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Week 5 Health and Society The Health Economic Cost-Effectiveness Analysis (CEA) Framework Describe the key elements of the Health Economic Evaluation (HEE) decision analytic framework for performing cost-effectiveness analysis. Be able to in...

Week 5 Health and Society The Health Economic Cost-Effectiveness Analysis (CEA) Framework Describe the key elements of the Health Economic Evaluation (HEE) decision analytic framework for performing cost-effectiveness analysis. Be able to interpret the results of a cost-effectiveness analysis of a healthcare intervention. ALL THE NOTES BELOW SUMMARISED CAUSE ITS TOO MUCH SUMMARY PICO PICO framework (Population, intervention, comparator, outcome and costs) → is a framework that structures questions in a way that will make it easier to search for and evaluate in medical research Week 5 1  P population being evaluated should be clearly defined I provide very specific details about the intervention being evaluated for cost-effectiveness → ‘the exactly how’ and the ‘exactly how much’ C O the outcome for a cost-effectiveness evaluation should be the one that best represents the ‘value’ of the intervention Week 5 2  C* costs refer only to monetary expenses associated with resource use such as the costs of meds, hospital stays and staff salaries. should all be measured in the same currency + with pricing relating to a single (constant) year ICER Used to assess the value of a healthcare intervention compared to an alternative (often the current standard of care or like a placebo) Calculated → difference in the costs of the 2 options divided by the difference in their health outcomes (where A represents the intervention and B the comparator + don't forget to always include both the monetary and health outcome as the units of an ICER) Eg: Week 5 3  Economic evidence and models Process of deciding whether to conduct a new HEE: 1. Check existing economic evidence a. literature search b. utilising existing studies 2. Assess applicability 3. Review clinical evidence a. if outcomes are unchanged → a simpler CMA might be sufficient b. if outcomes are improved → a full CEA is likely needed to assess the cost per unit of health benefit gained Decision tree concept Objective: To determine which option is more efficient in terms of costs and health outcomes It maps out the various expected pathways that are expected to occur throughout the population should it be exposed to each alternative Week 5 4  The decision tree tracks time from left to right; at the beginning, the population and problem is defined; then alternative pathways start: the population is mapped to receive either the intervention or the comparator. Any common and differing eventualities that might occur following these options are depicted - branching out like a tree, and the impact on resource use and health associated with these pathways are tracked. Finally the economic outcomes (costs and health outcomes) associated with each pathway are measured. For simple analyses, the tree itself can form the basis of the calculations - probabilities are assigned to each alternative pathway of events that may occur, and by multiplying the costs and outcomes by the probabilities, the total estimated costs and outcomes associated with each pathway can be calculated. Even when more complex mathematical functions are required to generate estimates of costs or outcomes, the decision tree is still a useful tool to conceptualise the problem. There are two main evidence frameworks that may be used to inform the estimate of costs and outcomes: trial-based (or within-trial) economic evaluation, and 'modelled' economic evaluation. Framework 1: 'trial-based' or 'within-trial' economic evaluation Sometimes referred to as 'economic analysis alongside a clinical trial'. This is when the economic data e.g. information on economic outcomes (e.g. quality of life measures that can translate to utility, survival or another Week 5 5  patient-relevant outcomes and information on resource use, e.g. doctor consultations, medications and hospitalisation costs) are directly observed and measured as part of a clinical trial (preferably an RCT). At the end of the study, costs and outcomes, as identified in the study, can be added up for each arm of the study and used directly to calculate an incremental cost-effectiveness ratio. Figure 2: Example of the measures taken in a within-trial economic evaluation. While many clinical studies publish economic analyses alongside the clinical paper or 'piggy-backed' onto the trial, these analyses tend to be simplified or for indicative academic results only. Trial-based economic analyses are rarely comprehensive enough to be used for decision-making purposes. Consider the advantages but also the disadvantages of trial-based evaluations in the table below. Table 1: Advantages vs Limitations of within-trial economic evaluation Advantages of within-trial economic Limitations of within-trial economic evaluation evaluation Internal consistency is a single source of Limited to patients and interventions evidence for the effectiveness and cost in a trial. data. Assumptions about clinical pathways are not Increases cost and complexity of required. clinical trials. Statistical analysis is available Limited to the outcomes measured (IPD, variable distributions, tests for and the time horizon of the trial. differences, etc.). Framework 2: An economic model An economic model is a constructed mathematical framework, generally supported by computer software, which uses multiple data inputs and calculations to generate estimates of costs and outcomes for the Week 5 6  alternatives presented in an economic decision, which have not been directly measured in clinical studies. The