Handout for pilot 'blackout' presentation
PTE Blackout Handout
Summary
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Infection (meningitis, encephalitis) 3. Neurofibromatosis type-1 – autosomal dominant genetic disorder which leads to cutaneous Café-au-lait spots, axillary freckles and peripheral neurofibromas.
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Tumour (primary or metastases) 4. Aicardi syndrome – rare X-linked genetic disorder leading to aplasia of the corpus callosum.
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Brain malformations 5. Migrational disorders – there can be abnormalities (partial or complete) in the migration of neurons to the surface of the brain, resulting in abnormal development of the grey matter.
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Drug withdrawal (previous anticonvulsant 8. Infection (congenital CMV, Rubella..)
or alcohol use) 9. Metabolic disorders (LCAD deficiency, urea cycle defects ..)
This on-demand teaching session is aimed at medical professionals looking
Description
Learning objectives
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Brain infection (encephalitis/ 3. Neurofibromatosis – genetic condition which
meningitis) causes tumours to arise around nerve tissue
5. Masses/ tumours (primary or 4. Perinatal ischaemia – this is disrupting the
metastatic) blood supply to the baby’s brain at the time of
6. Alcohol withdrawal delivery.
7. Substance abuse 5. Congenital pelvic malformations – can
8. Metabolic disorders, such as disrupt epidural arteries leading to
hypoglycemia, hepatic or renal cerebral hypertension and seizures.
failure, hypernatremia, dehydration
9. Damage to the nervous system 6. Hypoxic ischaemic encephalopathy
– describe for neonatal blackout
10. Systemic autoimmune diseases,
such as lupus
11. Brain tumours
Learning Objectives:
- Understand the differences between syncopal and non-syncopal causes of blackout
- Distinguish epilepsy from other
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
BLACKOUT By MedRxBlackout refers to a transient loss of consciousness. This is a very common presentation in acute medicine, accounting for 3% of all A&E admissions and 1% of hospital admissions. Therefore, it is a presentation medicalstudentsshouldbeawareof!Inthishandout,we will go through the differential diagnosis of a blackout and the important aspects of a blackout history and examination. We will also cover three important conditions for blackout: seizures, hypertrophic obstructive cardiomyopathy (HOCM) and subclavian steal syndrome. Using this Contents handout 1. The differential diagnosis of a blackout The content in this handout a. Syncopal causes is quite detailed. The most b. Non-syncopal causes important aspects are the 2. The history of a blackout differential diagnosis (section a. HPC 1), the ‘essential advice’ in b. PMH red and any writing in bold – c. DH prioritise these first! At the d. FH same time, the content is not e. SH exhaustive and should not be 3. Blackout conditions seen as covering every detail important ones. This handout a. Detailed condition - epilepsy is for purely educational b. Brief condition - HOCM purposes and should not be c. Brief condition - Subclavian steal used when treating syndrome patients. PAGE 2The essential differential diagnosis of a blackout The causes of a blackout can be split into two: Syncopal causes (arising from a lack of blood supply to the brain) Non-syncopal causes (not involving a lack of blood supply) Cardiac Syncopal causes of blackout. Syncopal causes of a blackout involve a loss of blood supply to the brain. In general, there are four broad things which can cause a lack of blood supply (Fig.1). 1. Firstly, problems in the heart can stop blood being pumped out effectively to the brain. This category includes arrythmias, structural cardiacbrovascular pathologies such as HOCM and a massive pulmonary embolus. 2. Secondly, problems in the blood vessels connecting the heart to the brain can compromise blood supply – this includes vertebrobasilar insufficiency, subclavian steal syndrome and aortic dissection. 3. Thirdly, neural reflexes can cause a lack of blood supply to the brain – this includes vasovagal syncope and carotid sinus hypersensitivity. 