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19. Endocarditis: Osler’s Challenge
Keywords
EndocarditisInfectionEchocardiogramAntibioticsDukeValveJanewayRoth’s spotsSplinter hemorrhagesCase
Weakness, fever at home, myalgias, cough, headache
Pertinent History
This patient presented to the emergency department (ED) at 9 pm with several complaints, including weakness, fever to 102 °F, cough, and headache. He is concerned about the flu, as his girlfriend is sick at home and was recently diagnosed with flu by an urgent care physician. His symptoms have been going on for 5 days, and he is able to eat and drink. He denies carbon monoxide exposure or trauma. He has not noticed chest pain, shortness of breath, or neck stiffness, and he has no focal neurologic deficits. However, he has noted generalized weakness and myalgias.
Past Medical History (PMH)
Hypertension.
Meds
Hydrochlorothiazide.
Surgical History (SH)
Smoker, 20 pack year history. Regular alcohol use. Remote IV drug use, but the patient has not used for over 2 years.
Pertinent Physical Exam
Blood Pressure 150/89 mm Hg, Heart Rate 105 beats/minute, Temperature 99.9°F, RR 18 breaths/minute, SpO2 98% RA.
Except as noted below, the findings of the physical exam are within normal limits.
Cardiovascular:
Tachycardia with regular rhythm, normal heart sounds, and normal distal pulses. No murmur is heard on initial examination.
Pertinent Diagnostic Testing
Test | Results 21:33 | Units | Normal Range |
|---|---|---|---|
WBC | 13.3 | 103/mm3 | 3.8–11.0 103/mm3 |
Hgb | 14.2 | g/dL | (Male) 14–18 g/dL (Female) 11–16 g/dL |
Na | 132 | mEq/L | 135–148 mEq/L |
K | 4.2 | mEq/L | 3.5–5.5 mEq/L |
BUN | 40 | mg/dL | 6–23 mg/dL |
Cr | 1.5 | mg/dL | 0.6–1.5 mg/dL |
Glucose | 168 | mg/dL | 65–99 mg/dL |
pH | 7.34 | – | 7.35–7.45 |
Lactate | 1.9 | mmol/L | <2.0 |
Chest X-Ray (CXR)
Multiple consolidations are present. The heart border is normal, and there are no pleural effusions present.
Plan
Antibiotics including ceftriaxone IV and azithromycin PO for community-acquired pneumonia, along with IV fluids, followed by reevaluation.
Update 1: (2215)
The patient’s hemodynamic status has not improved. HR is now 108 beats/minute, and temperature is 100.4 °F. He has received antibiotics and one liter of normal saline. With concern for sepsis from pneumonia, a second liter of normal saline is provided, along with acetaminophen 1 g PO. The patient does not appear to be in distress.
Update 2: (2302)
The HR has improved to 95 beats/minute, and the temperature has decreased to 99.5 °F. A reexamination reveals a grade II/VI murmur. Reevaluation of chest X-ray showing multilobar findings is concerning, along with remote history of IV drug use. A bedside ultrasound (US) reveals findings concerning for a tricuspid valve lesion (vegetation) on the periapical four-chamber view.
Tricuspid Valve Vegetation on Apical 4 Chamber View
Image courtesy of Sambita Basu, MD
Update 3: (2312)
Three sets of blood cultures are ordered from separate sites due to concern for endocarditis. Cardiology and Infectious Disease consultants recommend obtaining comprehensive echocardiogram with admission. Internal medicine is consulted for admission.
Update 4: (2338)
Patient to internal medicine floor.
Learning Points: Endocarditis
Priming Questions
- 1.
When should endocarditis be considered?
- 2.
How is the diagnosis made, and what roles do laboratory and imaging studies play?
- 3.
How should the Duke Criteria be used in the ED?
- 4.
What is the treatment for endocarditis, and what is required in the ED?
Introduction/Background
- 1.
