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Paediatrics > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Symptoms of HF

A
  • Breathlessness
  • Sweating
  • Poor feeding
  • Recurrent chest infections
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2
Q

Signs of HF

A
  • Poor weight gain or faltering growth
  • Tachypnoea
  • Tachycardia
  • Heart murmur, gallop rhythm
  • Enlarged heart
  • Hepatomegaly
  • Cool peripheries.
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3
Q

Signs of RHF

A
  • Ankle oedema
  • Sacral oedema
  • Ascites.
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4
Q

Pathophysiology of Atrial Septal Defect

A
  • Low pressure chambers compared to ventricles. So amount of shunt is less and less pulmonary circulation.
  • Leads to stretching of Right atrium and causes dilation - leading to arrhythmias in later life.
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5
Q

Types of ASD

A
  • Secundum ASD - 80% = centre of the atrial septum involving foramen ovale
  • Partial AVSD = defect of atrioventricular septum
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6
Q

Symptoms ASD

A
  • None normally
  • Recurrent chest infection or wheeze
  • Arrythmias
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7
Q

Signs of AVSD

A
  • Poor feeding
  • Failure to thrive
  • Tachypnoea
  • Common in Trisomy 21 - all will get screening at birth.
  • Gallop rhythm
  • Hepatomegaly and oedema.
  • Murmur arises from the valvular regurgitation rather than septal defects.
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8
Q

Physical signs of ASD

A
  • Not always causes a murmur and will be pulmonary flow murmur not cardiac.
  • Ejection systolic murmur best heard at left upper sternal edge - due to inc flow across pulmonary valve because of left to right shunt.
  • Fixed widely split second heart sound - due to rv stroke volume being equal in both inspiration and expiration
  • Partial AVSD - an apical pan systolic murmur from AV regurg
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9
Q

Ix of ASD

A
  • Chest radiograph - Cardiomegaly, enlarged pulmonary arteries, and inc pulmonary vascular markings
  • ECG -
    • Secundum ASD - partial right bundle branch block. Right axis deviation due to RV enlargement
    • Partial AVSD - superior QRS axis - due to defect in middle part of heart where AV node is. Displaced node conducts to ventricles superiorly giving abnormality in axis.
  • Echo - Mainstay of diagnostic investigations
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10
Q

Management of ASD

A
  • Management only when there is significant ASD - enough to cause RV dilation
  • Secundum - Cardiac catheterisation with insertion of occlusion device
  • Partial -surgical correction
  • Undertaken about 3-5 years of age in order to prevent RHF and arrhythmias later in life.
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11
Q

Small VSD

A
  • Asymptomatic up to 3mm
  • Loud pan systolic murmur at lower left sternal edge - louder = smaller defect as more pressure.
  • Quiet pulmonary second sound
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12
Q

Ix Small VSD

A
  • Chest radiograph - normal
  • ECG - normal
  • Echo - precise anatomy of defect.
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13
Q

Management small VSD

A
  • Lesions more often than not close spontaneously
  • Prevention of bacterial endocarditis while it is still present - good dental hygiene.
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14
Q

Large VSD Signs

A
  • Heart failure with breathlessness, and faltering growth after 1 week old.
  • Recurrent chest infection
  • Tachypnoea
  • tachycardia
  • Enlarged liver from heart failure.
  • Active precordium -
  • Soft pan systolic murmur or no murmur - implying large defect if none
  • Apical mid-diastolic murmur - from inc blood flow across mitral valve after blood circulated through lungs
  • Sound pulmonary second sound - raised pulmonary arterial pressure.
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15
Q

Large VSD Ix

A
  • Cardiomegaly
  • Enlarged PA
  • Inc pulmonary vascular markings
  • Pulmonary oedema

ECG - biventricular hypertrophy

Echo - Anatomy defect and pulmonary hypertension

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16
Q

Management of large VSD

A
  • Diuretics with captopril
  • Additional calorie input
  • Surgery - 3-6 months of age
  • Manage heart failure and faltering growth - prevent permanent lung damage from pulmonary HTN and high blood flow.
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17
Q