components of an economic model include: A conceptual model – e.g. a decision tree or health state diagram; sets out the disease-specific events and processes within the system in which the decision problem exists. A working model – e.g. this is the actual software, programming and calculations When is an economic model needed? An economic model is needed when the observed data alone is insufficient to predict the incremental costs and incremental outcomes, for the correct population and comparator, in the relevant context. For example: When the population has different risk characteristics, and the effect's magnitude may differ, we need to translate the treatment effect to make it applicable to the population. When the follow-up time is too short to capture all the differences in outcomes (or costs); therefore we need to extrapolate outcomes and costs over a longer time horizon. When the effect outcome is a surrogate measure; therefore, we need to transform surrogate outcomes into an outcome. When the comparator isn’t the relevant comparator in the real-world decision; therefore, we need to combine data from different sources for an indirect comparison. When the setting is in a different healthcare system (e.g. with a different pattern of resource use); therefore, we need to model/re-assign the way of resource use. When there are missing details (e.g. resource use, adverse events, etc.) that will affect overall comparative costs or outcomes; then we need to add or combine data from different sources. Week 5 7  As you can see, there are many reasons why economic modelling beyond the clinical study evidence is frequently necessary to estimate cost- effectiveness. Detailing the preferred approaches or concerns with each of the different modelling functions is beyond the scope of this introductory course. We will look more closely at just one modelling function (extrapolation) to get a sense of the challenges that are involved. Extrapolation Extrapolation is needed when clinical studies do not observe health outcomes or resource use for an adequate duration of time to quantify the total difference in costs and outcomes between decision arms. This can be particularly important in disease areas where the full benefits of treatment may extend many years beyond treatment initiation, such as in the case of cancer or chronic diseases. Extrapolation typically uses the available limited or short-term data to estimate long-term outcomes. What assumptions will be made within an extrapolation? One of the critical questions that need to be considered when understanding how extrapolation should proceed over time after the available data is: Is the treatment effect (i.e. the effect of the intervention that is driving the difference in outcomes) likely to continue to increase? To stay the same? Or to diminish? Consider the image below, where the first depiction of survival represents the data from two treatment arms that have been directly observed in clinical trials (Hlatky, Owens & Sanders 2006). Week 5 8  Figure 3: Different assumptions that are made with different extrapolation approaches. While there are numerous paths that these curves could follow, the key distinction between the extrapolation proposals in (B), (C) and (D), is that the treatment effect of the superior treatment is : (i) increasing, (ii) remaining steady, or (iii) decreasing, respectively. Week 5 9  The assumption of an increasing treatment effect (as depicted in (B)) assumes that the difference between the arms continues to grow. i.e., the treatment continues to effectively reduce the risk of death (or an event) so that the rate is less than in the comparator arm. This assumption is associated with the greatest incremental benefit in outcomes (i.e. the greatest area under the curve), and so is the most 'optimistic'. For this assumption to be reasonable, the intervention would need to have had some curative effect. This might include scenarios where risk was permanently reduced compared to the alternative, or where the cohort must continue to be exposed to the intervention such that it remains working (e.g. it may be a medicine that is taken indefinitely, such as blood pressure medications etc.). The assumption of a maintained or steady treatment effect (as depicted in (C)) assumes that the difference between the arms as observed at the end of the trial period is maintained into the future (neither shrinking nor growing) as the risk of events after the trial becomes the same in both arms. The patients who benefited from reduced risk in the trial period reverted to a risk rate in the comparator arm. This may represent when therapy is provided for an extended period of time (e.g. as in the observed time) but then stopped (perhaps because of concern about the safety of continuous exposure). The benefits of the treatment - e.g. in 'holding' a disease or delaying disease progression are maintained but do not continue to increase once the therapy is ceased. The assumption of a decreasing treatment effect (as depicted in (D)) assumes that the benefits observed at the end of the trial period diminish following the trial and are reversed such that the survival converges to become the same in both arms. This would represent the case where therapy is discontinued at the end of the study period. The effect it had in suppressing a disease (e.g. cancer or infection) stops, and the disease 'rebounds' and becomes increasingly active such that the treated group is at increased risk. After some time, the overall death rate 'catches up' to the comparator. This assumption is associated with the lowest incremental benefit or the most 'pessimistic' outlook. Increasing, maintained or decreasing treatment effects are all potentially plausible in different medical