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With the introduction of penicillin in the 1940s, the mortality rate from infective endocarditis (IE) decreased from 100% to about 30%.1 Despite newer antibiotics and other medical advances, the mortality rate remains 16% to 46%, and the annual incidence for the general population is 24 to 62 cases per million.2–11
Infective endocarditis has changed over the decades from a disease infecting rheumatic heart defects to an iatrogenic and self inflicted entity. With advances in invasive medical techniques and an increase in intravenous drug use, the prevalence of staphylococcus aureus has now surpassed streptococcus as the most common cause of IE.11–13 In addition, there is an increasing prevalence of resistant bacteria, poor compliance with treatment regimens, and risk of complications years later.8–10,14
The initial presentation to the emergency department (ED) is usually vague and non-specific, especially among intravenous drug users, and the number of missed diagnoses is unknown.15 The following case illustrates IE and its presentation and management.
A 23 year old woman presented to the ED complaining of lower extremity pain and swelling for five days. The patient was seen at an outlying ED six days previously, with a three week history of subjective fever and cough. She was diagnosed with multilobar, community acquired pneumonia and was prescribed levofloxacin. The fever continued; she developed bilateral knee and ankle pain, and a rust coloured sputum. The patient denied rashes, insect bites, chest pain, or vaginal discharge. Her medical history was negative for sexually transmitted diseases, heart murmurs, rheumatic fever, intravenous drug use, or recent dental work.
On physical examination, her pulse was 144 beat/min, blood pressure 109/46, respirations 28 breath/min, temperature 39.4°C, pulse oximetry 99% on room air. She had a normal mental status. Her mucous membranes were dry and her jugular veins were flat. She had no cardiac murmurs or gallops. She had bibasilar crackles and decreased breath sounds bilaterally although was not in respiratory distress. Her right third metacarpophalageal joint was swollen and tender, and she had mild bilateral swelling of the ankles without erythema, warmth, or tenderness. She had no rashes, peripheral oedema, Osler’s nodes, splinter haemorrhages, Janeway lesions, or Roth’s spots.
ED management included normal saline bolus for suspected dehydration, acetaminophen, laboratory investigations, and chest radiograph. After two litres of intravenous fluids, repeat vital signs were: pulse 102 beat/min, blood pressure 100/52, respirations 28 breath/min, temperature 37.7°C. A repeat cardiac examination revealed a II/VI systolic murmur at the left lower sternal border. Her chest radiograph showed focal confluence of opacities peripherally in the middle lung zones and lung bases that were consistent with infection or septic emboli. Her white blood cell count was 16.5 with 67 segs, 16 bands, 10 lymphocytes, and 7 monocytes. Her urine pregnancy test and urine analysis were negative. Her electrolyte panel was normal but sedimentation rate was 95.
The patient was prescribed immediately intravenous nafcillin and gentamicin. While in the ED, a transthoracic echocardiogram and computed tomography of the chest were ordered, and the internal medicine team was consulted. Computed tomography showed innumerable peripheral opacities, many of which displayed central cavitations; consistent with septic emboli (fig 1). The transthoracic echo showed large mobile masses on the tricuspid valve. Under the modified Duke criteria, the patient’s new murmur and echocardiogram results met two major criteria, categorising the diagnosis as “definite” infective endocarditis.7,16,17
Once admitted, a transoesophageal echocardiogram showed vegetations on all tricuspid leaflets, severe tricuspid regurgitation, and evidence of early right sided dilatation. Blood cultures from all four bottles grew staphylococcus aureus, sensitive to oxacillin (MSSA). The cardiothoracic surgical team evaluated the patient and recommended valve replacement surgery. The patient refused surgery and was discharged home after completing a six week course of intravenous antibiotics.
Since the publication of the Duke criteria in 1994, many studies have validated the sensitivity, emphasised the use of echocardiography, and offered suggestions for modification of the criteria.11,17–19 The modified Duke criteria now include three major (new murmur, positive blood cultures, vegetations found on echocardiogram) and six minor (predisposition, fever, vascular phenomena, immunological phenomena, microbiological findings, other echocardiographic evidence) criteria. To date, no studies have validated whether this improved criteria has decreased the mortality rate. In addition, there are no studies in the ED literature that quantify the misdiagnosis of IE. Many other studies have shown that the transthoracic approach is much easier to perform but inadequate in up to 20% of adult patients because of body habitus, chronic obstructive pulmonary disease, or chest wall deformities. Because of increased sensitivity, transoesophageal echocardiogram is recommended as the test of choice.11,20–22
In conclusion, emergency physicians must recognise the unchanged mortality rate with IE and understand the importance of early, reliable diagnosis. The most common initial presentation to the ED for endocarditis is intermittent fever and malaise.22 Likewise, 15%–20% of left sided infected patients and 50%–65% of right sided infected patients will not have a murmur on initial examination.22,23 This emphasises the importance of searching for risk factors in the history, looking for other physical examination findings, understanding the modified Duke criteria, and using transoesophageal echocardiograms. Emergency physicians must always include IE in the differential diagnosis for unexplained or persistent febrile illness.
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