Authors: Ijeoma Ikedum (1), Mexan Mapouka (2), Folasade Arinze (1)
Categories: Case Report, discitis, epidural abscess, Salmonella, vertebral abscess, vertebral osteomyelitis
Source: Case Reports in Infectious Diseases
Doi: 10.1155/crdi/6378392
Authors: Ijeoma Ikedum, Mexan Mapouka, Folasade Arinze
Spinal epidural abscess (SEA) is a serious but rare condition that is often challenging to diagnose early due to atypical presentations, especially in patients without common risk factors such as immunosuppression or sickle cell disease. This case report describes a 49-year-old woman with a history of alcohol use disorder who presented with flank pain and other nonspecific symptoms, initially misdiagnosed as musculoskeletal pain. MRI eventually revealed a SEA caused by nontyphoidal Salmonella (NTS), requiring surgical intervention and antibiotics. The discussion highlights the difficulty of diagnosing SEA, especially in patients without classic risk factors, emphasizing the need for high clinical suspicion, thorough history-taking, and timely use of MRI. Prompt imaging, neurosurgical consultation, and antibiotic administration are critical for effective management and favorable outcomes. Strategies for improving early diagnosis include using decision guides for emergent MRI and repeat imaging if initial results are nondiagnostic. This article aims to provide clinicians with an overview of SEA caused by NTS, emphasizing the importance of maintaining a high index of suspicion, critically examining reported risk factors, and exploring potential approaches for earlier diagnosis.
Spinal epidural abscess (SEA) is an uncommon but serious condition associated with significant morbidity that often eludes early diagnosis. According to Strohecker and Grobovschek, “the problem with SEAs is not treatment, but early diagnosis, before massive neurological symptoms occur” [1]. It traditionally presents as a triad of back pain, fever, and neurological deficits [2–4]. However, early diagnosis is often challenging due to atypical presentations in most cases. Staphylococcus aureus is the most common cause of SEA and accounts for about two-thirds of cases caused by pyogenic bacteria [2]. Gram-negative bacilli are less commonly isolated. Salmonella, a gram-negative bacillus, causes infections that can be categorized into two those leading to enteric fever (caused by S. Typhi and S. Paratyphi) and nontyphoidal Salmonella (NTS) infections, which primarily result in gastrointestinal illness. Enteric fever, caused by typhoidal strains, typically presents with sustained fever and systemic symptoms over a longer duration, unlike acute gastroenteritis and watery diarrhea commonly seen in NTS infections. Enteric fever has an average incubation period of 14 days, with symptoms persisting for up to 3 weeks. In contrast, NTS infections usually manifest within 6–12 h and resolve within 10 days, unless there is an underlying immunodeficiency, which can lead to more severe disease with invasive and extraintestinal complications.
SEAs due to Salmonella infections are exceedingly rare, and the available epidemiologic data on this condition are limited [5]. Diagnosis is notably challenging due to the myriad of potential risk factors and their varying contributions to the disease [6]. Reported risk factors for SEA due to NTS include autoimmune disease, malignancy, diabetes mellitus (DM), sickle cell disease, alcohol use disorder, human immunodeficiency virus (HIV), recent travel to endemic regions, immunosuppression, recent trauma or surgery, and ingestion of contaminated raw foods or water [7–12]. Atypical presentations and the absence of classic predisposing factors in many patients compound this complexity [13]. Early antibiotic treatment combined with urgent surgical intervention is critical in preventing neurological complications. This case report highlights a SEA caused by NTS in a patient with alcohol use disorder, emphasizing the need for a high clinical index of suspicion in patients with risk factors who present with atypical symptoms [3].
A 49-year-old woman with a medical history of alcohol use disorder presented to the emergency department (ED) with the sudden onset of left flank pain and shortness of breath. One week prior to presentation, she experienced a 3-day illness with fever, chills, and diarrhea. Initial computerized tomography (CT) scan of the abdomen and pelvis revealed nonobstructive nephrolithiasis. Chest CT angiography (CTA) revealed multilevel thoracic spondylosis. A provisional diagnosis of musculoskeletal pain was made. She received ketorolac and methocarbamol and was discharged home due to improvement in symptoms. She returned to the ED 4 days later with progressive, sharp mid-back, left flank, and upper abdominal pain. Associated symptoms included chills, nausea, and abdominal bloating without lower extremity weakness, loss of bladder, or bowel continence. She had no history of intravenous drug use, recent trauma, or steroid spinal injections. On admission, vitals were notable for a temperature of 98.9°F, heart rate of 90 beats per min, and respiratory rate of 18 breaths per min. A systolic murmur along the left lower sternal border was heard on cardiac auscultation. Abdominal examination revealed a soft abdomen with generalized tenderness. Examination of the cervical spine revealed pain with active range of motion in all directions, while reproducible tenderness was noted on palpation of the thoracic and lumbar spine. Cranial nerve examination was unremarkable. Motor strength was 5/5 in all muscle groups, and reflexes were normal and symmetric. Sensory testing revealed intact light touch, pain, temperature, and proprioception. The patient's tandem gait was normal.