scenarios - the reasoning for the assumed Week 5 10  course of effect in any health economic model should be biologically and medically supported. In particular, assumptions of indefinitely increasing treatment effect need strong supporting evidence. Depending on the expected effect, the health economist may generate the ongoing survival function by selecting different parametric functions statistically fitted to the observed data. If you are interpreting an economic evaluation that has extrapolated effect, even if you do not understand the extrapolation methods in detail, it is essential to clarify the assumption regarding ongoing treatment effect that underlies the extrapolated outcomes. Then it is easier to assess the plausibility of the claimed overall health outcome benefit of the treatment. Example An economic model that sought to identify the cost-effectiveness of the pharmaceutical 'nivolumab' in melanoma patients calculated ICERs using two different extrapolation methods for the same observed data. The results ranged from £13,753 per QALY to £52,466 per QALY (Laws et al. 2020). Good modelling practice must be used to determine the most appropriate assumptions and methods that will be applied. This may involve engaging: Epidemiologists to ensure the available data is properly understood and interpreted. Statisticians to ensure the mathematical modelling is correctly handled. Clinicians to ensure that the modelled assumptions and results have biological and clinical plausibility. Concept of equity in health economics Equity → refers to fairness in distributing resources, benefits, and burdens within a society. It can be measured in various ways but in taxation, equity will be divided into: Horizontal equity → indivs who are similarly situated in terms of their ability to pay should be treated equally Week 5 11  Vertical equity → recognises that indivs have diff abilities to pay and should be reflected in how taxes are structured Efficiency → practical and productive use of resources (ensures that resources are used in the most cost-effective way possible to achieve max output with min waste) Equity in health Measuring equity in health is def more challenging than doing it for resource distribution, it consists of complicated factors such as: socioeconomic factors geography culture edu occupation age Challenges of equity in health economics Health economics often prioritise efficiency OVER equity For eg: skin cancer clinic → efficient (delivers more QALYs at a lower cost) but it primarily benefits a more affluent population VS a maternal health service that is less efficient but addresses a more diverse + divergent population Just by looking at the number of QALYs for the least amount of resources, the skin cancer clinic will be picked for investment and = increase in health inequity but the more efficient option Affordability & Financial Analysis CEA → measures the incremental cost per health outcome gained but does not assess the total resource requirements for broad implementation (determines whether ongoing utilisation of a healthcare intervention is sustainable) Week 5 12  Financial analysis → generally simpler than HEE; estimates the total cost of implementing a healthcare intervention across a population over a specific period Steps for financial analysis 1. Identify the time period when the intervention could realistically be introduced the administrative body that is interested will likely provide advice on the preferred budget period 2. Estimate the size of the population who would be eligible for the intervention (e.g. a pharmaceutical or medical procedure) Typically this might be estimated using any epidemiological data available Alternatively, if the new intervention is going to directly replace an existing product or service then existing market data on the comparator product may inform the estimated number of patients. Estimate whether this population will change over time Consider whether other changes in clinical practice will impact the affected population (e.g. increased screening and effective early interventions for some conditions may impact requirements for end- stage treatments a few years later.) Tabulate the estimated total eligible population each budget year for a five year period. 3. Estimate the 'uptake rate' of the intervention in the eligible population i.e. what proportion of patient who could utilise the intervention are likely to choose to have it? This may be quite subjective or uncertain, but should be given some thought: Interventions for which there is no alternative active treatment option typically have higher uptake rates Week 5 13  Higher uptake rates may be expected for interventions helping serious conditions with poorer prognosis Interventions that are associated with more side-effects or poorer risk-benefit ratios may have lower uptake rates The extent to which sales representatives actively promote the intervention, and media dissemination of information about the condition or intervention may increase uptake rates. For medical devices or interventions where proceduralists need to have additional training or experience, uptake rates may be dependent on the access to training and the busyness of the clinic Consider whether the uptake rate will likely change over time as the intervention becomes more well known, or whether other changes in clinical practice will impact the future uptake rate? 4. Combine the projected eligible population and uptake rate estimates (i.e. multiply the eligible patient numbers by the estimated uptake for each year and tabulate for each year of the analysis) 5. Estimate the average 'quantity' of the intervention that will be used, per patient If it is a pharmaceutical - consider the dosing schedule and how long it will be used for in each patient (on average) For other interventions - will they be repeated - and if so, how frequently - or are they one-offs? Multiply by the estimated patient numbers and add 'total expected usage' to the tabulated analysis. 