Septic pulmonary embolism (SPE) usually originates from a patient’s heart, most commonly in the setting of tricuspid valve endocarditis, or from the peripheral veins (often secondary to septic thrombophlebitis), which together account for the majority of SPE. Less common origins include the head and neck (post-angial sepsis, mastoiditis), pelvis (thrombophlebitis) and infected arteriovenous shunts. Prompt identification of the septic focus is perhaps as important as the diagnosis of SPE itself, as resolution of the condition depends on the elimination of the source. Although the initial focus of infection is generally clinically apparent, occasionally it remains elusive. We report an instance of SPE secondary to seeding from oral abscess caused by methicillin-resistant Staphylococcus aureus (MRSA) septicaemia.
We present the case of a 26-year-old woman with asthma who was admitted to the emergency department at Mediclinic City Hospital, Dubai, United Arab Emirates (UAE), with a high-grade fever and pleuritic chest pain. At presentation, she had been taking 1 g co-amoxiclav (Augmentin®, GlaxoSmithKline) b.i.d. for 3 days, which had been prescribed by her general practitioner (GP) for an abscess on the buccal mucosa behind the angle of the mouth. An initial chest radiograph showed features of bilateral lower lobe consolidation and subsequent radiographs and a computed tomography (CT) scan of the chest showed multiple thick-walled cavitating nodules in both lung fields, which suggested SPE. The blood cultures carried out at admission and the swab from the patient’s oral abscess confirmed the presence of MRSA. The pulmonary lesions healed with appropriate antimicrobial therapy, but the oral abscess led to MRSA septicaemia, seeding of the lungs and multiple cavitating pulmonary nodules, which were similar to reported instances of septic emboli due to periodontal disease.1 To our knowledge, this presentation of SPE is rare.
A 26-year-old woman was admitted to the emergency department at Mediclinic City Hospital with complaints of fever, cough and pleuritic chest pain. She had a history of asthma that had been well controlled and she was not taking any steroids treatment for the condition. Over the past 3 days, the patient had been taking Augmentin, as prescribed by her GP, for the treatment of an oral abscess. In the emergency department, she mentioned that she was uncomfortable but she did not look particularly unwell. Her vital signs were recorded on admission and were as follows: blood pressure 125/76 mmHg, pulse 106/min and regular, temperature 38.9°C and oxygen saturation 98% in room air. The patient underwent a full blood count (FBC), C-reactive protein (CRP) test and chest radiography (Figure 1) at admission. The FBC showed an elevated white blood cell count of 21.4 K/µl with predominant neutrophilia, CRP was 273.5 mg/l and chest radiography showed bilateral lower lobe consolidation.
She was initially given intravenous (i.v.) ceftriaxone in the emergency department, pending results of blood culture, and was then transferred to the medical ward. Over the next 24 hours, the patient’s condition deteriorated and her temperature did not stabilize. She complained of worsening pleuritic chest pain; thus, chest radiography was repeated and showed worsening right middle lobe consolidation and left pleural effusion was now noticeable (Figure 2).
The patient underwent CT of her thorax (Figure 3), which showed multiple thick-walled cavitating nodules that were mainly seen in the periphery of both lungs with left lower lobe consolidation and bilateral pleural effusion with no evidence of hilar or mediastinal lymphadenopathy. The results of the tests were consistent with a diagnosis of SPE.
The patient’s blood cultures tested positive for MRSA but were sensitive to vancomycin, linezolid (Zyvox®, Pfizer) and clindamycin. MRSA was also cultured from pus drained from the abscess on the patient’s face. She was prescribed i.v. vancomycin and within 48 hours her temperature and clinical condition improved considerably.
The patient then completed 10 days of i.v. vancomycin as an in-patient and was discharged with a prescription for oral doxycycline for 1 week. She had a follow-up appointment in the clinic 2 weeks after her discharge, at which time she was asymptomatic and repeat CT of the thorax showed considerable improvement (Figure 4). Although the evidence suggests that the course of treatment should be i.v. antibiotics for 4 weeks, the patient had improved clinically, which was confirmed using radiology. Therefore, it was decided to change the patient’s prescription to oral antibiotics and maintain follow-up appointments in an outpatient setting.