Pathophysiology Persistent Ductus Anteriosus

A
  • Ductus anteriosus connects Pulmonary Artery to Descending aorta
  • Closes shortly after birth
  • Failed to close in PDA by 1 month after expected date of delivery - Preterm infant can have this due to prematurity and not congenital HD.
  • Flow of blood from aorta to pulmonary artery following fall in pulmonary vascular resistance after birth
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18
Q

Clinical features PDA

A
  • Continuous murmur beneath the left clavicle
  • Murmur continues into diastole because the pressure in the pulmonary artery is lower than that in aorta throughout cardiac cycle.
  • Pulse pressure is increased, causing a collapsing or bounding pulse
  • Symptoms Tunisia; but where duct is large, be inc pulmonary blood flow with heart failure and pulmonary hypertension.
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19
Q

Ix PDA

A
  • Chest radiograph and ECG normal
  • Echo - most readily identified.
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20
Q

Management PDA

A
  • Closure is recommended
  • With a coil or occlusion device via cardiac catheter at about 1 YO
  • Occasionally surgical ligation is required.
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21
Q

Left to right shunts

A

ASD
VSD
PDA

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22
Q

Right to left shunts

A

Tetralogy of fallot
Transposition of greater arteries

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23
Q

Outflow obstruction in a well or sick neonate

A

well - Pulmonary and Aortic stenosis - asymptomatic with murmur
Sick - coarctation of aorta - collapse with shock

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24
Q

Presentation of right to left shunts

A

cyanosis usually in first week of life.

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25
Q

Hyperopia nitrogen washout test

A
  • Infant placed in 100% oxygen ventilator for 10 mins.
  • If PaO2 from a blood gas remains low (15kPa or 113mmHg) a diagnosis of cyanotic congenital heart disease can be made if lung disease and persistent pulmonary hypertension of newborn have been excluded.
  • If PaO2 >20kPa it is not cyanotic heart disease.
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26
Q

Management of cyanosed neonate

A
  • Stabilise airway, breathing and circulation with artificial ventilation if necessary
  • Start prostaglandin infusion
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27
Q

S/E prostaglandin

A

apnoea, jitteriness and seizures, flushing, vasodilation and hypotension.

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28
Q

Duct dependent definition

A

Most infants with cyanotic heart disease, presenting in first few days of life are duct dependent - There is reduced mixing between pink oxygenated blood and blue deoxygenated blood from the body

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29
Q

4 anatomical features of ToF

A
  • A large VSD
  • Overriding of the aorta with respect to the ventricular septum
  • Subpulmonary stenosis causing right ventricular outflow tract obstruction
  • Right ventriclar hypertrophy.
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30
Q

Symptoms of ToF

A
  • Severe cyanosis
  • Hypercyanotic spells
  • Irritability and inconsolable crying because of severe hypoxia and breathlessness and pallor because of tissue acidosis.
  • Short murmur during a spell.
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31
Q

Signs of ToF

A
  • Clubbing of the fingers and toes will develop in older children
  • A loud harsh ejection systolic murmur at the left sternal edge from day 1 of life.
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32
Q

Ix of ToF

A
  • Chest radiograph - small heart possibly with untitled apex (boot shaped) due to RV hypertrophy
  • ECG - normal
  • Echo - cardiac catheterisation may be required to show the detailed anatomy of coronary arteries.
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33
Q

Management ToF

A
  • Surgery at 6 months - closing VSD, and relieving right ventricular outflow tract obstruction
  • Infants who are very cyanosed - require a shunt - artificial tube between the subclavian artery and pulmonary artery.
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34
Q