6. Consider the unit cost (price) of the intervention and estimate the direct intervention costs (per patient and across the estimated population that will use the intervention each year of the analysis) 7. Also consider any additional costs that may be directly associated with providing the intervention for example; if the intervention is an infusion there would be additional costs associated with aministration (consumables and supervision etc.), Week 5 14  similarly for procedures (admission, anaesthetic and/or theatre costs etc.) add the total additional costs that would be expected as an additional row to the analysis 8.Consider any cost offsets that may be directly associated with providing the intervention for example; if the intervention is replacing an alternative (i.e an active comparator such as an alternative pharmaceutical or procedure) estimate the expected average cost-savings per patient associated with no longer requiring the alternative add a row reporting the total savings expected across the population who will utilise the new intervention to the tabulated analysis. 9. Calculate the net costs or cost-savings expected each year (i.e. the total costs of the intervention + administration, then subtract any cost-savings) BUT take note that financial analysis is a projection and inevitability there will be uncertainty about the size of the population, uptake.. → so important!! to consider SCENARIO ANALYSES/SENSITIVITY ANALYSES that explore alternative estimates and assumptions about them Affordability vs Sustainability Although one intervention may seem cost-effective on its own (affordability), the duration/total resource requirement may make it less cost-effective instead (sustainability), so need to be aware of this and compare costs carefully Eg: Influenza Vaccine: Cost-effective but requires substantial resources for widespread distribution, possibly making it unaffordable on a large scale. Gene Therapy for Rare Disease: Less cost-effective but more affordable due to the small number of patients, making it a potentially desirable policy choice to improve health equity HnS Seminar Week 5 15  1. ICER (Incremental cost-effectiveness Ratio) Benefit gained vs money lost (cost-benefit ratio) How much do we have to pay for how much benefit we get > DIFFERENCE IN COSTS/DIFFERENCE IN OUTCOMES calculates the AMOUNT YOU HAVE TO PAY (COST) per unit of benefit COST-EFFECTIVENESS PLANE Week 5 16  X axis -> incremental benefits/outcomes reached Y axis -> incremental cost Week 5 17  LAMBDA = Gradient of the line = incremental costs/outcomes -> In quadrants C and D, you need to consider the trade-off. How much decrease in health is worth us saving money, how much is an increase in health worth in terms of monetary value? Public health level Not the same as on individual levels cuz “worth it” is different Esp in quadrant C -> Need to have a tighter threshold for how much cost you will accept LAMBDA -> rank all interventions and fund from the lowest ICER until you run out of money. STEPS: Use a formula to calculate GDP per capita Adjust ICER depending on national economic outlook, competing budget pressures Do emperical studies to ask citizens about their “willingness to pay” for health outcomes. ICER UNCERTAINTY Important to characterise or describe an uncertainty around any estimated ICER Consider WHERE the uncertainty is present and where it is relevant (isit within the primary data, within modelling methods, interpretation of the evidence or final results) Week 5 18  `Stochastic- not the focus of CEA Presenting uncertainty All economic evaluations should present a sensitivity analysis Examines how ICER is affected by a variation in a specific input parameter 1. Deterministic sensitivity analyses 2 ways > univariate (change one variable at a time and see how much one parameter changes the outcomes, in this case, how much it changes the ICER) > multivariate (change multiple variables at a time WHAT ARE THE THINGS THAT ARE MOST DETERMINISTIC IN CHANGING THE OUTCOMES 1. Probabilistic sensitivity analyses Use simulated models to tell what are the range of possible outcomes when people use a particular intervention Week 5 19  When there is uncertainty in the input, the value is selected at random from a defined probability distribution Input a set of parameters -> stimulates what a real person would do. simulation looks at how ppl interact with that particular intervention and then give you the expected outcomes (presents it in a scatter plot of incremental cost vs incremental effectiveness) Cons of ICER Generally conducted to show how it affects an average person in society (but not individualised to your own individual factors) Look at affordability of intervention (a VERY EXPENSIVE intervention can still have a pretty good ICER if it is SUPER EFFECTIVE at achieving its outcomes. Hence, it does not tell you how affordable it actually is. Need to look at it separately.) How does it change equity in healthcare? -> choose interventions that are both efficient and equitable. Sometimes the most efficient use of resources is not the most ethical or equitable. Decision making using economic evaluation Economic evaluation is only easy when there are no non-economic concerns about the intervention and ALL OTHER CRITERIA FOR FUNDING HAVE BEEN MET. Summary Healthcare intervention with ICER below accepted threshold SHOULD BE FUNDED If funding is between a choice of interventions, the one with the lower ICER is preferred. Then look at uncertainty of the ICER and use sensitivity analyses Professionalism and Leadership Lecture: Leadership in Medicine Week 5 20  Describe the principles of medical leadership as outlined in the RACMA leadership framework. Medical leader communication advocate scholar collaborator professional → value systems, patient first behaviour, reflective practice, ethical practice manager → people and performance medical expert Explain key leadership theories, including followership and adaptive leadership and how they may apply to teamwork within interprofessional healthcare teams. 