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Flashcards in Infections in heart Deck (13):

Rheumatic fever

summary intro

This systemic infection is still common in developing countries but increasingly rare in the West. Peak incidence: 5–15yrs. Tends to recur unless prevented. Pharyngeal infection with Lancefield group A β-haemolytic streptococci triggers rheumatic fever 2–4wks later, in the susceptible 2% of the population. An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue (antigenic mimicry) and may cause permanent damage to the heart valves.


diagnosis of RF

Use the revised Jones criteria (may be over-rigorous). There must be evidence of recent strep infection plus 2 major criteria, or 1 major + 2 minor.


Evidence of group A β-haemolytic streptococcal infection:

    • Positive throat culture (but this is usually negative by the time symptoms of rheumatic fever appear)

    • Rapid streptococcal antigen test

    • Elevated or rising streptococcal antibody titre (eg aso or DNase b titre)

    • Recent scarlet fever


MAJOR criteria of RF

    • Carditis: Tachycardia, murmurs (mitral or aortic regurgitation, Carey Coombs’ murmur,), pericardial rub, ccf, cardiomegaly, conduction defects (45–70%). An apical systolic murmur may be the only sign.

    • Arthritis: A migratory, ‘flitting’ polyarthritis; usually affects larger joints (75%).

    • Subcutaneous nodules: Small, mobile painless nodules on extensor surfaces of joints and spine (2–20%).

    • Erythema marginatum: (fig 1) Geographical-type rash with red, raised edges and clear centre; occurs mainly on trunk, thighs, arms in 2–10% ([link]).

    • Sydenham’s chorea (St Vitus’ dance): Occurs late in 10%. Unilateral or bilateral involuntary semi-purposeful movements. May be preceded by emotional lability and uncharacteristic behaviour.Cardiovascular medicine103


Minor criteria for RF

    • Fever

    • Raised esr or crp

    • Arthralgia (but not if arthritis is one of the major criteria)

    • Prolonged PR interval (but not if carditis is major criterion)

    • Previous rheumatic fever



    • Bed rest until crp normal for 2wks (may be 3 months).

    • Benzylpenicillin 0.6–1.2g im or penicillin V 250-500mg 2-3 times daily po for 10 days (if allergic to penicillin, give erythromycin or azithromycin for 10 days).Cardiovascular medicine104

    • Analgesia for carditis/arthritis: aspirin 100mg/kg/d po in divided doses (max 8g/d) for 2d, then 70mg/kg/d for 6wks. Monitor salicylate level. Toxicity causes tinnitus, hyperventilation, and metabolic acidosis. Alternative: NSAIDs ([link]). If moderate-to-severe carditis is present (cardiomegaly, ccf, or 3rd-degree heart block), add oral prednisolone to salicylate therapy. In case of heart failure, treat appropriately ([link])

    • Immobilize joints in severe arthritis.

    • Haloperidol (0.5mg/8h po) or diazepam for the chorea.


Prognosis with RF

60% with carditis develop chronic rheumatic heart disease. This correlates with the severity of the carditis

Recurrence may be precipitated by further streptococcal infections, pregnancy, or use of the Pill.

Cardiac sequelae affect mitral (70%), aortic (40%), tricuspid (10%), and pulmonary (2%) valves.

Incompetent lesions develop during the attack, stenoses years later


Infective endocarditis

summary intro

Fever + new murmur = endocarditis until proven otherwise.

Any fever lasting >1wk in those known to be at risk must prompt blood cultures.

Classification: 50% of all endocarditis occurs on normal valves. It follows an acute course, and presents with acute heart failure ± emboli.

Chief cause: S. aureus.

Risk factors: dermatitis; iv injections; renal failure; organ transplantation; dm; post-op wounds. Entry is usually via the skin. Mortality: 5–50% (related to age and embolic events).

Endocarditis on abnormal valves tends to run a subacute course. Risk factors: aortic or mitral valve disease; tricuspid valves in iv drug users; coarctation; patent ductus arteriosus; VSD; prosthetic valves. Endocarditis on prosthetic valves may be ‘early’ (during surgery, poor prognosis) or ‘late’ (haematogenous).



Constitutional symptoms are common (fever/FUO, weight loss, fatigue).
■ Exam reveals a heart murmur. The mitral valve is more commonly affected
than the aortic valve in non–IV drug users; more right-sided involvement is
found in IV drug users (tricuspid valve > mitral valve > aortic valve).

Osler’s nodes (small, tender nodules on the finger and toe pads),

Janeway lesions (small peripheral hemorrhages),

Splinter hemorrhages (subungual petechiae;

Roth’s spots (retinal hemorrhages),

focal neurologic defi cits from embolic stroke, and other
embolic phenomena are also seen.


diagnosis of IE

Major criteria:

    • Positive blood culture:

        • typical organism in 2 separate cultures or

        • persistently +ve blood cultures, eg 3, >12h apart (or majority if ≥4)

    • Endocardium involved:

        • positive echocardiogram (vegetation, abscess, dehiscence of prosthetic valve)


        • new valvular regurgitation (change in murmur not sufficient).