Management of Hypercyanotic spells

A
  • usually self-limiting and followed by a period of sleep. If prolonged - 15 min - should be given treatment
    • Sedation and pain relief - morphine
    • IV propranolol - works as both a peripheral vasoconstrictor and by relieving the subpulmonary muscular obstruction that is the cause of reduce pulmonary blood flow.
    • IV volume administration
    • Bicarbonate to correct acidosis
    • Muscle paralysis and artificial ventilation in order to reduce metabolic demand.
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35
Q

Pathophys Transposition of great arteries

A
  • Aorta connected to the RA - deoxygenated blood to the body
  • PA connected to RV - oxygenated blood returned to lungs
  • Leading to two parallel circulations - unless there is mixing of blood between them and is incompatible with life.
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36
Q

Signs and Symptoms of TOGA

A
  • Cyanosis
  • Day 2 - when ductal closure leads to a marked reduction in mixing of desaturated and saturated blood.
  • Cyanosis
  • S2 is loud and single
  • No murmur - but may be a systolic murmur from inc flow or stenosis within left ventricular outflow tract. (pulmonary)
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37
Q

Ix TOGA

A
  • Chest radiograph - Narrow upper mediastinum, with an egg on side appearance on the cardiac shadow - Sur to anteroposterior relationship to great vessels.
  • ECG - normal
  • Echo - abnormal arterial connections
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38
Q

Management of TOGA

A
  • Maintaining patency of ductus anteriosus with a prostaglandin infusion
  • Balloon atrial septostomy - passed through umbilical or femoral vein and then on through the RA and foramen vale. Balloon inflated in LA and pulled back through the atrial septum. This tears atrial septum and renders flap cable of foramen ovals incompetent and so allows mixing of systemic and pulmonary venous blood within atrium.
  • Switching back in neonatal period in first few days of life.
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39
Q

Eisenmenger syndrome

A
  • If high pulmonary blood Flow due to large left-to-right shunt or common mixing is not treated at an early stage, then pulmonary arteries become thick walled and the resistance to flow increases
  • Gradually, those children that survive become less symptomatic as the shunt decreases
  • 10-15 years of age, shunt reverses and teenager becomes blue.
  • Adult will die with RHF at a variable age, usually in 4th or 5th decade.
  • Treatment aimed at prevention, and to prolong transplantation needs.
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40
Q

Types of outflow obstruction

A
  • Aortic Stenosis
  • Pulmonary Stenosis
  • Adult type coarctation of aorta
  • Coarctation of aorta
  • Interruption of aortic arch
  • Hypoplastic left heart syndrome
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41
Q

Pathophys Aortic stenosis

A

Aortic valve leaflets are partly fused together, giving restrictive exit from left ventricle

42
Q

Physical signs of AS

A
  • Small volume, slow rising pulses
  • Carotid thrill
  • Ejection systolic murmur maximal at the upper right sternal edge radiating to the neck
  • Delayed and soft aortic second sound.
  • Apical ejection click.
43
Q

Ix AS

A
  • Chest radiograph - Normal or promenant LV with poststenotic dilation of ascending aorta.
  • ECG - LV hypertrophy
44
Q

Management AS

A
  • Regular clinical and echocardiographic assessment
  • High resting pressure gradient - >64mmHg across aortic valve will undergo balloon valvotomy
  • Aortic valve replacement later in life.
45
Q

Pulmonary stenosis signs

A
  • Asymptomatic
  • Ejection systolic murmur beast heard at the upper left sternal edge
  • Ejection click best heard upper left sternal edge
  • Prominent RV impulse of heave if severe
46
Q

Ix PS

A
  • Chest radiograph - normal
  • ECG - RV hypertrophy
47
Q

Management PS

A
  • Pressure gradient >64mmHg intervention required
  • Transcatheter balloon dilatation is the treatment of choice in most children.
48
Q

Adult type Co-arctation of aorta

A
  • Not duct dependent
  • More severe over time
49
Q

Symptoms + Signs of Adult type Co-arctation of aorta

A
  • Asymptomatic
  • Systemic hypertension in the right arm
  • Ejection systolic murmur at upper sternal edge
  • Collaterals heard with continuous murmur at the back
  • Radio-femoral delay - blood bypassing the obstruction via collateral vessels in the chest wall and hence the pulse in legs is delayed
50
Q

Ix of Adult type Co-arctation of aorta

A
  • Chest radiograph - Rib notching - due to development of large collateral intercostal arteries running under ribs posteriorly to bypass obstruction. 3 sign with visible notch in the descending aorta at the site of coarctation.
  • Ecg - LV hypertrophy
51
Q

Management of Adult type Co-arctation of aorta

A

Stent insertion when severe via cardiac catheter.

