Yr4 GenMed - Tutorials Flashcards
Outline a flowchart for interpreting spirometry results.
What is Dyspneoa/SOB?
- What does the patient mean when they say they are short of breath? (4)
Shortness of breath
- Cortical perception of abnormal work of breathing
- Working Harder to Breathe
- Not due to abnormalities in PaO2 or PaCO2
- Can be associated with low or normal paO2
- Can be associated with low, normal or high PaCO2
- Means different things to different people
Clinical Guides to Breathlessness
- History?
Clinical Guides to Breathlessness
- Examination?
- 11 Investigations?
- Need to give the respiratory rate as an exact number – don’t say they are tachypnoeic.
- Auscultation – comment on air entry first (inspiratory: expiratory ratio) then comment on added sounds.
Consider 3 pulmonary causes & cardiovascular causes? Others?
- 12 Ddx?
Pulmonary Causes
1. COPD
2. Pulmonary fibrosis
3. Suppurative Lung Disease
Other
Chronic Kidney Disease – fluid overload, anaemia, ?
What would you be looking for on examination?
What investigations would you order for this patient?
- Two types of natriuretic peptides can be measured to check for possible heart failure.
- Brain natriuretic peptide (BNP) is a protein that’s a type of hormone. A hormone is a chemical messenger in your bloodstream that controls the actions of certain cells or organs. BNP has “brain” in its name because that’s where researchers first discovered it. Your heart makes and releases BNP into your bloodstream when it’s working harder than normal to pump blood.
- The BNP tells your blood vessels to open wider and your kidneys to get rid of water and salt through urine (pee). This helps reduce the workload on your heart by lowering blood pressure and reducing the amount of blood your heart has to pump.
- N-terminal pro b-type natriuretic peptide (NT-proBNP) is a protein that’s an “ingredient” for making the BNP hormone. Like BNP, your heart makes larger amounts of NT-proBNP when it has to work harder to pump blood.
- Unusual to have such an elevated BNP in only right sided heart failure
- BNP – elevated in acute kidney failure & pregnancy
What is the general formula for approaching ABGs?
- A-a O2 gradient formula?
pH 7.25, PaCO2 60mmHg, PaO2 50mmHg, HCO3 27
What is the MOST Likely Cause in Patients presenting to ED
with this ABG on room air?
Acidosis, PaCO2 UP = Respiratory, PaO2 = LOW, HCO3 = 22-29, normal, Uncompensated, A-a O2 gradient = 25
- 150 - (1.25x60 + 50) = 25
- Low O2 = V/Q mismatch, Hypoventilation, Low inspired oxygen, Shunt
- Acute respiratory acidosis from hypoventilation because the A-a O2 gradient is normal = hypoventilation = narc overdose
pH 7.27, PaCO2 34mmHg, PaO2 92mmHg, HCO3 16
Interpret the ABG.
Acidosis, PaCO2 = low = therefore = metabolic
- A-a O2 gradient = normal
- Most common cause of an acute metabolic acidosis is GI/ Diarrhoea = loss of alkali
- Also think blood loss/lactic acidosis
pH 7.35, PaCO2 60mmHg, PaO2 50mmHg, HCO3 34
- Interpret the ABG.
pH 7.47, PaCO2 28mmHg, PaO2 75mmHg, HCO3 23
- Interpret the ABG.
Alkalosis, PaCO2 is LOW so its respiratory = Acute respiratory alkalosis, no change in bicarb = uncompensated = Acute
Hyperventilation = Anxiety attack this wouldn’t be hyperventilation because the PaO2 isnt high enough
When the A-a O2 is high = there is a v/q mismatch (doesn’t occur in hyperventilation)
- Acute asthma, pneumonia & PE
What are the features of increased pulmonary pressures on CXR?
Pulmonary hypertension is currently defined as a resting mean pulmonary arterial pressure of >20 mmHg at right heart catheterisation, which is a haemodynamic feature that is shared by all types of pulmonary hypertension.
Outline the treatment of:
1. Heart Failure?
2. Pulmonary Hypertension?
3. COPD?
4. Complex sleep apnoea?
Its January 2025….3 am
Mr B 72 y.o man on the ward
Called by nursing staff
Complaining of sudden deterioration in breathing…..
What are the 4 General Rules for Clinical Assessment of the Acutely Dyspnoeic Patient?
Examination?
Clinical Assessment of the Acutely Dyspnoeic Patient - General Rules
1. How Sick is the patient? - ABCD
2. Gather Information - Rate of Onset, Why in Hospital, Medication and Fluid Chart, Associated Symptoms
3. Prioritise and Stabilise
4. Initial Thoughts - Cardiac / Respiratory / Pulmonary Vascular / Fluid Balance / Anaphylaxis / Metabolic / Sepsis
Which investigations for an acutely dyspnoeic patient?