4. Finally, postural hypotension can cause a lack of blood supply. Normally, when we stand up from a seated position, vasoconstriction and increased heart rate (driven by the SNS) prevent a sudden drop in blood pressure. Therefore, anything that decreases this sympathetic response or decreases Reflex the intravascular volume can cause hypotension upon standing (postural hypotension)andhencesyncope.Thisincludesdehydration,anti-sympathetic drugs and autonomic dysfunction. Non - Syncopal causes of blackout. Non syncopal causes of a blackout are those postural causes which do not involve a decrease in blood supply, and cause syncope through an alternative mechanism. These include the following: • Intoxication (alcohol, sedatives) • Head trauma • Hypoglycaemia • Seizure PAGE 3 Taking a blackout history History of presenting complaint PMH With a blackout presentation, the easiest way to structure your HPC is Diabetes chronologically – ask what happened before, during and after the this could predispose to incident. Before hypoglycaemia, which remember is one of our 1. Was there a trigger? non-syncopal causes of a a. Head turning could indicate vertebrobasilar ischaemia blackout. It can also cause b. Long period of standing etc could indicate vasovagal autonomic dysfunction and c. No trigger could indicate cardiomyopathy/ arrythmia hence orthostatic 2. Was there any preceding symptoms? hypotension. a. feeling faint, nausea, stomach pain, going pale – vasovagal b. No symptoms – more likely cardiomyopathy/ arrythmia Cardiac c. Arrythmias can also cause palpitations this could relate to arrythmias or HOCM During Epilepsy 3. How long were they out? of course puts seizures to a. Arrythmia blackouts are short lived (seconds) the top of your differential b. Vasovagal blackouts are also short lived (seconds) list c. Seizures can last longer 4. Did they move (convulsions)? Psychiatric a. Seizures – stereotypical movements eg tonic, clonic. could predispose to non- epileptic seizures, or panic b. Note jerking movements can also occur in vasovagal syncope attacks which can cause 5. Did they bite their tongue? Were they incontinent? hyperventilation and c. These are classical of seizures blackout. After Anaemia 6. How quickly did they recover? d. Seizures have a prolonged (minutes to hours) post-ictal phase could contribute to hypoxia Recovery from syncopal causes is normally within seconds which could exacerbate a loss of blood supply to cause a blackout Social history 1. Alcohol – remember intoxication is a non-syncopal cause 2. Stimulant drugs – cocaine and amphetamines can cause tachyarrhythmias Family Cardiovascular disease raises possibility of any Drug history cardiac or cerebrovascular In general, the most common reasons for medications contributing to differentials blackout are that they cause hypoglycaemia, seizures or orthostatic Cardiovascular disease hypotension. could indicate inherited 3. Drugs causing hypoglycaemia: insulin, sulphonylureas (gliclazide) arrythmias such as HOCM or 4. Drugs causing seizures: channelopathies such as Anticonvulsant medications being withdrawn, brugada syndrome, long QT syndrome. Fluoroquinolone antibiotics lower seizure threshold Epilepsy 5. Drugs causing orthostatic hypotension : Antihypertensives – remember raises possibility of seizures these block the SNS response and hence can cause orthostatic hypotension Vasodilators (eg GTN spray) – these can cause hypotension Diabetes TCAs – can cause orthostatic hypotension remember can cause Steroid cessation – Addisonian crisis and hence orthostatic hypotension hypoglycaemia or autonomic dysfunction . PAGE 4 Epilepsy What causes it? Epilepsy is a medical condition in which patients The majority of the time, there is no have repeated seizures. A seizure is usually detectable cause for epilepsy. However, the possible causes can be split into defined as ‘a sudden alteration of behaviour due to a temporary change in the electrical acquired vs congenital functioning of the brain’. Causes Acquired causes Congenital causes The causes/ predisposing conditions for 1. Tuberous sclerosis – genetic condition which repeated seizures (epilepsy) are as causes hamartomas to arise throughout the body. follows: Hamartomas in the brain (cortical tubers) can cause 1. Head trauma seizures. 2. Stroke or brain haemorrhage 2. Sturge Weber syndrome – rare vascular disorder 3. Hypoxic brain injury with three major features: port wine stain (birth mark on 4. Brain infections – meningitis, face), leptomeningeal angioma (causing seizures) and encephalitis, abscess glaucoma. 