52
Q

Pathophysiology Coarctation of aorta

A
  • Due to arterial duct tissue encircling the aorta just at the point of insertion of the duct.
  • When duct closes, aorta also constricts causing severe obstruction to LV outflow.
53
Q

Symptoms Coarctation of aorta

A
  • A sick baby, with severe heart failure
  • Absent femoral pulses
  • Severe metabolic acidosis
54
Q

Ix Coarctation of aorta

A
  • Chest radiograph - cardiomegaly from HF and shock
  • ECG - normal
55
Q

Management Coarctation of aorta

A

Surgical repair soon after diagnosis.

56
Q

Pathophysiology + Management Interruption of aortic arch

A
  • No connection between the proximal aorta and distal arterial duct.
  • Associated with DiGeorge syndrome
  • Complete correction with closure of a VSD and repair of aortic arch is usually performed first few days of life.
57
Q

Hypoplastic LHS

A
  • Underdevelopment of entire left side of heart
  • Antenatal detection at US screening
  • Duct dependent systemic circulation
  • No flow though left side of heart so ductal constriction leads to profound acidosis and rapid cardiovascular collapse
  • No absence or weakness in any pulses.
  • Surgery straight away, again at 6 months and then again at 3YO
58
Q

Types of syncope

A
  • Neurally mediated syncope - drop in BP with preceding dizziness or lightheadedness, sweating or pallor - e.g. seeing needles, stressors.
  • Cardiac syncope - arrhythmic from HB, SVT, VT or other associated syndrome
59
Q

Suggestive causes that syncope is cardiac

A
  • Symptoms of exercise
  • Fhx of sudden unexplained death palpitations
60
Q

Main types of paediatric arrhythmias

A
  • SVT
  • Congenital Complete HB
61
Q

SVT

A
  • Most common childhood arrhythmia
  • HR - 250-300bpm
  • Presents with HF and can lead to pulmonary oedema and poor cardiac output
  • Electric cardio version - with synchronised direct shock,
  • Maintenance therapy after.
  • Treatment stopped at 1 YO
62
Q

Complete Congenital HB

A
  • Anti-Ro or Anti-La antibodies in maternal serum.
  • Prevents normal development of the electrical conduction system in developing heart - with atrophy and fibrosis of AVN
  • Few become symptomatic wit pre syncope or syncope
  • Symptoms treated with insertion of endocardial pacemaker
63
Q

Epidemiology of Rheumatic Fever

A

affects children between the ages of 5 and 15, with girls being affected slightly more commonly than boys.
Rheumatic fever can return later in life if left untreated,

64
Q

Biological RF RF

A

Age: rare in children under 4 years.
Sex: more common in females.
Ethnicity: for example, there is a higher prevalence of rheumatic fever among indigenous groups in Australia and New Zealand.
Immune status: immunocompetent vs immunocompromised.
Genetic susceptibility: as indicated by findings from twin studies.
Prior or untreated infection with Group A Streptococcus.
Virulence of the infective organism.

65
Q

Social Rf Rf

A

Low socioeconomic status: due to poor access to healthcare and antibiotics.
Overcrowding and poor housing: associated with poor hygiene and sanitation.
Climate: higher incidence over the winter months. In hot countries, streptococcal infection is more likely to present as a skin infection versus pharyngitis.