1. Democratic → follow the majority (the leader considers team members’ opinions before making decisions) 2. Autocratic → use it in the right time (leader makes decision without seeking input from team members) 3. Bureaucratic → by the book 4. Laissez-faire → stepping back and letting ppl do things on their own, just check back in with them 5. Authoritative → have enormous amounts of influence Transactional leadership style that focuses on the exchanges or transactions between leaders and their followers Transformational leadership Week 5 21  focuses on inspiring and motivating followers to achieve their full potential and contribute to the organisation’s long-term vision and goals Adaptive leadership recognises the constant presence of change and uncertainty in organisations and the broader environment; adaptive to change and skilled at dealing with them Followership is also a form of leadership being an active, engaged and responsible member of a team Recognise and distinguish between leadership and management skills in medical leadership. Leadership skills vision and strategic thinking inspiration and motivation management empowerment and development communication Management skills operational planning and organisation resource management process implementation and improvement performance monitoring and evaluation problem solving and decision-making All doctors are required to lead due to their professional knowledge and ability but not all doctors will have a management authority role based on position. Clinical Practice Week 5 22  Clinical Pearl: Higher Centre/Cognitive Testing Describe deficits in higher centre functions, such as aphasia, apraxia, agnosia, neglect, memory impairment, and executive function. Demonstrate a systematic neurological examination of a simulated patient’s higher centres and speech. Interpret clinical data from patient interviews and neurological higher centres examination to develop relevant differential diagnoses. Science and Scholarship Neurological Emergencies Describe clinical presentations of neurological emergencies. Outline the appropriate investigations for, and management of, neurological emergencies. Focal neurological deficits TIA Scenario 1 weak earlier, transient left-hand clumsiness for 10 mins 30 mins ago sudden onset right eye blindness, now resolved neurological exam normal → Carotid stenosis Treatment antiplatelet → aspirin and clopidogrel risk stratification: ECG, CTB, CTA large vessel stenosis new AF These may req admission as well early MRI brain and TIA clinic follow up Stroke Simplified stroke presentations Week 5 23  ACA contralateral leg>arm weakness MCA contralateral hemiparesis (arm/face>leg) hemisensory loss heimianopia aphasia (left), inattention (right) PCA contralateral hemianopia Brainstem/cerebellar (SCA, AICA, PICA) ataxia, vertigo, cranial nerve palsies dysarthria, dysphagia crossed sensory changed ipsilateral sensory loss on the face contralateral sensory loss on the body ataxic hemiparesis Hyperacute stroke treatment Thrombolysis (for large or small vessel occlusions) alteplase, tenecteplase imaging → non-contrast CT, CTA, MRI Endovascular clot retrieval (large vessel occlusion) imaging → non-contrast CT, CTA, MRI Scenario sudden onset of right-sided neurological symptoms global aphasia, right homonymous hemianopia, hemiplegia and sensory loss Week 5 24  → Left MCA occlusion Haemorrhage Scenario 65F has HTN, AF on warfarin 1hr dysarthria, right facial droop and mild right arm weakness headache and vomiting, drowsy, eyes deviated left, no response to pain on the right in a cortical lesion → eyes deviate to same side of lesion; brainstem lesion → eyes can deviate away from the side of the lesion BP 190/100, INR 1.9 (time taken for blood to clot); 1.1 and below is good → Intracerebral haemorrhage Treatment of intracerebral haemorrhage BP control reversal of antithrombotic effect Dabigatran (anticoagulant) Week 5 25  effect reversed by Idarucizumab → binds to Dabigatram and neutralises its effects Apixaban/Rivaroxaban (anticoagulants that inhibit factor Xa) Andexanet alfa → binds to the drugs and reduces their abilities Warfarin (anticoagulant) reversed by: vitamin K → helps the body produce clotting factors again fresh frozen plasma (FFP) → provides clotting factor directly prothrombin complex concentrate → concentrated dose of clotting factors surgery imminent herniation, hematoma removal Seizure most seizures self-abort but if greater than 5 mins, intervention may be req the longer a seizure persists, the less likely it will stop on its own Treatment 1. Benzodiazepine (Diazepam, midazolam, clonazepam) Week 5 26  IV/IO preferable, but use alternative route if not available if benzodiazepine use is indicated (>5mins) → give as early as possible, use the right dose, use the best available route 2. Antiseizure medication ASM Levetiracetam, valproate, phenytoin 3. General anaesthetic Midazolam infusion, propofol Scenario 1 ED with fever and cough, swab is positive for influenza A a crash is heard and the patient is found unresponsive with eyes open and symmetric clonic activity of arms and legs Take note that in the case of a seizure, DO NOT stick anything in their mouth or try to restrain them; when seizure stops, roll them