Treatment of Acute Respiratory Failure?
Options for Oxygen Therapy? (5)
Interpret the following Spirometry:
FEV1 = 72% predicted
FVC = 96% predicted
FEV1/FVC ratio = 62%
FEV1 improves by 3% following bronchodilator
Flow volume loop obstructive
- Compare obstructive vs. restrictive patterns on spirometry?
FEV1/FVC ratio <72% = obstructive pattern
Diagnosis: COPD, moderate severity, no acute bronchodilator response therefore less likely to be an asthmatic component.
5 Differences between obstructive and restrictive spirometry.
What on spirometry would suggest an asthmatic component?
Acute Bronchodilator Response
- 10 mins after Salbutamol or other rapid acting bronchodilator
- Acute bronchodilator response not the same as reversibilty
- >12% improvement in FEV1
- AND >200ml
- highly suggestive of asthmatic component
How would the following appear on flow volume loops:
- Upper airways obstruction?
- Tracheal obstruction?
- Vocal cord dysfunction?
- Intrathoracic tumour?
What is Dyspepsia?
- List 6 Causes of dyspepsia?
-
The concept of dyspepsia
- Persistent or recurrent pain or discomfort centred in the upper abdomen
- Felt to be related to stomach or duodenum
- May be associated with fullness, early satiety, bloating or nausea.
- Sometimes concurrent bowel symptoms
Causes of dyspepsia
1. Functional dyspepsia
2. Gastro-oesophageal reflux disease
3. Peptic ulcer
4. Malignancy
5. Biliary disease, pancreatic disease
6. Non-GI: drugs, endocrine disorders
What is Functional “non-ulcer” dyspepsia?
- 2 types?
Functional “non-ulcer” dyspepsia
- Dyspepsia in absence of obvious organic cause
- Considered to be related to changes in gastric motility and visceral hypersensitivity
- Can be sub-divided into epigastric pain syndrome (visceral hypersensitivity) and post-prandial distress syndrome (motility changes)
- Need a negative scope before you can call it a functional problem.
- Motility – eg. diabetic gastroparesis
Outline the treatment for Functional Dyspepsia (8).
List 12 Alarm symptoms in a patient with Dyspepsia?
- Outline an approach to dyspepsia.
Alarm symptoms in a patient with Dyspepsia
1. Unintended weight loss
2. Persistent vomiting
3. Progressive dysphagia
4. Odynophagia
5. Anaemia
6. Haematemesis/melaena
7. Palpable abdominal mass or lymphadenopathy
8. Family history of upper gastrointestinal cancer
9. Previous gastric surgery
10. Jaundice
11. Age over 45-50 yrs
12. Use of aspirin/NSAIDs
What diagnosis is the most likely in this man?
- Definition?
- 6 Causes?
= Peptic Ulcer
List 7 Presentations of peptic ulcers?
- List 10 Causes of Upper GI Tract bleeding?
Presentations of peptic ulcers
1. Dyspepsia - DU pain typically 2-3 hours after a meal and relived by food or antacid. Pain often wakes patient late at night (acid secretion without food buffer). GU pain tends to occur sooner after a meal and less likely to awaken at night.
2. Anorexia and weight loss common - Many ulcers are asymptomatic and symptoms are not specific or sensitive
3. Iron deficiency
4. Vomiting
5. Anorexia
6. GI bleeding
7. Perforation
What are 8 Clinical indicators for major bleeding in Peptic Ulcer Disease?
- Name 2 Risk-Stratification Tools for Upper Gastrointestinal Hemorrhage.
- Systolic BP < 100mm supine - Can be 40% volume loss
- Postural drop > 10mm Hg - ?15% blood volume loss
- Pulse > 100 per minute - Resting tachycardia with <15% volume loss
- Haemoglobin<80g/L
- Syncope (collapse)
- Variceal haemorrhage
- Comorbidity– age>60yrs, organ dysfunction (heart, kidney, respiratory etc), anticoagulation
- Rebleed in hospital
Peptic Ulcers
- Evaluation?
- Treatment?
Evaluation of peptic ulcers
- Usually diagnosed by endoscopy
- For gastric ulcers, usually do biopsies at time to exclude cancer
- Usually also rescope in 10 weeks or so to confirm healing
- May get HP serology as well if not biopsied at time of scope
Role of Proton pump inhibitors in PUD?
- Long term side effects?
Proton pump inhibitors for PUD
- On the whole very well tolerated
- Best taken on empty stomach before a meal
- Once daily dose for peptic ulcers. Twice daily for some indications like refractory reflux
- Rebound acid hypersecretion can occur on cessation
- Long term concerns: increased infections (C.dif [OR 1.7], pneumonia [OR 1.27]), malabsorption (osteopaenia, magnesium, iron, B12), medication interactions (clopidogrel)
- More recently ?dementia link, chronic renal disease, cardiac risk
Other than PPIs, name 3 other acid-peptic medications which may be used in the treatment of PUD?