66
Q

Jones Criteria RF

A

In order to establish a diagnosis of rheumatic fever, there must be:

Evidence of recent group A Streptococcus infection

Positive throat swab
Positive rapid streptococcal antigen test
Raised streptococcal antibody titre (ASO or DNAse B titres)
Recent episode of scarlet fever
plus either:

two major criteria
or one major criterion and two minor criteria

67
Q

Major criteria RF

A

Polyarthritis
Carditis
Sydenhams Chorea
Erythema Marginatum

68
Q

Polyarthritis

A

Multiple joints are affected, predominantly the larger ones, which become red, hot and swollen. Individually, each joint is usually affected for less than a week.

The arthritis is described as a “flitting” arthritis because it migrates to other joints within the next 1-2 months.

69
Q

Carditis RF

A

In rheumatic fever, every layer of the heart can be affected, resulting in a pancarditis.

Endocarditis, Pericarditis, Myocarditis

70
Q

Sydenhams chorea

A

Sydenham’s chorea is a rare, and late-presenting sign of rheumatic fever, appearing around 2-6 months after the initial streptococcal infection.

It consists of involuntary, semi-purposeful movements of the body which may be unilateral or bilateral. Occasionally the chorea is preceded by emotional lability or behaviour which is out of character for the patient.

71
Q

Erythema Marginatum

A

is a pink macular rash predominantly affecting the trunk and limbs while sparing the face. It expands outwards, leaving a pale centre and is described as a “geographical rash” because its borderlines resemble those drawn on a map

72
Q

Subcutaneous nodules

A

Hard, mobile, pea-sized nodules, typically found on the extensor surfaces (e.g. back of the elbows) or the spine. They are often painless and normally disappear within one month.
Subcutaneous nodules are a rare finding in rheumatic fever and are usually only seen when severe carditis is present

73
Q

Minor criteria RF

A

Polyarthralgia

Pain present in multiple joints. This is not included in the criteria if polyarthritis is already present.

Prolonged PR interval on ECG

This is only used as a criterion if there are no signs of pancarditis.

History of rheumatic fever

A previous history of rheumatic fever is a risk factor for subsequent flare-ups.

Fever

Typically, temperatures of more than 39 degrees centigrade.

Raised inflammatory markers

This includes markers such as CRP, ESR and leukocyte (white cell) count.

74
Q

Ddx Rf

A

Joint symptoms

Systemic-onset juvenile idiopathic arthritis (JIA), also known as Still’s disease
Reactive arthritis
Henoch-Schönlein purpura (HSP)

Cardiac disease

Cardiomyopathy
Kawasaki disease
Infective endocarditis

Chorea

Wilson’s disease
Adverse drug reactions
Huntington’s disease (very rare in children)

Skin changes

Adverse drug reactions
Lyme disease/erythema migrans
Erythema multiforme

75
Q

Ix RF

A

ECG: may show prolonged PR interval and tachycardia.
Vital signs: fever may be present.

Throat swabs: testing for cultures of group A Streptococcus, although usually negative by the time the symptoms appear.

Rapid streptococcal antigen test (RAST): may be performed before cultures if streptococcal infection is suspected. Results are obtained quicker than for throat cultures but may be less accurate.16 RAST tests can give false negatives, in which case, cultures are then performed as well.

Anti-streptococcal antibodies: check for elevated antibody levels or a rise in levels. The sample should also be repeated in 2 weeks. Levels tend to stay elevated for at least 6 months.

Blood tests: FBC (WCC may be raised), ESR and CRP, troponin (raised in myocarditis), rheumatoid factor and anti-CCP (to exclude other diagnoses).

Chest X-ray: to rule out heart failure.

Doppler echocardiogram: may be used to aid diagnosis of carditis in acute rheumatic fever.

76
Q

Most common antibodies in RF

A

The most common antibody tests used for rheumatic fever are anti-streptolysin O (ASO) and anti-DNAse B.