Minor criteria:

    • Predisposition (cardiac lesion; iv drug abuse)

    • Fever >38°C

    • Vascular/immunological signs

Vascular phenomena: Septic emboli, septic infarcts, mycotic aneurysm, Janeway lesions.
Immunologic phenomena: Glomerulonephritis, Osler’s nodes. Roth’s spots.

    • Positive blood culture that does not meet major criteria

    • Positive echocardiogram that does not meet major criteria.

How to diagnose:

Definite infective endocarditis: 2 major or 1 major and 3 minor or all 5 minor criteria (if no major criterion is met).



summary intro

Infl ammation of the pericardial sac.

Can compromise cardiac output via tamponade or constrictive pericarditis


Central chest pain worse on inspiration or lying flat ± relief by sitting forward.

A pericardial friction rub may be heard.

Look for evidence of a pericardial effusion or cardiac tamponade

Fever may occur.


causes of pericarditis

• Idiopathic

• Collagen Vascular disease

Infection (viral, bacterial, TB, and fungal)


Dressler’s syndrome, postcardiotomy syndrome

• Malignancy (e.g. breast, bronchus, lymphoma)

• Uraemia due to acute renal failure

Autoimmune disease (e.g. SLE, RA, Wegner’s, scleroderma, PAN)

• Granulomatous diseases (e.g. sarcoid)


Drugs (hydralazine, procainamide, isoniazid)

• Trauma (chest trauma, iatrogenic)



Investigations for pericarditis


    • May be normal in up to 10%.

    • ‘Saddle-shaped’ ST-segment elevation (concave upwards), with variable T inversion (usually late stages) and PR-segment depression (opposite to P-wave polarity). Minimal lead involvement to be considered, typically including I, II, aVL, aVF, and V3–V6.

    • ST segment is always depressed in aVR, frequently depressed or isoelectric in V1, and sometimes in depressed in V2.

    • May be difficult to distinguish from acute MI. Features suggesting pericarditis are:

        • Concave ST elevation (versus convex)

        • All leads involved (versus a territory, e.g. inferior)

        • Failure of usual ST evolution and no Q-waves

        • No AV block, BBB, or QT prolongation.

    • Early repolarization (a normal variant) may be mistaken for pericarditis. In the former, ST elevation occurs in pre-cordial and rarely in V6 or the limb leads and is unlikely to show ST depression in V1 or PR segment depression.

    • Usually not helpful in diagnosing pericarditis post MI.

    • The voltage drops as an effusion develops and in tamponade there is electrical alternans, best seen in QRS complexes.


    • May demonstrate a pericardial collection.

    • Useful to monitor LV function in case of deterioration due to associated myopericarditis.

    • We recommend every patient has an Echo prior to discharge to assess LV function.

Other investigations depend on the suspected aetiology

All patients should have:

    • FBC and biochemical profile

    • ESR and CRP (levels rise proportionate to intensity of disease)

    • Serial cardiac enzymes (CK, CK-MB, troponin). Elevations indicate sub-pericardial myocarditis

    • CXR (heart size, pulmonary oedema, infection).


Management for Acute Pericarditis

    • Admit? Depends on clinical picture. We recommend admission of most patients for observation for complications especially effusions, tamponade, and myocarditis. Patients should be discharged when pain free.

    • Bed rest.

    • Analgesia: NSAIDs are the mainstay. Ibuprofen is well tolerated and increases coronary flow (200–800mg qds). Aspirin is an alternative (600mg qds PO). Indometacin should be avoided in adults as it reduces coronary flow and has marked side effects. Use PPI (lansoprazole 30mg od) to minimize GI side-effects. Opioid analgesia may be required. Colchicine used as monotherapy or in addition to NSAIDs may help settle pain acutely and prevent recurrence.

    • Steroids: these may be used if the pain does not settle within 48h (e.g. prednisolone EC 40–60mg PO od for up to 2 weeks, tapering down when pain settles). Use in conjunction with NSAID and taper steroids first before stopping NSAID. It is also of value if pericarditis 2° to autoimmune disorders.

    • Colchicine: evidence suggests that either used as monotherapy or in conjunction with NSAIDs it may help to settle pain acutely and prevent relapses (1mg/day divided doses). Stop if patient develops diarrhoea, nausea. (1mg stat, 500mcg q6h for 48h).

    • Pericardiocentesis: this should be considered for significant effusion or if there are signs of tamponade (see Cardiac emergencies p.[link]).

    • Antibiotics: these should be given only if bacterial infection is suspected.

    • Oral anticoagulants: should be discontinued (risk of haemo-pericardium). Patient should be given IV UFH, which is easier to reverse (IV protamine) if complications arise.