Other acid-peptic medications
1. H2 antagonists: ranitidine, nizatidine
2. Sucralfate- coating agent in stomach. Occasionally used for bile-gastritis
3. Misoprostol: prostaglandin E analog. Shown to reduce risk of NSAID induced ulcers. Developing role for small intestinal NSAID
injury.
What is Helicobacter pylori and what association does it have with PUD?
- Risk factor?
- Prevalence?
- Disease associations? (5)
Helicobacter pylori
- Gram negative spiral flagellated bacterium
- Socioeconomic level seems to be the major determinant of risk of infection
- In Australia, 25-30% of population infected, prevalence increases with age
- Most infections probably acquired in early childhood
Helicobacter pylori and PUD
- Testing? (4)
- Treatment? (3)
Testing for HP
1. Serology (good if you have never been treated for HP). No preparation needed
2. Stool antigen test
3. Breath test which relies on HP urease activity - Need to avoid antibiotics for 4 weeks and PPI for 1-2 weeks
4. Endoscopic biopsy for histology or rapid urease test or culture - Need to avoid antibiotics for 4 weeks and PPI for 1-2
weeks
What role does Aspirin and NSAIDs play in the development of peptic ulcers?
- 2 COX enzymes?
Aspirin and NSAIDs in PUD
- These can be absorbed across gastric mucosa but the main problem seems to be systemic (post-absorption) inhibition of GI mucosal cyclo-oxygenase (COX)
- Enteric coated agents or rectal delivery still produces risk
- Endoscopic evidence of ulceration occurs in 15-30% of chronic users
- In a low risk subject, 0.5% risk per year of serious complicated ulcer
- 50–60% of NSAID-associated peptic ulcers, presenting for the first time as a complication, have been silent previously.
- Potent agents can induce damage after 7 days
- Reasonable to test for and eradicate HP in NSAID/aspirin naïve patients
- Eradication of HP not adequate alone in setting of complicated ulcer
- ?role of misoprostol
Describe the work-up for a patient with apparently negative H.pylori, NSAID negative peptic ulcers?
What are the subtypes of diabetes according to prevalence?
Classify the types of Diabetes Mellitus.
Which 10 conditions are associated with Syndrome of Insulin Resistance?
- Overflow hypothesis of insulin resistance?
How does visceral adiposity lead to insulin resistance?
Outline the criteria for the diagnosis of Diabetes (4).
- 3 Criteria for Pre-diabetes?
Outline an approach to New diagnosis of diabetes?
List 5 Reasons for suboptimal glycaemic control in an Existing diabetic patient?
- What are the goals for outpatient treatment of diabetes? Glycaemic targets? (3)
- Approach to individualisation of Glycaemic targets?
Reasons for suboptimal glycaemic control in Existing Diabetic Patients
1. Concurrent illnesses - Infection (pneumonia, diabetic feet), myocardial infarction
2. Treatment - Non-adherence & Suboptimal treatment
3. Poor understanding of treatment goals
4. Loss to follow-up
5. Social stressors
Classification of Hypoglycaemia? (3)
Outline the 3 Types of Insulin Treatments available for T1DM.
- Examples of each?
- Rationale?
What are the pros & cons of Injected Insulin regimens vs. Continuous insulin infusion regimens for TIDM?
Outline the Australian TIIDM Glycaemic Management Algorithm.
- Role of weight loss?
- Monotherapy?
- Dual therapy?
- Multiple therapies?
- Review intervals?
-
Which diabetic medication for a patient with TIIDM &:
- ASCVD?
- High risk indicators?
- Heart failure?
- CKD?
What is the “Incretin effect” in diabetes?
In healthy humans, the incretin glucagon-like peptide 1 (GLP-1) is secreted after eating and lowers glucose concentrations by augmenting insulin secretion and
suppressing glucagon release. Additional effects of GLP-1 include retardation of gastric emptying, suppression of appetite and, potentially, inhibition of β-cell apoptosis.
Outline the mechanism of action of GLP-1 therapies in the management of diabetes.
- DPP-4 inhibitors?
- GLP-1 analogues?
List some of the common adverse effects associated with the incretin therapies such as liraglutide, saxagliptin, exenatide.
Outline 3 effects of SGLT2 Inhibitors in lowering blood glucose levels for diabetic patients?
- Why chart them in the AM?
SGLT2 Inhibitors Cause:
1 - Glucosuria → lower blood glucose levels and weight loss.