77
Q

Management RF

A

Bed rest - limitation of exercise

Penicillin - benzylpenicillin followed by penicillin V (phenoxymethylpenicillin for 10 days)

If allergic - erythromycin or azithromycin

High dose aspirin - to limit inflam response

Corticosteroids - those with severe carditis and no response to abx

Acute HF - ACE inhibitor and diuretics. or Pericardiocentesis in presence of fluid

Chorea - Diazepam or haloperidol. Diazepam is preferred over haloperidol as it is not associated with the extrapyramidal side-effects which may occur with haloperidol.

78
Q

Prophylaxis RF

A

The current recommended first-line prophylactic treatment is benzathine penicillin G, given every 4 weeks as an intramuscular injection.

the patient can take oral penicillin instead of having the injections, but they must take these every day for the duration of prophylaxis and this may make compliance difficult

79
Q

How long prophylaxis RF

A

If carditis is not a feature of the acute episode, and there is no evidence of valvular disease, then prophylaxis may be given for only 5 years, or until age 21 (whichever is sooner).

If carditis is present during the acute episode but there is no valvular disease, then prophylaxis should be given for 10 years.

Where there is both carditis and persistent valvular disease, prophylaxis should be continued for life, or at least up to the age of 40.

80
Q

Complications RF

A

Carditis (e.g. infective endocarditis)
Heart failure
Pericardial effusions
Valvular disease (especially the mitral valve)
Atrial fibrillation (from severe untreated mitral stenosis)
Pulmonary hypertension
Thromboembolic events, such as strokes (a consequence of atrial fibrillation)

81
Q

Most common valve lesion in RF

A

Mitral regurgitation is the most common valve lesion in rheumatic fever overall, whereas mitral stenosis is the most common long-term cardiac complication

82
Q

Type of bacteria RF

A

Rheumatic fever develops as a complication of infection with Group A beta-haemolytic Streptococcus. It is not contagious.

83
Q

Pathophysiology IE

A

Infective endocarditis arises from three key factors occurring simultaneously:

Transient bacteraemia
Damage to valvular tissue
Formation of vegetations

When the valve is damaged (e.g. by trauma or the infecting organism itself), the endothelium is exposed, leading to an aggregation of platelets and fibrin at the affected site.

The circulating pathogen binds to this platelet-fibrin matrix and continues to proliferate.

84
Q

Causative pathogen if gram + IE

A

Staphylococci (e.g. Staph aureus)
Streptococci (e.g. Strep viridans, Strep intermedius, Groups A, B, C, D, G)
Enterococci

85
Q

Gram - IE

A

HACEK organisms*
Non-HACEK organisms (e.g. Pseudomonas aeruginosa, Neisseria elongata)
*Haemophilus spp., Aggregatibacter actinomycetemcomitans, Cardiobacterium spp., Eikenella corrodens, Kingella kingae

86
Q

Fungi IE

A

Candida
Aspergillus

87
Q

Intrinsic RF IE

A

Valvular stenosis or regurgitation: congenital or acquired

Hypertrophic cardiomyopathy

Structural heart disease with turbulent flow (e.g. VSD, PDA): but NOT isolated ASD or fully repaired VSD or PDA

Prosthetic heart valves: these will require replacement if infected

Previous infection (infective endocarditis/rheumatic fever) causing structural damag

88
Q

Extrinsic RF IE

A

Intravenous drug use (right-sided endocarditis)
Invasive vascular procedures (e.g. central lines)
Poor oral hygiene/dental infections

89
Q

Clinical findings IE

A

Fever
Tachycardia
New or changing heart murmur
Splinter haemorrhages: nailbed petechial haemorrhages
Osler’s nodes (tender subcutaneous nodules in the fingers) and Janeway lesions (painless erythematous macules on the palms): see Table 2
Roth spots (boat-shaped retinal haemorrhages, pale in the centre)
Clubbing: typically a late sign
Mild splenomegaly
Bi-basal lung crepitations: heart failure in severe cases

90
Q

Osler nodes vs Janeway lesions

A

Painful (Osler’s Ow!) - Painless

Typically affects fingers/toes - Typically affects palms/soles

Nodules - Macules/papules

Purple-pink with a pale centre - Erythematous/haemorrhagic

Localised immune-mediated response - Septic emboli

Subacute endocarditis - Acute endocarditis
Last hours to days- Last days to weeks

91
Q

Ix IE

A

Basic observations (vital signs): signs of infection (fever, tachycardia).