Infectious endocarditis (IE) is a disease associated with infection of the endocardial surface (heart valves, mural endocardium, or septum). Cardiac effects include valvular insufficiency, myocardial abscess, and congestive heart failure. Infective endocarditis can cause a wide number of systemic findings and symptoms, which makes diagnosis difficult. There is no standard diagnostic test beyond echocardiogram and blood cultures in the ED, and the diagnosis truly depends on consideration of the disease [1–10]. Duke’s Criteria are the standard diagnostic criteria [3, 4, 11]. William Osler put it best in an 1885 lecture: “Few diseases present greater difficulties in the way of diagnosis than malignant endocarditis, difficulties which in many cases are practically insurmountable” [12]. This remains true today [13, 14].
Heart Anatomy
Wapcaplet (https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg), “Diagram of the human heart (cropped)”, https://creativecommons.org/licenses/by-sa/3.0/legalcode
- 2.
Several categories of disease are present:
Native valve endocarditis (NVE) , acute or subacute [1, 2, 14–17].
The presentation and course of NVE is characterized by acute or subacute infection. Acute IE is aggressive and typically involves normal valves. It often is due to Staphylococcus aureus or group B streptococci. Subacute NVE usually involves abnormal valves and is more indolent over months.
Prosthetic valve endocarditis (PVE) , early or late [1, 2, 14–20].
PVE causes 20% of IE cases. Close to 4% of mechanical or bioprosthetic valves will become infected over their lifespan (mechanical valves are infected more commonly with in the first 3 months). Early PVE occurs within 60 days of implantation, commonly due to coagulase negative staphylococci, gram-negative bacilli, or Candida. IE occurring after 60 days is late PVE, with S. aureus being the most common cause.
Intravenous drug abuse endocarditis (IVDA IE) [1, 2, 14–20].
Up to 75% of patients with IVDA and IE have no underlying cardiac defect, with 50% of infections including the tricuspid valve. These are usually infected with S. aureus.
Other types of IE include pacemaker IE and nosocomial IE (NIE). Pacemaker IE is most commonly used due to S. aureus and can be challenging to treat. NIE occurs after 48 hours of hospitalization or is associated with healthcare environment exposure within 4 weeks of a performed procedure.
- 3.
IE is rare, with an annual incidence of up to 10 cases per 100,000 persons [1, 2, 10]. Approximately, 40,000–50,000 new cases occur in the US each year, with most cases occurring in urban settings (higher rates of intravenous drug use) [6, 10].
- 4.
Risk factors include prior endocarditis (the most common risk factor), structural heart damage, IV drug abuse (IVDA), poor immune function (vasculitis, HIV, diabetes, malignancy), nosocomial factors (surgical hardware placement, poor surgical technique, hematoma development), and poor oral hygiene [1, 2, 6, 10, 20].
- 5.
The risk of IE in IV drugs abusers is 2–5% per year, with a mean age of 30 years at time of diagnosis. In those with a history of IVDA and fever, close to 15% of patients have endocarditis [1, 2, 7–10, 17].
- 6.
Males are more commonly affected (1.5–3:1 male to female), and adults are more commonly affected. The age of those affected has steadily increased, with currently more than 50% of patients being greater than 50 years old [1, 2, 7–10, 17].
- 7.
Before antibiotics, this disease was associated with 100% mortality. Mortality is still high, with 1-year mortality approaching 20–40% and in-hospital mortality approaching 22% [1, 2, 7–10, 20].
Physiology/Pathophysiology
- 1.
Normally, valvular endothelium is resistant to microbial colonization. Trauma to the endothelium can result from high-pressure flow gradients and states of turbulent flow, which occur in patients with existing valvular or cardiac structural defects (rheumatic disease, congenital heart disease, prior endocarditis, prosthetic valve). Hypercoagulable or chronic inflammatory states (vasculitis, malignancy) can also result in vegetation formation along valves. IV drug use results in particulate matter bombardment along the cardiac structures, as well as vasospasm [1, 2, 7–10, 21–23].