- β-cell: ↓ insulin, ↑ glucagon → ↑ Lipolysis
- ↓ Steatosis (NAFLD)
2 - Natriuriesis → lower total body water and decreased heart failure = ↓ blood pressure
3 - Tubuloglomerular feedback activation → ↓ fibrosis and CKD progression
Commencing insulin on a naïve patient
- What are the safe doses of Optisulin and Novorapid for starting a basal-bolus regime?
- What are the safe doses for started a patient on mixed insulin?
- How can insulin doses be calculated using a weight-based regimen?
Starting basal-bolus regime - Safe doses:
1. Optisulin 6 - 10 units nocte – use lower dose (6-7 units) if elderly, frail, renal or hepatic impairment, low-normal BMI. Can increase by 2-3 units every 1-2 days in hospital (2-3 days in community)
2. Novorapid 3 – 4 units with meals
Mixed insulins - safe doses
1. Novomix-30: 6 to 10 units once or twice daily with meals, depending on BGLs, BMI, age, renal function, frailty and oral intake
2. Ryzodeg: 6 to 10 units once or twice daily with meals, depending on BGLs, BMI, age, renal function, frailty and oral intake
- Timing of Ryzodeg administration can be changed (eg if once daily, it can be taken with lunch one day and with dinner the next day, as long as the meal it is taken with is the main meal for the day)
What are 4 goals/principles of inpatient diabetes management?
- What about for TIDM?
- Why is inpatient diabetes management so important?
T1DM patients
- If they are cognitively capable (ie no altered GCS due to sepsis, uraemia, stroke, head trauma or sedation, and no psychiatric concerns), it is often safer to allow T1DM patients to have some autonomy over their inpatient diabetes management
- Ask about their insulin doses and chart a range.
- Eg Novorapid 0 – 6 units tds with meals instead of a fixed dose 4 units tds
- Why is perioperative inpatient diabetes management so important?
- What information is useful when making an inpatient diabetes referral?
- How do we manage diabetic medications perioperatively?
Perioperative management of diabetes medications
1 - If patient is on a morning operating list and fasting from midnight
- Reduce evening long-acting insulin to 70% of the dose.
- Patient not to have any of their morning diabetes medications.
- Consider ward-based insulin/dextrose infusion (not DKA one) with specific BGL parameters on when to be starting the infusions
2 - If patient is on an afternoon operating list and allowed to have a light early breakfast
- Can have morning diabetes medications
Diabetes - Case 1
- 69 yo woman, T2DM for last 9 years
- Normally on metformin XR 1000mg bd and gliclazide 60mg mane
- Admitted with unilateral headache, visual impairment and jaw claudication
- Temporal artery biopsy – Giant Cell Arteritis
- Commenced on prednisolone 60mg mane
What information would you like to know? What would you do next? Effect of Steroids in Diabetic patients?
- Add insulin at same time as steroid – ideally both should be in the morning.
- Might need to cease gliclazide temporarily due to risk of hypoglycaemia.
Diagnosis?
Severity? (7 factors to consider)
- Causes of Diabetic Ketoacidosis?
- Management of DKA? 3 Factors to consider?
- 5 Main concerns re: rapid correction of hyperglycaemia?
- Protocol?
Precipitating Causes of DKA
1. New diagnosis of DM
2. Infection
3. Poor adherence to treatment
4. Other
5. Unknown
Commence DKA protocol – 3 factors to consider
1. Fluid replacement
2. Insulin
3. Potassium
Main concerns: Rapid correction of hyperglycaemia can lead to:
1. Hypoglycaemia
2. Cerebral oedema
3. Hypokalaemia
4. Gastroparesis
5. Macular oedema
How cna SGLT2 inhibitors cause DKA?
SGLT2 inhibitors and DKA epidemiology
- Rare adverse reaction: Up to 1 in 1,000 patients (0.2 to 0.8 cases per 1,000 patient years in T2DM)
- Could be life-threatening
- Always consider it if non-specific symptoms: Nausea, vomiting, anorexia, abdominal pain, excessive thirst, dyspnoea, confusion, unusual fatigue or sleepiness
How can you prevent euDKA in SGLT2 inhibitor use?
- What are safe ketone levels?
Safe Ketone Levels
- <0.6 mmol/L is a normal range
- 0.7 – 2.0 mmol/L – consider prolonged fasting (starvation ketoacidosis) or insulin bolus requirement (usually 2-3 units, depending on BSLs and oral intake)
- If hyperglycaemic >15 mmol/L with these ketones, suggest venous blood gas to exclude diabetic ketoacidosis
- >2.0 mmol/L and hyperglycaemia– high risk of diabetic ketoacidosis. Need urgent VBG to assess for acidosis
Outline a flowchart for the definition of MI based on troponin rise.
Universal Definition of MI
- What are the 5 Types?
- What are you looking for on CXR in a patient with chest pain? (3)
What are you looking for on CXR in a patient with chest pain?