into recovery position TIME the seizure + DONT give IV benzodiazepines immediately as most seizures stop Scenario 2 more forgetful in last month, emotionally liable, not sleeping well generalised convulsive activity → ambulance called unresponsive 15mins later when ambulance arrived → begin seizing again IM midazolam given with reduction of jerking but patient does not wake up in ED 20 mins later, still not rousing, subtle left face/arm twitching Week 5 27  Scenario 3 previously healthy but recent relationship breakdown after dropping out of uni course presented to ED due to unpredictable limb jerking movements while giving Hx → he develops continuous irregular repetitive flinging and jerking movements of all limbs he appears frightened and teary but is still talking to me Week 5 28  → Psychogenic nonepileptic seizure diagnostic clues → bilateral tonic-clonic activity with maintained awareness, back arching, hip-thrusting, distractibility, inconsistent movements, waxing-waning patterns treatment avoid sedatives edu psychotherapy Altered mental status Examination of impaired awareness GCS → 15 (eyes, voice and movement) Scenario 1 day 1 post-op, pain has been diff to control frequent use of PRN opioids on routine check → falling asleep, diff ans qns BP 100/65, HR 60, RR 6, T 36.2 Pinpoint pupils → Opioid overdose (naloxone may lead to rapid reversal of altered mental status) Patient may have toxic-metabolic encephalopathy Wernicke’s encephalopathy hypoglycaemia, hyponatraemia, hypocalcemia, hypercalcemia resp failure (esp CO2 retention) medications (anticholinergics, some antibiotics, valproate) recreational drugs sepsis Week 5 29  renal or hepatic failure Scenario 2 65M, hypertension and sleep apnoea visiting hospital when he suddenly collapsed, unresponsive BP 180/90, HR 115 irregular, RR 9 all limbs extend to supraorbital pressure → sign of severe brain injury; significant brainstem dysfunction when opened manually, both eyes are deviated out and the left is higher pupillary light reactions are sluggish bilaterallly CT ANGIOGRAPHY SHOULD ALWAYS BE PERFORMED IN UNEXPLAINED LOSS OF CONSCIOUSNESS Scenario 2 85M with subdural haematoma fall with headstrike and a moderate right subdural haematoma non-surgical management → admitted for observation Week 5 30  moderate pain on review 1 hr ago but had been orientated now is very drowsy, grunting only and resistive to care repeat CT → NO change in haematoma size, while on the scanner, irregular twitching of the right foot noted → EEG carried out → suggestive of nonconvulsive status epilepticus where a person experiences prolonged or recurrent seizures without the typical convulsive movements (like jerking of the limbs) seen in generalized tonic-clonic seizures. Instead, the seizures are more subtle, often presenting with changes in behavior, mental status, or consciousness. RF ppl with known epilepsy or just had a convulsive seizure prolonged delay to return to normal post-generalised convulsive seizure unexplained altered mental status with myoclonus (esp lateralised), automatism, nystagmus, sustained head/eye deviation diagnosis → EEG; but if unavailable → risk-benefit analysis for benzodiazepines or ASMs Neuromuscular weakness Scenario 1 25F with no medical hx 2 weeks of diplopia, 1 week of dysarthria and diff standing from a chair Week 5 31  In ED: coughing after sipping after and is speaking in short phrases Myasthenic crisis Dysarthria, dysphagia, dyspnoea speaking in phrases tachypnea, increased WOB measure FVC: if12 hrs management ICU monitoring BP and volume status management Nimodipine (calcium channel blocker) → prevent vasospasm secondary to subarachnoid haemorrhage Neurosurgical aneurysm treatment (clipping or coiling) Scenario 2 thunderclap headaches over last 2 weeks no neurological symptoms RCVS recurrent thunderclap headaches may be provoked → valsalva, sexual activity, exercise, swimming Week 5 34  RF illicit drugs (cocaine, marijuana) antidepressants, immunosuppressants, nasal decongestants pregnancy, OCP complications stroke convexity subarachnoid haemorrhage ICH Other thunderclap headache causes aneurysmal subarachnoid haemorrhage reversible cerebral vasoconstriction syndrome arterial dissection cerebral venous thrombosis intracerebral haemorrhage CNS vasculitis pituitary apoplexy spontaneous intracranial hypotension (CSF leak) Scenario 3 fever with headache, photophobia ED: BP 105.60, HR 105, 6 39.2 irritable, disorientated to date, neck stiffness Week 5 35  Bacterial meningitis fever with headache → high suspicion bacterial meningitis is rapidly fatal do not delay antibiotics excessively pending lumbar puncture antibiotics coverage depends on local pathogens and indiv RF intravenous dexamethasone (corticosteroid) before/with antibiotics Scenario 4 32F with obesity, psoriasis episodic migraine since puberty increasing headaches in last few weeks, now daily and unremitting blurry vision, sometimes vision goes dark with postural changes pulsing sound in the ears in ED: visual acuity 6/60 in each eye Week 5 36  severe disc swelling + hemorrhages → sign of raised ICP CT/MRI dilation of the optic nerve sheets → papilloedema Week 5 37  clot can be seen in the right transverse sinus → cerebral venous thrombosis massive midline shift + large mass seen → glioblastoma Raised ICP Idiopathic intracranial hypertension Week 5 38  secondary intracranial hypertension venous sinus thrombosis mass lesion drug induced (vitamin A, tetracyclin) meningitis leptomeningeal carcinomatosis management acute neuroimaging is req → evaluate for secondary causes lumbar puncture with therapeutic drainage can prevent irreversible blindness CSF analysis helps to exude secondary causes (infection, inflammation, malignancy) BUT THE MAIN DISORDERS THAT ARE TRUE EMERGENCIES