12-lead ECG: to exclude first degree AV block (Figure 1). This may be seen in aortic root abscesses, which are a rare complication of infective endocarditis.

Urine dipstick: microscopic haematuria.

Full blood count: to exclude anaemia (↓Hb) and check white cell count (WCC) to track the progress of the infection and response to treatment.

CRP/ESR: inflammatory markers, used together with WCC (CRP more so). CRP may lag slightly behind WCC.

Urea & electrolytes: baseline renal function and creatinine clearance is required if starting on nephrotoxic antibiotics such as gentamicin.

Transthoracic echocardiogram is the first-line imaging investigation in endocarditis and should be performed as soon the diagnosis of endocarditis is suspected.

Transoesophageal Echo - more invasive

Chest Xray - initial infection screen and HF

CT - good if root abscess is present and if pt considered for surgery

92
Q

Diagnosis of IE

A

Duke criteria

93
Q

Major duke criteria

A

Positive for typical microorganisms on two or more separate occasions including Strep viridans, Strep bovis, HACEK group, Staph aureus, Community-acquired enterococci (in the absence of a primary focus)

Persistently positive cultures for microorganisms consistent with IE: ≥2 positive blood cultures of blood samples drawn >12 h apart or all of 3 or a majority of ≥4 separate cultures of blood (with first and last samples drawn ≥1 h apart)

A single positive culture for Coxiella burnetti or high antibody titre (>1:800)

94
Q

Minor Duke Criteria

A

Minor Duke criteria include:

Risk factors for infective endocarditis (see risk factors section)

Fever > 38oC

Vascular phenomena: septic emboli, Janeway lesions, conjunctival haemorrhage, intracranial haemorrhage

Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots, positive rheumatoid factor

Microbiological evidence: positive blood cultures which do not meet the major crit

95
Q

Definitve endocarditis

A

Direct evidence of infective endocarditis by histology or culture of organisms (e.g. from a vegetation)
TWO major criteria
ONE major + THREE minor criteria
FIVE minor criteria

96
Q

Possible endocarditis

A

Endocarditis is possible when there are:

ONE major and ONE minor criterion
THREE minor criteria
In other words, there is some evidence of endocarditis but not enough to make a definite diagnosis.

97
Q

Rejected IE

A

A diagnosis of endocarditis is rejected when there is:

A firm alternative diagnosis or
Sustained symptom resolution after <4 days of antibiotics

98
Q

Management IE

A

prolonged courses of antibiotics

treatment should last for at least six weeks in patients with prosthetic valves and two to six weeks for native valve endocarditis.

The start of the antibiotic course is taken from the first day a negative set of blood cultures is obtained

99
Q

Indications of surgery IE

A

Heart failure (i.e severe valve disease, pulmonary oedema or cardiogenic shock)
Uncontrolled infection
Prevention of embolism (large vegetations)

100
Q

Prophylaxis IE

A

Currently, in the United Kingdom, the National Institute for Health and Care Excellence (NICE) does not recommend using prophylactic antibiotics against endocarditis for patients underging dental procedures, or procedures affecting the gastrointestinal, genitourinary or respiratory tracts.

101
Q

Complications of IE

A

Valve destruction
Heart failure (secondary to valve regurgitation)
Arrhythmias and conduction disorders (e.g. AV block)
Myocardial infarction
Pericarditis
Aortic root abscess

Emboli (e.g. stroke, splenic infarction)
Immune complex deposition (e.g. glomerulonephritis)
Septicaemia
Death

102
Q
A

Paediatrics (17 decks)

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