1. Respiratory causes of chest pain
2. Cardiomegaly/ Heart failure
3. Widened mediastinum = aortic dissection
- 3 Causes of Troponin Elevation >50ng/L (unless early)?
- 9 Causes of Mild Troponin Elevations (es hs trops: 15-50ng/L)?
Measure troponin at presentation then 2 hours later.
Trops peak at 18 hours from onset of chest pain.
Suspected Acute Coronary
Syndrome Clinical Pathway?
What is a TIMI Score in suspected ACS?
TIMI
- TIMI Risk Score for UA/NSTEMI estimates mortality for patients with unstable angina and non-ST elevation MI.
- Can be used to help risk stratify patients with presumed ischemic chest pain. However, it was originally derived in patients with confirmed unstable angina or non-ST elevation myocardial infarction.
- UA/NSTEMI can sometimes be missed. Traditionally, the TIMI Risk Score for UA/NSTEMI can correlate the risk of adverse outcome in chest pain patients.
4 Investigations to consider for possible angina?
- Sensitivity & Specificity of non-invasive tests for the detection of coronary artery disease?
Investigations to consider for possible angina
1. ECG - A normal ECG doesn’t rule out ACS!
2. Echo +/- Stress (Exercise or Dobutamine)
3. Myocardial perfusion scan
4. CTCA
Severity Grading of Aortic Stenosis?
Intervene only with symptomatic severe aortic stenosis.
PBS Criteria for Prescribing Statins?
- Role of statins in delaying Aortic Stenosis progression?
Role of statins in delaying the progression of aortic stenosis = nil - this is a surgical problem
- Would still prescribe for other prevention
What medications are given for Radial angiography?
- What can be seen on this angiogram? Management options for a patient who also has severe aortic stenosis?
- Would you stent the LAD first or prioritise fixing her aortic stenosis with a TAVI valve?
- Does she need dual-anti-platelets? Which ones? How long for?
Radial Angiography
- 5F diagnostic
- 6F Intervention
- Dedicated radial catheters
- Radial cocktail:
1. Heparin 3000units
2. GTN 200mcg
3. Light sedation - midazolam and fentanyl
Angiogram - Shows severe stenosis at the bifurcation of the LAD - Management options – Stent (doesn’t require GA) or bypass graft (if she’s having a surgical/mechanical valve replacement anyway but if high surgical risk then valves fixed with TAVI = tissue valve, not a long lasting as mechanical valves).
ECG Interpretation?
Tx?
- Narrow-complex tachycardia
- Irregularly, Irregularly = likely AF
- V4, V5, V6 (lateral lead) = ST Depression – typically rate related ischemia but could be true ischemia (ask if any angina in the past few weeks)
What are 2 Risk Assessments to perform on a patient with AF to determine their suitability for anticoagulation?
If >2 on CHADS-VASC then anticoagulate unless your 2 points come from female gender and age >65yrs
Atrial Fibrillation
- Aetiology in Australia?
- 3 Consequences?
**Management of Atrial Fibrillation **
- Goals?
- 3 Rate Control medications?
- 4 Rhythm Control medications?
- 6 Key Points?
Rate Control
1. Digoxin
2. Beta blocker (Metoprolol)
3. Ca Channel Blocker (Verapamil)
Rhythm Control
1. Amiodarone
2. Flecainide
3. Sotalol
4. Dronedarone
Sotalol
- What is it?
- MOA?
- Indications?
- Precautions?
Sotalol is a methane sulfonanilide beta adrenergic antagonist used to treat life-threatening ventricular arrhythmias and to maintain sinus rhythm in atrial fibrillation or flutter.
- MOA: Sotalol is a competitive inhibitor of the rapid potassium channel. This inhibition lengthens the duration of action potentials and the refractory period in the atria and ventricles.
Amiodarone
- What is it?
- MOA?
- Indications?
- Precautions?
Amiodarone is a class III antiarrhythmic indicated for the treatment of recurrent hemodynamically unstable ventricular tachycardia and recurrent ventricular fibrillation.
- Amiodarone is a benzofuran derivative, anti-arrhythmic drug used commonly in a variety of settings.4 Most known for its approved indication in life-threatening ventricular arrhythmias, it is also used off-label in the outpatient and inpatient setting for atrial fibrillation.
Flecainide
- What is it?
- MOA?
- Indications?
- Precautions?
Flecainide is a class Ic antiarrhythmic agent used to manage atrial fibrillation and paroxysmal supraventricular tachycardias (PSVT).
The main contraindications for treatment with flecainide are ischemic heart disease, hypertension with left ventricular hypertrophy (LVH), congestive heart failure, hypertrophic cardiomyopathy, degree 2 and 3 atrioventricular blocks, complete bundle branch block and significant liver and kidney disease.
Digoxin
- What is it?
- MOA?
- Indications?
- Precautions?
