Cardiovascular Flashcards

(56 cards)

1
Q

Pathophysiology of Infective Endocarditis

A

Turbulent flow through abnormal valve
Congenital abnormality, Nodules from RHD, Heart valve trauma, etc
Platelets and fibrin attach to damaged valvular epithelium forming sterile vegetations
Transient bacteraemia arising from mouth, skin, gut, urinary tract etc seeds bacteria onto sterile vegetations.
Common causative agents
• Viridans Streptococci (Mouth)
• S.aureus (Skin/Nose)
• Enterococcus (Gut)
• HACEK
Valves have little blood supply therefore WBC can’t effectively get to site of infection
Infected vegetations enlarge and shed infected emboli and lead to valvular destruction
• Embolic phenomena > Infarct
Impaired valve function > Heart failure

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2
Q

Risk factors for developing Infective Endocarditis

A
Recent dental, endoscopic or operative procedure
Valve disease
Prosthetic valves
Past ARF
Heart disease/operations
IVDU
Immunosuppresion
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3
Q

Clinical Presentation: Symptoms of Infective Endocarditis

A

Fever + New murmur = IE until proven otherwise
Fever + Fatigue
Acute Heart Failure
Embolic Phenomena

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4
Q

Clinical Presentation: Signs of Infective Endocarditis

A

General manifestations of sepsis
Malaise, anorexia, weight loss, fever, rigor, night sweats, anaemia, clubbing, splenomegaly
Cardiac Manifestations
• New/Changing murmur
Secondary to valve destruction. May progress to heart failure and pulmonary oedema
• New harsh pansystolic murmur + acute deterioration
Due to IV septum perforation/rupture of a sinus of valsalva aneurysm into the RV
• Tachycardia/Hypotension
Secondary to sepsis
• Heart-block
• Intracardiac abscess
• Pericarditis
Manifestations of immune complex deposition
• Clubbing
• Skin: petechiae, splinter haemorrhages, Osler’s nodes, Janeway lesions
• Eyes: Roth’s spots, conjunctival splinter haemorrhages, retinal flame haemorrhages
• Renal: Microscopic haematuria, glomerulonephritis, renal impairment
• Cerebral: Toxic encephalopathy
Musculoskeletal: Arthralgia, arthritis

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5
Q

Outline Dukes Classification for diagnosis of Infective Endocarditis

A

Dukes Classification
Specificity 99%, Sensitivity 92%
• Major Criteria
○ 2 x positive blood culture with typical microbe
Persistently positive blood culture; single positive culture for Coxiella Burnettii
○ Evidence of endocardial involvement (Positive ECHO)
Oscillating intracardiac mass (vegetation); abscess; new partial dehiscence of prosthetic valve; new valve regurgitation
• Minor Criteria
○ Predisposing condition/IVDU
○ Fever >38 degrees
○ Vascular phenomena/stigmata
○ Positive blood culture not meeting above criteria
○ ECHO abnormality not meeting above criteria

Definite IE: 2 major criteria, or 1 major criteria and 3 minor criteria, or 5 minor criteria
Possible IE: Findings that fall short of definite endocarditis but are not rejected
Rejected diagnosis: Firm alternative diagnosis, sustained resolution of clinical features with <4 days of antibiotic therapy

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6
Q

DDx for Infective Endocarditis

A

Rheumatic Fever
Atrial Myxoma
Other cardiac neoplasms
SLE

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7
Q

What investigations should you order if you suspect Infective Endocarditis and why do you want each of them?

A
Blood cultures
Need three sets at least 20 minutes apart before treatment is started
FBC ?Leucocytosis ?Thrombocytopenia ?anaemia
ESR/CRP (high)
CXR ?Heart failure
Echo ?vegetations ?regurg ?abscess
Other
	• ECG
	• Urinalysis ?haematuria ?proteinuria 
	• U&amp;Es (baseline)
Serum Ig ?Polyclonal elevation
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8
Q

Management of Infective Endocarditis

A

Key points
• NVE vs PVE ?duration
• Strep vs Staph vs Entero vs HACEK ?Abx
• Cardiac surgery?

