Psychological Support
  87. 87. Some points about this case • Highlighted the importance of patient understanding • On questioning, Mrs X claimed to have no medical conditions • On further questioning, hypertension treatment was mentioned… • Mrs X then confirmed she had high blood pressure but that she ‘felt fine’ • She had made no connection between hypertension and the possible risks - ‘why would that effect my brain?’ • Patient understanding…
  88. 88. • Patient now worried about returning home to house where she lives alone • Again, understanding firstly of the risks of having another stroke, but also what and how the medication she is on should help her
  89. 89. Case 2 • 62 year old man having breakfast with his wife when he develops a severe headache and weakness in left arm. What other relevant information might we need?
  90. 90. Relevant information • Pain Info Severe pain localised to head • Onset Over 2 hours • Duration Ongoing • Seizure post-admission • Trauma? No evidence of trauma
  91. 91. Other relevant information • Past medical history: -History of Hypertension and hyperlipidaemia -Hip operation in past 4 weeks -Has smoked all his life -No previous stroke • Medication history Wafarin 5mg daily
  92. 92. Investigations • Vital signs • CT • FBC, Electrolytes • Echocardiograph – to show cardiac mural thrombus • ECG – possible AF • Plain Chest Radiograph • Prothrombin Time & Partial Thromboplastin Time
  93. 93. • Normal bloods • Clear Echo, ECG, CXR • Slightly prolonged PT&PTT – Related to Warfarin • BP 160/100 – Not severely hypertensive, so do not treat hypertension as emergency – lack of evidence as to whether this is helpful Results
  94. 94. CT
  95. 95. Intracerebral Haemorrhage
  96. 96. Management • Anticonvulsants (Seizures most common with ICH than other strokes) • Maintain perfusion of the brain - Keep hydrated (Consider saline) - Consider intubation if airway patency becomes a problem • IV vitamin K & Prothrombin complex - Reverse anticoagulation treatment • Send Type & Screen bloods to blood bank • MDT
  97. 97. Thank you

×