Digoxin is a cardiac glycoside used in the treatment of mild to moderate heart failure and for ventricular response rate control in chronic atrial fibrillation.
- Digoxin is indicated in the following conditions:
1) For the treatment of mild to moderate heart failure in adult patients
2) To increase myocardial contraction in children diagnosed with heart failure
3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.
What is usually performed for an AF ablation?
- What is the evidence for AF ablation vs. pharmacotherapy? Which trials?
PVI = Pulmonary Vein Isolation +/- atrial substrate modification
What are the indications for catheter ablation for AF? What level of evidence is each suggestion founded on?
List the oral options for anticoagulation in AF.
- Which is preferred?
- CHADS-VASc risk of 0?
- CHADS-VASc risk of 1?
- CHADS-VASc risk of >2?
- Outline 5 reasons for the underuse of Warfarin?
Oral Anticoagulation Options for AF
Warfarin (Coumadin or Marevan)
VS.
NOAC (Novel Oral Anticoag)
- Factor Xa inhibitors
1. Apixaban (Eliquis)
2. Rivaroxaban (Xarelto)
- Direct Thrombin Inhibitors
1. Dabigatran (Pradaxa)
Others under development - Is there a preferred anticoagulant for AF? = Yes and No - Warfarin out of favour whilst NOACs compare favourable compared to Warfarin.
- Which NOAC should I use? = There are no head to head studies comparing NOACs
Vitamin K Antagonists
- MOA?
- How long for INR to be therapeutic?
- Is there a pro-coagulant effect?
- List the limitations of VKA therapy.
Vitamin K Antagonists
- Warfarin (Coumadin or Marevan) is most commonly prescribed
- Derived from Coumarin
- Inhibits Vit K dependent synthesis of clotting factors = 2, 7, 9, 10, Protein C, Protein S, Protein Z
- 48-72 hours for INR to be therapeutic
- Pro-coagulant effect - Protein C
What are the Guidelines for the Management of Bleeding with NOACs?
- What are the Reversal agents for Warfarin? NOACs?
- List 9 conditions the use of NOACs should be used with caution in?
Reversal Agents
Warfarin
- Vit K (0.5-5mg) time of onset = 24/24
- Blood products = Prothrombin complex concentrate & FFP
NOAC
- Dabigatran (Idarucizumab)
- Rivaroxaban/Apixaban (developed but not available)
CASE: 90 year old female comes into ED following a fall at home and now has a very painful right hip.
- What would you check for clinically if you suspect a NOF?
- What are the clinical features?
- What pain relief would you consider?
- What is important in the history for the Anaesthetist, Orthopaedic reg, Geriatrician?
What would you check for clinically if you suspect a NOF?
Leg is shortened & externally rotated
What pain relief would you consider?
- Tapentadol = oral only so not fast enough action PLUS patient may need to go to theatre later so need to fast them so not a good option
- IV morphine OR sublingual fentanyl
- Regional block = lower chances of systemic side effects – especially delirium in the elderly
o Eg. Femoral nerve block (medial to lateral: Nerve, Artery, Vein, empty space, lymph nodes)
CASE: 90 year old female comes into ED following a fall at home and now has a very painful right hip.
- Differential Diagnoses for a NOF?
- Which investigations would you order?
- Does this lady need coags?
Differential Diagnoses of NOF
- Alternative fractures, such as of the pelvis (especially pubic ramus fractures), acetabulum, femoral head and femoral diaphysis, all need to be considered.
- Pathological fractures should be considered if there is not a significant history of trauma.
What is the blood supply of the head of the femur? Why is it important?
- The blood supply to the neck of the femur is retrograde, passing from distal to proximal along the femoral neck to the femoral head. This is predominantly through the medial circumflex femoral artery, which lies directly on the intra-capsular femoral neck.
- Consequently, displaced intra-capsular fractures disrupt the blood supply to the femoral head and, therefore, the femoral head will undergo avascular necrosis (even if the hip is fixed). Patients with a displaced intra-capsular fracture therefore require joint replacement (arthroplasty), rather than fixation.
- There is supply in the early days of life from the ligamentum arteriosum, which lies within the ligamentum teres, however this dramatically reduces in size in later life, and is of negligible importance in adults
What is a NOF?
- What are the two distinct areas of the neck of femur?
- What is the classification system for Intracapsular fractures?
Neck of femur (NOF) fractures can occur anywhere from the subcapital region of the femoral head to 5cm distal to the lesser trochanter.
What is the Management for NOF?
- Initial? Analgesia?
- Definitive?
- Geris mx?
- What is the surgical management for each of the Garden Grades of Subcapital Proximal Neck of Femur Fracture?