Streptococcus viridans group
• NVE: Benzyl-penicillin 1.2 g/4 h IV for 4 weeks
• PVE: Benzyl-penicillin 1.2 g/4 h IV for 6 weeks with Gentamicin for first 2 week
• Penicillin allergy: Vancomycin
Staphylococcus species
• MSSA
○ NVE: Flucloxacillin 2 g/ 6 h IV 4-6 weeks with gentamicin for at least 1st week
○ PVE: Flucloxacillin 2 g/ 6 h IV 6 weeks, Gentamicin for first 2 weeks + Rifampicin 600 mg bd PO for 6 weeks
• MRSA
○ NVE: IV Vancomycin for 4-6 weeks + Gentamicin for first week
○ PVE: Vancomycin + rifampicin for 6 weeks + gentamicin for 2 weeks
HACEK organisms
• NVE: IV cephalosporin (Ceftriaxone) for 4 weeks
• PVE: IV cephalosporin (Ceftriaxone) for 6 weeks
Coxiella burnettii
• NVE/PVE: Doxycycline for 3-4 years + second agent (co-trimoxazole, rifampicin, quinolone)
• Need to carefully monitor IgG titre
Usually require surgery

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9
Q

Clinical monitoring of Infective Endocarditis

A
• Signs of infection, persistent pyrexia and persistence of systemic symptoms
	• Persistent fever may be due to drug resistance, concomitant infection or allergy
	• Changing cardiac murmur
	• Signs of heart failure
	• Development of new embolic phenomena
	• Inspect IV access sites daily
	• Echo
	• ECG
Blood cultures
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10
Q

Define Heart Failure

A

The term heart failure refers to a clinical syndrome of signs and symptoms arising from the heart being unable to sufficiently pump blood to meet the bodies requirements. It is not a diagnosis, but rather the clinical manifestation of multiple, progressive forms of heart disease.

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11
Q

What are 4 ways in which Heart Failure can be classified ?

A

Left vs Right
Preserved EF vs Intermediate EF vs Reduced EF
Low output vs High output
Acute vs Chronic

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12
Q

What are the symptoms of left-sided Heart failure?

A
Left sided
	- Breathlessness (Dyspnoea)
		○ Exertional
		○ At rest
		○ Orthopnoea > PND
	- Fatigue
	- Nocturnal cough/wheeze
	- Nocturia
	- Cold peripheries
	- Weight loss
Muscle wasting
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13
Q

What are the symptoms of right-sided Heart Failure?

A
  • Peripheral oedema
    • Ascites
    • Nausea and anorexia
    • Facial engorgement
    • Neck pulsation
      Epistaxis
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14
Q

What are the causes/precipitants of heart failure?

A
Cardiac
	- Arrhythmia
	- Ischaemia/Infarction
	- Valve pathology
	- Hypertension
	- Cardiomyopathy
Respiratory
	- Chronic lung disease > Cor Pulmonale
	- PE
Medication
	- Non-compliance 
	- Discontinuation of diuretic
	- Commencement of drugs that cause salt and water retention > fluid overload
Other
	- Anaemia
	- Thyrotoxicosis
	- Infection + Fever
Anaesthesia + Surgery
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15
Q

Outline the NYHA classification of Heart Failure

A

I: Cardiac disease, but no symptoms and no limitation in ordinary physical activity
II: Mild symptoms (mild SOB and/or angina) and slight limitation of ordinary activity
III: Marked limitation in activity due to symptoms even during less than ordinary activity e.g. Walking short distances (20-100m). Comfortable only at rest
IV: Severe limitation. Experiences symptoms even at rest. Mostly bed bound patients

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16
Q

If Heart failure is suspected, what investigations would you order and why?

A

FBC ?Hb (anemia)
U&Es ?Hyperkalaemia (arrhythmia) ?hyponatremia (longstanding CHF/renal failure)
Pro-BNP ?cardiac vs non-cardiac dyspnoea
ECG - ECG ?arrhythmia ?ischaemia (old/new) ?LVH ?LBBB
CXR ?alveolar oedema ?kurly-B lines ?cardiomegaly ?distended pulmonary vessels ?effusion
Echo ?regional (infarct) vs global (Dilated cardiomyopathy) wall motion abnormalities ?valvulopathy ?Estimate EF
Coronary angiography r/o CAD

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17
Q

Outline the non-pharmacological and pharmacological management of chronic heart failure