Septic pulmonary embolism is an uncommon disorder that usually presents with insidious onset of fever, respiratory symptoms and lung infiltrates. Clinical and radiological features at presentation are usually non-specific, with the result that the diagnosis is frequently delayed.
Septic pulmonary embolism has been associated with risk factors such as i.v. drug abuse, endocarditis (especially tricuspid valve infection), pelvic thrombophlebitis, infected i.v. access sites and suppurative processes in the head and neck. There has recently been an increase in SPE in immunocompromised patients.2 SPEs arising from infections such as osteomyelitis, septic arthritis, cellulitis and occasionally pyomyositis have been increasingly described in children with MRSA infections, but these associations have not been previously described in adult patients.
In cases of SPE, the embolic blood clot or an infected thrombus detaches from its site of origin, which leads to an infarction in the pulmonary vasculature that also contains micro-organisms, inducing a focal abscess.2,3 Typically, multiple emboli occur, but solitary lung nodules can also occur and may be confused with neoplasm. Characteristically, lung abscesses are single, involve dependent pulmonary segments and are caused by gravitation. The same mechanism infrequently results in multiple lung abscesses, such as in the case of SPE. Lemierre’s syndrome (suppurative internal jugular vein thrombophlebitis), described by Lemierre in 1936, consists of acute pharyngotonsillitis, neck pain, fever and septic emboli to the lungs caused by Fusobacterium necrophorum.2
The normal progression of SPE is to enlarge and further destroy the lung; however, if treated with appropriate antibiotics, the cavitary and non-cavitary lesions will gradually decrease in size and either ultimately disappear entirely or form horizontal linear scars in the periphery of lung. S. aureus is the most common pathogen in SPE.
Radiography of the chest may reveal peripheral lung nodules with indistinct margins that have a tendency to cavitate but are often non-specific in appearance. Nodules of uniform size suggest a shower of emboli, but nodules of variable size indicate that the process is recurrent. A common outcome of SPE is necrosis of these nodules, leading to cavitation, and parapneumonic effusions may also be observed. CT of the chest can be useful in such cases for illustrating peripheral cavitary lesions.
Kuhlman et al.4 reviewed the CT scans of 18 patients with SPE and found that the most frequent pattern was multiple peripheral nodules of variable size from 0.5 to 3.5 cm.4 Other frequent findings included a ‘feeding vessel sign’, found in two-thirds of cases.5 In comparison with chest radiography, CT can better determine the extent of the disease because it identifies more parenchymal lesions that are presumed to be due to the same pathological process and can detect peripheral involvement.1 Another advantage of CT over chest radiography is the option of administering an i.v. contrast agent, which results in peripheral enhancement of these parenchymal nodules as well as easy delineation of lymphadenopathy relative to vascular structures in the hila and mediastinum. Contrast also allows better identification of feeding vessels that indicate the haematogenous origin of these nodules. It is concluded that CT can diagnose SPE even when conventional chest radiography fails to do so.5
In our case, sending blood cultures from the emergency department was crucial, as this expedited identification of MRSA and allowed the appropriate antibiotic to be initiated as early as possible. As a result, performing the blood culture for this patient the single most important investigation performed in the emergency department.
Anaerobic infections of the lung are characteristically polymicrobial, but the demonstration of only a single isolate from the abscess pus in this case may have been related to the intercurrent antimicrobial therapy with Augmentin.
Although a predisposing factor can usually be recognized in cases of SPE, the focus of infection for this case was clinically occult. However, the oral abscess, isolation of MRSA in both pus and blood and the absence of any other source of infection suggested that the oral mucosa was the primary source of SPE in our patient. CT is an important imaging modality for the diagnosis of SPE, as chest radiography can often be inconclusive.4