- Grade 1 = Dynamic hip screw & plate (know the blood supply is intact)
- Grade 2 = Dynamic hip screw & plate (1/5 failure rate resulting in necrosis, presents as increased groin pain approx. 4-6 weeks post-surgery)
- Intertrochanteric fracture = Dynamic hip & screw
- Grades 3 + 4 = Hemiarthroplasty (know the blood supply is not intact)
- Atypical Subtrochanteric = proximal nail
- Hemiarthroplasty = partial joint replacement because they know the head will necrose due to the lack of blood. (Grades 3 + 4)
What is the pathology? What is the management?
= Intertrochanteric fracture
- Also take a lateral hip x-ray!
Mx = Dynamic hip & screw for an Intertrochanteric fracture
Tutorial Case – Ms ET - Questions:
1. Does putting someone in a nursing home stop them from drinking?
2. Does being an alcoholic affect your decision-making capacity?
3. What do you think about younger persons being placed in residential aged care?
Encephalopathic – potentially reversible
Impaired cognition to make decisions
Not medically stable
- What is SAT and what do they do?
- What is meant by a “Guardian”? Which Act outlines it?
State Administrative Tribunal (SAT)
* Independent body that reviews a wide range of government decisions and determines disputes.
* Wide Jurisdiction extends to guardianship and administration, equal opportunity, vocational regulation, resources, and development (including town planning, and commercial and civil disputes).
- What do you think is meant by a ‘reasonable decision’?
- What conditions might affect someone’s ability to make ‘reasonable decisions’ about their lives? Think about 8 conditions that are static, potentially improving, or likely to progress.
Decision-making Disability
1. Neurodegenerative Disease - eg. Dementia
2. Delirium
3. Neurocognitive developmental conditions
4. TBI leading to Intellectual impairment/Acquired Brain injury
5. Stroke
6. Encephalopathies – Infective, Metabolic, Electrolyte imbalances
7. Substance abuse (acute intoxication or chronic use)
8. Mental illness (acute vs. chronic)
What is the difference between a Guardian and an Administrator?
- What decisions can a nominated guardian NOT make on behalf of the person they represent?
- When would these be sought?
Guardian – healthcare, lifestyle, living situation (everything but finances)
- Makes personal, lifestyle, and treatment decisions for a represented person with a decision-making disability.
- A guardian cannot: Vote, Make or change a will, Consent to a marriage
Administrator – finances but can’t change will
Least Restrictive Pathway
- Appointment of a guardian and/or administrator involves removing a person’s fundamental decision-making rights. Therefore, it is a LAST RESORT course of action undertaken by the SAT.
- Only considered after less restrictive measures of managing the person’s best interests have been found to be insufficient.
- What is a Public Advocate?
- What is a Public Trustee?
- What is the difference between plenary and limited orders?
What is the difference between plenary and limited orders?
- Plenary: Applies to all areas of the person’s life.
- Limited: Decision-making authority of the guardianship order limited to specific areas only (eg. medical, accommodation)
Assessing Capacity - Case 2
- What do we mean by EPA and EPG?
- Can the daughters do this?
What are your thoughts at this stage? What are the issues of concern?
Can you just discharge him home?
- What is Capacity?
- When might a healthcare professional be asked to asked to assess capacity?
- Is Competence assumed?
When might a healthcare professional be asked to asked to assess capacity?
In response to certain triggers:
1. To facilitate future planning (EPA, EPG, AHD)
2. Routine clinical care assessment (capacity to drive, capacity to consent to medical treatment)
3. Concerns from others re a person’s decision-making ability (by family, carer, service provider, GP, other doctors, social worker, lawyer) - assessment requested.
Assessing Capacity
- When assessing capacity, what is actually being assessed?
- What is the 6 step capacity assessment process?
- What must an assessment of decision-making capacity involve?
The six-step capacity assessment process
1. Identify the reason for assessing capacity (trigger).
2. Engage the person being assessed in the process.
3. Gather information to describe the context, choices and their
consequences.
4. Educate the person about the context, choices and their
consequences.
5. Assess capacity.
6. Take action based on results of the assessment.
Whatever the outcome of the assessment, keep a careful record of the whole process in the patient’s records.
What is Testamentary Capacity?
Outline the Hierachy of Treatment Decision-Makers?
Hierarchy of Treatment Decision-makers
* ‘Treatment’ refers to any medical, surgical or dental treatment or other
health care, including a life-sustaining measure or palliative care.
* A treatment decision is a decision to consent or refuse consent to
commencement or continuation of treatment.
* Treatment is regarded as urgent if needed to save a person’s life or
prevent the person from suffering significant pain or distress.
* Where a person requires urgent treatment and not practicable to
determine whether an Advance
Health Directive has been made or to
obtain a treatment decision from anybody in the hierarchy, the health
professional may provide the necessary treatment.
Which guidelines should you refer to for Stroke management?
- What are the 3 recommendations & 1 practice point for pre-hospital stroke care?