A

Correct underlying cause
- Rate control arrhythmias
- Thrombolysis for acute infarcts
- CABG/Angioplasty for ischaemia
- Medication review
- Control thyroid disease
- Pharmacological
1. Frusemide
Loop diuretic = symptom relief
Inhibit Na/K/Cl transporter at ascending LOH
IV vs Oral (2:1 effect)
SE: Low K+, ototoxic
Risk of hypotension after first dose: Falls risk, give at night
2. ACEi(>ARB)
Improves symptoms and prolongs life
Inhibits Ang I conversion to Ang II > Decreases water retention and decreases BP
SE: Dry cough, angioedema, hypotension
Warn of hypotension after first dose: Falls risk, give at night!
3. B-blocker
Not given initially > give only once NYHA stage 1 or 2
Lower BP
Negative chronotrope: SA node effects/AV node transmission
Negative Inotrope (short term): Stabilise with diuretics first!
Positive Inotrope (long term): Start low, go slow
4. Spironolactone
K+ sparing (aldosterone antagonist)
Can give if NYHA stage 4 or 4
Add if 1) K+ <3.2mmol/L, 2) predisposition to arrhythmia, 3) concurrent digoxin therapy, 4) pre-existing K+ loosing condition
SE: Hypotension, hyponatraemia, hyperkalaemia
5. Digoxin
Vasodilators

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18
Q

What medications should you avoid in managing chronic heart failure?

A

NSAIDs: Worsens renal function

Calcium Channel Blockers: Negative inotrope

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19
Q

What is the definition of Grade 1, Grade 2 and Grade 3 Hypertension?

A

Mild (Grade 1): 140-159/90-99
Moderate (Grade 2): 160-179/100-109
Severe (Grade 3): >180 systolic +/- >110 diastolic

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20
Q

What are the primary and secondary causes of hypertension?

A
Primary - Idiopathic (95%)
Secondary
	• Phaechromocytoma
	Paroxysmal sweating, palpitations and headache
	• OSA
	Daytime sleepiness etc
	• Renal artery stenosis/CKD
	• Coarctation of aorta
	• Adrenal tumour, Conn's or Cushing's 
	• Medication: COCP, NSAIDs
Pregnancy
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21
Q

What are the important points to ask in a history when a patient has hypertension

A
OPTICPR!
When the diagnosis was made
What reading were they getting prior to diagnosis
How was the BP being monitored
What treatments have they tried in the past? Side effects?
What treatments are they on now? Side effects?
What readings are they getting after treatment?
Complications
	• Stroke
	• Heart Failure
	• Peripheral vascular disease
	• Renal failure
Risk factors for Cardiovascular disease
	• DM
	• Hyperlipidaemia
	• FHx of CAD
Lifestyle factors (ask about attempts/success with any of these)
	• Obesity
	• Lack of physical activity
	• Excessive alcohol intake
High salt diet
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22
Q

In examining a patient with Hypertension, what are key signs/things not to miss?

A

Cardiovascular System
Blood pressure
Both arms, Lying/Standing
Signs of Cushing’s
Moon face, Weight gain, Purple striae, Buffalo hump, Proximal muscle weakness
Radio-femoral delay
Hypertensive Retinopathy (See opthalm notes)

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23
Q

What investigations should you do in patients with hypertension and why? (Think Ix for diagnosis, Ix for assessing end organ damage, Ix for ?secondary cause)

A

Ambulatory BP - at home BP record
U&Es/Cr ?renal disease
ECG ?LVH ?IHD
CXR ?Heart failure
Urinalysis ?proteinuria
Renal failure secondary to HTN; if positive, do a 24 hours urine collection and work out ACR
HbA1c ?CVS risk
Lipids ?CVS risk
Plasma Aldosterone/Renin activity ratio ?primary hyperaldosteronism
Conn’s - high PA/PRA ratio (think if hypokalaemia and not on diuretics)
24 hour catecholamines ?Phaechromocytoma
9am ACTH ?Cushing’s
Renal artery doppler ?Renal artery stenosis
Sleep study ?OSA

24
Q

You calculate the CVS risk for a patient with hypertension and get <10%, what treatment avenues should be explored?

A

CVD <10%
○ Lifestyle advice
○ Discuss harms and benefits of BP lowering and statin medications
Further assessment 5-10 years