5. Brain tumours 3. Vascular malformations – Arteriovenous 6. Neurodegenerative disease such malformations, cavernous hemangioma as AD 4. Abnormalities of cortical development (see Figure 1) a. Abnormal neuronal-glial proliferation b. Abnormal neuronal migration Abnormal cortical organisation PAGE 5 What are the Epilepsy symptotms Epilepsy is a medical condition in which patients There are many different types of have repeated seizures. A seizure is usually seizures, and the symptoms of epilepsy defined as ‘a sudden alteration of behaviour due depend on the type of seizure present. to a temporary change in the electrical The symptoms of different types of seizures are shown in table 1 functioning of the brain’. Type of seizure Symptoms Generalised tonic-clonic • What seizures look like in movies • Tonic phase (muscle tensing) • Followed by clonic phase (muscle jerking) • May be tongue biting, incontinence, groaning • Automatisms – stereotyped movements such as lip smacking, Temporal lobe (50%) swallowing, fiddling with objects • Mneomimic – feeling of familiarity (déjà vu) or unfamiliarity (jamais vu) • Auras – olfactory, auditory, affective • Focal clonic – jerking but in focalised manner Frontal lobe (30%) • Jacksonian march – contraction of muscles going along the Focal homunculus (ie hand to arm to face) • Versive movements – the eyes or head turning away from the midline • Posturing – fencing posture, or figure of 4 posture • Somatosensory symptoms such as tingling, shock sensation or Parietal lobe (10%) pain Occipital lobe (10%) • Visual symptoms such as flashing lights, spots, simple patterns Absence • Patient goes blank, is unaware and stares into space then goes back to normal • Lasts 10-20 seconds Atonic • Brief decreases in muscle tone – hence also referred to as ‘drop attacks’ • Occur in Lennox-Gustaut syndrome • Sudden and brief contractions of muscle Myoclonic (if you like opposite of an atonic) • Patient usually remains awake • Occur in juvenile myoclonic epilepsy Infantile spasms • Involves full body spasms • Also known as West syndrome PAGE 6 diagnosis and management What is the management? Diagnosis The management of epilepsy will be conducted by a Clinical neurologist and can broadly be split into conservative, The diagnosis of epilepsy is primarily a medical and surgical management. clinical one. Ultimately, a video form a relative is often the most useful piece of Conservative information in making a diagnosis 1.Keep a diary of when seizures occur to try and determine any EEG patterns or triggers EEGs can show abnormal electrical activity 2.Cutting down on alcohol - alcohol can increase seizure frequency in seizures. and risk of SUDEP However, in-between attacks EEGs will 3.Stop driving until seizure free for 12 months often be normal so a normal EEG cannot Medical exclude epilepsy Type of seizure Drug MRI Generalised tonic- First line - Sodium valproate MRI will generally be normal in epilepsy but Second line – lamotrigine or can be used to look for underlying clonic structural causes such as tumours. This levetiracetam investigation is particularly relevant in focal First line – lamotrigine or leviteracetam Focal Second line – carbamazepine, seizures rather than generalised one. oxcarbazepine, zonisamide Absence First line – Ethosuximide Second line – sodium valproate, Complications lamotrigine or leviteracetam Status epilepticus Atonic First line - Sodium valproate is defined as having a seizure lasting longer Second line – lamotrigine than 5 minutes or having more than 3 Myoclonic First line – sodium valproate seizures in 1 hour. This scenario is a medical Second line – lamotrigine, emergency as it can have life threatening leviteracetam or topiramate effects such as arrythmias or pulmonary Infantile spasms Prednisolone oedema. Treatment is with intravenous Vigabatrin lorazepam 4mg, repeated after 10 minutes if seizures continue. If seizures persist, then phenytoin or phenobarbital is used to stop them. In the community, buccal midazolam Surgical or rectal diazepam can be used to halt seizures. Surgical treatment can be used in medically refractory cases (seizures despite 2x therapies being used) or in cases with a clear structural cause. SUDEP stands for sudden unexplained death in Vagal nerve stimulation epilepsy. The factors which make SUDEP 50% of patients experience a 50% reduction in seizures more likely are alcohol consumption, having However 25% have no benefit and seizure freedom rarely occurs a longer seizure history, and missing doses of anti-epileptic medication. Possible Surgery mechanisms include cardiac arrythmias, Resection of a lesion causing seizures respiratory suppression causing pulmonary oedema and a generalised EEG suppression (such as tumour, AVM, cortical tuber) after