Complete blood count revealed white blood cells (WBCs) of 14.2 × 10 × 9/L (77% neutrophils). There were no abnormalities noted on urinalysis. There was no growth on blood cultures. Inflammatory markers were assessed. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured on Hospital day 4 and were 40 mm/hr and 16 mg/L, respectively. Transthoracic echocardiography (TTE) was negative for endocarditis. Magnetic resonance imaging (MRI) of the thoracic spine with and without contrast revealed a peripherally enhancing dorsal epidural fluid collection extending from T8 to T11, measuring approximately 0.7 × 1.3 × 6.5 cm. Severe thecal sac effacement was most pronounced at T8-T9 and T9-T10 (Figures 1(a) and 1(b)). Postcontrast T1-weighted sequences demonstrated abnormal enhancement in the left T9-T10 facet joint with associated joint effusion, paraspinal extension, and possible osseous erosion (Figures 1(c) and 1(d)).
Empiric treatment with intravenous vancomycin, ceftriaxone, and metronidazole was begun prior to transfer to a tertiary medical center. In addition, she underwent an emergent T9/T10 decompressive laminectomy and evacuation of an epidural abscess. NTS was isolated from surgical cultures. She had an uneventful recovery and was discharged to complete 8 weeks of oral ciprofloxacin. At the 1-month follow-up visit, she was participating in home physical therapy and reported occasional muscle spasms.
A timeline summarizing the patient's clinical course from initial symptom onset through follow-up is shown in Table 1.
SEA is a severe infection requiring urgent neurosurgical intervention to prevent permanent neurological deficits [1]. SEA caused by Salmonella species is extremely rare, with only a few cases reported [8, 9]. We summarized the detailed characteristics of thirteen patients, diagnosed with SEA due to NTS in the literature (Table 2). The majority of the patients were male, and there was a predominance of lumbar involvement.
Among the various reported risk factors for SEA due to NTS, our patient's only identifiable risk factor was alcohol use disorder. Alcohol was shown to have deleterious effects on leukocyte mobilization, phagocytosis, intracellular killing of bacteria, and T helper–1 lymphocyte-mediated cellular response [20]. Other literature suggests alcohol increases the risk of SEA by causing a chronic immunosuppressed state, impaired blood flow, and inducing the inflammatory response [6, 21]. Alcohol often coexists with other risk factors, including diabetes and obesity, further increasing the risk of SEA, as seen in one case reported in Table 2.
Interestingly, SEA can also occur in patients without any identifiable predisposing factors, making atypical cases more challenging to diagnose [22]. The classic triad of fever, back pain, and neurological symptoms is present in only a minority of patients diagnosed with SEA. Most patients tend to present with atypical or nonspecific symptoms, leading to unnecessary diagnostic delays and potentially resulting in neurological deficits. As shown in Table 2, 5 out of 13 reported cases of Salmonella SEA presented with atypical symptoms, contributing to challenges in timely diagnosis and treatment [14–17]. Significant delays in diagnosis have been reported in the literature and range from days to months, with 8 weeks being the longest time to diagnosis [23, 24]. We recommend careful history-taking, evaluating risk factors for which a direct role in the causation of SEA can be invoked, such as a prodromal diarrheal illness, as was the case in our patient.
There is no specific protocol for the early diagnosis of atypical SEA, and each case varies, relying heavily on physician judgment based on medical history, physical examination, laboratory tests, and imaging results [3]. Few studies have examined specific strategies for reducing delays in the diagnosis of SEA. Leukocytosis is not consistently present in patients with SEA, occurring in about 60%–80% of cases [15, 18]. Blood cultures are positive in only a proportion of SEA cases, with reported rates ranging from 44% to 60% in the literature [1]. In our review of published cases of Salmonella SEA (Table 2), nearly half of the patients [3–5, 15, 19, 25] did not have a positive blood culture, and the diagnosis was established through tissue aspirates or surgical specimens. Similarly, in our case, blood cultures were negative, and the causative organism was identified only from surgical cultures. Therefore, the absence of leukocytosis or positive blood cultures does not definitively rule out SEA. However, inflammatory markers such as CRP and ESR are typically elevated in patients with SEA. The elevation of these markers, especially in those experiencing severe back pain, should raise suspicion for the condition [10]. In our case, ESR was measured on Hospital day 4 and was 23 mm/hr. Although obtained later in the admission and not available during the early diagnostic phase, this finding is consistent with reports that inflammatory markers are typically elevated in SEA.
