Cardiology
A patient with known cardiac valve disease presents to ED with fever and shortness of breath worsening over the past 2 weeks. On examination, you note poor dental hygiene, and the patient informs you he underwent a tooth extraction about 3 weeks ago. You suspect infective endocarditis. Which of the following is the most likely causative pathogen?
Answer:
Streptococcus viridans (alpha-haemolytic Streptococcus) is a prominent member of the mouth flora and bacteraemia may result from poor dental hygiene or a dental procedure. Structurally weakened and damaged endocardium is susceptible to colonisation with an infective organism, especially if a thrombus has already been deposited.Infective Endocarditis
Cardiology
Last Updated: 8th September 2021
Infective endocarditis (IE) is an infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium.
- Acute: typically develops over a period of days to weeks and is characterised by spiking fevers, tachycardia, fatigue, and progressive damage to cardiac structures.
- Subacute: typically develops over the course of weeks to months and patients complain of vague constitutional symptoms.
Causative agents
- Native valve endocarditis (NVE)
- Patients who develop native valve endocarditis in the absence of intravenous drug use commonly present with viridans group streptococci, enterococci, or staphylococci, with other pathogens being less frequent.
- Intravenous drug users often present with right-sided valvular involvement and are more likely to have Staphylococcus aureus, streptococci, gram-negative bacilli, or polymicrobial infections. S. aureus is the most common causative organism and accounts for 60% to 90% of cases. The tricuspid valve is the most commonly affected, although the pulmonary valve is also susceptible to infection.
- Prosthetic valve endocarditis (PVE)
- Between 10% and 30% of all cases of IE occur in the context of prosthetic heart valves.
- Early prosthetic valve endocarditis (within 1 year of valve replacement) is often caused by S aureus or coagulase-negative staphylococci.
- Late prosthetic valve replacement tends to be caused by the same organisms as NVE, and non-surgical treatment in this group may be effective.
- The most common cause of infective endocarditis following dental procedures is Streptococcus viridans (alpha-haemolytic streptococci).
Pathophysiology
IE typically develops on the valvular surfaces of the heart, which have sustained endothelial damage secondary to turbulent blood flow. As a result, platelets and fibrin adhere to the underlying collagen surface and create a prothrombotic milieu. Bacteraemia leads to colonisation of the thrombus and perpetuates further fibrin deposition and platelet aggregation, which develops into a mature infected vegetation.
Risk factors
- Valvular heart disease
- Prosthetic valves
- Structural congenital heart disease
- Rheumatic heart disease
- Previous infective endocarditis
- Hypertrophic cardiomyopathy
- Intravenous drug use (IVDU)
Clinical features
All patients with bacteraemia should be suspected of potentially having IE, particularly those with an audible murmur.
- Acute IE
- Patients often present with signs and symptoms of peripheral or central emboli, or with evidence of decompensated congestive heart failure. Therefore, any patients who present with fever in conjunction with headache, meningeal signs, stroke symptoms, chest pain, dyspnoea on exertion, orthopnoea, or paroxysmal nocturnal dyspnoea need to be evaluated urgently for IE. Arthralgias and back pain may also result from peripheral septic emboli. Classic immunological features (e.g. Osler nodes, Roth spots) are uncommon due to rapid onset of disease process.
- Subacute IE
- Patients present with fever and chills, non-specific constitutional symptoms (night sweats, malaise, fatigue, anorexia, weight loss, myalgias), or palpitations. Physical examination is often non-specific, but subacute presentations are more likely to exhibit classic examination findings such as Janeway lesions (haemorrhagic, macular, painless plaques with a predilection for the palms and soles), Osler nodes (small, painful, nodular lesions usually found on the pads of the fingers or toes), splinter haemorrhages (commonly noted in the nails of the upper and lower extremities), or cutaneous infarcts. Palatal petechiae may also be present. Fundoscopy may detect Roth spots (oval, pale, retinal lesions surrounded by haemorrhage). Subacute IE must always be in the differential diagnosis of a patient with progressive fever and constitutional symptoms.
Investigations
- Lab tests
- Initial laboratory studies should include basic full blood count (FBC) and electrolyte panel, urinalysis and three sets of blood cultures from three different venepuncture sites 1 hour apart. Testing for rheumatoid factor and measuring erythrocyte sedimentation rate and complement levels may also be helpful.
- ECG
- An ECG should be undertaken, as progression of the infection may lead to conduction system disease.
- Echocardiography
- The decision to obtain a transthoracic echocardiogram (TTE) rather than transesophageal echocardiogram (TOE) is often difficult and has been considered by various guidelines. Any patient suspected of having native valve infective endocarditis should be screened with TTE. If negative and suspicion still remains, patients should undergo TOE. TOE is the preferred form of echocardiography in people with prosthetic material suspected to have infective endocarditis. TOE is also indicated in patients with a positive TTE, but where complications are suspected or likely, and before cardiac surgery during active infective endocarditis.
- Further imaging
- Computed tomography has been found to compare favourably with TTE in detecting valvular abnormalities in patients with IE, but it may miss small defects.
- MRI is the imaging modality of choice when investigating the cerebral complications of IE.
Management
Initial management is aimed at controlling airway, breathing, and circulation. It is vital to obtain blood cultures prior to the initiation of antimicrobial therapy, as one dose often masks an underlying bacteraemia and delays appropriate therapy. Subsequently, patients should undergo urgent echocardiography to determine the nature and extent of valvular lesions.
Broad-spectrum antimicrobial therapy is required empirically. Recommended antibiotic regimens may differ between countries and local guidance should be consulted. Discussion with an infectious diseases specialist should inform the optimal regimen. Consideration of the following factors influences the choice of empirical treatment:
- Previous antibiotic therapy received; native or prosthetic valve involvement
- Local epidemiology and knowledge of antibiotic-resistant and culture-negative pathogens
- Community, nosocomial, or non-nosocomial healthcare-associated infection.
Patients who are acutely ill or present with signs and symptoms of decompensated heart failure present the greatest challenge. Often, these patients are colonised with aggressive Staphylococcus aureus, and are at risk for decompensating quickly. Haemodynamic stability is the goal, and these patients often require urgent surgical intervention if the valvular lesion is beyond repair with medical treatment alone. Acutely ill patients presenting with decompensated heart failure will require surgery, with intravenous diuretics given to manage pulmonary oedema prior to the surgery.
Complications
- Congestive heart failure
- Systemic embolisation (emboli often involve the lungs, spleen, joints, brain, and coronary arteries)
- Valvular dehiscence, rupture or fistula
- Splenic abscess
- Mycotic aneurysms
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