25
You calculate the CVS risk for a patient with hypertension and get 10-20%, what treatment avenues should be explored?
○ Individualised lifestyle advice ○ Commence BP lowering +/- statin Further assessment in 1-2 years
26
You calculate the CVS risk for a patient with hypertension and get >20%, what treatment avenues should be explored?
○ Intensive lifestyle advice ○ BP lower + Statin + antiplatelet Annual review
27
If a patient has hypertension but no clinical CVD, what should their target BP be?
<140/85
28
If a patient has hypertension and T2DM/CVD/CKD, what should their target BP be?
<130/80
29
Outline the non-pharmacological management of Hypertension
``` • Diet: Reduce salt, fats and sugar • Physical activity: 30 min a day, green prescription • Weight: BMI <25 • Smoking cessation: ABC Reduce alcohol intake ```
30
Outline the escalation in pharmacologic management of hypertension you would go through for a patient aged <55 or who has T2DM
1. ACEi (half dose e.g. Cilazapril 2.5mg) 2. Increased ACEi (full dose e.g. Cilazapril 5mg) 3. Thiazide (half dose) (CONTRAINDICATED IN GOUT) 4. Add Calcium Channel Blocker (half dose e.g. Amlodipine 5mg 5. Increase thiazide to full dose 6. Increase CCB to full dose
31
Outline the escalation in pharmacologic management of hypertension you would go through for a patient aged >55 or who is black
``` ○ Thiazide (half dose) ○ ACEi (half dose ○ Increase thiazide (full dose) ○ Increase ACEi (full dose) ○ Add CCB (half dose) Increase CCB (full dose) ```
32
When would you add spironolactone in the management of hypertension?
In resistant hypertension when K+ is less than 4.5
33
When would you use a Beta-blocker in the management of hypertension?
Usually reserved for when there is inadequate control with other three main classes, or if there is a specific indication e.g. increased sympathetic drive, ACEi/ARB intolerance, heart disease
34
Outline an approach to thinking of the causes of palpitations
``` Cardiac • Arrhythmia ○ Tachyarrhythmia Supraventricular tachycardia (Afib/Aflut), Ventricular tachycardia (sinus tachycardia, ANVRT, AVRT), Supraventricular extrasystole, ventricular extrasystole ○ Bradyarrhythmia (rarer) Sinus bradycardia, sinus pauses, second- and third-degree AV block • Structural heart disease ○ Valvulopathy ○ Cardiomyopathy Non-cardiac • Psychosomatic ○ Anxiety, panic attacks ○ Depression, somatization disorder • Systemic ○ Hyperthyroidism ○ Hypoglycaemia ○ Fever ○ Anaemia ○ Hypovolaemia ○ Phaeochromocytoma • Medications/drugs ○ Alcohol, cocaine, heroin, amphetamines, caffeine, nicotine, synthetic drugs ○ Recent withdrawal of B-blockers Vasodilators, anticholinergics, hydralazine ```
35
What are key question to ask in a history when the presenting complaint is palpitations?
``` Circumstances prior to beginning of palpitations • Activity Rest, sleeping, exercise, change in posture, after exercise • Position Supine/Standing • Predisposing Factor Emotional stress, exercise, squatting/bending Onset of palpitations • Sudden vs gradual • Preceding symptoms Chest pain, SOB, vertigo, fatigue etc During episode • Describe what you notice • Fast or slow? • Regular or irregular • Tap rhythm out on table • Duration End of episode • Sudden vs gradual • Associated symptoms Background • Age of first episode • Number of previous episodes • Prior treatment • Frequency in last year/month • Previous cardiac disease • Previous psychosomatic disorders • Previous systemic diseases • Previous thyroid dysfunction • FHX: cardiac disease, tachycardia, SCD • Medications Drug abuse ```
36
What are some known triggers of Atrial fibrillation?
``` Heart Failure Hypertension Ischaemic Heart Disease PE Mitral valve disease Pneumonia Hyperthyroid (thyrotoxicosis) Caffeine Alcohol Post-op Hypokalaemia Hypomagnesaemia ```
37
If on examination, you feel someones pulse is irregularly irregular, whats the ddx?
Atrial fibrillation Ventricular ectopics Heart-block with ventricular escape Atrial flutter
38
What investigations do you need to order for someone who is found to have an irregularly irregular pulse?
``` ECG U&Es (baseline/K+/Mg2+) Cardiac enzymes CXR LFT TFT Echo ```
39
Outline the management of a patient who presents with acute AF (<48 hours) and is symptomatic/unstable.
Call for help ABCDE approach DC cardioversion (if haemodynamically unstable/unconscious) Pharmacological cardioversion: Amiodarone
40
