A Case of Lower Extremity Weakness and a Recent Neck Wound

Author: Elizabeth Kersten Wolpaw, MD and Andy Homer, MD (@UWashEM – EM Resident Physicians, University of Washington) // Edited by: Alex Koyfman, MD (@EMHighAK – EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER – Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center)

Case

A previously healthy 48 year old man presented to the emergency department (ED) with acute onset of lower extremity numbness and weakness. He had developed numbness of his legs around 4pm the day prior with subsequent weakness. By the time he presented to the ED, he was unable to move his legs and was insensate from his chest down. The patient denied fevers, IV drug use, or prior diagnosis of diabetes. He initially denied recent trauma but upon further questioning, he did recall having a metal toolbox fall on him and scrape the back of his neck approximately three to four weeks prior during which he had sustained a wound several millimeters deep which had since healed. He reported having persistent pain and intense itching in the area which was relieved only by scratching with a spoon or rubbing his back against the wall “like a bear.” The patient had been evaluated in the emergency department and then by his primary care provider for his neck pain and was counseled that it was most likely cervical strain.

On arrival to the ED, he was afebrile with normal vital signs. Physical exam demonstrated absent lower extremity motor function bilaterally, with slight weakness in his right arm and normal strength in his left. He was insensate from the nipple line down. A foley catheter was placed and drained 1.5 liters of urine. Labs demonstrated a leukocytosis of 21.2 K/UL as well as markedly elevated erythrocyte sedimentation rate and C-reactive protein. Gadolinium-enhanced MRI of the C and T spine showed multiple intramuscular abscesses of the right cervical paraspinous musculature as well as epidural abscesses extending from C3 to C7 and T3 to T9.

Incidence and Pathophysiology

Spinal epidural abscess (SEA) occurs in 0.2 to 2 cases per 10,000 hospital admissions, an incidence that has doubled over the past two decades due to an aging population, increased spinal instrumentation (notably spinal and epidural anesthesia), and the rising popularity of intravenous drug use^1,2. Men are affected about twice as often as women¹. A meta-analysis including 854 patients with SEA found that diabetes was the most common risk factor (occurring in 15% of patients), followed by intravenous drug use (9%) and chronic alcohol abuse (5%)¹.

Half of SEA cases are due to hematogenous dissemination of bacteria into the epidural space¹. In one third of cases, bacteria invade the epidural space through contiguous spread. In the remainder of cases, the source of infection cannot be identified.

Staphylococcus aureus accounts for two-thirds of spinal epidural abscess cases. Coagulase-negative staphylococci (especially in association with spinal procedures), gram-negative bacteria (often related to UTI’s), and Pseudomonas aeruginosa (especially in IV drug users) are less common causative pathogens. Spinal cord injury likely occurs both through mechanical compression and vascular occlusion from septic thrombophlebitis with resultant hypoxia³.

Diagnosis

The most common presenting symptoms of SEA are back pain (in about three fourths of patients), fever (in approximately half), and neurologic deficit (in around one third)². However, the “classic triad” of back pain, fever, and neurologic deficit occurs in the minority of patients. One study of 63 patients with SEA found that, while 98% of patients had one or more of these risk factors, only 13% had all three⁴.

The disease course progresses through four defined stages, from localized back pain (Phase I), to radicular pain radiating from the affected area (Phase II), to motor and sensory deficits (Phase III), and finally paralysis (Phase IV)⁵. The rate of progression through stages varies widely – from hours to months².

In most cases of spinal epidural abscess, clinical findings suggestive of spinal abscess lead to further laboratory and imaging work-up which may support the diagnosis (see image below for a common algorithm used). Definitive diagnosis is required before treatment with surgical drainage is considered. Suggestive laboratory findings include leukocytosis (present in two thirds of cases) and elevated inflammatory markers, such as ESR and CRP (present in nearly all cases). Blood cultures are positive in about 60% of cases, though bacteremia does not confirm the infectious source or mode of spread.

CT, myelography, and MRI with IV gadolinium are all more than 90% sensitive in diagnosing spinal epidural abscess. MRI is the current gold standard, as it can delineate the extension of abscess in all planes and is best at differentiating infection from malignancy.

Treatment

Treatment of SEA consists of surgery (decompressive laminectomy and debridement of infected tissue) with systemic antibiotics. Surgery should be performed as soon as possible given the unpredictable rate of disease progression in any given patient. A few retrospective studies have reported similar outcomes in patients treated with antibiotics alone as compared to those treated with antibiotics and surgical drainage². However, in these studies the patients receiving antibiotics alone generally had smaller abscesses and minimal if any neurologic deficits. The majority of retrospective studies on this topic support the use of both systemic antibiotics and surgery.

Antibiotic choice should be guided by the results of blood cultures or cultures of the abscess fluid itself. Pending culture results, broad empiric coverage should be initiated. This generally consists of vancomycin to cover staphylococcus and MRSA specifically, as well as a third- or fourth-generation cephalosporin to cover gram-negative bacilli. Duration of antibiotic coverage is usually 6 weeks or more because osteomyelitis co-occurs in most cases of spinal epidural abscess.

Despite advances in diagnostic and treatment modalities, 15% of patient with SEA are left with paresis or complete paralysis and nearly half have some form of neurologic deficit¹.

Case Resolution

Ultimately, the patient was believed to have developed a SEA from hematogenous spread of bacteria originating from either his initial soft tissue wound or subsequent scratching of his back and neck. Following his MRI, he was taken to the OR expeditiously for decompressive laminectomy and debridement of infected tissue. Frankly purulent material was drained from the epidural space. Cultures of blood and infected tissue grew MSSA. Post-operatively, the patient had no immediate improvement of his neurologic deficits. However, over the following months he did slowly regain strength and some sensation in his lower extremities.

Take-Home Points

• In approximately half of all cases, the diagnosis of spinal epidural abscess is missed on initial presentation². Because delays in diagnosis can lead to irreversible neurologic deterioration, it is important to maintain a high index of suspicion for SEA, especially among patients with predisposing conditions.
• Few patients with SEA present with the “classic triad” of back pain, fever, and neurologic deficit. However, the vast majority have at least one of these symptoms.
• Elevated inflammatory markers are sensitive but not specific markers of SEA. MRI with IV gadolinium remains the gold standard diagnostic imaging modality.
• Once the diagnosis is made, broad spectrum antibiotics (generally vancomycin and a third- or fourth-generation cephalosporin) should be initiated and the patient should be taken to the OR for decompressive laminectomy as soon as possible.
  

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References / Further Reading

1. Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients. Neurosurg Rev 2000;23:175-204.
2. Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012-2020.
3. Hlavin ML, Kaminsky HJ, Ross JS, Ganz E (1990) Spinal epidural abscess: a ten-year perspective. Neurosurgery 27:177–184
4. Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med 2004;26:285-91.
5. Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999;52:189–96.