a seizure (post-ictal). Corpus callosotomy – can be used in Lennox Gastaut syndrome Hemispherectomy – used in Sturge Weber syndrome PAGE 7 What causes it? HOCM HOCM is caused by mutations to genes important in HOCM is an autosomal dominant genetic cardiac muscle. The most common mutations cardiomyopathy characterised by depend on the age of the patient: hypertrophy of the cardiac muscle tissue of Adolescents and older the leftventricleanddisarray ofthecardiac sarcomeric proteins such as troponin or myocytes. This hypertrophy tropomyosin. disproportionately affects the septum of the heart, leading to outflow obstruction. In prepubertal children mitochondrial gene mutations Symptoms Signs Most patients with HOCM are 1. Ejection systolic murmur heard asymptomatic and any symptoms that Syncope loudest at the lower left sternal border – this do occur are relatively non-specific Palpitations may be associated with a thrill (could be found in many Chest pain 2. A fourth heart sound cardiomyopathies or heart defects): Diagnosis 1. ECG – can show signs of left ventricular hypertrophy 2. Echocardiogram – can show asymmetrical septal hypertrophy or systolic anterior movement of the anterior leaflet or the mitral valve 3. Genetic testing – can establish the affected genes Management There are various management options for HOCM depending on the severity of the obstruction and symptoms: 1. Beta blockers 2. Alcohol septal ablation (via a catheter) 3. Surgical myomectomy (removing part of the obstructing heart muscle) 4. Implantable cardioverter defibrillator 5. Heart transplant As well as what should be given in HOCM it is just as important to consider what should not be given. ACE inhibitors and nitrates can worsen left ventricular outflow obstruction so should be avoided. Other things to avoid are intense exercise, dehydration and heavy lifting. PAGE 8subclavian What causes it? steal syndrome Subclavianstealsyndromeisararecauseofsyncope Age Sedentary lifestyle caused by stenosis of the proximal left subclavian Smoking hyperlipidaemia artery (before the origin of the vertebral artery). In Alcohol Hypertension order to compensate for the lack of blood supply to Poor diet Diabetes the arm when it is being used, retrograde flow occurs in the vertebral artery, resulting in a lack o f supply to the posterior circulation of the brain. Lack of posterior circulation: Vertigo Symptoms Diplopia Visual loss The typical symptoms of subclavian steal Syncope syndrome occur during a period of arm activity. The symptoms can arise for one of Lack of blood supply to the posterior circulation (as the vertebral to the arm: blood flow reverses) or due to a lack of Arm claudication: arm pain, blood supply to the arm (due to inadequate parasthesia blood flow from retrograde flow) Diagnosis Management The management of subclavian steal syndrome 2. Initial investigation – duplex ultrasound to can be split into conservative, medical and show retrograde vertebral blood flow in surgical management. exercise 3. Definitive diagnosis – CT/MR angiography Conservative: Control modifiable risk factors for example Based on these investigations, the Subclavian sedentary lifestyle, diet, smoking steal syndrome severity can be graded: Medical 4. Pre-subclavian steal – reduced anterograde Antiplatelet therapy flow rather than frank retrograde flow Statins 5. Intermittent alternating flow – anterograde flow in the diastolic phase and Surgical retrograde flow in the systolic phase Percutaneous angioplasty +/- stenting – smaller 6. Advanced disease – there is permanent or more proximal occlusions retrograde flow Bypass techniques – longer or distal occlusions. Complications There are no specific complications of subclavian steal syndrome, however syncope caused by subclavian steal syndrome can lead to falls which can cause head injury. PAGE 9References 1. Farne, H., Norris-Cervetto, E. and Warbrick-Smith, J. (2015). Oxford cases in medicine and surgery. Oxford ; New York: Oxford University Press. 2. Anon, (n.d.). Zero To Finals – Tools for Medical School. [online] Available at: https://zerotofinals.com. 3. NT Contributor (2018). Stroke 4: immediate treatment of acute stroke and TIAs | Nursing Times. [online] Nursing Times. Available at: https://www.nursingtimes.net/clinical-archive/neurology/stroke-4-immediate- treatment-of-acute-stroke-and-tias-15-01-2018/. 4. updated :March 9, V.D. and 2021 (n.d.). Syncope | Definition, Causes, History Taking | Geeky Medics. [online] Available at: https://geekymedics.com/syncope/. PAGE 10