How do you administer Amiodarone to pharmacologically cardiovert a patient in AF? What do you need to rule out before hand?
IV infusion 5mg/kg over first hour with ECG monitoring, subsequent infusion given if required up to maximum of 1.2g in 24 hours. Infuse via a large or central vein in 5% glucose solution Need to rule out hyperthyroidism
41
What monitoring is required when giving amiodarone? (Before treatment, 6 months, annually)
Before treatment: ECG, CXR, TFT, LFT, K+, PFT[DLCO] 6 months: TFT, LFT Annually: ECG, CXR
42
Outline the management of a patient who is in acute AF (<48 hours) but is asymptomatic and haemodynamically stable
Correct Mg2+ and K+ Rhythm Control (DC cardioversion/Flecainide (CI: Structural heart disease, IHD)/Amiodarone) Rate Control (1st-line: B-blocker or CCB) Start thromboprophylaxis (LMWH>Warfarin or Dabigatran) Use no anticoagulation if stable sinus rhythm has been restored, no risk factors for emboli and if AF recurrence likely
43
Outline the management of a patient who is in acute AF (>48 hours) but is asymptomatic and haemodynamically stable
``` Do not cardiovert unless TOE has proven no intracardiac thrombus Rate Control (1st-line: B-blocker or CCB) If rhythm control is required, must be anticoagulated for >3 weeks first before elective cardioversion ```
44
Outline the management of chronic AF
Rate control just as good as rhythm control! Rate control - 1st line: B-blocker or CCB (CCB: Diltiazem, not verapamil!) - If this fails, add digoxin (Digoxin is very effective but really hard on kidneys, beware in kidney disease; need to monitor levels) - If this fails, try amiodarone Rhythm control - May be appropriate if; ○ Symptomatic/Unstable ○ Congestive Heart Failure ○ Younger patient ○ First presentation ○ Persistence despite corrected precipitant - DC cardioversion or - Elective Pharmacological Cardioversion ○ 1st line: Flecainide (CI: structural heart disease/IHD) - Refractory cases ○ AVN ablation with pacing ○ Pulmonary vein ablation ○ Maze procedure Anticoagulation - CHA(2)DS(2)VASc and HASBLED
45
What is a SVT? What are the different types of SVT?
``` SVT is a narrow complex tachycardia arising from above the ventricles. Sinus tachycardia • Physiological sinus tachycardia • Inappropriate sinus tachycardia • Sinoatrial node re-entrant tachycardia (SANRT) Atrial tachycardia • Focal atrial tachycardia • Multifocal atrial tachycardia* • Atrial flutter* • Atrial fibrillation* Atrioventricular arrhythmia • AVNRT Slow-fast (common), Fast-slow (uncommon), Slow-slow (atypical) • AVRT (WPW) Junctional tachycardia (rare) *=irregula ```
46
Outline the escalation of management in a patient with a SVT (AVNRT/AVRT)
Sonsider transiently blocking AVN, if SVT is actually of atrial origin, AV node blockade will unmask rhythm, so then treat that rhythm e.g. AF AV node block can be achieved by... ○ Vasovagal manoeuvres (Valsalva or carotid sinus massage) ○ IV Adenosine (6mg IV push > 12mg after 1-2 min if ineffective > 12mg again if ineffective after 1-2 min ) ○ If ineffective, use CCB (Verapamil) (2.5-5mg IV over 1-2 minutes > repeat every 5-10 minutes up to total dose 15mg; Give slowly as can cause hypotension; Never give if 1) also taking B-blocker 2) ?digoxin toxicity or 3) wide complex tachycardia) ○ If ineffective, try vagal manoeuvre again If ineffective contact CCU ?DC cardioversion
47
What is a broad approach to bradycardia
Physiological Drug-induced (B-blockers, amiodarone, CCB's, digoxin) Cardiac (Heart block, IHD, valvular disease, cardiomyopathy) Non-cardiac (Vasovagal, Hypothyroidism, adrenal insufficiency, hyperkalaemia, hypoxia, hyperthermia, increased ICP (Cushings triad))
48
What arrhythmia's causes bradycardia?
Junctional bradycardia | All types of heart block but mostly type 1 and type 2
49
What groups of patients should be screened for hyperlipidaemia?
``` Those at risk of hyperlipidaemia • Family history of hyperlipidaemia • Corneal arcus <50 years old • Xanthomata/Xanthelasmata Those at risk of CVD • Known CVD • Family history of CVD <60 years old • DM or impaired glucose tolerance • Hypertension • Smoker • Increased BMI • Low SES Indian/Asian background ```
50
What are the types of hyperlipidaemia?
``` Common primary hyperlipidaemia (70% of hyperlipidaemia; Increased LDL only) Familial primary hyperlipidaemia (Multiple types) Secondary hyperlipidaemia (Caused by Cushing's syndrome, hypothyroidism, nephrotic syndrome or cholestasis; Increased LDL) Mixed hyperlipidaemia (Increased LDL and triglycerides; Caused by DM, metabolic syndrome, alcohol and CKD) ```