WHERE MINS COUNT: 1. STROKE 2. CONVULSIVE STATUS EPILEPTICUS Eating Disorders Identify and differentiate between common eating disorders such as anorexia nervosa, bulimia nervosa, and binge-eating disorder. Outline the diagnostic criteria for the common eating disorders outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Discuss the risk factors, including genetic, psychological, social, and cultural factors, that contribute to the development of eating disorders. Describe the underlying biological, psychological, and social factors involved in the development and maintenance of eating disorders. Discuss the physical consequences of eating disorders on various organ systems and potential long-term health consequences. Week 5 39  Explain the importance of early identification, appropriate referral, and collaboration with mental health professionals in the management of eating disorders. Identify challenges and potential complications in the management of eating disorders and the importance of long-term follow-up and support. ED are much more common than we think, can affect anyone at any stage, there are often associated mental health disorders, EARLY TREATMENT AND SUPPORT IS ESSENTIAL!!! Stats >1 million Aus are currently living with an eating disorder (~4%) Aus adolescents who diet are 5x more likely to develop an ED 50% of Aus adolescents engage in disordered eating manually >80% diagnosed with an ED have at least one or more psych disorder AN → anorexia nervosa BED → binge eating disorder BN → bulimia nervosa Week 5 40  RF females children and adolescents (13-17 yo) competitive sports, occupations, performing arts minority groups hx of dieting or dieting as of current ppl who want to lose weight mental health conditions on restrictive diets due to medical conditions hx of trauma Week 5 41  comorbidities that cause weight loss or focus on body weight/shape personality traits of perfectionism or compulsiveness Yellow flags → not diagnostic but raises your concerns for an ED psychological preoccupation with eating, food, body shape, weight intense fear of weight gain heightened anxiety around meal times disturbed body image or extreme body dissatisfaction rigid thinking around food (good and bad food) depression, anxiety, low self-esteem, shame, guilt heightened sensitivity to comments or criticism around food, body or exercise physical sudden weight change paeds → unexplained decrease in growth curve cold sensitivity, fatigue, lethargy, fainting, dizziness, palpitations, OH, dyspnea, oedema altered mental cycle signs of frequent or self-induced vomiting lanugo osteoporosis or osteopenia behavioural dieting behaviour +/- compulsive exercising evidence of binge eating evidence of purging obsessive or pattern following rituals around food, prep and eating Week 5 42  changes in food preference ‘clean eating’ avoidance of social situations involving food gives excuses to avoid food What can we do to take note of ppl at risk of developing an ED screening tools SCOFF questionnaire S – Do you make yourself Sick because you feel uncomfortably full? C – Do you worry you have lost Control over how much you eat? O – Have you recently lost more than One stone (6.35 kg) in a three-month period? F – Do you believe yourself to be Fat when others say you are too thin? F – Would you say Food dominates your life? ED screen for primary care EDEQ ALWAYS CONDUCT A MENTAL HEALTH RISK ASSESSMENT FOR THESE PATIENTS Types of ED Binge eating disorder Week 5 43  Bulimia nervosa Anorexia nervosa Week 5 44  Avoidant restrictive food intake disorder (ARFID) other specific feeding and eating disorder unspecified eating disorder rumination disorder Complications of having an ED Social isolation Financial distress Employment and study impacts Relationship breakdowns Restricting will lead to: cardiac → bradycardia, hypotension, HF GI → gastroparesis, constipation hypolgycaemia hypothermia infections insomnia conc diff muscular injuries dizziness Week 5 45  seizures, muscle cramps amenorrhea osteoporosis high cholesterol levels dry skin, brittle hair and nails renal failure vit deficiencies death Binging will lead to: electrolyte disturbances → vomiting and laxative use dehydration insulin resistance and DMT2 tooth enamel decay and cavities intestinal obstruction or perforation parotid swelling related to prolonged vomiting oesophageal rupture pancreatitis → can lead to the overproduction of digestive enzymes → and if these enzymes are activated prematurely in the pancreas, they can start to digest pancreatic tissue → inflammation hepatitis → can lead to accumulation of fat in liver cells → can lead to non-alcoholic fatty liver disease → inflammation + liver damage When will ED present as an emergency Week 5 46  Management ppl and professions involved psychologist or psychiatrist gp sch fam inpatient team dietician social worker management pathway GP consult → risk identified → risk assessment → MHCP+GPMP or ED management plan (EDMP) GPMP allows access to 10 subsidised psych visits per calendar year Week 5 47  MHCP (mental health) not everyone will be eligible for a EDMP; there is a strict criteria that has to be met according to the DSM5 (but don't have to memorise this) EDMP allows up to 40 subsidised psych visits per calendar year AND allows up to 20 subsidised dietician visits per calendar year Treat the comorbidities depression and anxiety can compound issues neurodivergent patients will need diff approaches substance misuse disorders need appropriate support family, financial and social problems need to be addressed Consider pharmacotherapy antidepressant/anti-anxiety medications PPIs antipsychotics and benzodiazepines (in some situations only) Platforms that can also help Week 5 48  Alcohol Use Disorder Explain the mechanisms