Once SEA is suspected, a gadolinium-enhanced MRI should be obtained. However, it should be noted that the sensitivity in diagnosing SEA is 91% [23, 24]. It could be nondiagnostic early in the disease course, as seen in one of the patients summarized as follows, where a repeat MRI identified an abscess 8 weeks later. Image-guided biopsy or fluid sampling should be performed to confirm the diagnosis and guide antimicrobial treatment. In some cases, blood cultures may identify the causative pathogen, eliminating the need for invasive sampling. Lumbar puncture is generally contraindicated in patients with suspected SEA due to the potential risk of spreading the infection into the subarachnoid space [11]. Both Alerhand et al. and Tetsuka et al. [16, 26] highlight the limitations of relying on the classic triad and instead advocate for structured diagnostic algorithms. Alerhand's framework is tailored to the ED and prioritizes rapid identification based on risk factors, inflammatory markers, and a low threshold for emergent MRI. In contrast, Tetsuka et al. provide a broader algorithm applicable across care settings, emphasizing the integration of clinical risk assessment, inflammatory markers, and the critical role of early and repeated gadolinium-enhanced MRI. Together, these reviews underscore the importance of algorithmic approaches in reducing diagnostic delays and improving outcomes in SEA.
While gadolinium-enhanced MRI remains the gold standard imaging modality for the diagnosis and follow-up of spinal infections due to its high sensitivity, CT also plays an important complementary role. CT is particularly valuable in the detection and characterization of osseous changes, including vertebral body necrosis and terminal plate destruction, which often develop later in the course of the disease (3–6 weeks after symptom onset). In patients with contraindication to MRI or when bone involvement is suspected, CT can provide critical diagnostic information and guide surgical planning [27–29].
The management of SEA due to NTS involves both surgical and medical therapy. Empiric intravenous antibiotics should be initiated promptly once SEA is suspected, ideally after obtaining blood cultures, as delays in treatment are associated with neurological deterioration (25). Although the 2015 IDSA guidelines recommend fluoroquinolones such as ciprofloxacin for 6–8 weeks as the preferred therapy for Salmonella vertebral osteomyelitis and related spinal infections [25], our review of published cases demonstrates that 11 out of 13 patients were treated primarily with ceftriaxone, often in combination with surgical decompression. The frequent use of ceftriaxone may reflect clinician preference for broad-spectrum β-lactam coverage, availability, or concerns about the increasing prevalence of fluoroquinolone-resistant NTS strains and the intracellular persistence of Salmonella and its contribution to treatment failure and relapse [30]. We included a case of relapsed SEA, necessitating a switch to different antibiotics and a delay in treatment in Table 2 [31]. Successful treatment typically includes urgent surgical debridement to achieve adequate source control, particularly in patients with neurological compromise and combination with intravenous antibiotics [10]. Radiology-guided drainage may be considered in those who are poor surgical candidates or for small abscesses [7, 18, 31]. Medical therapy alone has been used in selected patients with very poor predictors, such as persons who are unable to tolerate surgery due to extremely poor medical conditions, those with paralysis for > 48–72 h, or if surgery is not indicated for source control [23]. However, medical therapy alone has also been successfully used in patients without neurologic deficits and with a known causative organism with susceptibilities for guiding antibiotic therapy [11, 14]. Close monitoring for signs and symptoms of relapse after completion of antimicrobial therapy is essential for managing SEA.
SEA is a critical condition with significant morbidity that can be challenging to diagnose early, particularly with atypical presentation. This case report of a 49-year-old woman with a history of alcohol use disorder who developed SEA due to Salmonella underscores the importance of maintaining a high index of suspicion in patients with nonspecific symptoms. Timely MRI and prompt neurosurgical consultation were crucial for effective management in this case. Our literature review highlights the diverse manifestations of SEA and the diagnostic difficulties, particularly in patients without classic risk factors. Early diagnosis relies on thorough history-taking, clinical judgment, and appropriate imaging. More extensive studies should be conducted to evaluate the cost-effectiveness of early MRI and the potential benefits of repeat imaging when initial results are nondiagnostic. Developing comprehensive guidelines for managing atypical SEA presentations could improve early diagnosis and outcomes for patients with this rare but serious condition.