51
What is the management of hyperlipidaemia
Lifestyle advice (aim BMI <25-20, diet, increase exercise) 1st line: Statins 2nd line: Ezetimibe 3rd line: Alirocumab
52
What is the pathophysiology of acute rheumatic fever?
Occurs due to an autoimmune mechanism related to molecular mimicry. Production of cross-reactive antibodies gives immune recognition and response against pathogen, but produce antibodies which recognise both host and microbial antigens. - Human cardiac myosin and streptococcal M protein are likely important antigens in the pathogenesis of rheumatic heart disease. Antibodies cross react with collagen or cardiac valvular endothelia antigens, then T cells infiltrate leading to inflammation (arthritis) or long-term damage (carditis then RHD) - Auto antibody-mediated neuronal cell signalling in cerebrospinal fluid may be part of pathogenesis in chorea Recurrent ARF attacks due to repeated streptococcal infections leads to increased scar formation in the valve. After initial attacks of ARF and carditis, the valve scars and then is neovascularised which perpetuates disease.
53
What are the major and minor criteria for diagnosis of acute rheumatic fever?
Major - Arthritis ○ Mono arthritis or asymmetrical migratory polyarthritis ○ Most common presenting complaint in ARF (75% of first presentations) ○ Extremely painful and unable to weight bear ○ Polyarthritis is usually asymmetrical and migratory - Carditis ○ Tachycardia, murmurs (mitral or aortic regurgitation), pericardial rub, CCF, Cardiomegaly, conduction defects. - Sydenhams chorea ○ GAS bacteria react with basal ganglia to cause this. ○ Involves jerky, uncontrollable and purposeless movements of hands, arms, shoulder, face, legs and trunk. ○ Can be a standalone criterion - Erythema marginatum (rare) ○ Rash with red, raised edges and clear centre, occurring mainly on the trunk, thighs and arms. ○ Not itching or painful - Subcutaneous nodules ○ Rare (<2% of cases) ○ Small, mobile, painless nodules on extensor surfaces of joints and spine Minor - Fever >38C - Arthralgia - Hx of ARF - Raised CRP (>30mg/L) or ESR (>50mg/L) Prolonged PR interval on ECG
54
What investigations would you do for a patient with ?acute rheumatic fever.
``` FBC ?WBC ESR/CRP Blood cultures if febrile Anti-strep serology (ASO, Anti-DNase B) CXR ECG ?PR prolongation ECHO ``` Tests for considering alternative diagnosis include serology for reactive arthritis, ANA ?autoimmune arthritis Rpeat blood culture ?IE, joint aspirate ?septic arthritis, joint XRay, choreform movements - copper levels, caeruloplasmin, ANA, drug screen and consider MRI or CT head
55
Outline the management of acute rheumatic fever
Admission to hospital ASAP after symptom onset Confirm diagnosis Refer to rheumatic fever register once diagnosis made for prophylaxis program and public health for contact tracing otify Public health service Antibiotics: - Oral penicillin V 250mg 2-3 times daily while diagnosis is being established - First dose IM benzathine penicillin 900mg or 450mg if <30kg should be given in patient and education given about secondary prophylaxis. Can stop oral penicillin once this dose is given. Repeat every 28 days Penicillin allergy: Erthromycin ethylsuccinate 40mg/kg per day in 2-3 divided dose, maximum 1g/day Ongoing management of symptoms - Arthritis/arthralgia ○ 1st line: Paracetamol ○ 2nd line: NSAID (Naproxen) - Fever (no specific treatment required) - Carditis/Heart Failure ○ Heart failure medication if required ○ Valvular surgery - Sydenham’s Chorea ○ Generally self limiting within weeks (almost all patients by 6 months) Sever chorea: carbamazepine PO 7-20mg/kg/day TDS or valproic acid 15-20mg/kg/day TDS. Both for several weeks and then trial off medication
56
Outline the options for secondary prophylaxis of Acute RHeumatic Fever and the time periods
Secondary Prophylaxis - 1st line: IM benzathine penicillin every 4 weeks - 2nd line: Oral penicillin twice daily - 3rd line: Oral erythromycin twice daily if allergy Time period - ARF + no/mild carditis: Minimum 10 year or until 21 years old (which ever is longer) - ARF + moderate carditis: Minimum 10 years after most recent episode or untill 30 years (which ever longer) - ARF + severe carditis: Minimum 10 years after most recent episode or until 30 years (whichever is longer) then review by specialist to consider lifelong