Which scoring/scaling system should be used for stroke identification (pre-hospital)?
- Which one is used in Perth?
Which score/scale to use?
- Approximately 34 different LVO prediction instruments
- Most prediction instruments were derived from elements of the NIHSS
- Significant heterogeneity
- Cincinnati Prehospital Stroke Screen, Los Angeles Motor Scale (LAMS), Los Angeles Prehospital Stroke Screen, Rapid Arterial Occlusion Evaluation (RACE)
- RACE is currently used in Perth for stroke bypass
- Australian studies for NIHSS-8 and ACT-FAST designed for use by ambulance.
What is the RACE Matrix for Stroke management in Perth?
- Pre-hospital management for all patients?
- When is a stroke bypass to an Acute Stroke centre indicated?
- When is a stroke bypass to a Neurovascular unit indicated?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- 1 strong, 1 weak recommendation, and 3 practice points regarding rapid assessment of stroke in the ED?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around brain imaging for suspected stroke in the ED?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around thrombolysis?
- Which fibrinolytic agent should be used? What dose? Alternative?
- What time frame can we still use thrombolysis for ischaemic stroke?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around Neurointervention (thrombectomy) - 3 strong recommendations?
- Timeframe?
- Should these patients also receive thrombolysis?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around feeding and swallowing in patients post-stroke?
- 6 consensus practice points?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around Antithrombotic therapy post-stroke?
- When can acute antiplatelet therapy be given after alteplase?
- Is routine use of anticoagulation in patients without cardioembolism following TIA/stroke recommended?
- Role of aspirin?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around Acute blood pressure lowering therapy post-stroke?
- What systolic BP should you aim for in patients with intracerebral haemorrhage?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around Surgery for ischaemic stroke and management of cerebral oedema?
- When should a hemicraniectomy ideally be performed?
- Role of corticosteroids for management of stroke patients with brain oedema and raised intracranial pressure?
- Role of osmotherapy & hyperventilation?
Consensus-based recommendation
1. In stroke patients with brain oedema and raised intracranial pressure, osmotherapy and hyperventilation can be trialled while a neurosurgical consultation is undertaken.
2. For selected patients with large cerebellar infarction threatening brainstem and 4th ventricular compression, decompressive surgery
should be offered.
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around medical intervention for Intracerebral haemorrhage (ICH) management?
- Mx of stroke patients with warfarin-related intracerebral haemorrhage?
- Should platelet transfusions be administered to stroke patients with ICH previously receiving antiplatelet therapy?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around routine surgical evacuation for stroke patients with supratentorial intracerebral haemorrhage?
- Role of haematoma evacuation?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around oxygen therapy in stroke patients? Who should get supplemental oxygen?
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around neuroprotective agents like hypotehermic cooling?
- Can patients continue their statins?
- What are the guidelines around Glycaemic therapy?
- What are the guidelines around pyrexia management?
Neuroprotection
1. For stroke patients, putative neuroprotective agents, including hypothermic cooling, are not recommended outside the context of research.
2. Patients with acute ischaemic stroke who were receiving statins prior to admission can continue statin treatment.
Glycaemic therapy
1. All stroke patients should have their blood glucose level monitored for the first 72 hours following admission, and appropriate glycaemic therapy instituted to treat hyperglycaemia (glucose levels greater than 10 mmol/L), regardless of their diabetic status.
2. For stroke patients, an intensive approach to the maintenance of tight glycaemic control (between 4.0-7.5 mmol/L) is not recommended.
Clinical Guidelines for Stroke Management 2017: Early assessment and management
- What are the guidelines around patent foramen ovale management? (2)
- What are the recommendations for anticoagulant therapy for stroke patients with AF? (4)
- 3 practice points for stroke patients with AF?
Patent Foramen Ovale Management
1. Patients with ischaemic stroke or TIA and PFO should receive optimal medical therapy including antiplatelet therapy or anticoagulation if indicated.
2. In patients with ischaemic stroke aged <60years in whom a patent foramen ovale is considered the likely cause of stroke after thorough exclusion of other aetiologies, percutaneous closure of the PFO is recommended.
Anticoagulation therapy
1. For patients with ischaemic stroke or TIA, with atrial fibrillation (both paroxysmal and permanent), oral anticoagulation is recommended for long-term secondary prevention.
2. Direct oral anticoagulants (DOACs) should be initiated in preference to warfarin for patients with non-valvular atrial fibrillation and adequate renal function.
3. For patients with valvular atrial fibrillation or inadequate renal function, warfarin (target INR 2.5, range 2.0-3.0) should be used. Patients with mechanical heart valves or other indications for anticoagulation should be prescribed warfarin.
4. For patients with ischaemic stroke, the decision to begin anticoagulant therapy can be delayed for up to two weeks but should be made prior to discharge.