- 2.
This damage to the endothelium increases the risk of sterile thrombus formation, consisting of fibrin and platelets [21–23].
- 3.
Microbes may attach and grow on this thrombus in episodes of bacteremia, viremia, or fungemia. These episodes most commonly occur in patients with periodontal disease and other sites of infection such as pneumonia, pyelonephritis, and cellulitis. Bacteremia results in the delivery of organisms to the valve surface. However, organisms must be able to attach and adhere to the valve (Table 19.1) [1, 2, 21–23].
- 4.
The most common valve affected is the mitral valve, followed by the aortic valve, the aortic and mitral valves combined, the tricuspid valve, and the pulmonic valve. IVDA IE most commonly affects the tricuspid valve [1, 2, 7–10, 14, 17].
Most common causative organisms in IE
Organism | Features |
|---|---|
S. aureus | Most common cause of IE overall (including acute, IVDA IE, PVE) Over half of IE cases do not have an underlying valve disorder 35–60% of bacteremia due to S. aureus are complicated by IE, with increased incidence of methicillin-resistant Staphylococcus aureus (MRSA) associated with IE A large percentage of bacteremia are due to an infected peripheral or central line Mortality approaches 50% |
Coagulase-negative Staphylococci | Usually presents with subacute IE Similar presentation to S. viridans (below) Causes 30% of PVE and < 5% of NVE One form is S. lugdunensis, which is extremely aggressive compared to other forms (positive blood culture highly suggestive of endocarditis) |
Streptococcus viridans | Accounts for 50–60% of subacute IE cases Many of the clinical signs and symptoms are due to immunologic phenomena with this form |
Streptococcus intermedius | Acute or subacute infections Accounts for close to 15% of IE cases due to Streptococcus May invade and form abscesses, especially in the central nervous system (CNS) |
Group A, C, G strep | Resembles S. aureus with high mortality and acute presentation Group A responds to penicillin Group C and G require synergistic combination of antibiotics |
Group B strep | Acute disease in pregnant and older patients with comorbidities Mortality approaches 40% Common complications include metastatic infection, arterial thrombi, and heart failure, which may require valve replacement |
Group D strep | Most are subacute, with sources including the gastrointestinal (GI) or genitourinary (GU) tract Third most common cause of IE Often resistant to antibiotics |
Nonenterococcal group D | Subacute presentation Often due to large bowel pathology (cancer, inflammatory bowel disease) Sensitive to penicillin |
Bartonella | More common in homeless patients with poor hygiene Blood cultures may be negative |
Pseudomonas | Most commonly presents in the acute form, except for right-sided disease Surgery typically required for treatment |
HACEK (Haemophilus aphrophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella) | Often results in subacute form Account for 5% of IE Most common gram-negative organisms in IE May cause complications such as arterial emboli and congestive heart failure Treatment often requires ampicillin, gentamicin, and surgery |
Fungal | Often results in subacute form Candida albicans is the most common cause of NVE and PVE Fungal IVDA IE often due to Candida parapsilosis or tropicalis |
Polymicrobial | Pseudomonas and enterococci are most common combination Also found in IVDA IE Cardiac surgery mortality rate higher in polymicrobial infections |
Making the Diagnosis
Endocarditis is a deadly disease, but our patient presented with flu-like symptoms. Plus, there are so many risk factors for IE, many of which are extremely common! Remember Osler’s quote? The key seems to be knowledge of risk factors and potential presentations…
Can’t Miss Diagnoses in Patients with Flu-like Symptoms
Endocarditis
Myocarditis
Spinal epidural abscess
HIV/AIDS
Necrotizing fasciitis
Tickborne illness
Encephalitis/meningitis
Tuberculosis
Malaria, dengue fever
Thyroid disease (thyrotoxicosis)
Heat stroke
Ingestion/toxicologic—carbon monoxide
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