by which alcohol affects the central nervous system and reward pathways, leading to reinforcement and addictive behaviours. Discuss the genetic and environmental factors that influence an individual's susceptibility to, and risk for, Alcohol Use Disorder (AUD). Summarise the role of psychosocial factors such as stress, peer influence, and co-occurring mental health disorders in the development and maintenance of AUD. Outline the diagnostic criteria for AUD as described in the DSM-5. Differentiate between mild, moderate, and severe AUD based on the severity and number of symptoms displayed. Outline the physical and mental health complications associated with chronic alcohol misuse, such as liver disease, cardiovascular disorders and psychiatric comorbidities. Outline the principles of managing alcohol withdrawal syndrome and the complications associated with detoxification. Describe evidence-based interventions and treatment modalities for AUD, including behavioural therapies, medications, support groups, and relapse prevention strategies. Effect of alcohol on the CNS This is caused by: Alcohol is able to bind to GABAa receptors in which GABA binds to and GABAa receptors are inhibitory neurotransmitters receptors in the brain Week 5 49  → when GABA (produced by the presynaptic neuron) binds, it allows the influx of chloride ions into the neuron, allowing for hyperpolarisation → making it less likely for the neuron to fire an AP Alcohol binds and increases the receptor’s activity → contributes to the sedative and anxiolytic effects of alcohol alcohol can also acts on other neurotransmitter systems such s glutamate, glycine, acetylcholine and serotonin Effect of alcohol on the reward pathway nucleus accumbens → alcohol, cocaine, amphetamines and cannabis binds here ventral tegmental area → opiates, alcohol, nicotine bind to receptors Both areas joined by the medial forebrain bundle Binding of these → dopamine Increase of these substances → increases brain stimulation reward threshold AUD is the most common substance use disorder in Aus dependence (impaired impulse control) is a chronic relapsing, remitting disease Factors that influence risk for AUD Week 5 50  RISK FACTORS 1. Biological a. genetics → fam hx of AUD b. neurobiology → ADHD c. gender → men more likely d. age → earlier onset on drinking alcohol → higher likelihood of AUD e. In-utero exposure 2. Psych a. mental health b. personality traits → impulsivity, risk-taking behaviour c. coping mech 3. Social a. cultural b. peer pressure c. bullying d. socioeconomic status e. family dynamics (alcohol abuse or dysfunctional fam environment) Week 5 51  RESILIENCE access to +ve adult role models positive fam relationships positive attitudes to and completion of schooling social grp and interests peer attitudes to alcohol, tobacco and other drugs Diagnosing AUD DSM-5 vs ICD-11 Complications of AUD and AWS AUD Week 5 52  wernicke encephalopathy due to a srs deficiency of thiamine (vit B1) CONFUSION ATAXIA NYSTAGMUS Korsakoff dementia usually followed after this → can possibly have anterograde amnesia Pancreatitis → alcohol metabolism in the pancreas produces toxic metabolites and ROS BM suppression → alcohol has a toxic effect on the BM, it can directly damage it Osteoporosis → chronic alcohol use inhibits osteoblasts and increases activity of osteoclasts, alcoholic also often have deficiencies in calcium and vit D Hypogonadisms → alcohol can directly damage the Leydig cells in the testes, it can also interfere with the release of GnRH hormone Infertility → reduced testosterone levels in men and affected menstrual cycle for women AWS (alcohol withdrawal syndrome) Week 5 53  sympathetic overdrive → tremor, tachycardia, increased BP, diaphoresis, anxiety, restlessness/agitation, insomnia nausea, vomiting headache photophobia/sonophobia hallucinations (auditory, visual, tactile) delirium seizures Management of AUD Week 5 54  relapse prevention counselling → non-governmental organisations, DASSA psychology self-help grps: AA, SMART recovery residential rehab medications: naltrexone (opioid antagonist), acamprosate (glutamate modulator) Management of AWS benzodiazepines → usually diazepam thiamine multivitamin check and supplement Mg correct electrolyte abnormalities as req symp medications → paracetamol +/- NSAIDs, antiemetics engage in relapse prevention services consider relapse prevention pharmacotherapy Clinical connections Week 5 55  INR normal (how quickly your blood clots) exhausted, dizzy, hot and cold shivery shakes (full on rigors and sweating), off my food, couple of vomits patient takes warfarin (for valve replacement) ddx sepsis meningitis haemorrhage stroke TIA SOL (esp tumour) Week 5 56  Looking at the risk of getting an ischaemic stroke cause of AF Neuro hx finds it hard to concentrate and feeling a bit down the last 2-3 days feels off but hard to describe for vision for speech, mumbles more, seems harder to pronounce words Week 5 57  no tremor noticed, just feels weak balance feels off headache → comes on gradually, gets worse, worse on waking up or putting head down, generalised Vomiting last 2 days as soon as he woke up felt a bit better about an hour after no bile or no blood Driving hx did not hit anything today but very close these days he had been feeling like he had been walking into things a lot and dropping things vestibular neuritis can cause vertigo Staph aureus most common pathogen to cause infective endocarditis; strep imp for dental procedures; enterococci Dexamethasone → a corticosteroid that is good with inflammation like brain swelling Four-factor prothrombin complex concentrate if fella is uncontrollably bleeding and INR is high HINTS examination → helps to diff btw a central or a peripheral cause of vertigo Week 5 58 Week 5 59